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IABDM Certification Exam for Dental Assistants 2020
Question Page Question Page 1 2-3 31 279 2 4-5 32 283-294 3 6-7 33 295-348 4 8-21 34 349-350 5 22-28 35 351-353 6 29-49 36 354-356 7 50-51 37 357-370 8 52-58 38 371-372 9 59-75 39 373 10 76-89 40 374-375 11 90-96 41 376 12 97-100 42 376-382 13 101-103 43 383 14 104-116 44 384-387 15 117-132 45 388-390 16 133 46 390 17 134 47 390 18 135-137 48 391-406 19 138-147 49 407 20 148-149 50 408-413 21 150 51 414-415 22 150-165 52 416-418 23 166-174 53 418-420 24 175-178 54 421-425 25 178 55 425-430 26 178-179 56 431-435 27 180 57 436 28 181-273 58 436-437 29 274-278 59 437-445 30 279 60 446-447 2
1.) A rubber dam, when properly applied and sealed completely, can significantly reduce the patient’s exposure to mercury vapor.
A. True B. False
https://www.ncbi.nlm.nih.gov/pubmed/9823089
Mercury levels in plasma and urine after removal of all amalgam restorations: the effect of using rubber dams. Berglund A1, Molin M. Author information Abstract OBJECTIVE: The aim of the present study was to determine whether removal of all amalgam restorations might significantly affect mercury levels in plasma and urine and whether the use of rubber dams might reduce patient exposure to mercury during amalgam removal.
METHODS: All amalgam restorations were removed from 18 subjects during a single treatment session in which a rubber dam was used and from 10 subjects when a rubber dam was not used. All amalgam restorations were removed by the same dentist using high-speed cutting, water coolant, and high-volume evacuation. The levels of mercury in plasma and urine were analyzed both before and during the subsequent twelve months after amalgam removal. In order to determine whether removal of all amalgam restorations might cause an exposure large enough to significantly increase the mercury levels in two indicator media for mercury exposure, i.e., plasma and urine, and to determine if the removal might cause a significant decrease in the mercury levels found over time, the one-tailed, paired Students' t- test was used. For each individual, the pre-removal levels were compared with both the levels found in plasma on d 1 and in urine on d 10, and also with the levels found 1 y after removal. Furthermore, in order to examine whether the use of rubber dams had any effect on the mercury levels found after removal, the changes in the mercury levels found were compared between the groups using the Wilcoxon-Mann- Whitney rank sum test. 3
RESULTS: After removal of all amalgam restorations, only the non-rubber dam group showed significant increases in the mercury levels found in plasma (p = 0.012) and urine (p = 0.037). However, one year later, the mercury levels in plasma and urine had sunk significantly below the pre-removal levels for both groups. When the changes in the mercury levels found were compared between the groups, the non-rubber dam group showed a significantly higher increase of mercury in plasma than the rubber dam group the day after removal (p = 0.0010). Compared to the pre-removal mercury levels in plasma and urine, the levels found 1 y after removal of all amalgam restorations were on average 52 +/- 23% (range 4-89%) lower in plasma and 76 +/- 21% (range 20-94%) lower in urine.
SIGNIFICANCE: The study showed that dental amalgam had a statistically significant impact on the mercury levels found in plasma and urine in the patients tested, and that the use of a rubber dam during removal of all amalgam restorations significantly reduced the peak of mercury in plasma following removal.
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2.) The EPA does NOT require dental offices have mercury separators.
A. True B. False
https://www.epa.gov/eg/dental-effluent-guidelines
Dental Effluent Guidelines
EPA promulgated pretreatment standards in 2017 to reduce discharges of mercury from dental offices into publicly owned treatment works publicly owned
treatmentworksA treatment works that is owned by the state or
municipality. (POTWs). The Dental Office Category regulation is codified at 40 CFR Part 441.
Dental offices discharge mercury present in amalgam used for fillings. Amalgam separators are a practical, affordable and readily available technology for capturing mercury and other metals before they are discharged into sewers that drain to POTWs. Once captured by a separator, mercury can be recycled.
EPA expects compliance with this final rule will annually reduce the discharge of mercury by 5.1 tons as well as 5.3 tons of other metals found in waste dental amalgam to POTWs.
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Background Frequent Questions Reporting Requirements Documents Additional information
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Background Related Information
Mercury in Your Environment
Mercury is a potent neurotoxin that bioaccumulates in fish and shellfish. Mercury pollution is widespread and a global concern that originates from many diverse sources such as air deposition from municipal and industrial incinerators and combustion of fossil fuels.
Key facts about dental clinics and mercury:
Dental clinics are the main source of mercury discharges to POTWs. EPA estimates about 103,000 dental offices use or remove amalgam in the United States; almost all of these send their wastewater to POTWs. Dentists discharge approximately 5.1 tons of mercury each year to POTWs; most of this mercury is subsequently released to the environment.
Mercury-containing amalgam wastes may find their way into the environment when new fillings are placed or old mercury-containing fillings are drilled out and waste amalgam materials that are flushed into chair-side drains enter the wastewater stream. Mercury entering POTWs frequently partitions into the sludge, the solid material that remains after wastewater is treated. Mercury from waste amalgam therefore can make its way into the environment from the POTW through the incineration, landfilling, or land application of sludge or through surface water discharge.
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3.) Traditional clinic masks (tied paper or disposal masks) offer no protection from exposure through mercury vapor inhalation. A. True B. False
https://www.ncbi.nlm.nih.gov/pubmed/2406428 https://www.osha.gov/laws-regs/standardinterpretations/1985-11-15
Particulate inhalation during the removal of amalgam restorations. Nimmo A1, Werley MS, Martin JS, Tansy MF. Author information Abstract An aerosol that contains amalgam particles is created when a high-speed hand- piece is used to remove an existing amalgam restoration. Those particles smaller than 10 microns are considered to be fully respirable. This means that a significant percentage of the particles have the potential to travel to the terminal alveoli, where they may become lodged. Long-term exposure to fully respirable particles may compromise a person's respiratory function. Amalgam restorations were placed in the typodont teeth of a mannequin designed to simulate the head and the respiratory tract of a patient. The amalgam restorations were removed under three experimental conditions: dry cut (control), wet cut (water spray) with high-velocity evacuation, and wet cut with high-velocity evacuation and a rubber dam. Particulate exposure was evaluated in the simulated respiratory tracts of the patient and the dentist that were equipped with ambient particle sizing samplers. Use of water spray and high-velocity evacuation significantly reduced patient exposure to particles. The use of a rubber dam, together with water spray and high-velocity evacuation, was responsible for a further significant reduction of exposure to particles when compared with water spray and high-velocity evacuation alone. The dentist, however, was exposed to moderate levels of fully respirable particles for all conditions tested. It is therefore recommended that all dental personnel wear face masks while removing existing amalgam restorations.
SUBJECT: Use of Chemical Cartridge Respirators for Protection Against Mercury Vapor
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A chemical cartridge respirator for protection against mercury vapor manufactured by the Mine Safety Appliance Company (MSA) has received approval from the Mine Safety and Health Administration (MSHA) and the National Institute for Occupational Safety and Health (NIOSH), TC- 23C-629 (Mersorb).
The respirator cartridge is equipped with a passive end-of-service-life indicator (ESLI) which changes color from orange to black before breakthrough occurs. Under NIOSH policy, the mercury respirator can only be approved when the cartridges are installed at the belt-mounted position so the ESLI is visible to the wearer.
We have received a request from MSA concerning the use of their mercury cartridges on the face- mounted position on a half-mask. MSA claims that the color indicator changes color in a much shorter time than that of the service life of the cartridge, and there is sufficient margin of safety against breakthrough even if the wearer does not perform frequent monitoring of the color change of the cartridge during the work shift. The Mersorb cartridge has also received an approval for use in an environment which contains both mercury vapor and chlorine gas.
We contacted NIOSH to request the certification test data. The test results indicated that when the cartridges were tested at a mercury vapor concentration of 21.5 mg/M3 (saturation concentration at room temperature) no breakthrough (0.05 mg/M) was observed after a test period of 500 to 690 minutes. The color change occurred from 31 to 305 minutes after the onset of the test.
Since the mercury cartridges were tested at concentrations about 210 times the OSHA permissible exposure limit (PEL) for mercury (0.1 mg/M3), the actual service life would be much longer at lower concentrations. It appears that the end-of-the-service-life indicator offers sufficient margin of safety against breakthrough.
In view of the above facts, it is concluded that the use of the MSA Mersorb cartridge on the face- mounted position on the half-mask would be acceptable provided the following conditions are met in addition to the limitations which appear on the approval label:
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4.) Measuring mercury vapor levels using a mercury vapor analyzer is a valid test for mercury levels in the air.
A. True B. False
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3033235/ https://www.ncbi.nlm.nih.gov/pubmed/16678246
Rapid methods to detect organic mercury and total selenium in biological samples
Dong-Ha Nam1 and Niladri Basu 1
Author information Article notes Copyright and License information Disclaimer
This article has been cited by other articles in PMC.
Abstract Go to:
Background Mercury (Hg) is a ubiquitous heavy metal that is neurotoxic to humans and wildlife[1]. It is ranked as a top three priority pollutant by the U.S. EPA's CERCLA program[2]. In the U.S., more than 50% of water bodies are under fish consumption advisories largely due to Hg contamination[3]. In addition, Hg levels in the tissues of most fish-eating wildlife are within 10-fold of levels known to cause overt damage[4,5]. Mercury's fate and toxicity depends upon its chemical speciation. In particular, organic Hg (generally found as methyl Hg, MeHg) is of health concern since it penetrates lipid bilayers, biomagnifies through aquatic food chains, and about 95% of the ingested dose is absorbed into the blood stream[1]. Methyl Hg can also cross the blood brain barrier by conjugating with L-cysteine and exploiting the methionine- uptake pathway[6]. As Hg has a high affinity for protein thiols, multiple neural components are vulnerable to its toxic action[7]. In an effort to assess Hg concentrations in biological samples, various analytical schemes are used[8-10]. Mercury strongly absorbs light at 253.7 9 nm and total Hg can be quantified via established spectroscopic methods. Recently, commercial vendors (e.g., Milestone Inc., BrooksRand, Perkin Elmer) have provided direct mercury analyzers to the market which permit rapid and straightforward analysis of total Hg. However, the detection of organic Hg is still hindered by sample treatments steps that are time consuming, wet chemistry digestions that generate ample chemical waste, and/or need for complex instrumentation. One common method to assess organic Hg involves pretreatment of sample with acid followed by alkaline digestion, and then extraction with an organic solvent (benzene or toluene) and finally back-extraction into an aqueous solution using cysteine or thiosulphate[4,10-12]. Organic Hg compounds may be quantified on the basis of separation techniques (e.g., GC, HPLC) with a sensitive detector (e.g., ECD, CV-AAS, ICP-MS). Selenium (Se) is an essential micronutrient. It is postulated that the presence of Se within cells may mitigate Hg toxicity by forming an inert crystalline Hg-Se complex[13,14]. Further, strict Hg-Se molar ratios of 1:1 have been observed in biological tissues from several organisms[15], though few Hg monitoring studies co-report on Se levels. The essential role of Se in physiology has encouraged the development of analytical methods for its quantification at trace levels. Among available techniques, fluorescence- based methods are considered to be easier and more cost-effective than conventional spectroscopic techniques (e.g., ICP-MS, GFAAS or HGAAS)[16] though few have outlined in detail key methodological considerations for the assessment of total Se in biological samples[17-19]. Owing to the need to determine both organic Hg and total Se in biological samples, there is a need to develop and apply of fast and reliable analytical methods. Here we detail a series of methods that may be used to simply and rapidly detect organic Hg (< 1.5 ml total sample volume, < 1.5 hour) and total Se (< 3.0 ml total volume, < 3 hour) in a range of biological samples. Go to:
Experimental Figure Figure11 provides a graphical schematic of the procedure to extract and detect organic Hg. About 10 to 50 mg of Standard Reference Materials (DOLT-3: dogfish liver, TORT-2: lobster hepatopancreas; both from the 10
National Research Council of Canada, NIST 1566b: oyster tissue from National Institute of Standards and Technology, USA) was homogenized in 50 mM Tris-HCl buffer (pH 8.5) containing protease (Subtilisin A, 99%; 100 μg), and next incubated at 50°C for 1 hr. Following this digestion step, NaOH (40%; 125 μL), cysteine (1%; 50 μL), CuSO4 (0.5 M; 50 μL), acidic NaBr (3.1%; 500 μL), and toluene (500 μL) were sequentially added to the digest and vortexed. Following centrifugation at 13,000 g for 5 minutes at room temperature, the top toluene layer was transferred to a test tube and mixed twice (60-80% of toluene) with Na2S2O3 (5 mM; 150 μL) to permit back- extraction of organic Hg into an aqueous phase. The aqueous phase was re- centrifuged (13,000 g for 2 minutes) and then placed into another test tube (1.5 mL tube) for organic Hg analysis. The final extracts, once obtained, can be analyzed for Hg content within a few days. All samples (SRMs for total Hg, extracts for organic Hg) were directly analyzed by a DMA-80 (DMA-80 Milestone, Inc., Shelton, Connecticut, USA) as we have previously outlined elsewhere[20,21]. Briefly, the direct mercury analyzer liberates mercury by introducing samples into a controlled heated environment. Nickel and quartz boats are used to introduce solid and liquid samples, respectively, into the machine's autosampler. The autosampler delivers the sampling boats into a quartz catalytic tube, where it is dried and then thermally decomposed in a continuous flow of ultra pure oxygen. Combustion products are carried off and further decomposed in a hot catalyst bed. The remaining decomposition products are carried by oxygen to a gold amalgamator that selectively traps mercury vapour. After the system is flushed with oxygen to remove any remaining decomposition products, the amalgamator is rapidly heated to release the mercury vapour from the gold trap. Then, flowing oxygen carries the mercury vapour through absorbance cells positioned in the light path of a single wavelength atomic absorption spectrophotometer. Absorbance is measured at 253.7 nm as a function of mercury concentration. This method is endorsed by the U.S. Environmental Protection Agency (EPA Method 7473). Here, the detection limit for the direct Hg analyzer was 0.020 ng and ranged from 0.010 to 0.029 ng. Total and organic Hg concentrations are expressed as μg/g (ppm) dry weight.
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Open in a separate window Figure 1 12
Schematic procedure of organic mercury analysis († Direct Mercury Analyzer; Time estimates are based on the analysis of one sample, though several can be batch processed). A simplified microplate-based fluorometric assay (total volume < 3 ml) for biological samples has been developed, based on the tube-based method of Sheehan and Gao[18] developed for urine and plasma. The method involves sample digestion (HNO3-HClO4 and HCl), conjugation as a piazselenol (2,3- diaminonaphthalene, DAN), and cyclohexane extraction (Figure (Figure2).2). Approximately 10 to 50 mg of SRMs (DOLT-3, TORT-2, NIST 1568a: rice flour, NIST 1577b: bovine liver, NIST 1515: apple leaves, selenite and selenate stock standard solution) and lemon shark (Negaprion brevirostris) samples were digested in the presence of 400 μL of HNO3(70%) and 100 μL HClO4(40%) for 80 min at 195°C, followed by the addition of 500 μL of HCl for 30 min at 150°C in a borosilicate tube. These acid digestions facilitate the oxidation of all forms of Se (particularly selenide and selenate) into selenite (selenous acid). To the digest, 10 mM of EDTA with sequential additions of 6.3 mM of DAN in 0.1 M HCl (500 μL) and 1 mL of cyclohexane was added to form a fluorescent complex as a 4,7-dichloro-5,6-benzopiazselenol (Cl2- Se-DAN complex) in an organic phase. Though endogenous metals present in working solutions may interfere with DAN, the interference may be masked by the addition of 10 mM of EDTA, which we tested here (250 μL; tested ranged from 1 to 100 mM). The fluorophore extracts, which reflect total Se, can be determined by fluorescence spectroscopy (emission at 560 nm; excitation at 360 nm) using 96 well microplates. Samples should be measured within a few hours of extraction. Concentrations of total Se in shark kidney samples obtained by the fluorometric assay were compared to values obtained using a conventional graphite furnace atomic absorption spectroscopy method as previously described[21]. The detection limit of total Se for the fluorometric assay ranged from 2 to 3 ng, with standard curve linearity for total Se concentrations up to 600 ng (Figure (Figure33).
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Open in a separate window Figure 2 14
Schematic procedure of total selenium analysis († Fluorescence Spectrometry; Time estimates are based on the analysis of one sample, though several can be batch processed).
Open in a separate window Figure 3 Relationship between predicted and measured total Se (ng) values in DOLT-3 using the fluorescence method described here. Go to: 15
Results and Discussion Average recovery rates from the certified values of DOLT-3, TORT-2, and NIST 1566b for total Hg were 98.9 ± 4.3% (n = 61), 97.5 ± 5.5% (n = 23), and 95.4 ± 4.9% (n = 3), respectively (Table (Table1).1). For organic Hg, the average recovery rates from the certified values of DOLT-3, TORT-2, and NIST 1566b were 98.6 ± 5.7% (n = 47), 97.9 ± 4.7% (n = 19), and 97.2 ± 9.6% (n = 4), respectively (Table (Table1).1). For total Hg and organic Hg, the relative standard deviation (RSD) was lower than 10% for all replicate measures. These results confirm the accuracy and precision of this method. The recoveries are similar to values published previously[4,20,21].
Table 1 Recovery rates of organic and total mercury concentrations in the certified reference materials
Standard Reference Organic mercury (μg/g dry wt.)† Total mercury (μg/g dry wt.)† Materials (SRM)
Expected Observed N Recovery Expected Observed N Recovery value value (%) value value (%)
DOLT- (Dogfish liver) 1.59 ± 1.57 ± 47 98.6 ± 5.7 3.37 ± 3.33 ± 61 98.9 ± 4.3 3 0.12 0.06 0.14 0.15
TORT- (Lobster 0.152 ± 0.149 ± 19 97.9 ± 4.7 0.27 ± 0.26 ± 23 97.5 ± 5.5 2 hepatopancreas) 0.013 0.009 0.06 0.02 16
Standard Reference Organic mercury (μg/g dry wt.)† Total mercury (μg/g dry wt.)† Materials (SRM)
Expected Observed N Recovery Expected Observed N Recovery value value (%) value value (%)
NIST (Oyster tissue) 0.0132 ± 0.0128 ± 4 97.2 ± 9.6 0.0371 ± 0.0354 ± 3 95.4 ± 4.9 1566b 0.007 0.0015 0.0013 0.0022
Open in a separate window † Detection limit: 0.020 ng by DMA-80 For total Se (Table (Table2),2), the recovery rates were within the certified values (± 18%) for DOLT-3 (n = 35; 103 ± 18%), TORT-2 (n = 20; 99.2 ± 15.7%), NIST 1568a (n = 8; 102 ± 16%), and NIST 1577b (n = 8; 97.3 ± 11.7%). Total Se was not detected from apple leaves (NIST 1515; 0.050 μg/g) which is likely due to the low concentration (close to detection limits) of Se in this material. Selenite (which is converted from all forms of Se) reacts with DAN to yield a fluorescent Se-DAN complex. The recovery rates of selenate standard stock solution (even at higher levels such as 100 or 250 μg/g) were similar to those from the selenite solution (Table (Table2).2). This indicates that the outline methodology is efficient at converting all selenate into selenite. In addition, Se concentrations in shark kidney samples (n = 10) that were measured using the fluorometric method described here were comparable to those observed obtained using graphite furnace atomic absorption spectroscopy (GFAAS) method (r = 0.978; p < 0.001) (Figure (Figure4).4). Results of the current assay may provide a rapid and reliable analytical approach for measuring total Se, although the fluorophore stability results remained to be resolved. 17
Table 2 Recovery rates of total selenium in the certified reference materials
Standard Reference Materials (SRM) Total selenium (μg/g)†
Expected value Observed value N Recovery (%)
DOLT-3 (Dogfish liver) 7.06 ± 0.48 7.27 ± 1.09 35 103 ± 18
TORT-2 (Lobster hepatopancreas) 5.63 ± 0.67 5.58 ± 0.77 20 99.2 ± 15.7
NIST 1568a (Rice flour) 0.38 ± 0.04 0.39 ± 0.06 8 102 ± 16
NIST 1577b (Bovine liver) 0.73 ± 0.06 0.71 ± 0.08 8 97.3 ± 11.7
NIST 1515 (Apple leaves) 0.050 ± 0.009 ND 4 -
Selenite (Standard stock solution) 100 89.3 3 89.3
250 239 3 94.7 18
Standard Reference Materials (SRM) Total selenium (μg/g)†
Expected value Observed value N Recovery (%)
Selenite (Standard stock solution) 100 86.2 4 86.2
250 229 3 91.6
Open in a separate window ND: Not detected, † Detection limit: 2 - 3 ng by fluorescence spectroscopy
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Open in a separate window Figure 4 Pearson correlations of total Se in lemon shark kidneys measured between fluorometric assay and atomic absorption spectroscopy (GFAAS). Go to:
Conclusions Overall, the outlined approaches provide an easy, rapid (< 1.5 hr for organic Hg, < 5 min for total Hg, < 3 hr for total Se), reproducible, and cost-effective 20 platform for measuring organic Hg and total Se. As the methods are down- scaled, they require very small quantities of sample (10-50 mg) and can be performed on precious materials, and they generate less chemical waste than conventional approaches. Go to:
Competing interests The authors declare that they have no competing interests. Go to:
Authors' contributions DN and NB designed the study, analyzed data, and drafted the manuscript. Both have read and approved the final manuscript.
Mercury vapor levels in exhaust air from dental vacuum systems. Stone ME1, Cohen ME, Debban BA. Author information Abstract OBJECTIVE: This study was undertaken to determine mercury (Hg) vapor levels in the air exhausted from dental vacuum systems.
METHODOLOGY: Hg vapor concentrations from the dental vacuum system exhaust ports of three dental clinics were measured utilizing the Jerome 431-X mercury vapor analyzer and the United States Occupational Safety and Health Administration's (OSHA) method ID-140 in units of ng Hg/m3. Air velocity measurements and temperatures were determined with a constant temperature thermal anemometer. Hg emissions per unit time were then calculated in ng Hg/min. Ambient Hg concentrations from a location approximately 1000 feet away from the closest clinic sampled in this study were measured with an Ohio Lumex Inc. RA-915+ Hg vapor analyzer.
RESULTS: 21
Mean Hg vapor concentrations analyzed with the Jerome 431-X were: 46,526, 72,211, and 36,895 ng/m3 for clinic I (110 chairs), clinic II (30 chairs) and clinic III (2 chairs), respectively. Mean Hg vapor concentrations utilizing OSHA method ID-140 were 45,316, 73,737, and 35,421 ng/m3, respectively. Air flow values were: 11.6, 1.8, and 0.5 standard m3/min, respectively. Hg emission data utilizing air flow measurements were calculated to be 532,684, 131,353, and 18,079 ng/min, respectively, (P<0.001). There was no statistical difference between the two methods used to measure Hg vapor concentrations. The mean Hg concentration in ambient air approximately 1000 feet from the nearest clinic sampled was 13.2 ng/m3.
CONCLUSION: The two different methods used to measure Hg vapor concentrations provided similar estimates of Hg concentrations from the exhaust air of three dental vacuum systems. Hg vapor release to the atmosphere from dental vacuums can be substantial and can exceed human exposure limits.
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5.) Extra water spray, while removing amalgam fillings is used to
A. Keep the handpiece cool B. Cool the amalgam C. Keep the mouth from drying out D. Lowers levels of Hg vapor E. A & C F. B & D
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3270415/
A Safe Protocol for Amalgam Removal
Dana G. Colson *
Author information Article notes Copyright and License information Disclaimer
This article has been cited by other articles in PMC.
Abstract Go to:
1. Introduction In dentistry, there is a lot of controversy about the topic of silver mercury fillings; are they safe or not safe? There are many articles written on the pros and cons of these types of fillings. It is difficult to quantify and to assess the effects in each individual. It is not easy to identify silver mercury fillings as the cause if illness presents or if the fillings contributed to illness, except in extreme toxicity cases. Refer to the beginning sections of this review paper concerning the science and mechanism of how mercury interconnects with body tissues and functions. Environmental doctors investigate heavy metal toxicity as part of their overall wellness regiment to help their patients with health concerns. These doctors look at sources of metals when the patient's lab reports/diagnostic tests show high levels of mercury and other metals. They investigate what sources are contributing and how to reduce the burden on the body. The doctor may prescribe the safe removal of silver mercury fillings so as not to create an additional burden on the body and to help their patient heal. Thus, 23 when removing amalgams, additional steps help ensure that the patient is protected. Go to:
2. Introduction of Amalgam in Dentistry Dental amalgam restorations, also called silver mercury fillings, were introduced to North America in the 1830s and have been the standard restorative filling for our molars and premolars. At that time there was a lot of controversy about its intraoral use. Silver mercury fillings began to take over the cast gold and gold foil restorations. These were excellent and lasted for years; however they were labour intensive and the cast gold required a lab process that centrifuged gold into a wax pattern to fit the tooth accurately. This was a two-appointment process with added expense. Gold foil restorations were often traumatic to the pulp of the tooth, creating necrosis and requiring root canal. The addition of amalgams as a restorative filling was a welcomed opportunity to offer at a substantial cost reduction as the mercury was triturated with a pellet containing silver, copper, tin, and zinc. This created a substance that could be placed into the cleaned out tooth structure where decay had been present. It was packed, condensed, and allowed to harden within a few minutes and then carved intraoral chairside. Today the extra, unused amalgam is placed in a container for safe disposal. This restoration is easily burnished to tooth structure to recreate the tooth to its original shape and size. The onset of amalgam allowed people to keep their teeth, rather than having them extracted if money did not allow for gold restorations. Keeping teeth enabled people to have better digestion and supported a more balanced quality of life. Today, with the increase of chemicals such as pesticides, preservatives, processed ingredients in food, and diverse contaminants in our environment; sensitivities, allergies, and other illnesses are increasing rapidly. The Brain Wash postulates that the toxins in our society are not additive but synergistic. For example, the average apple contains residue of eleven different neurotoxins and is sprayed with pesticides seventeen times prior to being picked from a tree [1]. Our food intake of many pesticides and additives is most often unknown. The level of materials such as mercury that our bodies could tolerate several decades ago may not be what we can sustain today. 24
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3. Amalgam and Composite Fillings Silver mercury amalgam restorations are comprised of 50% mercury, with the balance being silver, copper, tin, and zinc [2]. Over time the exposed surface changes. The fillings corrode, and surface texture becomes rough. People who chew gum create a smooth, shiny surface on their fillings. Mercury vapor is released by chewing grains, nuts, seeds, and gum, as detected using mercury vapor analyzers [3]. A study in 2010 looked at the wearability of composite (white) restorations compared to amalgams. It showed that over 12 years, the group of patients that were not prone to decay, with resin/composite-filled restorations, were better off than the group of patients with silver amalgam restorations [4]. Today with awareness of diet, home care, and education, the majority of people who seek preventative dental care are less prone to decay. The author has worked with alternative restorations for over 27 years. The advantage of white composite restorations is that composite binds to composite and the base of the tooth rarely needs to be disturbed once the amalgams are removed. Dental restorative materials have various components, and individual Material Safety Data Sheets (MSDSs) are available from the manufacturer. If an individual has concerns or is sensitive to materials, one can refer to these reference sheets. For example, there are many composites and bonds available today without bisphenol A. Psychological benefits are also a positive factor for patients. People feel that they now have a mouth without the “scars” of the past. They are no longer self-conscious when smiling, laughing, and singing. With the introduction of composite restorations, many modifications have been made with the materials and applications due to the extensive ongoing technology and research. The concerns with good marginal seals and prevention of recurrent decay have been diminished. Wear and polishability of the composite materials with nanohybrid particulates can withstand stronger chewing forces. Composites are technique sensitive, and various aids can be used to ensure a proper seal of the restorative material to the tooth structure and to create tight contacts to the adjacent tooth to prevent food impaction between teeth. Today we aim for minimally invasive dentistry to 25 maintain integrity of the tooth structure, and white composite materials are ideal for these restorations. Go to:
4. Considerations prior to Amalgam Removal When examining a patient for amalgam removal upon request, many factors must be looked at including the rate of wear/attrition on their teeth, pressures exerted, type of diet consumed on a daily basis, their oral hygiene, and other metals in their mouth. Often amalgam restorations exist under crowns and amalgam tattoos (discoloration along the gum) are noted. Amalgams have also been used to seal the apex of root canal treated teeth. If heavy pressures are exerted by an individual or there is evidence of grinding and clenching, then the longevity of a composite restoration may be compromised. The size of the restoration will also influence the choice of materials. Tooth cusps often fracture over time, as well as with excessive pressure, requiring an indirect restoration to be fabricated by a lab. Today the increasing trend is to work with a computer-generated restoration to secure/repair the tooth in the long term. Bite plates to prevent grinding and clenching help preserve these new restorations from excessive wear and pressure. When the patient is seen for an initial exam, a thorough medical and dental history is taken. Records including radiographs and intraoral pictures are taken, and a comprehensive exam follows. Previous films are requested or brought in by the patient. Lengthy conversations ensue to make sure that the patient is properly prepared and that we are working with their physician, in a timely manner, to complement the detoxification process that their doctor has prescribed and is administering. The physician evaluates the overall health of the body and the ability of the individual to eliminate toxins. For example, if a patient has a leaky gut, physicians restore this prior to removal as it is difficult to flush out toxins [5]. If a woman is pregnant or breast feeding, amalgam removal does not occur until she has completed breast feeding her child [6]. It has been reported that the mercury concentration in the blood of the fetus can be thirty times greater than the mother's blood [7]. Supplements are helpful and are prescribed on an individual basis by the physician. Vitamin C intake is recommended, often with other supplements, prior to and following amalgam removal. Once the amalgam restorations have been 26 removed, the physician continues to work with the patient to help with the detoxification of mercury that is stored in the body. Go to:
5. Chairside Procedures The following steps are taken when removing silver mercury fillings, to ensure minimal if any absorption sublingually, or through the mucosal tissues, and to minimize mercury vapor absorption through the blood/brain barrier [8–10]. In office, the patient is prepared as follows, prior to amalgam removal: i. the patient is draped with a plastic apron under the dental bib to cover their clothing; ii. a dental dam (“raincoat”) is customized to fit the existing tooth/teeth to prevent particulates from contacting the oral mucosa; iii. underneath the dam, activated charcoal or chlorella is placed, along with a cotton roll and gauze. This helps to intercept particles and to chelate dissolved metals that seep under the dam. Often the particles are found on the sublingual tissues and lateral borders of the tongue. This must be prevented as this is the fastest absorption route into the body; iv. the patient's face is draped under the dam, with a liner; v. goggles for the eyes and hair cap or bonnet protection are placed; vi. oxygen is supplied to the patient with a nasal mask and the mercury vapor ionizer is turned on. The vapor ionizer is a specialized air filtration system that is used to bind mercury vapors that are attached by the negative ion flow and are then carried to a positively charged ionizer plate at the opposite end of the room. The operators also protect themselves with a filtered mask, eye and hair protection, and face shields. The removal of amalgam commences as follows: i. a new dental bur is used in the handpiece to ensure easy removal; 27 ii. high volume suction and a continual addition of water spray are supplied to the site where the amalgam is being extracted; iii. if possible, the amalgam restoration is sectioned and then scooped out to eliminate as much mercury vapor release as possible [11]. The vitality of the tooth is always a concern and the less trauma to the tooth, the healthier the pulp, which supplies blood vessels and nerve supply to the tooth. The deeper the restoration, the greater the chance of pulpal degeneration, causing necrosis and subsequent abscess at the apex of the tooth, as well as bone loss. Once the amalgam is removed completely, i. the oxygen and protective coverings are taken away; ii. an immediate inspection under the dental dam occurs. The gauze, cotton roll and activated charcoal/chlorella are wiped away. Gauze is then used to inspect the floor of the mouth and tongue to make sure no particulates seeped under the dam; iii. once all mucosal tissues are fully inspected and cleaned, the mouth is flushed with copious amounts of water, again to ensure no ingestion or absorption of amalgam particulates. The tooth is then restored to a healthy state of form and function. Materials are taken into consideration as discussed previously on an individual need. Often environmental healthcare providers give direction on the preferred choice of materials to be used through biocompatibility testing. It is the dentist's ultimate responsibility to advise the patient about the strengths and limitations, if they cannot tolerate some materials. It has been the author's experience that once the amalgam materials have been removed and the patient detoxes under the supervision of their physician, the range and variety of materials increase, allowing the dentist to create the best prognosis for the tooth. Dentists by law in Ontario [12] and elsewhere in Canada must have a certified amalgam separator on the wastewater lines in dental offices in their practices and must use a certified hazardous waste carrier for the recycling and disposing of amalgam waste. Go to: 28
6. After Amalgam Removal A 2011 Norwegian study showed a 3-year followup after amalgam removal with precautions in a treatment group compared to a reference group. It showed significant reductions in intraoral and general health complaints [13]. The following is a list of outcomes that I repeatedly hear from my patients over the years. Although I have not scientifically collected them, after amalgam removal and detoxification, they have also been reported in the literature. Comments include that a. patients no longer have a metallic taste in their mouth; b. patients feel as if they have more energy; c. patients are able to concentrate better and make decisions easier (the “brain fog” is gone); d. their body responds better to other treatments, as if a barrier has been lifted. To achieve effective results one must include an integrative approach with a physician and health care team with attention to detoxification and diet over several months, with laboratory tests to monitor progress. Go to:
Disclosure Dr. D. G. Colson is a D.D.S. at Dr. Dana Colson & Associates as well as the author of “Your Mouth: The Gateway to a Healthier You.”
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6.) Heating an amalgam filling by tooth brushing, or polishing by a dental hygienist or dental assistant, can create mercury vapor release in excess of OSHA’s "ceiling limit" standards of exposure.
A. True B. False https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5352807/ http://www.dentistrytoday.com/hygiene/1212--sp-1049442323 https://www.youtube.com/watch?v=jni5WHsKDKE
Increased mercury emissions from modern dental amalgams
Ulf G. Bengtsson1 and Lars D. Hylander 2
Author information Article notes Copyright and License information Disclaimer
This article has been cited by other articles in PMC.
Abstract Go to:
Introduction The vast majority of mercury containing fillings consists of two principal ingredients; liquid mercury and a metal powder referred to as the alloy. The mixing ratio is approx. 50 wt% of each with small variations, although alloys with high content of spherical alloy particles requires somewhat less mercury (Anusavice et al. 2012). This mixing is referred to as trituration by dental science. The term alloy, when used in physics, refers to one or more elements, at least one being a metal, which are dissolved into each other. When used by dental science, alloy refers to a mixture of solid metal particles, not including mercury apart from very small amounts sometimes added (pre- amalgamation). When the bulk of mercury is added to the alloy powder, reactions take place and the resulting compound is called dental amalgam. Amalgams are mixtures of mercury and one or more other metals, which may be dissolved into the mercury or being metal particles just glued together by mercury (Hylander and Plath 2006). Silver, being the main component of the presently dominating alloy, has resulted in the name silver fillings of these 30 restorations. Considering that mercury, not silver, is the dominating metal in the final filling, they should rather be termed mercury fillings. The alloy/mercury mixing ratio is set by the manufacturer at a ratio, where the mercury has been claimed to be firmly bound to the alloy in the dental amalgam. Although this assumption has been proved to be erroneous (Homme et al. 2014), there is no consensus on acceptable emissions from dental fillings and there is no awareness of differences in mercury losses from conventional amalgams and non-ɣ2-amalgams, respectively. In addition, a limited number of dentists prefer a softer mix, using an increased amount of mercury. This is known in dental science as the “wet technique” (Möller 1978; Bergdahl 1973). The excess mercury will be removed in the oral cavity when the mix is squeezed/packed into the prepared tooth cavity. This squeezing out/packing is referred to as condensation by dental science but has nothing to do with the term as used in physics. The wet technique requires the use of bulk mercury and alloy. As a consequence of the ban on the use of bulk mercury in dentistry agreed upon in the Minamata Convention, this technique will be prohibited in the future. However, many manufacturers still provide bulk alloy and mercury. One manufacturer gives two alternative mixing ratios, 1:1 and 1:1.2, the latter suitable for dentists preferring the wet technique (Nordiska Dental 2017). Study of the microstructure of the amalgam filling reveals that it is not homogenous, but it consists of a number of different phases; ɣ1, ɣ2, ɛ and more (Anusavice et al. 2012). Depending on the copper content, the fillings are termed either low copper amalgams or high copper amalgams. These expressions refer to the now withdrawn standards ISO 1559 Ed.1 and Ed.2, which stipulated 6% Cu max. and 30% Cu max., respectively. When increasing the copper content, the ɣ2-phase slowly disappears and at around 12%, it has almost disappeared. Amalgams with a copper content resulting in no ɣ2-phase are called non-ɣ2 amalgams (non-gamma-two). The ɣ1-phase, present in both low and high copper amalgams, is transformed to the β1-phase with considerably less mercury. This phase transformation goes on for years constantly generating free mercury (Schmalz and Arenholt- Bindslev 2009; Mahler et al. 1973). Standards for the composition below refers to the alloy ingredients, not the final filling material. 31
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Methods used and types of amalgams This study is based on observations of droplets rich in mercury found on dental fillings, challenging the dominating assumption that mercury in amalgam is firmly bonded to the alloy. The observations were photographed with a light microscope (×252 magnifying), analyzed with a scanning electron microscope (SEM) and a literature review was performed to explain the phenomena and possible implications of these observations at the surface of dental amalgam fillings. The study includes two groups of dental amalgam: conventional amalgams and non-ɣ2-amalgams. Copper amalgam is included in the background description to clarify its specific properties.
Conventional amalgams Due to the fact that the alloy of conventional amalgams contains max. 6% copper, they are also known as low copper amalgams. These are rich in the ɣ2-phase, known for its poor corrosion resistance (Anusavice et al. 2012). ISO 1559, 1st ed. 1978 (now withdrawn), stated:
Silver: 65% min.
Tin: 29% max.
Copper: 6% max.
Mercury: 3% max.
Zinc: 2% max.
Non-ɣ2-amalgams The first one of these non-ɣ2-amalgams was patented by a Canadian inventor (Youdelis 1967). It later became known as Dispersalloy and its alloy partly contains particles with a spherical form. This spherical alloy for dental applications, used in many of today’s mercury fillings, was invented by the American Dental Association (Marjenhoff and George 1992). Grantees of the US Public Health Service was not allowed to protect their inventions before 1980, so the ADA never had the opportunity to patent it. 32
These new amalgams were initially not in accordance with the standard above, so ISO 1559 Ed. 2, 1986 (now withdrawn), was released updating the composition requirements to include alloys with high copper contents that already had been on the market for more than 10 years:
Silver: 40% min.
Tin: 32% max.
Copper: 30% max.
Mercury: 3% max.
Zinc: 2% max. The present standard is ISO 24234 Ed.2, 2015, and includes other compositions, which have been on the market in violation of ISO 1559 Ed.2:
Silver: 40% min.
Tin: 32% max.
Copper: 30% max.
Indium: 5% max.
Palladium: 1% max.
Platinum: 1% max.
Zinc: 2% max.
Mercury: 3% max. The mercury in the alloy standards above is there to allow for pre- amalgamation to aid the final mixing, the trituration, with mercury. ISO standards do not regulate the market for mercury fillings but products already on the market drive the development of these standards.
Copper amalgam One outdated member of the family of mercury containing filling materials is the copper amalgam. It must not be mistaken for the low or high copper versions mentioned above. 33
Copper amalgam is provided as small round or square tablets consisting of approx. 70% mercury and approx. 30% copper. Sometimes it is spiked with approx. 1% of cadmium (Örstavik 1985). Cadmium amalgam with cadmium and tin has been in use. It was discontinued when found that cadmium was one of the worst metals that could be used in a dental alloy and therefore already in 1849 recommended to not use (Hodgen 1924). When restoring a dental cavity with copper amalgam, small pieces of amalgam are placed in a spoon and heated over an open flame until droplets of mercury are visible on the surface of the metal, see Fig. 1.
Fig. 1 Two tablets of copper amalgam in a spoon heated over an open flame ready to be crushed. With courtesy of the Norwegian TV Company NRK The tablets are then crushed and triturated with pestle and mortar and allowed to cool and is then inserted into the prepared cavity. In the Nordic countries, 34 it was predominantly used in children with extensive caries, but was sometimes also used in adults. The latest documented use in Sweden is from 1981 and in Norway it was used as late as 1994 (Kromberg and Röynesdal 1994). It was sold in Europe as late as 2001 (Produits Dentaires SA 2001). Copper amalgam is known for its high corrosion rate, giving it increased antibacterial effects (Örstavik 1985). In a document from the Nordic Institute of Dental Materials (NIOM), the head of the institute calculates that a child with copper amalgams in all molars (10 g) could be exposed to 2.3 g of mercury and 1.0 g of copper annually in a worst case scenario (Mjör 1981). Copper amalgam is still sold in India and the provider is also an exporter (Pyrax Polymars 2017). Even though its use may be limited, it is still regarded as a viable alternative by the Indian Dental Academy, a national leader in continuing dental education (Indian Dental Academy 2017). It is not mentioned in the Minamata Convention despite the fact that the use of copper amalgam is one of the few activities apart from Artisanal and Small-Scale Gold Mining (ASGM), where mercury is deliberately heated with extensive emission of mercury as a consequence. The Indian company confirms that it sells copper amalgam with approx. 70% mercury in the form of tablets to be heated. In the package insert, it is however stated that the tablets consist of equal amounts of mercury and copper. If the latter is true, this is a new dental alloy not previously accounted for in the scientific literature (Pyrax Polymars 2017). Go to:
Instability phenomena
Droplets on the surface of non-ɣ2-amalgams Polishing the surface of many high copper amalgams stimulates the formation of droplets rich in mercury, see Figs. 2 and and3.3. This formation happens even if the polishing takes place under cold water to avoid any rise in temperature and continues a number of hours after the polishing has stopped.
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Fig. 2 Droplets of mercury on the surface of modern, high copper non-ɣ2-amalgam, photographed with a light microscope (×252 magnifying). Photo: Ulf Bengtsson
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Fig. 3 A sphere of mercury on the surface of modern, high copper non-ɣ2-amalgam, documented with a scanning electron microscope (SEM). Note the strong signal from mercury as the electron beam passes the sphere. Photo: Ulf Bengtsson This phenomenon was first described by Rehberg and Scharschmidt in 1976 and has since been verified by a number of researchers (Rupp et al. 1979; Schneider and Sarkar 1982; Sarkar et al. 1991). Publication has mainly been done in the form of scientific meetings abstracts but to our knowledge no dental scientific journal paper has ever been devoted to this most striking phenomenon alone. Some abstracts are not even possible to get from the dental organization, who initially held the meetings. However, there has obviously been internal discussions taking place and some regard this as a polishing artefact. Observations of droplets have however been made on clinical fillings contradicting this notion (Fredin 1994). 37
One of the very few pictures of these droplets in the dental scientific literature can be seen in one of the big standard encyclopedias of dental materials accompanied by the text: “The small, very light, drop-shaped areas on particle phase are high in mercury owing to the freshly polished specimen (×1000).” (Anusavice et al. 2012). No further discussion of the phenomenon is offered. Another picture of droplets without comment is presented by Herö et al. (1983). A few papers, published outside of the dental community, have however dealt with this phenomenon. Both the formation of droplets and documentation of them is presented by a corrosion expert, outside of the dental community (Pleva 1994). In another study, the investigator has indeed seen small “globules” on all surfaces of fillings from extracted teeth, indicating that this is not just an in vitro phenomenon but indeed occurs in clinical situations. Unfortunately the type of amalgam was not accounted for (Fredin 1994). In 1985, one of the authors (UB) contacted the National Board of Health and Welfare in Sweden about findings of droplets on the surface of modern amalgams. The Swedish Institute for Metals Research was given the task of stripping these small droplets from the surface to determine their content of mercury. Through an extraction replica technique, five droplets were lifted from the surface and measurements ranged from 44.1 to 85.4% mercury (Lehtinen 1985). These findings gave rise to the suspicion that the formation of these droplets was accompanied by an increased emission of mercury vapor. A final examination project was initiated at Linköping University to study mercury vapor emission in amalgams, previously found to produce droplets, with low copper amalgams used as controls. It was concluded that, indeed, non-ɣ2 amalgams exhibit an increased emission of mercury vapor (Toomväli 1988). One would expect that droplets rich in mercury found on high copper fillings should have been published and discussed in journals commonly read by dental personnel, especially in an issue involving safety. As far as we can find, this has not happened. This is one of two phenomena of instability, introduced with the new non-ɣ2- amalgams. The other is described below. 38
Increased emission of mercury vapor in non-ɣ2-amalgams In 1994, it was shown that the amount of tin in the ɣ1-phase is related to the emission of mercury vapor (Mahler et al. 1994). Based on this paper, it is possible to identify the brands tested: conventional amalgams, amalgams with reduced amount of ɣ2- and non-ɣ2-amalgams. The result is clear; non- ɣ2-amalgams emit substantially more mercury vapor than the old, conventional ones used before the 1970s, see Fig. 4. Using the highest emitter of the low copper amalgams as a baseline, the high copper amalgams emits 3–43 times as much mercury vapor depending on brand. One of the most wide spread amalgams, DIS, emits ten times the amount of mercury vapor as compared with the highest emitter of the conventional amalgams, OPT, under the experimental conditions used.
Fig. 4 Mercury vapour loss (ng) between 0.5 and 30 min after abrasion. Left group (red cross- hatched bars): non-ɣ2-amalgams; third bar from right (blue hatched): reduced ɣ2- amalgam; right group (two white bars): old, conventional ɣ2–containing amalgams Diagram based on findings in Mahler et al. (1994). (Color figure online) Also Ferracane (1995) compared losses of mercury as related to the amount of ɣ1-phase. He confirmed the pattern of differences in mercury vaporization from amalgams of different composition. Using the highest emitter of the low 39 copper amalgams as a baseline, the high copper amalgams emitted 3–62 times as much mercury vapor depending on brand and the high copper amalgams had by far the highest emission of mercury vapor (Ferracane 1995). In an investigation measuring differences in mercury vapor emission in corroded and uncorroded samples, only one non-ɣ2-amalgam and one low copper amalgam was used. The pattern is once again confirmed with the non- ɣ2-amalgam emitting substantially more mercury vapor than the conventional one (Boyer 1988). Corroded samples emitted more mercury vapor than not corroded ones (Boyer 1988). In another investigation, using the same brands of amalgam as Mahler et al. (1994), the specimens were abraded, immersed in artificial saliva and mercury was then measured in the solution after 2h (Marek 1997). Also in this investigation, the mercury loss decreased with increasing tin content in the ɣ1-phase. In a second part of the test, when the specimens were treated differently in order to generate an oxide layer before testing, there was no relation between mercury loss and tin content. In the four investigations above, the main researchers in dental amalgam are all reaching similar results. When the reducing oxide layer is removed, the emission of mercury is inversely related to the amount of tin in the gamma-1 phase. This oxide layer is very fragile, so touching the surface with a piece of cotton wool will result in higher levels of mercury vapor. Unfortunately, we cannot find any openly published information/discussion on increased emission of mercury vapor from modern amalgams in any journal commonly read by dental personnel. On the contrary, several big national and international dental organizations have stated that mercury fillings are stable. Thereby, this is the second phenomenon of instability, introduced with the new non-ɣ2-amalgams, which needs to be considered when evaluating exposure and losses of mercury from dental amalgam. Increased emission of mercury vapor may be provoked by a slight touch of the filling surface as by chewing or polishing or by a slight increase of temperature such as consuming hot beverages or hot food. Go to: 40
Conclusion The non-ɣ2-amalgams are marketed as superior in strength and corrosion resistance. When trying to meet these goals for development, a strong sub- optimization has occurred. In experimental set ups, these amalgams, being introduced in the 1970s, emit about ten times more mercury vapor than the ones previously used. Ordinary dental personnel, politicians and other decision makers has not been informed about the instability of modern non- ɣ2-amalgams.
More than a decade ago, the ADA established recommendations for appropriate mercury hygiene within dental offices.
Recommendations1 are subject to periodic updates and change as new information and technology emerge. The ADA has established guidelines for the protection of dental healthcare workers and the environment. The National Institutes of Health has provided guidance2 concerning the reduction/elimination of mercury waste from healthcare facilities. Furthermore, dental service 3-5 branches within the US military have taken a leadership role regarding mercury workplace safety. This article reviews and elaborates on the ADA’s 15-point mercury safety guidelines. Common workplace violations are highlighted, and steps for correction are cited. Practitioners can utilize this information to assist in development of an office protocol. Restorative dentists who no longer offer amalgam services should not ignore mercury hygiene. Amalgam restorations are replaced or removed for a variety of reasons, including defective margins, recurrent caries, fractured tooth structure, and endodontic access. Even this more limited exposure to amalgam may pose a workplace or environmental risk. Dental1,6-12 personnel should not forget they are at greaterADA RECOMMENDATIONS risk of mercury exposure1 than the general population.
(1) “Train all personnel involved in the handling of mercury or dental amalgam regarding the potential hazard of mercury vapor and the necessity of observing good hygiene practices.” This can be accomplished with in-office staff training. Often, the employee designated as the OSHA educator will present information and training at a weekly or monthly staff meeting. State and local dental societies may offer such training to member dentists and their staff. These educational courses are a valuable tool to satisfy OSHA mandated guidelines for staff training on infection control and workplace safety from potential biohazards, including mercury. 13 Amalgam consists of approximately 50% mercury by weight. Mercury vapor release is of particular concern as a potential health risk. An estimated 75%14-16 to 80% of inhaled mercury vapor, which reaches pulmonary alveoli, will be absorbed into the blood. Prophylactic measures can be taken to substantially lower risks to dental personnel and the environment. Measures cited to follow will elaborate. (2) “Make personnel aware of the potential sources of mercury vapor in the operatory – that is, spills; open storage of used capsules; trituration of amalgam; placement, polishing or removal of amalgam; heating of amalgam-contaminated instruments; leaky capsules; and leaky bulk amalgam dispensers. Personnel also should be knowledgeable about the proper handling of amalgam waste and be aware of 41
environmental issues. Some state dental societies have published waste management recommendations applicable to their state.” The dental profession has moved towards routine use of pre-encapsulated amalgam. Loading of elemental mercury and alloy powder onto opposite ends of a measuring balance beam is now obsolete. Scrap (or waste) amalgam handling poses a greater problem.
Figure 1.
Scrap amalgam improperly stored in an unsealed open box, within a treatment room drawer. Also note the open spent amalgam capsules, which actually are of minor consequence in this unsafe and noncompliant situation. Proper storage and recycling of waste6,17,18 amalgam has been a challenge. Because the focus of concern has been patient safety with amalgam, some clinicians may underestimate the importance of environmental or workplace risk. These incorrect assumptions may result in unrealized hazards and liabilities. Some dentists improperly store scrap amalgam in open containers (Figure 1). Used amalgam- mix capsules containing small amounts of amalgam are sometimes improperly stored in an open, and not closed, manner. Waste amalgam and spent capsules may be inappropriately disposed of in the general office refuse, from which they later enter municipal landfills or incinerators.19,20 This source of mercury can enter ground water, or elevate the mercury level in the air. Adherence to ADA Recommendation No. 11 on methods for amalgam storage is advisable. (See discussion of Recommendation No. 11 later.)
Figure 2.
ISO (International Organization for Standardization) 11143 certified amalgam separator. These units protect municipal wastewater by collecting the 60% of waste 42
amalgam and mercury that bypasses standard dental unit primary and secondary traps. The Vermont Dental Society21 and the National Wildlife Federation have jointly published guidelines for environmental safety. Special amalgam separator/collector traps have been designed for dental wastewater.22 These are required in Germany, King County (Seattle), Washington, and many other regions. These separators have been specially engineered to remove elemental mercury23,24 and very small particulate amalgam, which will pass thorough standard dental operatory unit traps (Figure 2).
Figure 3.
Internal floor surface of amalgamator (assuming no defective open seam) has collected scrap amalgam and beads of elemental mercury. Over time, amalgamators become contaminated to the degree of a biohazard. They represent a source of mercury vapor for dental personnel. 25,26 Mercury-contaminated amalgamators present another problem (Figure 3). Debris on any surface or working part of an amalgamator may include scrap amalgam, as well as beads of free mercury. A defective gap or seam opening will permit debris to escape from the amalgamator. Otherwise, risk is limited to mercury vapor exposure directly from the contaminated amalgamator.
Because of release of mercury6 vapor, the World Health Organization (WHO) has cautioned against heating of dental amalgam. The WHO specifically recommends that coolants be employed when polishing or removing amalgam. Friction generates heat. Heat releases mercury vapor. The WHO states “open heating of amalgam should never be carried out…” (Note: In the case of crematoria, the WHO advises vapor collectors to protect air quality, as mercury is released from amalgam.)
Figure 4.
Scrap amalgam often collects on surfaces difficult to clean, such as the lumen of an amalgam carrier. Amalgam should be removed by ultrasonic cleaning tank, and collected and 43
handled in accord with ADA recommendations. Autoclave temperatures generate dangerously high levels of mercury vapor. The mechanism should never be “freed” by holding the instrument in an open flame. Heating amalgam-contaminated instruments often occurs when incompletely cleansed instruments are autoclaved. Scrap amalgam frequently clings to the lumen of amalgam carriers, causing the mechanism to stick (Figure 4). Amalgam adheres to crosshatched surfaces of amalgam condensers and carving and finishing instruments. Ultrasonic pre-cleaning prior to autoclaving is advisable. Examination of ultrasonic tanks often reveals amalgam debris. This potential source of mercury exposure must be collected, stored, and disposed of in a worker-safe and environmentally friendly manner. Residual waste amalgam27 subjected to high autoclave temperature will generate exceptionally high levels of mercury vapor. When venting autoclaves or any potential source of mercury vapor, proper air exchange is advised to protect employees. Furthermore, heating a “sticky” amalgam carrier under a flame is sometimes used to free the mechanism clogged by waste alloy. This will produce potentially dangerous levels of mercury vapor in the immediate vicinity.
Figure 5.
Left: New carbide bur has optimal cutting efficiency, which reduces preparation time and lowers the cutting temperature. Defective alloy may be removed in larger segments, which are more easy to collect, and present less surface area/volume for reduced mercury vapor release.Middle: After three autoclave cycles corrosion substantially dulls carbide bur. Preparation time and temperatures are elevated as cutting efficiency declines. Right:Smaller Additional slurry amalgam autoclave cycles haveparticulates corroded are the generated. carbide bur to the extent that at alloy removal the bur exhibited complete metal 44
fatigue. While in the patient’s mouth, the bur tip broke.
To reduce overhead costs, handpiece burs (even inexpensive single-use brands) may be used and sterilized multiple times (Figure 5). Handpiece cutting efficiency is dramatically reduced. In removing defective alloys, preparation time and cutting temperatures are elevated. These burs, subjected to excessive stress and corrosion of multiple cycles of autoclaving, exhibit metal fatigue. Cutting efficacy is dramatically reduced, prolonging cutting times and increasing operator exposure to mercury vapor and amalgam particulates. It becomes more difficult to segment defective alloy into larger and safer particle size (see section 5). Frictional heat is elevated with use of28,29 these defective, dull burs, which may not only elevate levels of mercury vapor, but insult pulpal tissue. No study has specifically addressed the relation of poor-cutting, defective burs, with regard to elevated levels of mercury vapor. However, this is easily extrapolated from research demonstrating relatively high release of mercury vapor from the very limited and less invasive procedure of amalgam polishing. (3) “Work in well-ventilated spaces, with fresh air exchanges and outside exhaust. If the spaces are air- conditioned, air-conditioning filters should be replaced periodically.” Many practices are in full compliance with this recommendation, with office space that has been initially designed with adequate ventilation ductwork, fresh air exchanges, and filtration systems. Numerous private companies will assist with facility design for optimal workplace ventilation.
In Sweden,3 the threshold limit for the breathing zone of dental personnel has been established at 30 µg Hg/m (cubic meter) air. Other nations may not have established safety thresholds, or there may be no monitoring of the air quality, even if standards are in place. Thus, currently in countries like the United States, it may be very difficult if not impossible to assess if a particular clinic affords its staff a safe breathing workplace environment. Some facilities definitely have inefficient ventilation. As examples, older clinic settings or special facilities (prison dental clinics where building design may focus primarily on staff and inmate security) may not address concerns related to ventilation. Similarly, some offices may compromise on fresh air exchange in an effort to decrease threat of burglary or other crime. Initial costs for proper ventilation and fresh air exchangers may seemingly be prohibitive when a clinical facility is being planned, and expenses are considered. (4) “Periodically check the dental operatory atmosphere for mercury vapor…” Dosimeters should be used for routine monitoring of air-mercury levels. Hand-held mercury vapor analyzers can be used for rapid hazard assessment after a spill or cleanup. Many state and local dental societies have these devices available for loan to member dentists. It would be cost-effective for groups of dentists to pool their resources to accomplish recommended monitoring. Private environmental firms will also provide this monitoring service. The site of mercury contamination may not be easily observable, and mercury cannot be detected by odor. It cannot be assumed that such contamination does not exist, or if it does, that it has no consequence. (5) “Use proper work area design to facilitate spill contamination and cleanup. Flooring covering should be nonabsorbent, seamless and easy to clean.” 45
Figure 6. Figure 7.
Scrap amalgam on Treatment room carpeted treatment-room floor flooring of tile and grout. Debris (bur shown for scale). Over time, collects on rough surfaced grout, scrap and waste amalgam including waste and scrap becomes imbedded in the carpet amalgam. and breaks into smaller and smaller particles. Carpet scuffed by foot traffic or wheels on an operatory stool releases mercury vapor into the breathing zone of dental personnel. Vacuuming brings mercury vapor into the breathing zone of cleaning staff. This is a significant area of noncompliance. Operatory flooring is too frequently carpeted, tile and grout, or seamed linoleum (Figures 6 and 7). Waste amalgam, as well as water-borne waste, may enter areas that are difficult if not impossible to clean. Foot traffic will scuff scrap amalgam, raising ambient mercury vapor levels in an operatory. Restorative dentists are encouraged to examine their protective eyewear after removal of a defective amalgam. Glasses are often speckled with amalgam slurry. A significant amount of slurry and particulate matter may escape onto the operatory floor over the course of a day. Seamless linoleum is an ideal floor covering to facilitate cleanup and prevent buildup of waste amalgam. Of significance, the smaller the particle of amalgam, the greater the ratio of surface area/volume. This means that minute micron-sized particles of amalgam have far greater potential for mercury vapor release. An equal mass of larger particle sized alloy is of far less risk. (6) “Use only precapsulated alloys; discontinue the use of bulk mercury and bulk alloy.” This is an important area of progress. In the past, dentists measured alloy powder and free elemental mercury in a balance beam device. The same amalgam mixing capsules and pistils were used repeatedly for years. Amalgam may even have been mixed in an open centrifuge. Excess mercury was forced through a “squeeze cloth” to achieve an ideal working consistency of alloy. Free mercury was either washed down the sink, into municipal sewage, or collected in a jar for the next amalgam mix. Mercury spills were commonplace, and falsely assumed to be of minimal consequence. Gloves and masks were rarely employed. Progress has been significant in terms of avoiding these problems. Despite modern precautions, trace amounts of mercury may adhere to the exterior of unused amalgam capsules because of flaws in the manufacturing process. Unopened capsules should always be handled with gloved hands, with the assumption that a potential risk exists. (7) “Use an amalgamator with a completely enclosed arm.” 46
Figure 8.
Protective safety cover of amalgamator has been completely removed. If encapsulated amalgam is improperly seated in amalgamator arms, the contents can be dispersed in an airborne fashion throughout the facility. This is an area where dentistry has made great progress. However, some dentists are employing older or defective amalgamators lacking a protective safety lid (Figure 8). Occasionally, an amalgam capsule may be improperly seated within the mixing arms. Upon depressing the “on” button, the capsule and partially mixed contents can be released into the air. An enclosed mixing arm more safely confines alloy contents to the amalgamator.
Over time, 25most amalgamators become mercury-contaminated to the level of a biohazard. Unserviceable units should be disposed25 of in accordance with local and state environmental regulations when such a protocol is established. (8) “Use care in handling amalgam. Avoid skin contact with mercury or freshly mixed amalgam.” Barrier techniques originally designed for infection control have largely eliminated this problem. Facemasks, face shields, gloves, and protective eyewear are nearly universally utilized.
Figure 9.
Clinician with protective eye wear, protective clothing, and surgical facemask. Facemask must secure to facial contours including facial hair. No standard mask will filter mercury vapor or amalgam particulates smaller than 10 µm. Filtration protection varies for different masks. Unfortunately, standard barrier techniques do not prevent pulmonary exposure to mercury vapor (Figure 9). The filtration pore size and a secure30 mask seal vary greatly from manufacturer to manufacturer with standard surgical masks. Some masks are far superior to others in filtering waste 47
amalgam particulate material. Masks should be changed frequently to assure effectiveness.31 No standard surgical mask can filter mercury vapor or amalgam particulate matter smaller than 10 µm. A poorly fitted mask, or one from an inferior manufacturer, will fare far worse. Several studies have examined the quantitative32,33 release and consequences to dental personnel of mercury vapor sourced to amalgam removal. Few research the problems of µm-sized amalgam particles, which31 have potential to travel through protective masks, and ultimately into terminal alveoli of the lungs. Protective gloves, face shields, and barrier clothing should also be employed for cleaning amalgam collection traps, freeing clogged suction lines, and removing instruments from ultrasonic cleaners prior to autoclaving. The US Navy and US Air4,5 Force have established protocols to dispose of waste amalgam collected from traps prior to recycling. (9) “If possible, recap single-use capsules from precapsulated alloy after use. Properly dispose of them according to applicable waste disposal laws.” 34 Recapping disposable capsules reduces mercury vapor emissions. Used capsules and scrap alloy sealed in a biohazard container can contribute to mercury air-contamination if incinerated with biomedical waste. Air quality and/or ground water may be compromised if amalgam-contaminated capsules are disposed of in standard municipal trash. State certified and bonded amalgam-recycling companies are ideally suited to handle and process amalgam waste.
Dentists have been found liable for costs incurred in mercury cleanup when an35,36 unlicensed amalgam waste handler improperly disposed of scrap amalgam in a community landfill. Dentists are advised to check a recycler’s EPA license number and insurance coverage. (10) “Use high-volume evacuation when finishing or removing amalgam. Evacuation systems should have traps or filters…” As stated, improved filtration systems have been developed to remove nearly all mercury/amalgam in wastewater from the dental37,23,24 operatory. Local, state, and national governments are increasingly requiring this level of filtration. Dentists in the past practiced without an assistant, and with little or no high-volume evacuation. When excessive debris, including waste amalgam, accumulated in the patient’s mouth, the patient was instructed to rinse into a cuspidor. The wastewater emptied directly into the public sewer system. The acceptance of four-handed dental practice, with high-volume evacuation, has lessened this source of mercury contamination. Unfortunately, quantities of waste amalgam and mercury may remain in plumbing traps, or office cabinet or drawer space from clinical practice of earlier times. This contamination may have environmental liability and workplace safety consequences for a practitioner many years later. The current dentist in that practice and/or facility may assume responsibility for previous oversight of mercury hygiene. Some dentists may prefer to prepare teeth without water spray to improve visibility. The absence of a water spray elevates the temperature and may damage pulpal tissue, as well as increase production of mercury vapor when removing amalgam. Dental professionals are exposed to approximately ten times the concentration of mercury vapor without this precaution.38 Handpiece water mist/spray also helps trap alloy debris into slurry, for ease in suctioning and removal. High-volume evacuation and water spray function together to reduce mercury vapor levels and waste particulate alloy from the breathing area of dental personnel. Marginally functional suction pumps and clogged vacuum hoses do not allow proper evacuation. These situations should be remedied. (11) “Salvage and store all scrap amalgam (that is, noncontact amalgam remaining after a procedure) in a tightly closed container, either dry or under radiographic fixer solution…” 48
Storage of scrap amalgam under water is associated with mercury going into solution. Disposal of mercury-contaminated water then becomes a problem. Scrap alloy stored in radiographic fixer solution will not have mercury go into solution. However, disposal of fixer solution may present a chemical waste problem in and of itself. This solution should be disposed of in accordance with environmental waste management laws and guidelines. Waste management companies that collect and process used radiographic fixer chemicals may not be equipped to handle mercury wastewater. If scrap amalgam is stored dry, mercury vapor may escape when the container lid is removed. This occurs each time the container is opened and closed. Adequate ventilation is essential. (12) “Where feasible, recycle amalgam scrap and waste amalgam. Otherwise, dispose of amalgam scrap and waste amalgam in accordance with applicable laws…” As stated, environmental law usually attaches legal liability for cleanup to the originator or generator of the biohazard waste (the dental practice). Ignorance of the related law is no defense. (13) “Dispose of mercury-contaminated items in sealed bags according to applicable regulations…” Again, municipal sewage, landfill, and incineration are not equipped to deal with mercury waste. Mercury-contaminated items require special handling and disposal by licensed carriers. Most state dental societies provide lists of such companies. (14) “Clean up spilled mercury properly using trap bottles, tapes or freshly mixed amalgam to pick up droplets, or use commercial cleanup kits. Do not use a household vacuum cleaner.”
Figure 10.
Example of commercially available mercury spill cleanup kit. This can be used by dentists offering amalgam services. Mercury cleanup and recovery works best on a flat, smooth, and nonabsorbent surface. It is advisable to train with a kit, prior to an actual mercury spill. Copyright Lab Safety Supply, Inc, Janesville, Wis. Reproduced with permission. Precapsulated amalgam has nearly eliminated the problem of mercury spills. Occasionally, a capsule is opened without a complete mix, or is defective, and free elemental mercury may spill. Protocol and training for mercury cleanup should be in place, prior to an event. Commercial prepackaged mercury cleanup kits are available for purchase (Figure 10). A household or industrial vacuum cleaner would obviously distribute spilled mercury, or mercury vapor from waste amalgam, throughout a defined breathing space. Vacuuming of operatory carpeting (which is 49
an inappropriate floor covering) is not advisable. Standard commercial vacuum bags do not adequately filter mercury vapor. Cleaning service personnel may have little knowledge of the potential risks. Again, it is recommended to cover treatment-room floors with a seamless, nonabsorbent material. (15) “Remove professional clothing before leaving the workplace.” Barrier techniques intended for infection control serve a dual function—protection from blood-borne pathogens, and mercury hygiene. Today, many dental offices utilize professional cleaning services for clinic gowns and scrubs. Offices may have on-site washers and dryers for personnel clothing. Disposable gowns and clothing shields are also available. Dental professionals should not wear contaminated clinical attire outside of the workplace (eg, lunch at aDISCUSSION local restaurant, or in their vehicle during a homebound commute).
Dentistry has made important progress in the area of mercury hygiene for workplace and environmental safety. Today, many practices are in compliance with the ADA recommendations. This article is intended to assist practices in addressing complete compliance, and can assist with in-service training. It is important to remember that during in-service training mercury hygiene techniques should be explained simply, and not in complex terms. A time for questions and answers should be provided. It is important38 to remember that auxiliaries may actually be at greater risk of mercury exposure than dentists. Some dental clinics offer on-site testing for mercury vapor levels and employee screening of urinary mercury levels. This 38,39is very significant, as a limited number of dental clinics demonstrate dangerously high mercury levels. The distribution of dentists with elevated levels of mercury is not uniform. While a majority display relatively low levels of urinary mercury, a smaller number demonstrate high levels. This implies compliance with mercury workplace safety guidelines is not universal for dentists and auxiliaries. A safe work environment should be a right, and not a privilege enjoyed by some but not all.
Amalgam has6,17,18 survived as a restorative material, in large measure, because of low cost and clinical reliability. The fees charged for amalgams have been questioned.40 When practitioners examine associated expenses involved with amalgam placement or removal, workplace and environmental safety should be considered. Increasing government regulations regarding dental mercury management are inevitable. These government directives will cost money to implement. It may be time to examine the trueCONCLUSION short- and long-term costs associated with the use of amalgam as a restorative material.
Organized dentistry is to be lauded for advancing workplace and environmental mercury hygiene safety. Local and state dental societies, the ADA, and the US military dental services have made contributions. Compliance with ADA mercury hygiene recommendations requires time, effort, and resources, but compliance is required. Debate regarding the continued use of amalgam as a restorative material is beyond the scope of this article. This is an issue of informed consent and personal choice. For now, all restorative dentists must address mercury safety.
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7.) Amalgam fillings do not release any measurable mercury vapor at mouth temperature.
A. True B. False https://www.ncbi.nlm.nih.gov/pubmed/1475757 https://www.youtube.com/watch?v=Bw94F94FZqA
Release of mercury vapor from dental amalgam. Berglund A1. Author information Abstract Because of its long-term clinical use there is more information and research data available about dental amalgam than about any other dental restorative material. However, on and off the safety of dental amalgam has been called in question and during the 80's the mercury controversy came to the fore, not only within the profession but also among the general public. Sources of mercury vapor contamination within dentistry were identified and attempts made to evaluate the contributions to the daily mercury uptake which can be attributed to dental amalgam. Mercury can be released from dental amalgam by evaporation and electrochemical corrosion as well as from amalgam particles which have been swallowed. A major route for mercury uptake from amalgam restorations is through inhalation of mercury vapor. The present study focused on experimental and analytical difficulties associated with the measurement of mercury vapor released in the oral cavity. A careful methodological study of the kind of source of mercury vapor that is prevalent and on the methods for measuring the intra-oral release of mercury vapor was carried out. With this as a basis quantitative determinations of the release rate of mercury vapor from amalgam restorations were made on healthy human subjects not occupationally exposed to mercury. The daily uptake of mercury from inhaled mercury vapor was calculated and salivary and urinary mercury levels were determined. In addition the release rate of mercury vapor from different types of amalgam was studied in vitro and in vivo. The findings may be summarized as follows: The only relevant measurable quantity when determining the mercury vapor released from amalgam restorations is the amount released per time unit, i.e. the amount of mercury vapor collected during intra-oral sampling is proportional to the sampling time. The diffusion of mercury atoms inside an amalgam restoration results 51
in the formation of a concentration gradient in the surface of the amalgam. This mercury diffusion is the rate-determining step for mercury vapor release in the long run. In the short run the mercury concentration gradient prevalent on the amalgam surface on the measuring occasion is the apparent rate-determining step. The daily uptake of mercury from inhaled mercury vapor released from dental amalgam seems to make a very small contribution to the total body burden of mercury, in comparison with what can be tolerated in the work environment. The in vitro results revealed obvious differences regarding the release rate of mercury vapor from dissimilar amalgam types.(ABSTRACT TRUNCATED AT 400 WORDS).
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8.) Of the following protective protocols, which is USED for the patient protection during mercury filling removal:
A. Alternative breathing source (i.e. oxygen mask) B. Wearing a disposable HAZMAT type suit C. Pre and post removal rinse D. Safety glasses E. Rubber Dam enhanced with HgX cream F. All of the above https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3270415/ https://iabdm.org/wp-content/uploads/2016/06/protect2016.pdf https://iabdm.org/wp-content/uploads/2017/04/ProtectProtocol-brochure.pdf
A Safe Protocol for Amalgam Removal
Dana G. Colson *
Author information Article notes Copyright and License information Disclaimer
This article has been cited by other articles in PMC.
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1. Introduction In dentistry, there is a lot of controversy about the topic of silver mercury fillings; are they safe or not safe? There are many articles written on the pros and cons of these types of fillings. It is difficult to quantify and to assess the effects in each individual. It is not easy to identify silver mercury fillings as the cause if illness presents or if the fillings contributed to illness, except in extreme toxicity cases. Refer to the beginning sections of this review paper concerning the science and mechanism of how mercury interconnects with body tissues and functions. Environmental doctors investigate heavy metal toxicity as part of their overall wellness regiment to help their patients with health concerns. These doctors look at sources of metals when the patient's lab reports/diagnostic tests show high levels of mercury and other metals. They investigate what sources are contributing and how to reduce the burden on the body. The doctor may prescribe the safe removal of silver mercury fillings so as not to create an additional burden on the body and to help their patient heal. Thus, 53 when removing amalgams, additional steps help ensure that the patient is protected. Go to:
2. Introduction of Amalgam in Dentistry Dental amalgam restorations, also called silver mercury fillings, were introduced to North America in the 1830s and have been the standard restorative filling for our molars and premolars. At that time there was a lot of controversy about its intraoral use. Silver mercury fillings began to take over the cast gold and gold foil restorations. These were excellent and lasted for years; however they were labour intensive and the cast gold required a lab process that centrifuged gold into a wax pattern to fit the tooth accurately. This was a two-appointment process with added expense. Gold foil restorations were often traumatic to the pulp of the tooth, creating necrosis and requiring root canal. The addition of amalgams as a restorative filling was a welcomed opportunity to offer at a substantial cost reduction as the mercury was triturated with a pellet containing silver, copper, tin, and zinc. This created a substance that could be placed into the cleaned out tooth structure where decay had been present. It was packed, condensed, and allowed to harden within a few minutes and then carved intraoral chairside. Today the extra, unused amalgam is placed in a container for safe disposal. This restoration is easily burnished to tooth structure to recreate the tooth to its original shape and size. The onset of amalgam allowed people to keep their teeth, rather than having them extracted if money did not allow for gold restorations. Keeping teeth enabled people to have better digestion and supported a more balanced quality of life. Today, with the increase of chemicals such as pesticides, preservatives, processed ingredients in food, and diverse contaminants in our environment; sensitivities, allergies, and other illnesses are increasing rapidly. The Brain Wash postulates that the toxins in our society are not additive but synergistic. For example, the average apple contains residue of eleven different neurotoxins and is sprayed with pesticides seventeen times prior to being picked from a tree [1]. Our food intake of many pesticides and additives is most often unknown. The level of materials such as mercury that our bodies could tolerate several decades ago may not be what we can sustain today. 54
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3. Amalgam and Composite Fillings Silver mercury amalgam restorations are comprised of 50% mercury, with the balance being silver, copper, tin, and zinc [2]. Over time the exposed surface changes. The fillings corrode, and surface texture becomes rough. People who chew gum create a smooth, shiny surface on their fillings. Mercury vapor is released by chewing grains, nuts, seeds, and gum, as detected using mercury vapor analyzers [3]. A study in 2010 looked at the wearability of composite (white) restorations compared to amalgams. It showed that over 12 years, the group of patients that were not prone to decay, with resin/composite-filled restorations, were better off than the group of patients with silver amalgam restorations [4]. Today with awareness of diet, home care, and education, the majority of people who seek preventative dental care are less prone to decay. The author has worked with alternative restorations for over 27 years. The advantage of white composite restorations is that composite binds to composite and the base of the tooth rarely needs to be disturbed once the amalgams are removed. Dental restorative materials have various components, and individual Material Safety Data Sheets (MSDSs) are available from the manufacturer. If an individual has concerns or is sensitive to materials, one can refer to these reference sheets. For example, there are many composites and bonds available today without bisphenol A. Psychological benefits are also a positive factor for patients. People feel that they now have a mouth without the “scars” of the past. They are no longer self-conscious when smiling, laughing, and singing. With the introduction of composite restorations, many modifications have been made with the materials and applications due to the extensive ongoing technology and research. The concerns with good marginal seals and prevention of recurrent decay have been diminished. Wear and polishability of the composite materials with nanohybrid particulates can withstand stronger chewing forces. Composites are technique sensitive, and various aids can be used to ensure a proper seal of the restorative material to the tooth structure and to create tight contacts to the adjacent tooth to prevent food impaction between teeth. Today we aim for minimally invasive dentistry to 55 maintain integrity of the tooth structure, and white composite materials are ideal for these restorations. Go to:
4. Considerations prior to Amalgam Removal When examining a patient for amalgam removal upon request, many factors must be looked at including the rate of wear/attrition on their teeth, pressures exerted, type of diet consumed on a daily basis, their oral hygiene, and other metals in their mouth. Often amalgam restorations exist under crowns and amalgam tattoos (discoloration along the gum) are noted. Amalgams have also been used to seal the apex of root canal treated teeth. If heavy pressures are exerted by an individual or there is evidence of grinding and clenching, then the longevity of a composite restoration may be compromised. The size of the restoration will also influence the choice of materials. Tooth cusps often fracture over time, as well as with excessive pressure, requiring an indirect restoration to be fabricated by a lab. Today the increasing trend is to work with a computer-generated restoration to secure/repair the tooth in the long term. Bite plates to prevent grinding and clenching help preserve these new restorations from excessive wear and pressure. When the patient is seen for an initial exam, a thorough medical and dental history is taken. Records including radiographs and intraoral pictures are taken, and a comprehensive exam follows. Previous films are requested or brought in by the patient. Lengthy conversations ensue to make sure that the patient is properly prepared and that we are working with their physician, in a timely manner, to complement the detoxification process that their doctor has prescribed and is administering. The physician evaluates the overall health of the body and the ability of the individual to eliminate toxins. For example, if a patient has a leaky gut, physicians restore this prior to removal as it is difficult to flush out toxins [5]. If a woman is pregnant or breast feeding, amalgam removal does not occur until she has completed breast feeding her child [6]. It has been reported that the mercury concentration in the blood of the fetus can be thirty times greater than the mother's blood [7]. Supplements are helpful and are prescribed on an individual basis by the physician. Vitamin C intake is recommended, often with other supplements, prior to and following amalgam removal. Once the amalgam restorations have been 56 removed, the physician continues to work with the patient to help with the detoxification of mercury that is stored in the body. Go to:
5. Chairside Procedures The following steps are taken when removing silver mercury fillings, to ensure minimal if any absorption sublingually, or through the mucosal tissues, and to minimize mercury vapor absorption through the blood/brain barrier [8–10]. In office, the patient is prepared as follows, prior to amalgam removal: i. the patient is draped with a plastic apron under the dental bib to cover their clothing; ii. a dental dam (“raincoat”) is customized to fit the existing tooth/teeth to prevent particulates from contacting the oral mucosa; iii. underneath the dam, activated charcoal or chlorella is placed, along with a cotton roll and gauze. This helps to intercept particles and to chelate dissolved metals that seep under the dam. Often the particles are found on the sublingual tissues and lateral borders of the tongue. This must be prevented as this is the fastest absorption route into the body; iv. the patient's face is draped under the dam, with a liner; v. goggles for the eyes and hair cap or bonnet protection are placed; vi. oxygen is supplied to the patient with a nasal mask and the mercury vapor ionizer is turned on. The vapor ionizer is a specialized air filtration system that is used to bind mercury vapors that are attached by the negative ion flow and are then carried to a positively charged ionizer plate at the opposite end of the room. The operators also protect themselves with a filtered mask, eye and hair protection, and face shields. The removal of amalgam commences as follows: i. a new dental bur is used in the handpiece to ensure easy removal; 57 ii. high volume suction and a continual addition of water spray are supplied to the site where the amalgam is being extracted; iii. if possible, the amalgam restoration is sectioned and then scooped out to eliminate as much mercury vapor release as possible [11]. The vitality of the tooth is always a concern and the less trauma to the tooth, the healthier the pulp, which supplies blood vessels and nerve supply to the tooth. The deeper the restoration, the greater the chance of pulpal degeneration, causing necrosis and subsequent abscess at the apex of the tooth, as well as bone loss. Once the amalgam is removed completely, i. the oxygen and protective coverings are taken away; ii. an immediate inspection under the dental dam occurs. The gauze, cotton roll and activated charcoal/chlorella are wiped away. Gauze is then used to inspect the floor of the mouth and tongue to make sure no particulates seeped under the dam; iii. once all mucosal tissues are fully inspected and cleaned, the mouth is flushed with copious amounts of water, again to ensure no ingestion or absorption of amalgam particulates. The tooth is then restored to a healthy state of form and function. Materials are taken into consideration as discussed previously on an individual need. Often environmental healthcare providers give direction on the preferred choice of materials to be used through biocompatibility testing. It is the dentist's ultimate responsibility to advise the patient about the strengths and limitations, if they cannot tolerate some materials. It has been the author's experience that once the amalgam materials have been removed and the patient detoxes under the supervision of their physician, the range and variety of materials increase, allowing the dentist to create the best prognosis for the tooth. Dentists by law in Ontario [12] and elsewhere in Canada must have a certified amalgam separator on the wastewater lines in dental offices in their practices and must use a certified hazardous waste carrier for the recycling and disposing of amalgam waste. Go to: 58
6. After Amalgam Removal A 2011 Norwegian study showed a 3-year followup after amalgam removal with precautions in a treatment group compared to a reference group. It showed significant reductions in intraoral and general health complaints [13]. The following is a list of outcomes that I repeatedly hear from my patients over the years. Although I have not scientifically collected them, after amalgam removal and detoxification, they have also been reported in the literature. Comments include that a. patients no longer have a metallic taste in their mouth; b. patients feel as if they have more energy; c. patients are able to concentrate better and make decisions easier (the “brain fog” is gone); d. their body responds better to other treatments, as if a barrier has been lifted. To achieve effective results one must include an integrative approach with a physician and health care team with attention to detoxification and diet over several months, with laboratory tests to monitor progress.
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9.) Mercury vapor is most easily absorbed by the body via:
A. Inhalation B. Swallowing C. Exposure to skin or mucous membranes https://www.cdc.gov/niosh/ershdb/emergencyresponsecard_29750021.html https://emedicine.medscape.com/article/1175560-overview
MERCURY (ELEMENTAL) : Lung Damaging Agent
CAS #: 7439-97-6
RTECS #: OV4550000
UN #: 2809 (Guide 172)
Common Names:
Elemental mercury Liquid silver Quicksilver
Agent Characteristics
APPEARANCE: Heavy, shiny, silver-white, mobile liquid metal, at room temperature. DESCRIPTION: Mercury exists naturally in the earth’s crust, and is released by degassing of the earth’s crust, volcanic emissions, and through evaporation. It can be obtained by heating mercury containing ores and condensing the vapors. Mercury is used in many industries, especially the electrical industry, and in many instruments such as thermometers and barometers. It has been used clinically, but because of its toxicity this use is diminishing. Most people are exposed to mercury through diet and dental fillings. Mercury is odorless. This card will only address elemental mercury. METHODS OF DISSEMINATION: o Indoor Air: Mercury can be released into indoor air as a liquid spray (aerosol) or as a vapor. 60
o Water: Mercury can be used to contaminate water. o Food: Mercury can be used to contaminate food. o Outdoor Air: Mercury can be released into outdoor air as a liquid spray (aerosol) or as a vapor. o Agricultural: If mercury is released into the air as a liquid spray (aerosol), it has the potential to contaminate agricultural products. If mercury is released as a vapor, it is highly unlikely to contaminate agricultural products. ROUTES OF EXPOSURE: Elemental mercury is toxic primarily through inhalation of mercury vapors. It is only slowly absorbed through the skin, although it may cause skin and eye irritation. Elemental mercury droplets may be absorbed through eye contact. Ingestion is not an important route of acute exposure as almost no elemental mercury is absorbed through the gastrointestinal tract.
Personal Protective Equipment
GENERAL INFORMATION: First Responders should use a NIOSH-certified Chemical, Biological, Radiological, Nuclear (CBRN) Self Contained Breathing Apparatus (SCBA) with a Level A protective suit when entering an area with an unknown contaminant or when entering an area where the concentration of the contaminant is unknown. Level A protection should be used until monitoring results confirm the contaminant and the concentration of the contaminant. NOTE: Safe use of protective clothing and equipment requires specific skills developed through training and experience. LEVEL A: (RED ZONE): Select when the greatest level of skin, respiratory, and eye protection is required. This is the maximum protection for workers in danger of exposure to unknown chemical hazards or levels above the IDLH or greater than the AEGL-2. o A NIOSH-certified CBRN full-face-piece SCBA operated in a pressure-demand mode or a pressure-demand supplied air hose respirator with an auxiliary escape bottle. o A Totally-Encapsulating Chemical Protective (TECP) suit that provides protection against CBRN agents. o Chemical-resistant gloves (outer). o Chemical-resistant gloves (inner). 61
o Chemical-resistant boots with a steel toe and shank. o Coveralls, long underwear, and a hard hat worn under the TECP suit are optional items. LEVEL B: (RED ZONE): Select when the highest level of respiratory protection is necessary but a lesser level of skin protection is required. This is the minimum protection for workers in danger of exposure to unknown chemical hazards or levels above the IDLH or greater than AEGL-2. It differs from Level A in that it incorporates a non-encapsulating, splash-protective, chemical-resistant splash suit that provides Level A protection against liquids but is not airtight. o A NIOSH-certified CBRN full-face-piece SCBA operated in a pressure-demand mode or a pressure-demand supplied air hose respirator with an auxiliary escape bottle. o A hooded chemical-resistant suit that provides protection against CBRN agents. o Chemical-resistant gloves (outer). o Chemical-resistant gloves (inner). o Chemical-resistant boots with a steel toe and shank. o Coveralls, long underwear, a hard hat worn under the chemical- resistant suit, and chemical-resistant disposable boot-covers worn over the chemical-resistant suit are optional items. LEVEL C: (YELLOW ZONE): Select when the contaminant and concentration of the contaminant are known and the respiratory protection criteria factors for using Air Purifying Respirators (APR) or Powered Air Purifying Respirators (PAPR) are met. This level is appropriate when decontaminating patient/victims. o A NIOSH-certified CBRN tight-fitting APR with a canister-type gas mask or CBRN PAPR for air levels greater than AEGL-2. o A NIOSH-certified CBRN PAPR with a loose-fitting face-piece, hood, or helmet and a filter or a combination organic vapor, acid gas, and particulate cartridge/filter combination or a continuous flow respirator for air levels greater than AEGL-1. o A hooded chemical-resistant suit that provides protection against CBRN agents. o Chemical-resistant gloves (outer). o Chemical-resistant gloves (inner). o Chemical-resistant boots with a steel toe and shank. 62
o Escape mask, face shield, coveralls, long underwear, a hard hat worn under the chemical-resistant suit, and chemical-resistant disposable boot-covers worn over the chemical-resistant suit are optional items. LEVEL D: (GREEN ZONE): Select when the contaminant and concentration of the contaminant are known and the concentration is below the appropriate occupational exposure limit or less than AEGL-1 for the stated duration times. o Limited to coveralls or other work clothes, boots, and gloves.
Emergency Response
CHEMICAL DANGERS: o Heating mercury vapor produces mercuric oxide, which is highly irritating to mucous membranes and more likely than elemental mercury vapor to adversely affect the lungs. o Elemental mercury reacts with most metals. o Elemental mercury reacts with many acids. o Elemental mercury reacts vigorously with ground mixtures of sodium carbide. o Mercury reacts with acetylenic compounds, ammonia, azides, oxygen, oxidants, and halogens. EXPLOSION HAZARDS: o A violent heat-producing (exothermic) reaction, possibly an explosion, occurs when mercury comes in contact with chlorine dioxide, lithium, rubidium, halogens, or acetylide. o Mercury and methyl azide are shock and electrical discharge sensitive. o Pure dry ammonia and mercury do not react even under pressure and heat, but if water is present, a compound forms that can explode during depressurization. o Upper and lower explosive (flammable) limits in air are not available for mercury. FIRE FIGHTING INFORMATION: o Mercury is non-combustible. o The agent itself does not burn, but it may react upon heating to produce corrosive and/or toxic fumes. o Fire will produce irritating, corrosive, and/or toxic gases. 63
o Use an extinguishing agent suitable for the type of surrounding fire. o Do not direct water at the heated metal. o Run-off may pollute waterways. o If the situation allows, control and properly dispose of run-off (effluent). INITIAL ISOLATION AND PROTECTIVE ACTION DISTANCES: o When any large container is involved in a fire, consider initial evacuation for 0.33 mi (500 m) in all directions. o This agent is not included in the DOT ERG2004 Table of Initial Isolation and Protective Action Distances. o In the DOT ERG 2004 orange-bordered section of the guidebook, there are public safety recommendations to isolate a mercury (Guide 172) spill or leak area immediately for at least 150 ft (50 m) in all directions. PHYSICAL DANGERS: o Vapors are heavier than air and will collect and stay in poorly- ventilated or low-lying areas. o Hazardous concentrations may develop quickly in enclosed, poorly- ventilated, or low-lying areas. NFPA 704 Signal: o Health: 1 o Flammability: 0 o Reactivity: 0 o Special:
SAMPLING AND ANALYSIS: o OSHA: ID140 o NIOSH: 6009 ADDITIONAL SAMPLING AND ANALYSIS INFORMATION:
References are provided for the convenience of the reader and do not imply endorsement by NIOSH. 64
o AIR MATRIX Chatterjee S, Pillai A, Gupta VK [2002]. Spectrophotometric determination of mercury in environmental sample and fungicides based on its complex with o-carboxy phenyl diazoamino p- azobenzene. Talanta 57(3): 461-465. Abstract.
NIOSH [1994]. Mercury: Method 6009. In: NIOSH Manual of Analytical Methods. 4th ed. Cincinnati, OH: U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, DHHS (NIOSH) Publication No. 94-113.
OSHA [1989]. Particulate mercury in workplace atmospheres, mercury: OSHA-SLTC Method ID-145. Salt Lake City, Utah: U.S. Department of Labor, Occupational Safety and Health.
OSHA [1991]. Mercury vapor in workplace atmospheres: OSHA-SLTC Method ID-140. Salt Lake City, Utah: U.S. Department of Labor, Occupational Safety and Health.
Singhvi R, Turpin R, Kalnicky DJ, Patel J [2001]. Comparison of field and laboratory methods for monitoring metallic mercury vapor in indoor air. J Hazard Materials 83(1-2):1-10.
Temmerman E, Vandecasteele C, Vermeir G, Leyman R, Dams R [1990]. Sensitive determination of gaseous mercury in air by cold vapour atomic fluorescence spectrometry after amalgamation. Anal Chim Acta 236:371-376. Abstract.
Yu JC, Zhang B, Lai Y-K [2000]. Direct determination of mercury in atmospheric particulate matter by graphite plate filtration– electrothermal atomic absorption spectrometry with Zeeman background correction. Spectrochim Acta B Atom Spectrosc 55(4):395-402. o OTHER No references were identified for this sampling matrix for this agent. 65
o SOIL MATRIX Barshick CM, Barshick S-A, Britt PF, Lake DA, Vance MA, Walsh EB [1998]. Development of a technique for the analysis of inorganic mercury salts in soils by gas chromatography/mass spectrometry. Int J Mass Spectrom 178(1-2):31-41. Abstract.
Götzl A, Riepe W [2001]. Mercury determination –– SPME and colorimetric spot test. Talanta 54(5):821-827. Abstract.
López-García I, Sánchez-Merlos M, Hernández-Córdoba M [1997]. Determination of mercury in soils and sediments by graphite furnace atomic absorption spectrometry with slurry sampling. Spectrochim Acta B Atom Spectrosc 52(14):2085-2092. Abstract.
Moreda-Piñeiro J, López-Mahía P, Muniategui-Lorenzo S, Fernández- Fernández E, Prada-Rodríguez D [2002]. Direct mercury determination in aqueous slurries of environmental and biological samples by cold vapour generation–electrothermal atomic absorption spectrometry. Anal Chim Acta 460(1):111-122.
Vedrina-Dragojevic I, Dragojevic D, Cadež S [1997]. Spectrofluorimetric method for the determination of the total mercury content in sediment and soil. Anal Chim Acta 355(2-3):151- 156. Abstract. o SURFACES No references were identified for this sampling matrix for this agent. o WATER EPA [1994]. Determination of metals and trace elements in water and wastes by inductively coupled plasma-atomic emission spectrometry, Method 200.7. In: Methods for the determination of metals in environmental samples supplement 1. Cincinnati, OH: U.S. Environmental Protection Agency. (EPA/600/R-94/111), National Technical Information Service, PB95-125472.
EPA [1994].Mercury by cold vapor AA Spectrometry – Manual, Method 245.1. In: Methods for the determination of metals in environmental samples supplement 1. Cincinnati, OH: U.S. 66
Environmental Protection Agency. (EPA/600/R-94/111), National Technical Information Service, PB95-125472.
Signs/Symptoms
TIME COURSE: Symptoms develop within a few hours of exposure to mercury. EFFECTS OF SHORT-TERM (LESS THAN 8-HOURS) EXPOSURE: Exposure to high levels of elemental mercury vapor produces acute health effects. Respiratory symptoms predominate, and they include cough and difficulty breathing or shortness of breath (dyspnea). Gastrointestinal effects, such as metallic taste, nausea, vomiting (emesis), diarrhea, and abdominal pain, are frequent. Central nervous system (CNS) effects are also common, and they include headache, weakness, and vision changes. EYE EXPOSURE: o Irritation INGESTION EXPOSURE: o Ingestion does not normally result in whole-body (systemic) toxicity. INHALATION EXPOSURE: o Acute exposure to high levels of elemental mercury vapor may cause inflammation of the lungs (chemical pneumonitis), difficulty breathing or shortness of breath (dyspnea), chest pain, and dry cough. Effects may improve or, conversely, worsen, leading to fluid accumulation in the lungs (pulmonary edema), respiratory failure, and death. Acute toxicity may also cause kidney damage (sometimes severe) and kidney failure, rapid heart rate (tachycardia), and high blood pressure (hypertension). The patient/victim may have a metallic taste, salivation, difficulty swallowing (dysphagia), abdominal cramps, and diarrhea. Central nervous system (CNS) effects include headache, weakness, and visual disturbances. SKIN EXPOSURE: o Skin (dermal) reactions associated with skin contact with elemental mercury liquid or vapor are rare. o Rash or inflammation of the skin (contact dermatitis) are possible. o Acute contact with the skin does not normally result in whole-body (systemic) toxicity.
Decontamination 67
INTRODUCTION: The purpose of decontamination is to make an individual and/or their equipment safe by physically removing toxic substances quickly and effectively. Care should be taken during decontamination, because absorbed agent can be released from clothing and skin as a gas. Your Incident Commander will provide you with decontaminants specific for the agent released or the agent believed to have been released. DECONTAMINATION CORRIDOR: The following are recommendations to protect the first responders from the release area: o Position the decontamination corridor upwind and uphill of the hot zone. o The warm zone should include two decontamination corridors. One decontamination corridor is used to enter the warm zone and the other for exiting the warm zone into the cold zone. The decontamination zone for exiting should be upwind and uphill from the zone used to enter. o Decontamination area workers should wear appropriate PPE. See the PPE section of this card for detailed information. o A solution of detergent and water (which should have a pH value of at least 8 but should not exceed a pH value of 10.5) should be available for use in decontamination procedures. Soft brushes should be available to remove contamination from the PPE. o Labeled, durable 6-mil polyethylene bags should be available for disposal of contaminated PPE. INDIVIDUAL DECONTAMINATION: The following methods can be used to decontaminate an individual: o Decontamination of First Responder: . Begin washing PPE of the first responder using soap and water solution and a soft brush. Always move in a downward motion (from head to toe). Make sure to get into all areas, especially folds in the clothing. Wash and rinse (using cold or warm water) until the contaminant is thoroughly removed. . Remove PPE by rolling downward (from head to toe) and avoid pulling PPE off over the head. Remove the SCBA after other PPE has been removed. . Place all PPE in labeled durable 6-mil polyethylene bags.
o Decontamination of Patient/Victim: 68
. Remove the patient/victim from the contaminated area and into the decontamination corridor. . Remove all clothing (at least down to their undergarments) and place the clothing in a labeled durable 6-mil polyethylene bag. . Thoroughly wash and rinse (using cold or warm water) the contaminated skin of the patient/victim using a soap and water solution. Be careful not to break the patient/victim’s skin during the decontamination process, and cover all open wounds. . Cover the patient/victim to prevent shock and loss of body heat. . Move the patient/victim to an area where emergency medical treatment can be provided.
First Aid
GENERAL INFORMATION: Initial treatment is primarily supportive of respiratory and cardiovascular function. Use caution when administering intravenous (IV) fluids when fluid accumulation in the lungs (pulmonary edema) is present. ANTIDOTE: There is no antidote for mercury toxicity. Chelation therapy may be warranted in some patient/victims following an assessment by a physician. EYE: o Immediately remove the patient/victim from the source of exposure. o Immediately wash eyes with large amounts of tepid water for at least 15 minutes. o Seek medical attention immediately. INGESTION: o Immediately remove the patient/victim from the source of exposure. o Ensure that the patient/victim has an unobstructed airway. o Do not induce vomiting (emesis). o Do not administer activated charcoal. o Ingestion of small amounts of mercury does not normally require treatment (decontamination). 69
o If transport is necessary, prepare the transport vehicle in case the patient/victim vomits. The vomit may contain elemental mercury that can contaminate the transport vehicle. Have a suction apparatus ready and prepare several towels and double-sealable plastic bags to quickly clean and isolate vomitus. Only a professional mercury clean- up kit with a self-contained vacuum system should be used to decontaminate the transport vehicle. Ordinary vacuum cleaners can vaporize elemental mercury and increase the concentration of airborne mercury. o Seek medical attention immediately. INHALATION: o Immediately remove the patient/victim from the source of exposure. o Evaluate respiratory function and pulse. o Ensure that the patient/victim has an unobstructed airway. o If shortness of breath occurs or breathing is difficult (dyspnea), administer oxygen. o Assist ventilation as required. Always use a barrier or bag-valve-mask device. o If breathing has ceased (apnea), provide artificial respiration. o Seek medical attention immediately. SKIN: o Immediately remove the patient/victim from the source of exposure. o See the Decontamination section for patient/victim decontamination procedures. o Seek medical attention immediately.
See ATSDR Medical Management Guidelines for Acute Chemical Exposures, Elemental Mercury https://www.atsdr.cdc.gov/MHMI/mmg46.pdf, for detailed recommendations.
Long-Term Implications
MEDICAL TREATMENT: Chelation therapy may be considered for the patient/victim after consultation with a physician. However, the decision to chelate for a particular patient/victim should be made only by professionals experienced in the use of chelation, preferably in consultation with the regional poison control center. Chelation therapy becomes less effective in 70
reducing the severity of poisoning and the risk of aftereffects (sequelae) as time after exposure increases. DELAYED EFFECTS OF EXPOSURE: Several days after the initial exposure, symptoms include heavy salivation (ptyalism), inflammation of the intestines (enteritis), and kidney (renal) damage. There can also be chronic central nervous system (CNS) effects, which develop as a result of the ability of absorbed elemental mercury to cross the blood-brain barrier. The acute mercury-induced lung damage usually resolves completely, but some cases of diffuse increased fibrous tissue in the lung (pulmonary fibrosis), restrictive lung disease, and chronic respiratory insufficiency have been reported. EFFECTS OF CHRONIC OR REPEATED EXPOSURE: Mercury is not classifiable as a carcinogen. It is unknown whether chronic or repeated exposure to mercury increases the risk of reproductive toxicity or developmental toxicity. Chronic or repeated exposure to mercury may cause lymphocyte aneuploidy. Menstrual disorders (dysmenorrhea) have been reported in female workers chronically exposed to mercury. An increased incidence of spontaneous abortion has been reported among wives of men chronically exposed to mercury. Mercury is known to cross the placental barrier. Repeated or continuous exposure to elemental mercury can result in accumulation of mercury in the body and permanent damage to the nervous system and kidneys. Classic health effects of poisoning include neurological and psychiatric effects, loss of kidney function, and inflammation of the upper airway and throat. Neuropsychiatric effects include tremor, anxiety, readily or frequently changing emotions (emotional lability), forgetfulness, insomnia, loss of appetite (anorexia), fatigue, and disturbances of thought and movement.
On-Site Fatalities
INCIDENT SITE: o Consult with the Incident Commander regarding the agent dispersed, dissemination method, level of PPE required, location, geographic complications (if any), and the approximate number of remains. 71
o Coordinate responsibilities and prepare to enter the scene as part of the evaluation team along with the FBI HazMat Technician, local law enforcement evidence technician, and other relevant personnel. o Begin tracking remains using waterproof tags. RECOVERY AND ON-SITE MORGUE: o Wear PPE until all remains are deemed free of contamination. o Establish a preliminary (holding) morgue. o Gather evidence, and place it in a clearly labeled impervious container. Hand any evidence over to the FBI. o Remove and tag personal effects. o Perform a thorough external evaluation and a preliminary identification check. o See the Decontamination section for decontamination procedures. o Decontaminate remains before they are removed from the incident site.
See Guidelines for Mass Fatality Management During Terrorist Incidents Involving Chemical Agents, U.S. Army Soldier and Biological Chemical Command (SBCCOM), November, 2001 for detailed recommendations.
Occupational Exposure Limits
NIOSH REL: 3 o TWA (mercury vapor): 0.05 mg/m (skin) 3 o Ceiling: 0.1 mg/m (skin) OSHA PEL: 3 o Ceiling: 0.1 mg/m ACGIH TLV: 3 o TWA (8-hour): 0.025 mg/m NIOSH IDLH: 10 mg/m3
DOE TEEL: 3 o TEEL-0: 0.025 mg/m 3 o TEEL-1: 0.1 mg/m 3 o TEEL-2: 2.05 mg/m 3 o TEEL-3: 4.10 mg/m 72
AIHA ERPG: o ERPG-1: Not appropriate. o ERPG-2: 0.25 ppm o ERPG-3: 0.5 ppm
Acute Exposure Guidelines [Interim]
10 min 30 min 60 min 4 hr
AEGL 1 NR NR NR NR (discomfort, non-disabling) – mg/m3
AEGL 2 3.1 2.1 1.7 0.67 (irreversible or other serious, long-lasting effects or impaired ability to mg/m3 mg/m3 mg/m3 mg/m3 escape) – mg/m3
AEGL 3 16 mg/m3 11 mg/m3 8.9 2.2 mg/m (life-threatening effects or death) – mg/m3 mg/m3
NOTE THAT VALUES ARE IN mg/m3, NOT ppm
NR = Not recommended due to insufficient data
Technical Support Documentpdf iconexternal icon
IMPORTANT NOTE: Interim AEGLs are established following review and consideration by the National Advisory Committee for AEGLs (NAC/AEGL) of public comments on Proposed AEGLs. Interim AEGLs are available for use by organizations while awaiting NRC/NAS peer review and publication of Final AEGLs. Changes to Interim values and Technical Support Documents may occur prior to publication of Final AEGL values. In some cases, revised Interim values may be posted on this Web site, but the revised Interim Technical Support Document for the chemical may be subject to change. (Further information is available through AEGL Processexternal icon).
Decontamination (Environment and Equipment)
ENVIRONMENT/SPILLAGE DISPOSAL: The following methods can be used to decontaminate the environment/spillage disposal: 73
o Do not touch or walk through the spilled agent if at all possible. However, if you must, personnel should wear the appropriate PPE during environmental decontamination. See the PPE section of this card for detailed information. o Keep combustibles (e.g., wood, paper, and oil) away from the spilled agent. o Use water spray to reduce vapors or divert vapor cloud drift. Avoid allowing water runoff to contact the spilled agent. o Do not direct water at the spill or the source of the leak. o Stop the leak if it is possible to do so without risk to personnel, and turn leaking containers so that gas rather than liquid escapes. o Prevent entry into waterways, sewers, basements, or confined areas. o Isolate the area until gas has dispersed. o Ventilate the area. EQUIPMENT: Agents can seep into the crevices of equipment making it dangerous to handle. The following methods can be used to decontaminate equipment: o Not established/determined
Agent Properties
Chemical Formula: Hg Aqueous solubility: Soluble Boiling Point: 674°F (356.72°C) Density: Liquid: 13.534 at 77°F (25°C) (water = 1) Gas: 6.93 (air = 1) Flammability: Not combustible Flashpoint: Not established/determined Ionization potential: Not established/determined 74
Log Kbenzene-water: Not established/determined
Log Kow (estimated): 0.62 Melting Point: -102°F (-38.87°C) Molecular Mass: 200.59 Soluble In: Organic solvents Specific Gravity: 13.6 at 77°F (25°C) Vapor Pressure: 0.002 mm Hg at 77°F (25°C) Volatility: Slightly volatile at room temperature. Significantly more volatile when heated.
Hazardous Materials Warning Labels/Placards
Shipping Name: Mercury Identification Number: 2809 (Guide 172) Hazardous Class or Division: 8 Subsidiary Hazardous Class or Division: Label: Corrosive Placard Image:
Trade Names and Other Synonyms
Colloidal mercury 75
Hg Hydrargyrum Kwik (Dutch) Mercure (French) Mercurio (Italian)
Mercury (Hg) Mercury metal Mercury vapor Metallic mercury Quecksilber (German) Quick silver
Who to Contact in an Emergency
In the event of a poison emergency, call the poison center immediately at 1-800- 222-1222. If the person who is poisoned cannot wake up, has a hard time breathing, or has convulsions, call 911 emergency services.
For information on who to contact in an emergency, see the CDC website at emergency.cdc.gov or call the CDC public response hotline at (888) 246-2675 (English), (888) 246-2857 (Español), or (866) 874-2646 (TTY).
Important Notice
The user should verify compliance of the cards with the relevant STATE or TERRITORY legislation before use. NIOSH, CDC 2003.
76
10.) A mercury safe practice is one in which: A. No amalgam fillings are placed B. Protective protocols are in place for preventing patient exposure to mercury during amalgam removal C. Dentist and staff are also protected with proper protocols D. Environmental mercury contamination is avoided by using an amalgam separator for the office wastewater E. All of the above
https://www.dentalwellness4u.com/layperson/mercurysafedentists.html https://www.sciencedirect.com/science/article/pii/S0377529113000059
Mercury Safe and Mercury Free Dentists: What They Do and Why They Do It Why Dentists are Mercury Free and Mercury Safe Dental schools still teach dentists to use mercury amalgam (silver) fillings and the American Dental Association (ADA) continues to tell the public they are safe. But recently more and more questions have been raised about the safety of the mercury vapor released from amalgam fillings by various forms of stimulatio n. This has resulted in a controversy and an ongoing debate about them - with some dentists saying they are safe and some saying they aren’t. This has now evolved to the point where over 50% of practicing dentists are no longer putting mercury amalgam fillings in their patients’ teeth. In fact, three countries, Norway, Sweden and Denmark have banned the use of these fillings in the dental practice.
The controversy has also made dentists rethink what they were taught in dental school. After extensive research (including reading Dr. McGuire’s book The Poison in Your Teeth: Mercury Amalgam (Silver) Fillings . . . Hazardous to Your Health), and information provided on the ADA’s website, many dentists have concluded that it would no longer be in the best interests of their patients to offer mercury amalgam as a filling material and became amalgam free.
In addition, because it has been proven that unsafe levels of toxic mercury vapor are released when amalgam fillings are unsfely removed, Mercury Safe dentists have made their offices as mercury safe as possible. To that purpose, these dentists use state-of-the art technology, equipment, and safe removal protocols, to protect their patients, their staff, themselves and the environment from excessive, and unnecessary, occupational exposure to mercury at the dental office. In doing so they've now made their practices both Mercury Free (amalgam silver filling free) and Occupationally Mercury Safe.
Becoming both a Mercury Free (amalgam/silver filling free) and Mercury Safe dental practice is a decision made by the individual dentist - but they all believe that deciding whether or not to have your existing mercury amalgam fillings removed and replaced must be your choice, and your choice alone. Because they place great importance on Patient Education, they feel it is their responsibility to educate their patients about the relationship of oral to overall issues and to provide them with the information required for them to make educated decisions. That is why many dentists provide Dr. McGuire’s books and why they also encourage patients to go to the ADA’s website (www.ada.org) to learn more about the pros and cons of removing, or keeping, mercury amalgam silver fillings. But again, every mercury safe dentist will make it clear that the decision to remove and replace mercuryt amalgam fillings can, and should only, be made by the patient.
Mercury Free and Mercury Safe Dentists: What's the Difference? Dentists who are both Mercury Free (amalgam/silver filling free) and Mercury Safe want their patients to know that there is a significant difference between the two. As a patient it is also very important to know the difference between the two - because more and more dentists are becoming Mercury Free but are still not Mercury Safe. 77
Strictly speaking, the term “Mercury Free” refers to dentists who do not put amalgam silver fillings in their patients’ teeth. This term was first used over 40 years ago by dentists who wanted to distinguish themselves from other dentists who believed that mercury amalgams were safe and continued to use them.
However, the term Mercury Free wasn’t a truly accurate description because even dentists who didn’t put in amalgam fillings still had to remove them – and the unsafe removal process released excessive and unnecessary amounts of toxic mercury vapor. But while being Mercury Free was a good beginning - it solved only part of the problem.
Over time, dentists who were Mercury Free developed protocols and equipment that allowed them to dramatically minimize a patient’s exposure to mercury during the amalgam removal process. In effect, using these protocols meant that their practices were not just Mercury (amalgam) Free - but also were now Mercury Safe – yet they erroneously continued to only use the term Mercury Free to describe themselves. But times have changed and the term "Mercury Free" is not only inadequate but confusing and misleading!
Today it is no longer enough for a dentist who is both Mercury (amalgam) Free and Mercury Safe to just promote his or her practice as only being Mercury Free. Why? Recently a survey showed that 52% of general dentists no longer use amalgam and call themselves Mercury Free. But, and this is important for every dental patient to know; not because they were concerned about safely removing them – but mainly because they no longer felt amalgam was a good filling material when compared to the newer composite fillings.
This of course has created a dilemma for patients who believed that dentists who said they were Mercury (amalgam filling ) Free meant they also used protocols to safely remove amalgam fillings. But patients are catching on and now look for dentists who will safely remove their amalgam fillings and now ask this question of the dentist: “Are you both Mercury Free and Mercury Safe?” Bottom line . . . you can’t assume that a dentist who advertises his or her practice as being Mercury - amalgam fiilling- Free, is also Mercury Safe – unless you ask!
The Main Difference between a Mercury Safe Dentist and a Dentist who is only Mercury Free Unsafe removal of amalgam/silver fillings can generate huge amounts of toxic mercury vapor, easily over 100 times more than the maximum levels of mercury vapor allowed by all government regulatory agencies. What really separates Mercury Safe Dentists from those who are 'only' Mercury Free, is their understanding that:
• When unsafely removed, amalgam fillings release excessive and unnecessary amounts of poisonous mercury vapor. • The mercury released from amalgam fillings negatively affects themselves, the patient, the staff, and the environment. • Patients absolutely need to be protected from exposure to toxic mercury vapor during the amalgam removal process.
Mercury Safe Dentists also have the specialized equipment, training, experience, and skills necessary to minimize their patients’ exposure to mercury during amalgam removal. If you want to protect yourself from excessive and unnecessary occupational exposure to mercury vapor at the dental office make sure your dentist is not just Mercury Free - but also Mercury Safe!
Abstract The rules governing the use of metallic mercury, a toxic and hazardous chemical, is in most jurisdictions identical to widely accepted standards and practices for handling 78
the same chemical in industry for the protection of humans and their work environment. There cannot be exceptions solely for the practitioner dentists and their patients. Any workplace must be safe for both workers and visitors. The latter being dental patients waiting in the dentist's work environment. We reviewed the literature for toxic health effects of elemental mercury upon humans and present information about the Minimata Convention convened by the United Nations Environment Programme. A study conducted among dentists in Singapore and their personal work environment almost 30 years ago contributed to the workplace standard for elemental mercury, which was reduced, and is still currently enforced as a global standard. We recommend that dentists, with a large alternative battery of restorative materials today, make selection of a restorative material a more seriously considered choice, and not to make use of amalgam without the proper use of personal protective equipment for themselves (members of the dental operating team) and their patients, (amalgam traps and judicious monitoring of their workplace air quality). Mercury is ubiquitous in our presence due to human activities; any reduction in the dentists' workplace contributes to a global reduction. Previous Next article in issue Keywordsarticle in issue Occupational health
Mercury toxicity
Safety of workplace 1. Introduction Mercury is ubiquitous. Mercury occurs naturally in the environment and exists in several forms [1]. Elemental mercury is used in many industrial processes and manufactured products, including but not limited to, manufacture of soaps, detergents, and fluorescent bulbs, in production of sulphuric acid, in gold mining, in batteries and so on. All forms of mercury, namely, metallic or elemental forms as used in dentistry for the manufacture of dental silver amalgam during restorative dentistry; organic forms as existing in fish, pesticides and other bonded-chemicals and inorganic mercury, at times mercuric oxide used as the red coating for traditional herbal 79
remedies, are present in our human environment through usage. Consequently mercury is present in our human environment from manufacturing to waste disposal and finally as waste in our midst. This mercury could be in the air we breathe, in the food we consume, also in antiseptics or antifungals we come in contact with daily as hand wash, or in vaccinations as the preservative Thiormersal® [2] found in vaccines. In the 1980s, the first author conducted a study of the neurobehavioral effects of mercury of 98 actively-practising Singapore dentist volunteers, dentists who were occupationally exposed to elemental mercury [3]. As the range of dental materials was then limited, some of these dentists used mercury and amalgam almost exclusively as the only restorative material for all posterior teeth in their practices, where aesthetics was not a prominent patient consideration. Note also that patients in those days were not as demanding with regards to anaesthetics as they might be today. Although the “controls” were also investigated, their mercury data remain unpublished as part of a doctoral thesis within the National University of Singapore Medical Library archive. 2. Human exposure to different forms of mercury This hygiene fact from the US Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry is well acknowledged
“A person can be exposed to mercury from breathing in contaminated air, from swallowing or eating contaminated water or food, or from having skin contact with mercury. Not all forms of mercury enter your body easily, even if they come in contact with it; so it is important to know which form of mercury you have been exposed to, and by which route (air, food, or skin). When you swallow small amounts of metallic mercury, virtually none (less than 0.01%) of the mercury will enter your body through the stomach or intestines, unless they are diseased. …When you breathe in mercury vapours, (from elemental mercury), however, most (about 80%) of the mercury enters your bloodstream directly from your lungs, and then rapidly goes to other parts of your body, including the brain and kidneys. Once in your body, metallic mercury can stay for weeks or months. When metallic mercury enters the brain, it is readily converted to an inorganic form and is “trapped” in the brain for a long time. Metallic mercury in the blood of a pregnant woman can enter her developing child [1]”. Mercury crosses the placental barrier easily to affect the developing foetus. What effects this may have is however only reflected in the case study reports. However 80
research conducted by the author showed neurobehavioral changes in test subjects even when they were exposed to very low levels of mercury, levels below that established for applications in industry and dentistry. In that study we examined 96 24–49 year-old dentists and compared them to 56 control subjects. The results however, apply only to adults [4]. In a case report of an accident involving four adults in 1983, including a pregnant woman and her new-born infant, Lien et al. reported that although the baby was born without reportable abnormalities within 26 days of the accidental exposure to mercury vapour, the baby had blood levels of mercury that were comparable to the mother indicating direct and free transfer of the metal across the placental barrier [5]. This study adds to the evidence that breathing in mercury vapour crosses the placental barrier and mercury crosses into the foetus when mother is exposed to mercury vapour. Likewise, mercury crosses the blood brain barrier easily to affect the developing foetus. What effects this may have, have not been fully elucidated. However, since in the research conducted on adults, even very low levels of exposure, levels below that established as safe by authorities, led to neurobehavioral changes in adults, the question of how much mercury is acceptable in air in the operatory as we use amalgam is raised. Hygiene considerations for mercury used in dentistry for the manufacturing of dental amalgam, comprising 50% metallic mercury, must have no exceptions from similar industrial applications in terms of health and safety regulations. Mercury used is identical for both dentistry and chlor-alkaline industry, or in the industry manufacturing fluorescent tubes or mercury-fumed street lighting bulbs, commonly seen along roads and highways. It is certain that mercury has extensive applications for products that result in human benefits. Along with this, humans are also exposed to the well documented toxic effects, similar as the mercury leaching from the dental amalgam fillings in our oral cavities and also a constant source of dentist's work environmental pollution wherever mercury is stored and used. Dufault et al. [6] reported that many food products are now made using such mercury- cell chlor-alkaline industry applications. They concluded that with respect to total mercury exposure in children and sensitive population, consumption of high fructose corn syrup also had insidious mercury ranging from 0.005 to 0.670 μg mercury/g 81
of sweetener. They reported that average daily consumption was approximately 50 g/person in the US in 2009. 3. What are the toxic effects of elemental mercury that require attention? The US's Centre for Disease Control, published this review in 1999 and updated that in 2006, stating
“The nervous system is very sensitive to mercury … Permanent damage to the brain has also been shown to occur from exposure to sufficiently high levels of metallic mercury. … Metallic mercury vapours or organic mercury may affect many different areas of the brain and their associated functions, resulting in a variety of symptoms. These include personality changes irritability, shyness, nervousness), tremors, changes in vision (constriction (or narrowing) of the visual field), deafness, muscle incoordination, loss of sensation, and difficulties with memory [1]”. Similarly, in the same review [1] based upon occupational exposure of elemental mercury at higher concentrations, as in the chlor-alkali industry, where chlorine and alkali are products from the electrolysis of seawater using pans of elemental mercury as the electrode, the toxic effects were stated as “Short-term exposure (hours) to high levels of metallic mercury vapour in the air can damage the lining of the mouth and irritate the lungs and airways, causing tightness of the breath, a burning sensation in the lungs, and coughing. Other effects from exposure to mercury vapour include nausea, vomiting, diarrhoea, increases in blood pressure or heart rate, skin rashes, and eye irritation. Damage to the lining of the mouth and lungs can also occur from exposure to lower levels of mercury vapour over longer periods (for example, in some occupations where workers were exposed to mercury for many years). Levels of metallic mercury in workplace air are generally much greater than the levels normally encountered by the general population. Current levels of mercury in workplace air are low, due to increased awareness of mercury's toxic effects. Because of the reduction in the allowable amount of mercury in workplace air, fewer workers are expected to have symptoms of mercury toxicity”. The confirmation of toxic effects relies upon animal studies, and not solely upon observations in humans, 82
“To protect the public from the harmful effects of toxic chemicals and to find ways to treat people who have been harmed, scientists use many tests. One way to see if a chemical will hurt people is to learn how the chemical is absorbed, used, and released by the body; for some chemicals, animal testing may be necessary” [7]. There is now sufficient data in global occupational safety databases to support this fact: mercury is highly toxic to humans, yet a controversy exists.
The US FDA webpage at the time of writing this article (2013) offered consumers the following hygiene advice:
“FDA has reviewed the best available scientific evidence to determine whether the low levels of mercury vapour associated with dental amalgam fillings are a cause for concern. Based on this evidence, FDA considers dental amalgam fillings safe for adults and children ages 6 and above. The amount of mercury measured in the bodies of people with dental amalgam fillings is well below levels associated with adverse health effects. Even in adults and children ages 6 and above who have fifteen or more amalgam surfaces, mercury exposure due to dental amalgam fillings has been found to be far below the lowest levels associated with harm. Clinical studies in adults and children ages 6 and above have also found no link between dental amalgam fillings and health problems [8]”. From the above, we see that amalgam restorations are deemed to be safe, by the FDA, in children 6 years old and above. However, there have been reports that eating and chewing releases mercury from fillings [9], [10]. It seems contradictory therefore that there should be regulations enacted for chronic inhalation exposure of mercury as enforced by the US Environmental Protection Agency (EPA) [11], when another US government agency the FDA deems it safe for amalgam to be used in fillings. While this political debate rages on globally, the authors here are of the view that mercury, whether used in dentistry or industry, is still mercury. Safe hygienic principles are required whenever the dentist's personal choice is to use dental amalgam as his restorative material. There cannot be any exceptions from industrial practice for the practising dentist for safe handling of mercury. A comprehensive review of the effect of mercury on humans and animals has been published in the Journal of the Federation of American Societies for Experimental Biology (FASEB) 1995 and the article is available free online at 〈 83
http://www.ncbi.nlm.nih.gov/pubmed/7737458〉. The effects of mercury on the immune system, kidney glomerular physiology, intestinal bacteria of both humans and animals, amongst others, are discussed. 4. Global conventions, regulations and the dental operatory environment A vast and substantial data had been presented to any interested reader for the safe handling of this toxic chemical: elemental mercury, because use of mercury is as old as antiquity. In the following section, we elaborate the rationale for the growing database of pharmacokinetics and pharmacodynamics attributes linked to mercury's safety and along with this the regulations to ensure the safety, health, rights and well- being of all workers, including the practitioner-dentist, and their patients. The patients may be told to be exposed to a lesser degree in the toxic environment of the dentist's operatory, but the rationale of public health administration based upon the scientific principles from hygiene, is that patient has a right to know of their environment, be this work environment or just for the visit to their dentist. In addition, the patients are duly required to be fully informed under clinical practice ethics as under clinical research situations, of what may happen to mercury that was implanted as dental amalgam restorations in their dentition – permanent or deciduous. The waiting room of the dental practitioner is required to be environmentally assayed for presence of safe levels of elemental mercury vapour on a daily or periodic basis whenever mercury is present in the clinic. We, as humans, have a right to know and to be duly informed of our environment – work or recreational or homes and places we visit from time to time, including a shopping centre. In a Singapore law, this is within the scope and ambit of our Workplace Safety and Health Act 2006, revised Chapter 354A in 2009. However, the safety of placement of mercury within the dental amalgam (device) for restorative purposes is not in this legislation, but is regulated separately as detailed above by the US FDA, as a Class II medical device. The environment of the dental clinic in the US is governed by the Occupational Safety and Health Administration (OSHA), which published a pamphlet about standards for dealing with mercury in the work environment [12]. The Singapore legislations, as revised Chapter 354A, were enacted after much consultation with the OSHA regulations. In this aspect, one will note the emphasis on air quality and methods of mopping up mercury spills. The current OSHA permissible exposure limit (PEL) for mercury vapour is 0.1 mg/m3 of air as a ceiling limit. A worker's exposure to mercury 84
vapour shall at no time exceed this ceiling level. From the perspective of hygiene, another index for assessing human exposure based upon personal dosimetry is preferred and more realistic, namely that of inhaled mercury toxicity. This is because the ceiling PEL may not be at all reflective of the practising dentist's real-time exposure. The preferred standard for safety is the EPA's “Reference concentration for Chronic inhalation exposure” [10] index computed by personal dosimetry breathing zone studies. Similar in design to the first author's dosimetry study of 1992, a more recent dosimetry study of 180 dentists, Ritchie et al. [13], reported that dentists were found to have on average urinary mercury levels four times that of control subjects, dentists were significantly more likely to have suffered from kidney disorders and that dentists were advised to put greater emphasis on the safe handling of dental amalgam within their practice environment by periodic hygiene surveillance using personal dosimetry monitoring. He further commented, 122 (67.8%) of the 180 surgeries visited had environmental mercury measurements in one or more areas above the Occupational Exposure Standard (OES) set by the Health and Safety Executive of UK. In the majority of these surgeries the high levels of mercury were found at the skirting and around the base of the dental chair. In 45 surgeries (25%) the personal dosimeter measurement (i.e. in the breathing zone of dental staff) was above the OES. Note the UK's OES is the same concentration as the EPA's Reference Concentration for Chronic Inhalation Exposure (RfC), at 25 μg/m3 air for 8 h a day, 40 h per week; this occupational hygiene standard for “lowest-observed-adverse-effect level” (LOAEL: 0.025 mg/m3 air) was derived from several studies, one of which was by the first author [3]. Note that the EPA's IRIS for the RfC stated “no-observed-adverse- effect level” (NOAEL) as “None” [8]. This means that mercury is very toxic at any concentration, even at the minimum lowest as yet undetermined because of limitation of our diagnostic tools. Mercury hygiene practice in dentistry should be similar to that in industry and should have the same regulations as they are about prevention of the same thing – mercury poisoning and long term health effects of mercury exposure amongst workers. To this end we should all realise that the United Nations Environment programme has a Global Mercury Partnership, the aims of which include promoting the development of national inventories of mercury uses and releases; developing strategies for enhanced 85
outreach and risk communication activities to reach at-risk populations, including sensitive populations; increasing public awareness and promotion of mercury-free products, technologies and processes, using and/or with environmentally friendly alternatives; promoting application and sharing of information on best available techniques and measures to reduce mercury emissions from point sources, among others [14]. In another United Nations convention, namely the Minamata Convention of 2013, it was specifically agreed that “Certain kinds of non-electronic medical devices such as thermometers and blood pressure devices are also included for phase-out by 2020. Governments approved exceptions for some large measuring devices where currently there are no mercury- free alternatives. Vaccines where mercury is used as a preservative have been excluded from the treaty as have products used in religious or traditional activities. Delegates agreed to a phase-down of the use of dental fillings using mercury amalgam”.
Independently, the European Union, the US and Japan have all declared bans on export of mercury since about 2008 [15].
What do all these activities mean to practising dentists in Singapore? It is quite obvious that over next decades it would be more difficult to obtain mercury and hence as a profession we need to work at being good at using alternative restorative products and remain as successful as before in restoring teeth. The United Nations Environment Programme (UNEP) has published a pamphlet on “Mercury Use in Healthcare Settings and Dentistry” and is available online as a downloadable portable document file [16]. In that document, dentists, including their clinic operatory support staff, will learn how to store mercury and how to mop up spills of mercury. It also advises removal of amalgam fillings in chunks rather than grinding it down completely, use of finer mesh to trap amalgam waste (100 rather than 40 units for sieve traps) which were endorsed for ISO 14011 Environmental Management audit procedures, namely, use amalgam traps that are certified ISO 11143. For a detailed description and management of dental amalgam wastes, some countries have legislations that waste water emitted from any dental clinic be subjected to audits for compliance, and cannot exceed 100– 2000 ppm of mercury in waste water [17]. 86
The UNEP also stated – not to place or remove amalgam fillings in pregnant ladies. It further stressed, “Treat extracted teeth with amalgam fillings as amalgam waste. Waste amalgam should be kept sealed in plastic containers. Waste amalgam may be disposed by licenced waste disposal companies who will recycle mercury and other metals”. Similarly, the American Dental Association has published a 2007 pamphlet on the “Best Management Practices for Amalgam Waste” and this is available online as a downloadable portable document file [18]. 5. Safe removal of dental amalgam restorations The measurable level of mercury in blood and plasma is correlated with the number of surfaces of fillings that are of amalgam in the oral cavity. Higher number of fillings of amalgam is correlated with a higher blood and plasma levels of mercury. Upon removal, within 3–48 h, there was a rise in the level of mercury in blood and plasma. Thereafter, there was a decline [19]. It is therefore important to follow a strict protocol to reduce patient exposure to mercury during removal. It had been recommended that hair covers, body drape, eye protection and rubber dam together with a high vacuum suction be used during amalgam removal [20]. Water coolant is important during removal as more mercury vapour is released from amalgams when the temperature increases. It may be important for signage be displayed so that everyone, workers and visitors are cautioned about the presence, from storing, using and disposing, of elemental mercury in the workplace, namely the dental clinic.
6. Dentist's choice in use of dental amalgam and informed consent documentation from patients as a good practice procedure Despite the advantages that bonding seems to provide, various studies comparing longevity of fillings of amalgam and composites have shown that amalgam is the more tolerant material and despite poor technique, such as poor moisture control during placement, is as lasting as composite restorations. Roulet [21] reported that amalgam shows excellent longevity data with studies up to 20 years; the average annual failure rate was 0.3–6.9%. Posterior composites were in the same range (0.5– 6.6%); however, the study times were much shorter (max. 10 years). However, it was pointed out that composite restorations took longer to place. A more recent study 87
comparing amalgams versus composites in posterior teeth showed that amalgam restorations lasted statistically significantly longer [22]. When composites failed, they deteriorated rapidly. It is no wonder therefore that dental schools continue to teach and practitioners continue to choose the use of amalgam restorations. Despite its advantages, informed consent is required in some jurisdictions (by regulations) during placement of dental amalgams, much similar to the clinical research environment. In Europe, the federal governments of Norway, Finland, Denmark, and Sweden have enacted legislation requiring that dental patients receive due process of documentation with regards to adequate informed consent information provided prior to their decision for receiving the type of dental restorative material that will be used and implanted. This is prior to the actual amalgam placement by the dentist. In the US, a few state governments have enacted similar informed consent legislation for dental patients receiving dental restorations. These state legislations were enacted by Maine, California, Connecticut, and Vermont. There is a similar need for informed consent procedure for dentists who use mercury amalgam restorative material as well as technical considerations in such information during removal of dental amalgam restorations [23]. While such regulations does not apply in Singapore and we have not yet enacted these regulations, it is in the prudent opinion of the author that we take and document full informed consent for using any restorative material. Informed consent here means giving a patient adequate information concerning the materials, providing adequate opportunity for the subject to consider all options, responding to the subject's questions, ensuring that the subject has comprehended this information, obtaining the subject's voluntary agreement to choose a material and continuing to provide information as the subject or situation requires. Patients should also be informed that bleaching teeth with amalgam restorations risks increasing the release of mercury vapour from amalgams [24]. Note that composites are not free of hazards. Composites leach oestrogenic monomers into the environment in concentrations at which biologic effects have been demonstrated in in vivo experimental models [25]. The US's Centres for Disease Control and Prevention published a free booklet “NIOSH Pocket Guide to Chemical hazards” from the US' National Institute for Occupational Safety and Health (NIOSH) which is applicable to the constant surveillance of the workplace for any air-borne mercury levels for alerting the 88
inhabitants of the clinic to dangerous levels and what preventive steps to be taken to control and avoid such hazardous situations. Note that the dental clinic could be located within a shopping centre or in the hospital with lots of humans potentially being exposed. The CDC has evidence to label elemental mercury inhalation as “Lung Damaging Agent”.
In this booklet and the Emergency Response Card [26], [27] data, the dental practitioner using dental amalgam is advised to read about measurement and monitoring methods, as in personal dosimeter for the operator and the dental chairside assistants. There are now rapid reading assays to gather such data. Next, the type of personal protective equipment, ranging from respirators and facemasks with filters, some reusable and others single use types, are also listed. This Emergency Response Card contains the different types of PPE to be used for the various alert levels. It is advisable for all practising dentists using mercury as restorative material, to read and train their staff for workplace hygiene maintenance on a weekly basis. The FDA has provided guidance that amalgams should be used in adults and children 6 years of age and above. Mercury is highly toxic. Its immediate effect from inhalation is as appropriately named “Lung Damaging Agent”. When mercury is allowed to enter the dental clinic, the chances of such exposure is ever present. The only way to prevent such occurrence is to eliminate the use of such materials for restorative dentistry applications. Amalgam has been used as fillings for about 150 years and has served dentistry well. As mercury is ubiquitous in the environment it will always be measurable in blood and urine. Though a number of patients have reported hypersensitivity to amalgams, the large majority of patients with amalgam fillings have not, albeit neurobehavioral deficits may affect those chronically exposed to mercury, such as dentists. When choosing to use amalgams, dentists should have the safety of their team members and patients in mind and should conduct audits with respect to amalgam hygiene and make the choice to be safe. Acknowledgement This paper was reviewed by a practising dental clinician with many years of experience in management of dental clinics, Associate Professor Sum Chee Peng, who made critical suggestions for additions, which were all incorporated because of their relevance. The authors herein wished to state their appreciations for the suggested 89
improvements. There is no conflict of interests, whether financial or otherwise with regards to the contents presented herein. The authors were not paid by any third party and declared that they received no financial contribution to write this publication with regards to the controversy regarding the legal status of dental amalgam as a medical device approved for use by humans in humans.
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11.) The purpose of using a rubber dam is to A. Prevent mercury amalgam particles from lodging in the oral mucosal tissue. B. Isolate the tooth or teeth being worked on C. Make it easier to evacuate the filling material and prevent amalgam particles from being swallowed D. Offer an isolated and dry field for placing the composite filling E. All of the Above https://www.rdhmag.com/articles/print/volume-38/issue-3/content/dammed-if- you-do-dammed-if-you-don-t.html
How a rubber dam during dental procedures improves treatment and quality of care By Staci Violante, RDH, BSDH, MSDH A dental or rubber dam, also known as a Kofferdam, is a thin, six-inch, latex or nitrile square sheet that is used in dentistry as a shield to isolate one or more teeth from the remainder of the mouth during a dental procedure. The rubber dam is used in dentistry mainly for endodontic, fixed prosthodontic (crowns and bridges), and restorative procedures. Aside from isolating the treatment or operative site, “the purpose of the rubber dam is to prevent saliva from interfering with the dental work, such as contamination of oral microorganisms during root canal therapy, or to keep fillingmaterials such as compositedry during placement and curing, and to prevent instruments and materials from being aspirated, swallowed, or damaging the mouth.”1 Consider this analogy: A doctor uses surgical drapes to isolate the area of the body being operated on to prevent bacterial contamination from occurring; this is the equivalent of a dentist using a rubber dam for a dental procedure where isolation is necessary.
The dental dam The dental dam is detained over a single tooth or multiple teeth by the appropriate rubber dam clamps over the anchor tooth. The tooth crowns protrude out from the rubber dam through the individual holes made by a hole punch, isolating the tooth to be treated from the rest of the patient’s mouth. This keeps the tooth dry and reduces the risk of 91 exposure to microorganisms. Listed below are several advantages and disadvantages of using a rubber dam during a dental procedure.2
The advantages of using a rubber dam:
enhances visibility of the treatment site since the dam retracts the cheeks and lips
reduces the risk of the patient swallowing instruments or debris
reduces the risk of contamination of oral microorganisms in the blood and/or saliva
provides a clean and dry operating field that is free of saliva, blood, and debris from the procedure, as well as achieves maximum bond strength when using restorative materials and cements
reduces mercury exposure when using amalgam materials in the mouth; 92
reduces aerosol splatters in the oral cavity from dental procedures;
protects dentists, hygienists, and patients from possible exposure to HIV, hepatitis, and other infectious diseases or blood-borne pathogens during procedures
The disadvantages of using a rubber dam:
additional application time, which can be difficult and time- consuming
additional cost of materials: stamp, dental clamps, rubber dam, frame
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rubber dam could break in the patient’s mouth, thus floss is placed around the clamp as a precaution for retrieval
could cause damage to the oral mucosa during placement and removal of the dam
patient may have discomfort or difficulty breathing due to blockage of the airway
if the rubber dam is latex, it could cause a latex allergy or episode to occur
may decrease communication between patient and operator
may increase patient anxiety
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many patients refuse the rubber dam
When using a rubber dam in any dental procedure, not only does it isolate the tooth or teeth and offer better visibility for the dentist to focus, but most importantly, the rubber dam also keeps bacteria and saliva far from the treatment area to prevent infection and contamination.
There are more significant advantages in using a rubber dam during dental treatment than not. A rubber dam essentially limits the spread of bacteria to the isolated tooth during a procedure, as well as prevents that same bacteria from being swallowed or absorbed internally. In fact, the rubber dam is mandatory for certain endodontic procedures in the United States, and according to the American Association of Endodontists, it should be the required standard of care. It is a recommended universal precaution in Centers for Disease Control and Prevention statements on infection control in dental care practice. Additionally, the rubber dam adds protection for dentists by decreasing liability should a patient swallow or choke on something during treatment.1
How to prompt patients to dam it! Generally, use of the rubber dam during dental procedures is not a problem for patients. However, persuading some patients to have a rubber dam placed before their procedures can be a daunting task. For patients who simply cannot breathe through their noses, having a rubber sheet over the face that blocks their airway can be extremely uncomfortable and claustrophobic. This can lead to difficulty breathing and may cause gagging. It is imperative that safety measures also be taken for patients with latex allergies. Latex-free options are available in all products today. A positive approach about rubber dam use by dentists and team members—along with their consistent use on patients—are major components that can work together to generate greater patient acceptance of them in the dental practice. 95
“Although some studies suggest that many dentists are foregoing the use of dental dams, most professional associations, including the American Dental Association, advocate their use and make a point of including them in training dental professionals.”3 When using a rubber dam in any dental procedure, not only does it isolate the tooth or teeth and offer better visibility for the dentist to focus, but most importantly, the rubber dam also keeps bacteria and saliva far from the treatment area to prevent infection and contamination.
Using a rubber dam for dental procedures should be mandated, but until then, when choosing to use a rubber dam, it is best to explain to the patient that the rubber dam will improve the completed treatment and the quality of care for the patient.
STACI VIOLANTE, RDH, BSDH, MSDH, graduated from the New York University College of Dentistry Dental Hygiene Program in 1997. She went on to complete her master’s degree at the Fones School of Dental Hygiene at the University of Bridgeport. She has been a practicing clinical dental hygienist for the past 20 years, as well as serving as clinical professor in the dental hygiene department at New York University College of Dentistry. She is currently pursuing her doctorate of health science in education.
References 1. Centers for Disease Control and Prevention. Guidelines for Infection Control in Dental Health-Care Settings—2003. MMWR. 2003;52(No. RR-17):1-76. https://www.cdc.gov/mmwr/PDF/rr/rr5217.pdf
2. Gilbert GH, Litaker MS, Pihlstrom DJ, Amundson CW, Gordan VV, DPBRN Collaborative Group. Rubber dam use during routine operative dentistry procedures: findings from the Dental PBRN. Oper Dent. 2010;35(5):491-499. doi: 10.2341/09-287C.
3. Glossary of dental clinical and administrative terms: rubber dam. Code on dental procedures and nomenclature. American Dental Association website. Accessed 96
2017. http://www.ada.org/en/publications/cdt/glossary-of-dental- clinical-and-administrative-ter#r.
4. Perrine GA. A simplified rubber-dam technique for preparing teeth for indirect restorations. J Am Dent Assoc. 2005;136(11):1560-1561.
5. Reuter JE. The isolation of teeth and the protection of the patient during endodontic treatment. Int Endod J. 1983;16(4):173-181.
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12.) Silver fillings can be composed of?
A. A. Hg Mercury A. B. Cu Copper B. C. Tn Tin C. D. Zn Zinc D. E. Ag Silver F. All of the above
https://www.epa.gov/mercury/mercury-dental-amalgam
What are Dental Amalgam Fillings? Sometimes referred to as “silver filling,” dental amalgam is a silver-colored material used to fill (restore) teeth that have cavities. Dental amalgam is made of two nearly equal parts:
liquid mercury, and a powder containing silver, tin, copper, zinc and other metals.
Amalgam is one of the most commonly used tooth fillings, and is considered a safe, sound, and effective treatment for tooth decay.
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Are Dental Amalgam Fillings Safe?
When amalgam fillings are placed in or removed from teeth, they can release a small amount of mercury vapor. Amalgam can also release small amounts of mercury vapor during chewing. People can absorb these vapors by inhaling or ingesting them. However, the U.S. Food and Drug Administration (FDA) considers dental amalgam fillings safe for adults and children over the age of six.
FDA regulates dental amalgam as a medical device. FDA is responsible for ensuring that dental amalgam is reasonably safe and effective. Among other things, FDA also makes sure the product labeling for dentists has adequate directions for use and includes applicable warnings.
Background: Since the 1990s, FDA, the Centers for Disease Control and Prevention (CDC) and other government agencies have reviewed the scientific literature looking for links between dental amalgams and health problems. CDC reported in 2001 that there is little evidence: 98
that the health of the vast majority of people with dental amalgam is compromised, or that removing amalgam fillings has a beneficial effect on health. In 2002, FDA published a proposed rule to classify dental amalgam as a class II medical device with special controls. In 2008, FDA reopened the comment period for that proposed rule. After reviewing all comments, FDA issued a rule in 2009.
More information from the FDA:
Website on dental amalgam
o Dental amalgam fillings page Press release announcing the final rule
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Are There Alternatives to Using Dental Amalgam Fillings? Presently, there are five other types of restorative materials for tooth decay:
resin composite glass ionomer resin ionomer porcelain gold alloys
The choice of dental treatment rests with dental professionals and their patients, so talk with your dentist about available dental treatment options.
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How Does Amalgam Waste Affect The Environment? Related Information
In its Amalgam Separators and Waste Best Management EXIT, the American Dental Association recommends a series of amalgam waste handling and disposal practices. 99
EPA's 2008 Health Services Industry Detailed Study: Dental Amalgam (PDF)(76 pp, 1 MB, About PDF) compiled information on mercury discharges from dental offices, best management practices (BMPs), and amalgam separators.
Fact sheet on Mercury Use in Dental Amalgam from the Interstate Mercury Education and Reduction Clearinghouse (PDF) (4 pp, 139 K, About PDF)
If improperly managed by dental offices, dental amalgam waste can be released into the environment. Although most dental offices currently use some type of basic filtration system to reduce the amount of mercury solids passing into the sewer system, dental offices are the single largest source of mercury at sewage treatment plants.
The installation of amalgam separators, which catch and hold the excess amalgam waste coming from office spittoons, can further reduce discharges to wastewater. Without these separators, the excess amalgam waste will be released to the sewers.
From sewers, amalgam waste goes to publicly-owned treatment works (POTWs)
Publicly-Owned Treatment WorksA water treatment facility, as defined by
Section 212 of the Clean Water Act, that is used in the storage, treatment, recycling,
and reclamation of municipal sewage or industrial wastes of a liquid nature, and is
owned by a municipality or other governmental entity. It usually refers to sewage
treatment plants. (sewage treatment plants). POTWs have around a 90% efficiency rate of removing amalgam from wastewaters. Once removed, the amalgam waste becomes part of the POTW's sewage sludge, which is then disposed:
In landfills. If the amalgam waste is sent to a landfill, the mercury may be released into the ground water or air. Through incineration. If the mercury is incinerated, mercury may be emitted to the air from the incinerator stacks. By applying the sludge to agricultural land as fertilizer. if mercury- contaminated sludge is used as an agricultural fertilizer, some of the mercury used as fertilizer may also evaporate to the atmosphere. 100
Through precipitation, this airborne mercury eventually gets deposited onto water bodies, land and vegetation. Some dentists throw their excess amalgam into special medical waste containers, believing this to be an environmentally safe disposal practice. If waste amalgam is improperly disposed in medical waste bags, however, the amalgam waste may be incinerated and mercury may be emitted to the air from the incinerator stacks. This airborne mercury is eventually deposited into water bodies and onto land.
Learn more about this issue, and about EPA's effluent limitation guidelines and standards to help cut discharges of mercury-containing dental amalgam, on our Dental Effluent Guidelines page. Learn more about what EPA and others are doing to reduce mercury pollution
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13.) Which statement is true:
A. Hg can be transported from the mother to the fetus during pregnancy and breast feeding B. Hg is only transferred from the mother to the fetus C. Hg is only transferred in breast milk D. Hg is neither transferred to the fetus nor present in breast milk https://www.cdc.gov/breastfeeding/breastfeeding-special- circumstances/environmental-exposures/mercury.html
Breastfeeding mothers should minimize exposure to mercury in their diets, at home, and at work.
Mercury is a naturally-occurring element in the environment and is also released into the environment through human activities such as burning coal and oil. Mercury collects in streams, lakes, and oceans, where fish and other animals are exposed. Small amounts of mercury are also used in making common household items like fluorescent bulbs and some thermometers. People who work in recycling plants, who manufacture items with mercury, and who handle dental amalgam might have some mercury exposure on the job.
How might mercury affect breastfeeding mothers and babies?
Mercury can pass from a mother to her baby through the placenta during pregnancy and, in smaller amounts, through breast milk after birth. Exposure to mercury can affect the infant’s brain and nervous system development during pregnancy and after birth.
How much and what types of fish are recommended for breastfeeding women to consume?
Although mercury naturally occurs throughout the environment, the mother’s diet is the primary source of mercury exposure for most breastfed infants before they are introduced to complementary foods. Most fish contain some level of mercury. When a mother eats fish, the mercury in the fish can be passed into her breast milk. However, the benefits of breastfeeding may be greater than the possible adverse effects of exposure to mercury through breast milk. 102
Although fish remains an excellent source of protein and essential vitamins and minerals for breastfeeding women, some care must be taken in how much and what kind to eat. The U.S. Food and Drug Administration (FDA) and the U.S. Environmental Protection Agency (EPA) have issued fish consumption guidanceexternal icon for pregnant and breastfeeding women and young children:
Download PDF pdf icon[359KB]external icon
Eat a variety of fish. If you eat fish caught by family or friends, check for fish advisoriesexternal icon. If there is no advisory, eat only one serving and no other fish that week. Try to avoid eating the “Choices to Avoid” fish or feeding them to children. It is best to eat a variety of fish from the “Best Choices” and “Good Choices” categories on this chartexternal icon.
For adults:
1 serving = 4 ounces of fish, measured before cooking. Eat 2 to 3 servings (between 8 and 12 ounces) of fish a week from the “Best Choices” list OR 1 serving (4 ounces) from the “Good Choices” list on this chartexternal icon.
For children:
A serving is 1 ounce at age 2 and increases with age to 4 ounces by age 11. Serve fish to children 1 to 2 times per week from a variety of fish. Portion 103
sizes should be smaller than adult portions and based on your child’s age and calorie needs. Currently there are no specific recommendations about the amount or frequency of fish consumption for infants (breastfed or non-breastfed) younger than age 2.
How can breastfeeding mothers and their families protect themselves from mercury at home?
Handling an intact lightbulb or thermometer that contains mercury does not cause mercury exposure. If a mercury-containing lightbulb or thermometer breaks, however, it can spill mercury onto surfaces and release mercury vapors into the air. If this happens, families should be advised to follow the EPA instructions on safe clean-up of a broken mercury-containing lightbulbexternal icon or broken mercury thermometerexternal icon.
How can breastfeeding mothers reduce their exposure to mercury at work?
Women who are concerned about mercury exposure at work should be advised to talk to their supervisor or safety officer to discuss ways to avoid or reduce exposure to mercury. Information on how to reduce mercury exposure in different jobs is available from the National Institute for Occupational Safety and Health (NIOSH), the Occupational Safety and Health Administration (OSHA),external icon and on this fact sheet pdf icon[PDF-77KB]external icon.
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14.) Dr. Weston Price discovered:
A. That 95% of American adults had some sort of dental foci infection B. That root canal teeth acted as silent focal infections C. A correlation between diet and dental health D. All of the above https://www.westonaprice.org/health-topics/dentistry/root-canal-dangers/
DNA Studies Confirm Dr. Weston Price’s Century-Old Findings Toxic dental materials have created much havoc in the dental profession, as well as in patient health, for nearly two centuries. Dental mercury fillings, nickel crowns (especially in children, called “chrome crowns”), root canals and cavitations have been the target of concern for a long time.
Dental mercury was first exposed as a health-compromising product in 1840. The dental profession finally overcame the perception that putting toxic mercury in the mouth might be detrimental to human health; organized dentistry still considers the current fillings containing 50 percent mercury as “state of the art.”
The toxicity of root canals was disclosed by Mayo’s Clinic and Dr. Weston Price jointly back in about 1910. Close to a century ago. Price’s textbook on root canals, published in 1922, upset the dental associations at that time, and still does today. The American Dental Association (ADA), denies his findings and claims that they have proven root canals to be safe; however, no published data from the ADA is available to confirm this statement. Statements, but no actual research.
My attention was drawn to the increase in autoimmune disease after the high-copper amalgams of 1975 were initiated as “state of the art” fillings, which ADA claimed released no mercury. On the contrary, 105
studies from Europe1 found that the high-copper amalgams released fifty times more mercury than previous amalgam!
In watching these changes regarding the onset of autoimmune disease, I noticed a blip in the statistics—an increase in amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease) in 1976 (See Figure 1).
Note in Figure 2 that the actual number of cases of multiple sclerosis increased tremendously, from an average of 8800 per year during the period 1970 to 1975, to an increase of up to 123,000 in one year. That year being 1976, the birth date of high-copper amalgams.
Figure 1 Figure 2
ROOT CANAL HAZARD Is mercury the only dental hazard that can create conditions favorable to autoimmune diseases? No. There are bacteria in root canals that favor destruction of the nervous system and many other systems, resulting in the creation of autoimmune reactions. 106
What is the common denominator? The formation of a hapten (see page 46). A hapten is a small molecule that can elicit an immune response only when attached to a large carrier such as a protein; the carrier may be one that also does not elicit an immune response by itself. In general, only large molecules, infectious agents, or insoluble foreign matter can elicit an immune response in the body.
Healthy cells have a code imprinted on them. It is called the Major Histo-compatibility Complex (MHC). This is your personal code called “self.” Your body considers other code or alteration of this code to be “non-self.” The immune system is trained to kill and eliminate any “non-self” invaders.
If an atom of mercury attaches to a normal healthy cell, a hapten is formed and the immune system immediately identifies that cell as “nonself.” The immune system then proceeds to kill the contaminated cell. If mercury attaches to a nerve cell, the result is a neurological disease, such as multiple sclerosis, Lou Gehrig’s disease, seizures or lupus. If mercury attaches to a binding site on a hormone, that endocrine function is altered. Mercury can attach to almost any cell in the body and create autoimmune diseases in those tissues.
Lately, it has become evident that toxins from anaerobic bacteria have the same ability to create non-self autoimmune diseases by interfering with the MHC. This is the project that Dr. Price began to study a century ago. Resistance from organized dentistry was the same then as it is today. Price wondered why dentistry was considered a “health” profession.
Price was concerned about the pathological bacteria found in nearly all root canal teeth of that time. He was able to transfer diseases harbored by humans from their extracted root canal teeth into rabbits by inserting a fragment of a root canal root under the skin in the belly area of a test rabbit. He found that root canal fragments from a person who had suffered a heart attack, when implanted into a rabbit, would cause a heart attack in the rabbit within a few weeks. Transference of 107 heart disease could be accomplished 100 percent of the time. Some diseases transferred only 88 percent of the time, but the handwriting was on the wall.
Dr. Price discovered that root canals had within them bacteria capable of producing many diseases. They had no place in the body. Which is more important? The life of the tooth or the life of the patient? This is still the primary argument facing us today.
ROOT CANALS AND NEUROLOGICAL DISEASE Considering the difficulty of culturing anaerobic bacteria, it was hard to identify them with 1920s technology. Most of the bacteria reported by organized dentistry at that time were aerobes of unknown significance. Today, with DNA analysis available, anaerobic bacteria (the dangerous kind) can be identified whether dead or alive by the presence of their tell tale DNA signatures.
Let’s go back to the graphs of ALS up through the year 2000. Note an increase in 1976 and another increase in slope in 1991. In 1990, the dental association “suggested” that dentists perform thirty million root canals per year by the year 2000. Dentists accomplished that goal by 1999. As I understand it, the bar has now been raised to sixty million per year.
The unexplained increase in MS (8800 to 123,000) coincided with the advent of high copper amalgams. The increase in ALS in the same year is suggestive of the same cause. ALS also increased in 1991 as more root canals were performed. Statistical coincidence?
The goal of dentistry is to save teeth. Root canals allow dentists to maintain many teeth for years instead of extracting them. But is this goal appropriate considering the biological expense exposed with DNA research? What is more important? To save the life of the tooth or that of the patient? 108
HAVENS FOR BACTERIA Dr. Price, while head of research for the now-defunct National Dental Association, took one thousand extracted teeth and reamed them out as dentists normally do, prior to filling the canals with wax. Price sterilized the canals with forty different chemicals far too toxic to be used in a live human situation; he wanted to see whether the canals could be permanently sterilized. After forty-eight hours, each tooth was broken apart, and cultured for the presence of bacteria. Nine hundred ninety out of one thousand cultured toxic bacteria just two days after treatment with chemicals designed to make the tooth sterile. Where did these bacteria come from?
An overview of the structure of a tooth (see Figure 4) shows the outer layer, known as enamel, the second layer, known as dentin, and the inner portion, known as the pulp chamber, where the nerve lives. On the outside of the tooth is what is called the periodontal ligament. Teeth are not attached directly to bone. Fibers come out of the tooth and intertwine with fibers coming out of the bone, and they unite to form what is called the periodontal ligament.
The second layer of the tooth, the dentin, is not really solid but composed of tiny dentinal tubules. In a front tooth, if all these tubules were attached end to end, they would reach over three miles.3 Note that the tubules have adequate space to house many thousands of bacteria (see Figure 5). This is where the bacteria were hiding in the thousand teeth Price tested. From the dentin tubules, bacteria can migrate either into the pulp chamber, where space is left as the gutta percha—a natural form of rubber used to fill the space inside the cleaned-out root—shrinks upon cooling, rebounding from the force applied to push the wax down the canal, and losing the liquid portion (see Figure 6), or into the periodontal ligament where a plentiful supply of food awaits them.
A tooth has one to four major canals. This fact is taught in dental school, but never mentioned are the additional “accessory canals.” Price identified as many as seventy-five separate accessory canals in 109 a single central incisor (the front tooth). Figure 7 shows one of these canals filled with necrotic (dead) tissue.
There is no way that any dental procedure can reach into these accessory canals and clean out the dead tissue. This necrotic tissue creates a home for multiple bacterial infections outside the tooth in the periodontal ligament. With added food supply from this area, the anaerobic bacteria can multiply and their toxins can contribute to the onset of disease (see Figure 8).
Of course, the root apex (terminal end) is the primary area of concentration of infection. Even though this may be the last area to show infection, dentistry generally considers a tooth sterile unless areas of bone resorption show up on X-ray. Upon cooling and shrinking of the gutta percha, space is left at the apex in which bacteria can thrive, where neither white blood cells of the immune system, nor antibiotics can reach them.
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Figure 4 Figure 5
Figure 6 Figure 7
Figure 8 111
TOXIC MICROORGANISMS Our first DNA studies examined bacteria retrieved from crushed root tips. We can identify eighty-three different anaerobic bacterial species with DNA testing. Root canals contain fifty-three different species out of these eighty-three samples. Some are more dangerous than others, and some occur frequently, some occasionally. Selecting those that occur more than 5 percent of the time, we found:
Capnocytophaga ochracea Fusobacterium nucleatum Gemella morbillorum Leptotrichia buccalis Porphyromonas gingivalis
Of what significance are these? Four affect the heart, three the nerves, two the kidneys, two the brain and one the sinus cavities. Shouldn’t we question the wisdom of supplying a haven for these microbes so close to our brain and circulatory system? Does this information validate the claims of “sterile” root canals?
Dentists claim they can “sterilize” the tooth before forcing the gutta percha wax down into the canal. Perhaps they can sterilize a column of air in the center of the tooth, but is that really where the problem is? Bacteria wandering out of the dentinal tubules is what Price was finding, and what we were finding in the crushed tooth samples. But does the problem end there? Hardly.
Just out of curiosity, we tested blood samples adjacent to the removed teeth and analyzed them for the presence of anaerobic bacteria. Approximately 400 percent more bacteria were found in the blood surrounding the root canal tooth than were in the tooth itself. It seems that the tooth is the incubator. The periodontal ligament supplies more food, therefore higher concentration of bacteria.
But the winner in pathological growth was in the bone surrounding the dead tooth. Looking at bacterial needs, there is a smorgasbord of 112 bacterial nutrients present in the bone. This explains the tremendous increase in bacterial concentration in the blood surrounding the root canal tooth. Try sterilizing that volume of bone.
Apparently, the immune system doesn’t care for dead substances, and just the presence of dead tissue will cause the system to launch an attack. Infection, plus the autoimmune rejection reaction, causes more bacteria to collect around the dead tissue. Every time a person with a root canal bites down, these bacteria are flushed into the blood stream, and they start looking for a new home. Chemotaxis, or the chemical attraction of a specific bacteria for a specific tissue, assists the anaerobes in finding new quarters in the heart, nervous system, kidney, brain, etc., where they will perform their primary damage.
Many of the bacteria in the surrounding bone are present in far more than 50 percent of the samples tested. Streptococcus mutans was found in 92 percent of the blood samples. It can cause pneumonia, sinusitis, otitis media, meningitis and tooth decay.
Streptococcus mitis was found 92 percent of the time. This microbe attacks the heart and red blood cells. It is a rather hearty bug, for it went to the moon (hiding in a camera) on an unmanned expedition, stayed there over two years in an environment without atmosphere, exposed to temperatures of 250 degrees Fahrenheit during the day, minus 250 in the shadow. Upon returning to Earth with the astronauts of Apollo 12, over two years later, this microbe was still alive.10 In humans, S. mitis binds to platelets and is involved in the pathogenesis of infective endocarditis. Want this guy living in your dead root canal tooth?
Of the top eight bacteria in the blood adjacent to root canal teeth, five affect the heart, five the nervous system, two the kidney, two the liver, and one attacks the brain sinus, where they kill red blood cells Of these, Prevotella intermedia (present in 76 percent of the samples) attacks heart, kidney and sinus; Strep intermedius (present in 69 percent of the samples) attacks heart, nerves, lungs, liver and brain. 113
DNA examination of extracted root canals has shown bacterial contamination in 100 percent of the samples tested. This is quite the opposite of official claims that root canals are 97 percent successful. Do they need a new definition of success?
CAVITATIONS Cavitations are the next big problem that result from dental procedures. Cavitations are areas of unhealed bone left over after a tooth extraction (see Figure 9).
Dentists are generally taught to remove a tooth and leave the periodontal ligament in the socket, a procedure which would be like delivering a baby and leaving the placenta in the uterus.
These socket areas with the ligament left in place rarely heal. After tooth removal, a cap of about 2 millimeters (one sixteenth of an inch) covers the extraction site, leaving a hole the size of the root of the tooth behind. In records of five thousand surgical debridements (cleaning) of cavitations, only two were found to be healed.14 When the periodontal ligament is left in the bone, the body senses that the tooth is still there, and the order for healing is canceled. These holes are lined with many of the same bacteria found in root canal sockets, but actually more different species. Whereas root canal teeth contain up to fifty-three different species of bacteria, cavitations yield up to eighty- two of the eighty-three we test for.
Of the five most frequently present bacteria found in cavitations, three affect the heart, two the nervous system and one the kidneys and lungs. They are as follows:
Streptococcus mutans (occurrence 63 percent of the samples), affects the nervous system, can cause pneumonia, sinusitis, otitis media and meningitis. It has also been blamed for causing dental decay in teeth, but this may be more the result of the fluid flow pulling bacteria into the tooth than actual active invasion by the bacteria.2 114
Porphyromonas gingivalis (occurring in 51 percent of the samples), damages the kidney, alters integrity of endothelial lining of blood vessels, and induces foam cells from macrophages, contributing to atherogenesis. It contains proteases that lyse red blood cells and extract nutrients (primarily iron) from the red blood cells. This action is called porin forming, which can destroy red blood cells rapidly. (By the way, P. gingivalis can both up and down regulate about five hundred different proteins critical to maintaining our normal biochemical actions.)
Candida albicans (present in 44 percent of the samples), in its yeast form is beneficial in the process of demethylation of methyl-mercury as well as its ability to destroy pathogenic bacteria in the intestinal tract. When converted into the fungal form by a shift in pH in the digestive system, candida can penetrate the intestinal wall, leaving microscopic holes that allow toxins, undigested food particles, bacteria and other yeasts to enter the blood stream. This condition is sometimes referred to as Leaky Gut Syndrome, which can lead to environmental intolerances.
Prevotella intermedia (occurrence rate of 44 percent) has as its primary concern coronary heart disease (CHD). P. intermedia invades human coronary artery endothelial cells and smooth muscle cells. It is generally located in atheromatous plaques. Cellular invasion of cardiac muscle is central to the infective process.11
ANTIBIOTICS So, if all these diseases of “unknown etiology,” that is, of unknown origin, are the result of bacterial invasion, why not just flood the body with antibiotics? They kill bacteria, don’t they? Ever hear of someone who was sick, was given antibiotics, and then got even worse? Most of us have heard the story. Perhaps the following information explains what happens in these cases, and why antibiotics cannot be used in infections of this nature. 115
Most antibiotics are “bactericidal”—think suicidal, or homicidal. Antibiotics kill. But this is not the same type of killing that John Wayne was noted for. When he fired at the bad guy, the bad guy fell over dead. Was then presumed to be buried. But when bactericidal antibiotics kill a bacterium, the bacterium explodes (see Figure 10).
The fragments are not eliminated immediately, for each piece is a lipopolysaccharide called endotoxin.12 By way of contrast, exotoxins are the toxic chemicals that are released by pathogenic bacteria, and endotoxins are toxic entities (fragments of the original bacteria) that are the result of the bacterial explosion caused by the antibiotic. Endotoxins present a huge challenge to the immune system, for now, instead of facing one bacterium, it has to process and eliminate perhaps one hundred endotoxins. With dozens of bacteria to confront from each single root canal or cavitation, no one antibiotic can kill all of them, and if there were one, the resulting dead bacterial corpses would overwhelm the body and produce either greater disease or death.
Broad spectrum antibiotics cannot be used for this reason. Sometimes even one capsule of antibiotic produces more problems than the immune system can tolerate. Plus, of course, it takes only two or three capsules to completely sterilize the gut of its four or more pounds of friendly bacteria.13 Antibiotics are far more powerful and potentially devastating than I ever thought they were. Antibiotics should be used with ultra caution, not routinely given for ten days or so after oral surgery, “just in case.”
There are other ways to get these microbes under control, and several are being tested at this time. It is advantageous to have intravenous vitamin C and occasionally a non-killing antibiotic is added to this solution. This combination does reduce the challenge to the immune system, but, overall, root canals represent the rock-and-hard-place situation. 116
Leave the root canal or cavitation in the body, and there is the potential of creating an unwanted autoimmune or degenerative disease that could be life threatening. Toxins and bacteria can both leak from these contamination sites wreaking havoc with a person’s cardiovascular, endocrine, nervous and immune systems. The public needs to be informed, so they can make educated choices in the trade-off between toxic convenience and health.
Removing the offending tooth presents problems that must be confronted, or other problems can be induced—problems not as dangerous as the continuous bacterial spill, but ones that need to be avoided if possible. In order to allow the immune system to focus on healing, all other offending dental materials should be removed (mercury, copper, implants, tattoos and nickel crowns) so that the immune system can deal with the bacterial challenge instead of the bacteria plus toxic metals. Nutrition should be calculated from the aspect of the blood chemistries commensurate with one’s ancestral diet and in line with the dietary principles formulated by Dr. Price. Recovery from a root canal is complicated, but your patient’s life is worth salvaging.
These studies in DNA analysis of bacteria in root canals and cavitations confirm the fact that Dr. Weston Price, despite being one century ahead of his colleagues, was absolutely correct in determining that bacteria-laden root canals have no place in the body of people interested in their health. This toxic waste spill can be stopped, but not with the assistance of dental associations, which continue to insist that the procedure of root canals is perfectly safe. The recent increase in suggested quota up to sixty million root canals per year is not in the best interest of their patients, nor can that action do anything but increase health costs for the innocent patient.
Price was right. Root canals are not worth the price.
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15.) Cavitations can form from:
A. Trauma to the jaw. B. Dentists introduction of bacteria into the socket with contaminated water C. Incomplete cleaning of the periodontal ligament D. All of the above https://youtube/14Y3zsfVtZc https://www.westonaprice.org/health-topics/dentistry/dental-cavitation-surgery
Dental Cavitation Surgery
JANUARY 31, 2012 BY LOUISA WILLIAMS145 COMMENTS 118
Appropriate Pre- and Post-Extraction Protocols When Surgical Intervention is Necessary The decision to pull a tooth is a very important and permanent one. It requires the active participation of the patient, the holistic physician/practitioner, and the biological dentist. If tooth extraction (or surgery of a former extraction site) is deemed necessary, individuals greatly enhance their chances of a positive outcome by adhering closely to pre- and post-cavitation surgery protocols. 119
A dental “focus” is defined as an area anywhere in the mouth— whether a tooth or an extraction site—that is chronically irritated and/ or infected. These “dental focal infections” can include impacted wisdom teeth, incompletely extracted wisdom (and other) teeth, failed root canals, failed dental implants, and devitalized teeth (from deep fillings, crowns or physical trauma). What makes chronic dental focal infections so particularly difficult to diagnose is their relative silence in the mouth. That is, in contrast to acute illnesses such as ear infections that can feel quite fiery and hot, typically dental foci “smolder” for years, manifesting only mild and intermittent symptoms of pain and swelling.
DENTAL FOCI AND DISTURBED FIELDS However, what is not silent are the “disturbed fields” which these dental focal infections typically cause in the body. For example, although a left lower (number 17) impacted wisdom tooth may manifest no significant pain or inflammation locally, the patient may be quite aware of distal symptoms related to this site. Chronic left shoulder pain and/or intermittent heart pain and palpitations are classic signs and symptoms of the disturbed fields secondary to this chronic dental focal infection (Figure 1).
Figure 1 120
Note that these symptoms are also ipsilateral; that is, on the same side as the dental focus. If, for example, a patient complains of chronic right-sided symptoms such as writer’s cramp (wrist tendonitis), right hip or shoulder pain, and right sciatica, a knowledgeable doctor or practitioner would first want to rule out an ipsilateral—that is, right- sided—dental focal infection (Figure 2). This tendency of dental foci to cause ipsilateral disturbed fields is therefore an excellent diagnostic clue that can be used in helping to determine the primary cause of a patient’s particular chronic one-sided symptoms.
Figure 2
CONSERVATIVE BIOLOGICAL DENTISTRY Good dentists do everything possible to try to save a tooth. They don’t recommend extraction—or even a root canal—until all other avenues of treatment have been exhausted. These can include ozone injections to try to heal infection in the tooth, laser treatments, isopathic remedies (Notatum 4X, Aspergillus 4x, etc.), and nutritional support (ubiquinol/CoQ10, crystal sulfur/MSM, Schuessler’s cell salts, original Quinton Marine Sea Plasma, etc.). 121
Additionally, both biological dentists and holistic physicians and practitioners endeavor to first adequately diagnose what’s wrong with the tooth (or socket) in order to determine the underlying problem. For example, if a patient is eating excessive sugar this could be the true cause of pain and inflammation manifesting in a first molar. This tooth has a reflexive relationship with the pancreas and stomach. By changing one’s diet (and nothing is more motivating than the thought of a root canal or the loss of a tooth) to a nutrient-dense one and avoiding refined sugar, along with supportive nutritional supplementation, the first molar can often be saved.
It should also be noted that it is essential in most cases to clear the teeth of any toxic dental materials such as mercury amalgam, and aluminum and nickel in conventional porcelain and gold crowns, before extracting teeth. Clearing the mouth of these heavy metals often removes a galvanic dental focus. This term refers to the intermittent pain or irritation (or no local symptoms) induced in a tooth from two different metals placed on or near a tooth.
DENTAL GALVANIC FOCI Dental galvanism, or electrogalvanism, can even occur from just one amalgam filling since these fillings themselves are a mixture of mercury, silver, copper, tin and zinc. However, galvanic dental foci typically arise from a highly positively charged gold crown placed on or near a highly negatively charged mercury amalgam filling. When mercury makes contact with gold in the mouth, a galvanic cell or “dental battery” is formed, with a current running between the mercury (functioning as an anode) and the gold (functioning as a cathode). The resulting anodic corrosion of mercury in these dental batteries has been measured at ten to twenty times higher than corrosion in a single amalgam filling alone.
As previously described, these strong electrical currents that create a dental galvanic focus can be relatively asymptomatic locally, but refer pain to distal parts of the body (ipsilateral disturbed fields), or they can cause intermittent mild irritation or pain in the tooth itself and 122 surrounding gums. Unfortunately many dentists misdiagnose galvanic pain and refer patients to endodontists for a root canal. This is very disturbing to see in a patient’s history since these galvanic foci could have been cleared conservatively by simply replacing the gold and mercury with metal-free alternative dental materials, and thus saving the tooth.
Therefore, if your dentist recommends a root canal for a sore or painful tooth, it is essential to get a second opinion. In fact, the ready recommendation of a root canal should be a red flag for any patient to seriously consider changing from a conventional dentist to a biological (holistic) one. Your health—and even your life—depend on it.
HIGH QUALITY X-RAYS ESSENTIAL A periapical view, which is a specific x-ray of the root of the tooth in question, is essential to diagnosis. If there is a clear radiolucency at the root of the tooth; that is, a black circular area, this is an indication of a cavitation or hole in the jawbone. This area of chronic ischemia (lack of blood supply) and infection is referred to by various terms (osteonecrosis, osteomyelitis, NICO, etc.), but broadly speaking it is a dental focal infection. When there is an obvious radiolucency apparent on x-ray there is very little one can do to save the tooth, although some dentists have been able to reduce and even clear very small cavitation areas through ozone injections. However, in most cases, when the x-ray is positive, the decision whether to do a root canal or extract the tooth then needs to be made.
If the periapical view of the tooth is negative; that is, no black radiolucency or other signs are apparent, then the biological dentist and physician endeavor to do everything possible to save the tooth with holistic therapies and supplements. However, it is important to remember that x-rays are not always definitive in determining dental foci. In fact, radiological evidence of a bone cavitation area is not even visible until as much as thirty to fifty percent of the jawbone is destroyed.1 So if symptoms continue despite holistic care, further imaging studies may be appropriate such as a 3-D Cone Beam 123
Scanner, which uses digital technology to record images, revealing much more than simple “flat” x-rays.
ROOT CANAL OR EXTRACTION? The irreversible decision of whether to have a root canal or extraction should only be made when both the dentist and doctor have exhausted all conservative measures to try to reduce the infection and save the tooth. When these efforts have failed over time, the first decision a patient must face is whether to have a root canal procedure or to extract the tooth. Dr. Weston A. Price, the quintessential holistic physician, always weighed the state of the tooth against the health of the patient: “. . . all pulpless teeth, root filled or not, harbor so much danger of becoming infected that they should be extracted, though the time as to when they should be extracted will depend on several contributing factors. If the patient belongs to a family in which there is a low defense for streptococcal infection, it had better be soon. . . If the patient is in another group with a very high defense and not much danger of overloads, and if it is a tooth that is greatly needed by that patient, I would advise you to do what I do: retain some of those root filled teeth, because I believe they are of more value to the patient in the mouth than out.”2
Price’s counsel, delivered during a 1926 dental conference, still holds the weight of truth today. That is, most biological dentists and practitioners find that if a patient is in excellent health, he or she can handle the stress of a root canal tooth. However, it is important for this tooth, as well as any associated ipsilateral disturbed fields in the body, to be monitored over time. If at any point positive signs and symptoms arise, and the patient’s health is compromised, then the decision as to whether the root canal tooth should be extracted must be reevaluated.
In contrast, if a patient has suffered from chronically ill health for many years, then the decision of whether to extract a devitalized or root canal tooth is clearer. In these cases surgery is typically very appropriate. Or, for example, if a patient receives a grave diagnosis such as breast cancer, it is important that all root canal teeth 124 anywhere in the mouth—but especially ipsilateral to the breast—be cleared in the face of this serious disease in order to try to save the patient (Figure 3).
Figure 3
However, even when it’s clear that a tooth can’t be saved, simple extractions can be as irresponsible and ineffective as when an untrained conventional dentist removes mercury amalgam fillings. What is required is a knowledgeable and skillful dentist and sufficient pre- and post-surgery treatment in a well-prepared patient. This type of surgery is termed “cavitation surgery.”
HISTORY OF CAVITATION SURGERY Cavitation has a dual meaning. As previously described, a cavitation is a cavity or hole of infection in a bone. In surgical nomenclature however, cavitation surgery is the term for the dental surgical procedure that removes diseased bone from within this cavity so that new healthy bone can grow back.
G.V. Black, DDS, MD (1836-1915), known as the “Father of Cavitation Surgery,” treated many of these areas of chronic osteitis (bone inflammation) at the turn of the twentieth century. In his two-volume 125 opus entitled Work on Operative Dentistry, Dr. Black characterized these cavitations in the jawbone as a progressive “death of bone” which was able to “soften the bone, often hollowing out the cancellous portions of large areas of bony tissue.”3 As described previously however, Black was amazed that even the larger jawbone cavitation areas full of necrotic (dead) debris could cause no visible redness, swelling or increase in patients’ temperature. However, when these bone cavitation lesions were “opened freely and every particle of softened bone removed until good sound bone forms…,” Black found that “. . . generally, the case makes a good recovery.”4 Thus, Dr. Black identified the serious pathological processes that are generated in infected teeth and bone, noted that these chronic dental focal infections were often relatively silent, and pioneered the cavitation surgery methods that are still being emulated today by trained biological dentists in the removal of these dental focal infections.
CHOOSING A BIOLOGICAL DENTIST Biological dentists who specialize in cavitation surgery attend continuing education courses to learn how to most expertly extract devitalized teeth, as well as how to effectively clean out extraction sites that harbor infection from previously incorrectly extracted teeth. The primary cause of these jawbone cavitations in extraction sites is the failure of the conventional dentist or oral surgeon to remove all of the periodontal ligaments when pulling a tooth. These remaining periodontal ligament pieces later act as a barrier to the creation of new blood vessels and, therefore, to the regrowth of new bone. Dr. Hal Huggins likens the severity of this dental omission to the failure of removing the placenta (afterbirth) after delivering a baby: “Bone cells will naturally grow to connect with other bone cells after tooth removal—providing they can communicate with each other. If the periodontal ligament is left in the socket, however, bone cells look out and see the ligament, so they do not attempt to ‘heal’ by growing to find other bone cells.”5
In these incomplete extractions, approximately two to three millimeters of bone will superficially grow over the socket area, but beneath the 126 bone a hole, or cavitation, will remain (Figure 4). As described previously, the term for the degeneration of bone in these cavitation areas, osteonecrosis, is defined as the death of tissue due to poor blood supply. Synonyms of osteonecrosis are inflammatory liquefaction, and, more familiarly, gangrene. Although this latter term may seem exaggerated since it conjures up ghastly images of partial amputations on the battlefield, for those of us who have witnessed a biological dentist spooning out oily black mushy bone from an osteonecrotic cavitation site, the term seems perfectly appropriate (Figure 5). Many dentists have this diseased tooth and bone tissues analyzed through pathology labs (contact Dr. Jerry Bouquot at (713) 500-4420, or [email protected]). In one clinical study of thirty-eight patients referred by me to Dr. Russ Borneman for cavitation surgery, one hundred percent showed positive histological (tissue-related) signs of ischemic osteonecrosis (bone death) and osteomyelitis (bone marrow infection), thus confirming the clear pathological tissue within these dental focal infections.6
Figure 4
It is essential to choose a well-trained and skillful dentist or oral surgeon to treat these ischemic cavitation sites. The best referral comes from your holistic doctor or practitioner if he or she is knowledgeable about dental focal infections. Referral from a family member, friend, or work colleague who has had success with a particular biological dentist can also be valuable. Additionally, going to 127 the websites of the three major biological dental organizations in the U.S. can help further narrow down the decision-making process of choosing the right professional for this very specialized surgery. These organizations are: the International Academy of Biological Dentistry and Medicine (www.iabdm.org); the International Academy of Oral Medicine and Toxiciology (www.iaomt.org); and the Holistic Dental Association (www.holisticdental.org). Also check the Hal Huggins website (www.hugginsappliedhealing.com)
PRE- AND POST-SURGICAL PROTOCOL Every biological dentist or oral surgeon has suggested procedures to follow before and after surgery. The following protocol is based on my experience over the past two decades preparing patients for surgery and treating them afterwards, and I hope can add to and support the biological dentist’s directions. With this protocol, along with carefully diagnosing for whom, as well as when, cavitation surgery is appropriate, and most important, the skill of a well-trained dentist or oral surgeon, I have had a ninety-nine percent success record since 1996.
PRE-CAVITATION CONSIDERATIONS In the majority of cases it is best to clear the mouth of heavy metals before cavitation surgery. In fact, this may even obviate surgery in some individuals who have galvanic-induced dental foci as described previously. Additionally, patients with non-toxic dental restorations heal much better from surgery than those with toxic metals in their mouth. In contrast however, mercury removal is often contraindicated in cancer patients (until the tumors are cleared and lab tests negative), whereas cavitation surgery to remove the root canals and other devitalized teeth can be clearly indicated, tolerated well, and even life- saving in this population of patients.
It is also important that liver detoxification pathways and kidney clearance functions are as optimal as possible. A simple Comprehensive Wellness Profile (CWP) from Direct Labs (www.directlabs.com) is a very affordable (over $500 worth of tests for 128 only $97) and easy blood test to run to determine the functioning of these, as well as other organs and systems, in the body. Of course, a complete history and exam should also be performed by the holistic doctor or practitioner and the biological dentist to further assist in making the decision if the patient is healthy enough to undergo dental surgery.
If an individual is very ill, it is often necessary to have this patient on his or her deepest homeopathic constitutional remedy for at least a month or two in advance, in order to facilitate immune, metabolic, and nervous system functioning before surgery. The new Sankaran sensation method of constitutional homeopathy is the single most curative modality known by this author to achieve health, and thus prepare an individual for a successful surgical outcome.
Another important assessment to make before surgery is to determine whether the patient has a major tonsil focus. Chronic tonsil focal infections and chronic dental focal infections feed into each other and further infect each other. Patients with a chronic tonsil focus who want to have their wisdom tooth cavitation sites treated, for example, often don’t heal well. This observation was made in the 1920s by Dr. Henry Cotton (1876-1933), a brilliant, if controversial, psychiatrist who specialized in researching the effect of focal infections in the onset of mental illness. In his book, The Defective, Delinquent, and Insane, Cotton asserted that in most cases the wisdom teeth were not infected because they were impacted but were impacted because they were infected, and that this “infection is transmitted from the tonsils.”7 Before these suspected primary tonsil focus patients have dental surgery therefore, it is important to reduce the tonsil focus through avoiding commercial pasteurized dairy (the typical allergy food that causes chronic upper respiratory infections and the tonsillitis in childhood that eventually coalesces to a more hidden chronic tonsil focal infection later in life), rubbing Notatum 4X drops over the tonsils on the upper anterior neck area, and to be on their constitutional homeopathic remedy according to the new Sankaran system. 129
Finally, vegans, and even many lacto-ovovegetarians typically do not consume enough protein to heal tissue, and thus, the surgical site, adequately. Lacto-ovo-vegetarians often become sensitive to the over- ingestion of eggs and dairy foods over the years, which greatly reduces their absorption of these normally utilizable protein foods. Lab tests and energetic testing can determine if a patient is deficient in protein, and if so, the encouragement of eating more eggs and dairy (if there is no allergy) as well as meat broths if the patient is willing, is often needed for at least one to two months in order to have a successful surgical outcome.
THE FIVE HEALING DAYS It is imperative for patients to take at least three days off after surgery, but the most optimal protocol is to take the day of, plus the following four days off, a time period I have labeled as the “Five Cavitation Surgery Healing Days.” Patients should plan to rest and avoid any strenuous physical activity during this time. In fact, any exercise (except slow and short walks) or vibration from extensive car and plane travel can delay, and even block, healing of the surgery site.
This rest and healing time is significant because if a “dry socket” forms from the invasion of bacteria in the area between the blood clot and the bone and the blood clot is lost, the surgery almost always must be redone at some later point. Dry socket is signaled by significant pain in the surgical site or the ipsilateral ear, and typically a foul odor. The standard treatment of antibiotics often does little because there is no blood flow in the area, and eugenol from the oil of cloves may actually further impair healing of the site. I typically recommend more Notatum 4X drops and laser treatments, as well as a castor oil pack on the suspected disturbed field (stomach, small intestine, liver, etc.) in the body. The best course of action though is for patients to take five full days off and follow this protocol carefully in order to allow complete healing of the site, and therefore only have to undergo this cavitation surgery procedure once. 130
Figure 5 – Necrotic bone on left, healthy bone on right.
The use of a therapeutic laser (830 nanometers and 100 milliwatts) is so effective during these five days in healing the inflamed nerves and soft (gums) and hard (bone) tissues, that it has become a sine qua non in my post-surgical protocol (available from [email protected]). Patients rent this laser so they can use it in the comfort of their own home, treating the surgical site for one minute at a time, anywhere from six to ten times a day. This laser is so healing to tissue that it often obviates the need for any pain medication, or at the least, considerably reduces the amount of pain pills needed.
Isopathic drops such as Notatum 4x and Aspergillus 4x (www.bioresource.com) are especially helpful post-surgically to augment healing in the site. Further, they can be dropped onto the surgical site at a protocol of two to three drops, three times a day during these five days, and then one or two times a day for one week afterward. When the laser is next applied over the site, these isopathic drops are then photophoretically driven into the surgical site for even deeper healing.
Acute homeopathic remedies are also an important component in this protocol. Arnica montana 30C is most commonly prescribed to reduce pain and heal the bruising post-surgery at a dose of two pellets, three 131 times a day, for five days, and then once a week thereafter. If the surgery was very deep and there is a chance that the maxillary (upper jaw) or mandibular (lower jaw) trigeminal nerve was injured, Hypericum perforatum 30C should also be taken at a different time of the day, but at a similar dosage schedule as the Arnica. If the surgery was particularly extensive and intense, patients may want to take the stronger 200C potency of both of these remedies. However, for those individuals who are already on their constitutional homeopathic remedy, usually redosing this remedy one to two times after surgery is all that is required.
One to two vials of the mineral-rich Quinton Marine Sea Plasma (www.originalquinton.com) taken daily after surgery further ensures healing of the gums, jawbone, and neighboring teeth during these five days. Patients should hold the contents of each vial in the mouth for approximately a minute or more before swallowing.
Finally, nutrient-dense bone broths are essential during these five recovery days. A clear broth from grass-fed organic beef, chicken, turkey, lamb, or from wild fish is especially important the first two days when the surgical incision has not fully closed and you don’t want any food particles to get lodged in there. Later you can purée vegetables (carrots, squash, turnips, onions, kale, etc.) to make a thicker soup to stave off hunger and supply more needed vitamins and antioxidants for further healing of tissues.
POST-SURGERY OFFICE VISIT Besides the post-surgery dental visit to check on healing of the site and to remove any stitches, it is important for the patient to also see a doctor or practitioner knowledgeable in focal infections. At that visit the surgical site is checked, any neighboring autonomic ganglia (groups of nerve areas that can hold bacteria and other toxins transported from nearby ipsilateral dental foci) are treated, and any related disturbed fields caused by the focal tooth (or extraction site) are addressed if necessary. This clean up of all the areas in the body disturbed or infiltrated by infection from the chronic focal infection ensures more 132 complete healing of the site, with no reflex “back flow,” or re- introduction of toxins or microbes, back into the dental focal area.
CONCLUSION It is important that the decision whether to sacrifice a tooth or repeat surgery of an incompletely extracted site be made by the team of a doctor or practitioner knowledgeable about focal infections, a skillful and experienced biological dentist, and an informed patient. Appropriate pre- and post-surgery protocols can ensure a successful outcome and complete healing of the surgical site. For more information on diagnosing and treating dental focal infections please refer to my book, Radical Medicine
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16.) Which organism is usually found in dental and tonsillar foci:
A. Clostridium B. Candida C. Herpes D. Streptococcus https://www.ncbi.nlm.nih.gov/pubmed/8131787
Bacteriology of dental infections. Asikainen S1, Alaluusua S. Author information Abstract The most common dental diseases, periodontal disease and dental caries, are chronic infections caused by bacteria of normal oral flora. When these bacteria increase in number and irritation exceeds the host defence threshold, disease arises. The human oral flora comprises more than 300 different bacteria. During the last decade approximately 10 species, mainly Gram-negative anaerobes, have been noted as putative pathogens in periodontal disease. The Gram-positive and facultatively anaerobic mutans streptococci are aetiologically the most important bacteria in dental caries. Data have rapidly increased on the association of these bacteria with certain periodontal diseases or caries, on phenotypic and genotypic characteristics, pathogenic mechanisms, antibiotic susceptibility patterns and transmission among family members. Chronic dental infections have been the focus of renewed interest because of recent advances in oral microbiology as well as in medicine. We now know that in addition to oral streptococci, recently classified, fastidious periodontal anaerobes can be detected from various extra-oral infections. Oral bacteria may spread into the blood stream through ulcerated epithelium in diseased periodontal pockets and cause transient bacteraemias, which are regarded as increased risk, especially for immunocompromised patients or persons with endoprotheses. In these patients, routine antibiotic prophylaxis is recommended for invasive dental care procedures. Also the new association between dental infections and myocardial/cerebral infarction have offered new challenges for cooperation between dental and medical researchers.
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17.) Homeopathic remedies can be an effective antibacterial:
A. True B. False https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4908854/ Complementary therapies are now becoming the rule rather than the exception in the management of headache and facial pain. It is incumbent on physicians to be aware of and to have a working knowledge of these increasingly popular modalities. A number of unconventional medical methods are being used in dentistry. These include regulation thermography, homeopathy, nosode therapy, acupuncture, magnetic field therapy, ozone therapy, Mora therapy, and lymph drainage.[1] Homeopathy is a safe and natural alternative that is effective in both adults and children. Homeopathic remedies are used in dentistry to improve the psychological or emotional condition of patients without the side effects of conventional drugs.
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18.) 3 Main sources of Mercury exposure are:
A. Occupational exposure, food (mainly Fish) and silver/mercury fillings B. Industrial coal energy production, food and gold mining C. Cow meat, fluoride toothpastes and fish oils D. Liver, grass and berries https://people.uwec.edu/piercech/hg/mercury_water/sources.htm
Sources of Mercury
Natural
Natural sources of mercury include volcanoes, forest fires, cannabar (ore) and fossil fuels such as coal and petroleum. Active Volcano
Anthropogenic
Levels of mercury in the environment are increasing due to discharge from hydroelectric, mining, pulp, and paper industries. Incineration of municipal and medical waste and emissions from coal-using power plants also contribute to high levels of mercury.
Mercury released from ongoing human activity in the U.S. can be separated into four broad categories. The first category is “area sources”. Landfills, dental preparations, and laboratory use are defined as area sources. The second category is combustion processes. These include coal-fired power generation, medical waste incinerators, and municipal waste combustors. The third category is the manufacture of metals, alkali, and cement. Other industrial processes fall into the fourth category. 136
In the past, mining was a substantial source of mercury in some areas. For example, the hydraulic placer- gold mines of the Sierra Nevadas released several thousand tons of mercury to the environment from the 1860s to the early 1900s. The U.S Geological Survey (USGS) believes that high levels of mercury in fish, Coal Burning Power Plant amphibians, and invertebrates downstream of hydraulic mines are a result of historic mercury use.
Power plants are now the largest anthropogenic source of Mercury in the United States. To address this concern, new legislation has been proposed to cut emissions of pollutants from power plants. However, different parties disagree on how mercury should be regulated. In December 2004, the Environmental Protection Agency will reach its deadline for setting maximum achievable control technology (MACT) provisions for mercury under the Clean Air Act.
Mercury Contamination
Mercury in the air is deposited into the water. Bacteria in lake, stream, and ocean sediments then convert elemental mercury into organic mercury compounds such as methylmercury. 137
Mercury is able to travel long distances in the air. There is a global reservoir of airborne mercury circulating worldwide at any one time. Both natural and anthropogenic emissions contribute to the global mercury reservoir. It is estimated that the annual global input of mercury into the reservoir is 4,900 tons.
In 1995, it was estimated that forty percent (32 metric tons (t)) of mercury deposited form the air onto U.S. water and soil came from the global mercury reservoir. The other sixty percent came from anthropogenic sources in the U.S. There is uncertainty at this time as to how long some forms of mercury persist in the atmosphere.
The “recycling” of anthropogenic mercury also raises levels of mercury in the environment. Recycling takes places when mercury in water volatizes and contributes to the increase of atmospheric mercury concentrations.
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19.) Documented oral effects by dental amalgam mercury fillings do not include:
A. Gingivitis, Bleeding gums B. Burning mouth C. Oral tissue inflammation D. Bone loss E. Teeth whitening
https://iaomt.org/resources/dental-mercury-facts/dental-mercury-amalgam- side-effects/#_ednref11
Mercury Fillings: Dental Amalgam Side Effects and Reactions
Dental amalgam side effects and reactions as a result of the mercury in these fillings vary by patient due to individualized risk factors.
If everyone experienced the same reactions to and side effects of environmental toxicants, it would be obvious to everyone, as well as their doctors, that exposure to a specific toxic material results in a definitive outcome– the exact same illness. However, research has demonstrated that individuals respond to environmental toxicants like dental amalgam mercury in a way that is unique to their own bodies.
Dental Amalgam Mercury: What is it?
Millions of dentists around the world routinely use dental amalgam as a filling material in decayed teeth. Often referred to as “silver fillings,” all dental amalgams actually consist of 45-55% metallic mercury. Mercury is a known neurotoxin that can cause harm to humans, especially children, pregnant women, and fetuses. A 2005 World Health Organization (WHO) report warned of mercury: “It may cause harmful effects to the nervous, digestive, respiratory, immune systems and to the kidneys, besides causing lung damage. Adverse health effects from mercury exposure can be: tremors, impaired vision and hearing, paralysis, insomnia, emotional instability, developmental deficits during fetal development, and attention deficit and developmental delays during childhood. Recent studies suggest that mercury may have no threshold below which some adverse effects do not occur.”[1]
There is a global effort spearheaded by the United Nations Environment Programme to reduce mercury usage, including that of dental mercury,[2] and some countries have already banned its use.[3] However, amalgams are still used for about 45% of all direct dental restorations worldwide,[4] including in the United States. In fact, it has been 139 estimated that there are currently over 1,000 tons of mercury in the mouths of Americans, which is more than half of all the mercury being used in the U.S. today.[5]
Reports and research are consistent that these mercury-containing fillings emit mercury vapors,[6] [7] [8] and while these restorations are commonly referred to as “silver fillings,” “dental amalgam,” and/or “amalgam fillings,” [9] the public is often unaware that amalgam refers to the combination of other metals with mercury.[10]
Dental Amalgam Side Effects and Reactions Linked to Mercury in Fillings
Properly diagnosing “adverse health effects” related to dental mercury amalgam fillings is impeded by the intricate list of potential responses to the elemental form of the substance, which include over 250 specific symptoms.[11] The table below is a brief listing of some of the symptoms most commonly associated with inhalation of elemental mercury vapors (which is the same type of mercury continually emitted from dental amalgam fillings):
Symptoms most commonly associated with inhalation of elemental mercury vapors
Acrodynia or similar symptoms such as emotional instability, loss of appetite, general weakness, and skin changes[12]
Anorexia[13]
Cardiovascular problems/ labile pulse [frequent changes in heart rate]/tachycardia [abnormally rapid heartbeat] [14]
Cognitive/neurological/impairments/memory loss/decrease in mental function/difficulties with verbal and visual processing[15] [16] [17] [18] [19]
Delusions/delirium/hallucination[20] [21]
Dermatological conditions/ dermographism [skin condition characterized by raised red marks]/dermatitis[22] [23]
Endocrine disruption/enlargement of thyroid[24] [25]
Erethism [symptoms such as irritability, abnormal responses to stimulation, and emotional instability] [26] [27] [28] [29]
Fatigue[30] [31] 140
Symptoms most commonly associated with inhalation of elemental mercury vapors
Headaches[32]
Hearing loss[33]
Immune system impairments[34] [35]
Insomnia[36]
Nerve response changes/peripheral neuropathy/decreased coordination/decreased motor function/ polyneuropathy/ neuromuscular changes such as weakness, muscle atrophy, and twitching[37] [38] [39] [40] [41]
Oral manifestations/ gingivitis/metallic taste/ oral lichenoid lesions/[42][43][44][45] [46] [47]
Psychological issues/mood changes related to anger, depression, excitability, irritability, mood swings, and nervousness[48] [49] [50] [51]
Renal [kidney] problems/ proteinuria/nephrotic syndrome[52] [53] [54] [55] [56] [57]
Respiratory problems/ bronchial irritation/bronchitis/cough/ dyspnea [breathing difficulties]/ pneumonitis/ respiratory failure[58] [59] [60] [61] [62] [63] [64]
Shyness [excessive shyness]/social withdrawal[65] [66]
Tremors/mercurial tremors/ intention tremors[67] [68] [69] [70] [71]
Weight loss[72]
Not all patients will experience the same symptom or combination of symptoms. Moreover, in addition to the symptoms above, an extensive number of studies have documented risks for other health conditions associated with dental amalgam. In fact, scientists have associated the mercury in amalgam fillings with Alzheimer’s disease,[73] [74] [75] amyotrophic lateral sclerosis (Lou Gehrig’s disease),[76] antibiotic resistance,[77] [78][79][80] anxiety,[81] autism spectrum disorders,[82] [83] [84] autoimmune disorders/immunodeficiency,[85] [86] [87] [88] [89] [90] [91] [92] [93] [94] cardiovascular problems,[95] [96] [97] chronic fatigue syndrome,[98] [99] [100] [101] depression,[102] infertility,[103] [104] kidney disease,[105] [106] [107] [108] [109] [110] [111] [112] multiple sclerosis,[113] [114] [115] [116] Parkinson’s disease,[117] [118] [119] and other health problems.[120] 141
Dental Amalgam Side Effects and Reactions Factor #1: The Form of the Mercury
The different forms of elements are an essential factor in evaluating the gamut of symptoms related to environmental toxicants: mercury can exist in different forms and compounds, and these different forms and compounds can produce different side effects in humans that are exposed to them. The type of mercury used in amalgam fillings is elemental (metallic) mercury, which is the same type of mercury used in certain types of thermometers (many of which have been banned). In contrast, the mercury in fish is methylmercury, and the mercury in the vaccine preservative thimerosal is ethylmercury. All of the symptoms described in the previous section are specific to elemental mercury vapor, which is the type of mercury exposure associated with dental amalgam fillings.
Dental Amalgam Side Effects and Reactions Factor #2: Mercury’s Impact on Different Organs within the Body
Another reason for the wide-range of symptoms is that mercury taken into the body can accumulate in virtually any organ. In relation to dental amalgam fillings, the World Health Organization (WHO) has stated: “Dental amalgam constitutes a potentially significant source of exposure to elemental mercury, with estimates of daily intake from amalgam restorations ranging from 1 to 27 μg/day.”[121] Research has shown that this results in 67 million Americans aged two years and older exceeding the intake of mercury vapor considered “safe” by the U.S. EPA due to the presence of dental mercury amalgam fillings [or over 122 million Americans exceeding the intake of mercury vapor considered “safe” by the California EPA due to their dental mercury amalgam fillings].[122]
An estimated 80% of the mercury vapor from amalgam fillings is absorbed by the lungs and passed to the rest of the body,[123] particularly the brain, kidney, liver, lung, and gastrointestinal tract.[124] The half life of metallic mercury varies depending on the organ where the mercury was deposited and the state of oxidation.[125] For example, the half lives of mercury in the whole-body and kidney regions have been estimated at 58 days,[126] whereas mercury deposited in the brain can have a half life of up to several decades.[127]
Furthermore, mercury vapor taken into the body binds to sulfhydryl groups of protein and to sulfur-containing amino acids throughout the body.[128] Mercury vapor, which is lipid soluble, can cross the blood-brain barrier with ease and is converted into inorganic mercury in the cells by catalase oxidation.[129] This inorganic mercury is eventually bound to glutathione and protein cysteine groups.[130] Click here to learn more about the symptoms and effects of mercury vapor toxicity. 142
Dental Amalgam Side Effects and Reactions Factor #3: Delayed Effects of Mercury
Effects of toxic exposure are even more insidious because it can take many years for symptoms to manifest themselves, and previous exposures, especially if they are relatively low-level and chronic (as is often the case from mercury amalgam fillings), might not be associated with the delayed onset of symptoms. The concept of a delayed reaction after a chemical exposure is supported by the Occupational Safety and Health Administration (OSHA)’s acknowledgement about chemical exposure and subsequent illness: “This is particularly true for long-term health effects which develop over time, or after repeated [chemical] exposures. Many chronic diseases are characterized by long latency periods of 20-30 years or longer.”[131]
Dental Amalgam Side Effects and Reactions Factor #4: Allergies to Mercury
A 1993 study reported that 3.9% of healthy subjects tested positive for metal reactions in general.[132] If this figure is applied to the current U.S. population, this would mean that dental metal allergies potentially impact as many as 12.5 million Americans. Also pertinent is that, in 1972, the North American Contact Dermatitis Group determined that 5-8% of the U.S. population specifically demonstrated allergy to mercury by skin patch testing,[133] which would amount to approximately 21 million Americans today. Yet, these figures could be even higher because recent studies and reports tend to agree that metal allergies are on the rise.[134] [135]
Since most patients are not tested for mercury allergies prior to dental amalgam exposure, this means that millions of Americans are unknowingly allergic to the fillings in their mouths. A 2011 article by Hosoki and Nishigawa explained why dentists should be educated about this possible side effect: “Current data indicate that practicing dentists need to obtain further specialized knowledge about dental metal allergy in order to ensure the correct treatment of patients in their clinics.”[136]
Ionization of metals appears to play a major role in these types of allergies. While a “stable” metal is generally regarded as non-reactive, if ionization of the metal occurs, this can cause an allergic response. In the oral cavity, ionization can result from pH changes initiated by saliva and diet.[137] The electrolytic conditions can also cause corrosion of the dental metals and generate electrical currents in a phenomenon known as oral galvanism.[138] Not surprisingly, oral galvanism has been established as a factor in sensitivities to dental metals.[139] While the combination of mercury and gold has been recognized as the most common cause of dental galvanic corrosion, other metals used in dental restorations can similarly produce this effect.[140] [141] [142]
A gamut of health conditions has been linked to dental metal allergies. These include autoimmunity,[143] [144] chronic fatigue syndrome,[145] [146] [147] fibromyalgia,[148] [149] metallic pigmentation,[150] multiple chemical 143 sensitivities,[151] [152] multiple sclerosis,[153] myalgic encephalitis,[154] oral lichenoid lesions,[155] [156] [157] [158] [159] orofacial granulomatosis,[160] and even infertility.[161]
Dental Amalgam Side Effects and Reactions Factor #5: Genetic Predisposition
Genetics is an important factor to consider when evaluating risk for reactions to dental amalgam mercury fillings.
The issue of genetic predisposition to specific, adverse effects from mercury exposure has also been examined in several studies. For example, researchers have associated neurobehavioral consequences from mercury exposure with a specific genetic polymorphism. The researchers of a study published in 2006 linked the polymorphism, CPOX4 (for coproporphyrinogen oxidase, exon 4), to decreased visuomotor speed and indicators of depression in dental professionals.[162] Additionally, the CPOX4 genetic variation was identified as a factor for neurobehavioral issues in a study of children with dental amalgams. The researchers noted, “…among boys, numerous significant interaction effects between CPOX4 and Hg [mercury] were observed spanning all 5 domains of neurobehavioral performance…These findings are the first to demonstrate genetic susceptibility to the adverse neurobehavioral effects of Hg [mercury] exposure in children.”[163]
The ability of these specific genetic variants to negatively impact the body’s reaction to dental mercury exposure has even achieved attention in the mainstream media. A 2016 article by Greg Gordon of McClatchy News included interviews with some of the researchers of the studies mentioned above. Markedly, Dr. James Woods stated: “‘Twenty-five percent to 50 percent of people have these (genetic variants).’”[164] In the same article, Dr. Diana Echeverria discussed “a lifetime risk” of neurological damage related to this population, and she elaborated: “‘We’re not talking about a small risk.’”[165]
Another area of genetic susceptibility in relation to dental mercury risk that has merited attention is the APOE4 (Apo-lipoprotein E4) genetic variation. A 2006 study found a correlation between individuals with APOE4 and chronic mercury toxicity.[166] The same 144 study found that removal of dental amalgam fillings resulted in “significant symptom reduction,” and one of the symptoms listed was memory loss. The symptom of memory loss is quite interesting, as APOE4 has also been associated with a higher risk for Alzheimer’s disease.[167] [168] [169]
Importantly, the authors of a study which found a connection between number of mercury fillings and neurotoxic effects for those with APOE genotype explained: “APO-E genotyping warrants investigation as a clinically useful biomarker for those at increased risk of neuropathology, including AD [Alzheimer’s disease], when subjected to long-term mercury exposures…An opportunity could now exist for primary health practitioners to help identify those at greater risk and possibly forestall subsequent neurological deterioration.”[170]
Other than CPOX4 and APOE, genetic traits that have been examined for association with health impairments caused by mercury exposure include BDNF (brain-derived neurotropic factor),[171] [172] [173] metallothionein (MT) polymorphisms, [174] [175] catechol- O-methyltransferase (COMT) variants,[176] and MTHFR mutations and PON1 variants.[177] The authors of one of these studies concluded: “It is possible that elemental mercury may follow the history of lead, eventually being considered a neurotoxin at extremely low levels.”[178]
Dental Amalgam Side Effects and Reactions Factor #6: Other Considerations
Even with the recognition that allergies and genetic susceptibility can both play a role in reactions to dental amalgam, there are a variety of other factors tied into health risks of mercury as well.[179] In addition to the weight and age of the individual, the number of amalgam fillings in the mouth,[180] [181] [182] [183] [184] [185] [186] [187] [188] [189] [190] [191] [192] gender, [193] [194] [195] [196] [197] d ental plaque,[198] selenium levels,[199] exposure to lead (Pb),[200] [201] [202] [203] consumption of milk[204] [l05] or alcohol,[206] methylmercury levels from fish consumption,[207] the potential for mercury from dental amalgam fillings to be transformed into methylmercury within the human body,[208] [209] [210] [211] [212] [213] and other circumstances[214] [215] can play a role in each person’s unique response to mercury. For example, the tables below identify over 30 different variables that can influence reactions to dental mercury.[216]
Conclusion about Mercury Fillings / Dental Amalgam Side Effects and Reactions
Factors related to mercury vapor release from dental mercury amalgam fillings
Age of dental mercury amalgam filling 145
Factors related to mercury vapor release from dental mercury amalgam fillings
Cleaning, polishing, and other dental procedures
Contents of other materials mixed with the mercury, such as tin, copper, silver, etc.
Dental plaque
Deterioration of dental mercury amalgam filling
Habits such as brushing, bruxism, chewing (including gum chewing, especially nicotine gum), consumption of hot liquids, diet (especially acidic foods), smoking, etc.
Infections in the mouth
Number of dental mercury amalgam fillings
Other metals in mouth, such as gold fillings or titanium implants
Root canals and other dental work
Saliva content
Size of dental mercury amalgam filling
Surface area of dental mercury amalgam filling
Techniques and safety measures applied when removing dental mercury amalgam filling
Techniques used when placing dental mercury amalgam filling
Personal traits and conditions related to mercury exposure response
Alcohol consumption
Allergy or hypersensitivity to mercury 146
Factors related to mercury vapor release from dental mercury amalgam fillings
Bacteria, including mercury-resistant and antibiotic resistant
Burdens in organs and tissues such as kidney, pituitary gland, liver, and brain
Diet
Drug use (prescription, recreational, and addiction)
Exercise
Exposure to other forms of mercury (i.e. fish consumption), lead, pollution, and any toxic substances (presently or previously)
Fetal or breastmilk exposure to mercury, lead, and any toxic substances
Gender
Genetic traits and variants
Infections
Microbes in the gastrointestinal tract
Milk consumption
Nutrient levels, especially copper, zinc, and selenium
Occupational exposures to toxic substances
Overall health
Parasites and heleminths
Stress/trauma 147
Factors related to mercury vapor release from dental mercury amalgam fillings
Yeast
Moreover, the concept of multiple chemicals interacting within the human body to produce ill-health should now be an essential understanding required for practicing modern-day medicine. Researchers Jack Schubert, E. Joan Riley, and Sylvanus A. Tyler addressed this highly relevant aspect of toxic substances in a scientific article published in 1978. Considering the prevalence of chemical exposures, they noted: “Hence, it is necessary to know the possible adverse effects of two or more agents in order to evaluate potential occupational and environmental hazards and to set permissible levels.”[217]
This is especially important considering that individuals can be exposed to different substances through their home, work, and other activities. Furthermore, exposures experienced as a fetus are also known for their potential to contribute to health risks later in life.
Clearly, the precise way that a person’s body responds to an environmental toxicant is based on a spectrum of circumstances and conditions. The factors described in this article are only a fraction of numerous pieces in the puzzle of adverse health effects related to toxic exposures. The science behind dental mercury demonstrates that in order to fully understand environmental illness, we need to recognize that just as each toxic exposure is unique, so is each person impacted by such a toxic exposure. As we accept this reality, we also offer ourselves the opportunity to create a future where dentistry and medicine are more integrated with an open acknowledgement that each patient responds to materials and treatments differently. We also offer ourselves the opportunity to use safer products that reduce the overall toxic burden in our bodies and forge the path to renewed health.
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20) Dental Assistants and Dental Hygienist are subjected to mercury exposure, because:
A. High doses of mercury vapor are released when teeth with dental amalgam mercury fillings are cleaned with an ultrasonic scaler B. High doses of mercury vapor are released when teeth with dental amalgam mercury fillings are polished C. Both a and b are true
https://iaomt.org/for-professionals/occupational-mercury-exposure/
Why should dentists, dental hygienists, dental assistants, and other dental staff be concerned about occupational exposures to mercury from dental amalgam?
Dentists, dental staff, and dental students are exposed to mercury at a greater rate than their patients. Severe exposures from past practices include hand-squeezing of fresh amalgam, where drops of liquid mercury could run over the dentist’s hands and contaminate the entire office.1 Dangerous levels of mercury are still generated in the dental workplace, and research has clearly identified that exposure to these mercury levels can cause ill-health to dental workers,1,3,45,,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,2627,,28,29,30,31,32,33 and dental students.34,35,36 Another area that has received much attention is the possibility of reproductive hazards to female dental personnel, including menstrual cycle disorders, fertility issues, and pregnancy risks.37,38,39,40,41,42
Scientific research demonstrates that dental mercury amalgam exposes dental professionals, dental staff, dental patients, and fetuses to releases of mercury vapor, mercury-containing particulate, and/or other forms of mercury contamination.43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,666,7,68,69,707,1,72,73,74,75,76,77, 78,79,80 Mercury vapor, which is continually released from dental amalgam mercury fillings, is known to be released at higher rates during brushing, cleaning, clenching of teeth, chewing, etc.,81,82,83,84,85,86,87,88,89,90,91,92,93,94 and mercury is also known to be released during the placement, replacement, and removal of dental mercury amalgam fillings.95,96,97,98,99,100,101,102,103
Dental workers require protection from mercury exposures when working with dental mercury amalgam, and a variety of studies have specifically called for protective measures to be taken in the dental office as a means of limiting mercury releases.104,105,106,107,108,109,110,111,112,113,114,115
What can I do to protect myself? 149
Becoming a mercury-free dental office (i.e. an office that no longer places mercury/silver/amalgam fillings) is the first step. However, even if mercury is no longer used in your office, you will still have patients with existing mercury fillings. This means that you will want to take precautionary measures during dental procedures involving these fillings. We suggest that you learn more about IAOMT’s Safe Mercury Amalgam Removal Technique (SMART) and The SMART Choice to protect your health, as well as the other resources from the IAOMT on this website. You might also consider joining the IAOMT so that you can learn more about biological dentistry.
What are my rights as a worker?
Employee exposure to mercury is regulated in the United States by the 1970 Occupational Safety and Health Act116 and Workers’ Rights Handbooks117 from the United States Department of Labor’s Occupational Safety and Health Administration (OSHA), which establish that all employees have the right to know about the chemicals in their work environment. OSHA’s Hazard Communication Standard (HCS) states: “All employers with hazardous chemicals in their workplaces must have labels and safety data sheets
[SDS] for their exposed workers, and train them to handle the chemicals appropriately. The training for employees must also include information on the hazards of the chemicals in their work area and the measures to be used to protect themselves.”118 Employers must also evaluate workplaces for allowable airborne concentrations,119 and they are supposed to keep a 30-year record of employee exposures and medical records.120 Employees have the right to access this information, and more on workers’ rights in regards to chemical exposures can be learned at https://www.osha.gov/Publications/pub3110text.html121 and at https://www.osha.gov/Publications/osha3021.pdf122
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21.) A HgA1c can be lowered, by flossing and better oral hygiene.
A. True B. False https://www.mouthhealthy.org/en/az-topics/d/diabetes Practicing good oral hygiene and having professional deep cleanings done by your dentist can help to lower your HbA1c.
22.) Fluid within a healthy tooth flow: A. From the enamel to the pulp B. From the pulp to the enamel https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3063177/
Fluid Mechanics in Dentinal Microtubules Provides Mechanistic Insights into the Difference between Hot and Cold Dental Pain
Min Lin, 1 Zheng Yuan Luo, 2 Bo Feng Bai, 2 Feng Xu, 1 , 3 , * and Tian Jian Lu 1 , *
Adrian Thomas, Editor
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Abstract Go to:
Introduction Dental pain is a significant health problem which negatively affects the lives of millions of people worldwide and induces huge societal costs [1]. Although dental thermal pain has become an increasingly mature topic of study and the sensory responses of tooth to various stimulations have been studied for decades [2]-[7], frustration is mounting over the limited 151 breakthroughs in dental pain therapy, mainly due to the limited acknowledge of dental pain mechanism [8]. Studies of tooth microstructure have revealed that dentinal microtubules radiate from pulp wall to exterior cementum or dentine-enamel junction (DEJ) (Fig. 1 A and B) [9]. Most of the dentinal microtubules contain non- myelinated terminal fibrils and odontoblastic processes (extension of odontoblast) that are placed in an environment filled with dentinal fluid [4], [10], [11]. Based on the characteristics of tooth innervation system, three main theories have been proposed to explain the mechanisms underlying dental pain sensation [12]: (i) Neural theory, which assumes that changes in tooth surface temperature are conducted through enamel, dentin and finally to sensory receptors located at DEJ causing neuron excitation; (ii) Odontoblastic transduction theory, which assumes external stimulus is transmitted along odontoblasts and transferred to nerves via synaptic junctions between odontoblasts and nerves; (iii) Hydrodynamic theory, which attributes dental pain sensation to the stimulation of mechano-sensitive nociceptors as a consequence of dentinal fluid movement within dentinal microtubules. Among these hypotheses, the hydrodynamic theory is the most widely accepted explanation for dental pain sensation [3], [4], [7].
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Open in a separate window Figure 1 Physiological relevant structures. (A) Cut-away image of human tooth; (B) SEM image of dentine showing solid dentine material and dentinal microtubules (DMTs) running perpendicularly from pulpal wall toward dentine-enamel junction [9]. (C) Schematic of DMT innervation system and nerve firing (NF) in response to outward dentinal fluid flow (DFF). Terminal fibril 153
(TF) situated in tubule between odontoblast process and tubule wall [11]. Slightly outward displacement of odontoblastic process (OP) and its cell body (CB) in response to outward flow. The dash line indicates the original position of the odontoblast. The outward movement of the OP reduces the dimension of the channel available for the DFF, resulting in increased shear stress on the terminal bead (TB) although the volume flow is low [4]. (D) Slightly inward displacement of OP in response to inward flow. This movement tends to produce a smaller shear stress on the TB than that at its original position (dash line). (E) Physically realistic model for fluid dynamics simulation (inward flow). d t, d p and d f are diameters of DMT, OP and TF, respectively; R b is radius of TB; L is computational length. One side of OP surface is in contact with tubular surface [36], hence no dentinal fluid is allowed to pass through at this side. The TF and OP are modeled as rigid structures that do not deform due to DFF. We assumed that there is no synaptic structure between OP and TF [48], though different finding has been reported [36]. TB containing varying amounts of receptor organelles [35] is assumed as the sensory zone at the end of TF. The volume of TF is smaller as compared with odontoblast [36], and hence the movements of TF as caused by DFF is neglectable. External stimuli (e.g., thermal, mechanical and dental restorative processes) applied to human tooth cause either an inward (toward the pulp chamber) or outward (away from the pulp chamber) dentinal fluid flow in dentinal microtubules [13]–[16]. Dentinal fluid flow-induced shear stress on intradental nerve terminals may activate mechano-sensitive ion channels (e.g., ASIC3, TREK1 and TREK2) [17] and cause dental pain sensation [17]– [20]. Direct evidence for the hydrodynamic theory is that intradental neural discharge rate increases with increasing dentinal fluid flow velocity (cat tooth, in vivo) [4], [7]. However, the neural responses in tooth (human and cats, in vivo) have been found to be more sensitive to the outward fluid flow than to the inward fluid flow [3], [4], [7] and that cold stimulation evokes more rapid transient pain sensations whilst hot stimulation generally induces a dull lasting pain [21], [22], both outlive the hydrodynamic theory. Although the precise transduction mechanism remains unknown, the major differences between the effects of hot and cold stimulations have been identified: the former causes an inward fluid flow while the latter causes an outward fluid flow [4], [7], [16]. An initially high rate of outward fluid flow under cooling was found to correspond to short latency neural responses [23]. In addition, odontoblastic process movements as aspirated by dentinal fluid flow have been demonstrated [4], [24]. Hence, a better understanding of the fluid flow, odontoblastic process movement and the associated intradental nerve 154 responses would provide an insight into the mechanisms underlying the different responses of tooth to cold and hot stimulations. In the present study, the effects of dentinal fluid flow on the shear stress experienced by nerve terminals were firstly analyzed using a computational fluid dynamics (CFD) model. A modified Hodgkin-Huxley (H-H) model was then proposed to simulate the intrapulpal nociceptor transduction. We validated the developed models by comparing the simulated results with the experimental observations by Andrew & Matthews [4] and Vongsavan & Matthews [7]. Based on the simulated results, we explained in detail that dentinal fluid flow with different directions and odontoblastic process movements cause significantly different intradental neural responses. Finally, mechanistic insights into the difference between hot and cold dental pain responses were provided. Go to:
Results and Discussion The tooth is innervated almost exclusively by nociceptive afferents [25], [26]. The neural discharge thresholds expressed in terms of flow velocity in a single dentinal microtubule have been found to be 460.4 µm/s (in the case of outward flow) and −849.9 µm/s (in the case of inward flow) [4]. However, there exists no experimental method for determining the mean mechanical pain threshold of intradental nociceptors. Since the mechano-sensitive ion channels open at a specific mechanical threshold [27], the two critical flow velocities should generate the same maximum shear stress on the terminal bead (τ MSS), which was assumed to be the threshold shear stress, τ thr, in this study. Therefore, our strategy was to relate the two critical flow velocities with τ thr. The local channel diameter (distance between terminal bead and odontoblastic process) depends upon the odontoblastic process displacement, which, in turn, depends upon the velocity and direction of the fluid flow. For example, when an inward flow is applied, a higher rate of fluid flow will cause more significant odontoblastic process displacement, increasing thereby the dimension of the channel available for the fluid flow [18] (Fig. 1 D). The above-mentioned relationships were simplified and simulated as follows. One value was specified for the local channel diameter at the critical outward flow velocity of 460.4 µm/s and the corresponding τ MSS (predicted) was assumed to be τ thr. Then, the value of the local channel diameter at the 155 critical inward velocity of −849.9 µm/s was adjusted over several cycles of τ MSS predictions until the predicted τ MSS was the same as the one obtained at the flow velocity of 460.4 µm/s. The local channel diameter values corresponding to other flow velocities (except the two critical flow velocities) were obtained with linear interpolation. The predicted τ MSS as a function of flow velocities are shown in Fig. 2. It should be noted that the τ thr and the predicted τ MSS at other velocities vary with the specified local channel diameter value at the flow velocity of 460.4 µm/s (Figure S1). Nevertheless, such variation does not affect the predicted neural responses (Figure S2, Text S1).
Figure 2 Variation of TB MSS (simulated) and neural discharge rate (measured[4]) as a function of fluid velocity (negative for inward flow; positive for outward flow).
Velocity thresholds: V c1 = 460.4 µm/s, V c2 = −849.9 µm/s [4]. To qualitatively explain why the inward and outward flows evoke significantly different intradental neural responses, we plotted the τ MSS against the flow velocities, and the results are compared with the change of neural responses (Fig. 2). We observed that the τ MSS in the outward 156 flow case increases dramatically with increasing flow velocity, corresponding to the increase in neural discharge rate. In sharp contrast, the τ MSS in the case of inward flow was observed to be “inert” to the increasing flow velocity and the neural discharge rate is zero or low accordingly (Fig. 2). The results of Fig. 2 indicate that the distinct difference in intradental neural responses to different fluid flow directions may be attributed to odontoblastic process displacement. τ MSS is dependent upon the fluid velocity, which, in turn, is dependent upon the dimension of the channel available for the fluid flow. Reducing the channel diameter may result in a higher shear stress and thus the neural discharge rate, although the volume flow is low. The simulated results of the membrane potential and frequency response at the outward flow velocity of 611.6 µm/s are shown in Fig. 3 A. The simulated impulse frequency (N = 17) agrees well with the experimental measurements of Vongsavan ∼& Matthews [7] (N = 17 in Fig. 3 B) and Andrew & Matthews [4] (N = 15 in Fig. 3 C). It is known that the pain intensity is reflected by the frequency of the impulse, not by its exact magnitude or shape. Hence, the present model is capable of capturing the neural responses of intradental mechano-sensitive nociceptors.
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Open in a separate window 158
Figure 3 Response of nociceptor membrane potential in cat tooth to flow velocity of 611.6 µm/s. ∼ (A) Action potential simulated with the modified H-H model. (B and C) Experimental measurements by Vongsavan & Matthews [7] and Andrew & Matthews [4], respectively. N is the number of neural impulses in 5 s. To quantitatively explain the significant difference in intradental neural responses to different fluid flow directions, we modeled the neural discharge rate (in 5 s) under different fluid flow velocities. The results are shown in Fig. 4. Experimental observations show that nociceptors respond in a significantly different manner to dentinal fluid flow having different directions [4]. The neural discharge rate increases progressively as the outward flow velocity increases above the threshold. In contrast, the nociceptors show much less sensitivity to the inward flow. The simulated results are in good agreement with the experimental data. Our simulations reveal that the odontoblastic process displacement accounts for the difference in the response of intradental nociceptors to inward and outward flows. The outward flow tends to carry the odontoblastic process toward the dentinal microtubule, reducing the dimension of the space for the fluid flow (Fig. 1 C) and thereby, increasing the fluid velocity (around the terminal bead wall) and the τ MSS. In this case, the neural discharge rate will increase even though the fluid velocity is low at the boundary. Conversely, the odontoblastic process displacement in the inward flow case tends to increase the dimension of the space for the fluid flow around the terminal bead wall (Fig. 1 D), resulting in a lower τ MSS even though the fluid velocity at the boundary is relatively high. Therefore, the intradental nociceptors exhibit “low sensitivity” to the inward flow.
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Figure 4 Comparison of frequency response between experimental measurements[4] and model predictions. Note that cold stimulation (0 5°C) is reported to cause outward flow velocities range between 531.2 849.9 µm/s [2], [4], whilst hot stimulation ( 55°C) causes inward flow velocities range between∼ 354.1 779.1 µm/s [4]. ∼ ∼ Although thermal pain sensation ∼has been attributed to the activation of thermal-gated ion channels [28], it may not be exactly the case when dental pain evoked by thermal stimulation is considered [23]. It has been demonstrated that the sensory response of tooth to thermal agitation occurs before a temperature change can be detected in the pulp-dentine junction where most sensory structures are located [29]. If the hydrodynamic theory is a valid mechanism responsible for dental thermal pain, the difference in the subjective pain responses may result from the different dentinal fluid flow induced by cold and hot stimulations. Although fluid velocities were employed as the boundary conditions in the modeling of the τ MSS and the subsequent neural discharge, the difference between hot and clod dental pain sensations can still be revealed. Note that the cold stimulation (0 5°C)- induced outward flow velocities range between 531.2 849.9 µm/s [2], [4] whilst the velocity range of the inward flow becomes∼ ∼ 160
354.1 779.1 µm/s [4] in the case of hot stimulation ( 55°C). These experimentally reported inward and outward flow directions and their corresponding∼ magnitudes were consistent with those∼ employed as the boundary conditions in this study (Fig. 2 and and4).4). Based on the simulated results (Fig. 4), the explanations for the phenomenon that cold stimulation causes sharper and more shooting pain sensation than does hot stimulation may be summarized as follows. The intradental neural response was observed after a short latency (<1 s) of cold stimulation (0 5°C) [30], [31]. At this stage, the local temperature (where terminal bead is located) is still far from being capable of activating the thermo-sensitive∼ nociceptors [31]. Therefore, it appears unlikely that such response is originated from the thermo-sensitive nociceptors. Note that fluid flow could be detected before a noticeable temperature change could be found in DEJ and that the latency of the initiation of the dentinal fluid flow (<1 s) [4], [16] (induced by either hot or cold stimulation) corresponds to the latency of the neural response. In addition, the flow velocity induced by cold stimulation may easily exceed the threshold [2], [4], which may activate the mechano-sensitive nociceptors (Fig. 2 and and4).4). Therefore, the initial stage of cold-induced dental pain (sharp, shooting pain) may involve the activation of mechano-sensitive nociceptors by dentinal fluid flow. It should be mentioned that, after a long latency ( 30 s), the neural response (dull, burning pain) to cold stimulation may be attributed to the activation of thermo-sensitive nociceptors [22], [32]: ∼by then the temperature around the nociceptors may have exceeded the threshold. In the case of hot stimulation (55°C), a relatively long latency (>10 s) of the neural response was observed [30], [31]. During this stage, no neural discharge could be detected [4], [30], [31]. This does not contradict with the conclusion that the dentinal fluid flow may evoke the neural response, since hot stimulation can hardly initiate a high rate of the fluid flow [4] needed for the activation of mechano-sensitive nociceptors (Fig. 2 and and4).4). It is possible that after such a long latency, the temperature around the thermo- sensitive nociceptors reaches the threshold [31], triggering the nociceptors and causing pain sensation [30], [31]. In conclusion, we have developed a simulation framework coupling a CFD model with a modified H-H model for the quantification of dental pain sensation (in terms of neural discharge) evoked by dentinal fluid flow in 161 dentinal microtubules. By attributing to different dentinal fluid flow directions and the corresponding odontoblast movements, it is demonstrated that the proposed models are capable of explaining the experimental observation that intradental mechano-sensitive nociceptors are not “equally sensitive” to inward and outward flows of dentinal fluid [4], [7]. The mechanism underlying the phenomenon that cold stimulation evokes sharper and more shooting pain sensation than hot stimulation also involves dentinal fluid flow and odontoblast movement. To our best knowledge, this study is the first attempt to the quantitatively interpret dental thermal pain responses in terms of fluid mechanics and will be potentially guide lines for tooth hypersensitivity treatment. Go to:
Methods
Modeling of shear stress The dentinal microtubule innervation system is consisted of dentinal fluid, non-myelinated sensory nerve fibril and odontoblastic process, as shown schematically in Fig. 1 C and D. To compare the simulated results with existing experimental data, the diameter of the microtubule was selected as d t ≈0.73 µm (cat canine) [4]. The dentinal fluid has a composition similar to that of cerebrospinal fluid, with viscosity µ ≈1.55×10−3 Pa·s and density ρ ≈1010 kg/m3 [33]. Up to 50% of the microtubules located in the pulpal horn are innervated [25] and, in most cases, each microtubule contains only one beaded terminal fibril [11]. The terminal fibril extends about 100 µm into the microtubule above the pupal wall [34]. The diameter of the terminal fibril is d f ≈0.1 µm [34]. The terminal beads have varying amounts of receptor organelles and the diameter of the bead is d b ≈0.2 µm [35]. The microtubule is also penetrated by odontoblastic process, whose cell body lies at the opening of the microtubule on the pulpal wall [4], and there is only one odontoblastic process inside a microtubule accompanied by only one terminal fibril in most cases [36]. The extension of the odontoblastic process was found to be restricted to the inner half of the microtubule ( 200 µm) [34]. The outline of the odontoblastic process is smooth and not beaded [11], with diameter decreasing along its longitudinal direction, i.e., from∼ pulpal wall to DEJ [36]. For simplicity, the odontoblastic process diameter was assumed to 162
vary linearly with its longitudinal direction, given that its maximum d op (at pulpal wall) is smaller than 1 µm [18]. Outward fluid flow causes slight movement of odontoblasts toward the microtubule whereas inward flow causes the odontoblasts to move in the opposite direction [4] (Fig. 1 C and D). The movement of the terminal fibril can be neglected due to its small volume as compared with that of odontoblast [18], [36]. The movement of the odontoblastic process changes the dimension of the space for the fluid flow, affecting thus the shear stress on the terminal bead [18] (Fig. 1 C and D). To model the effect of odontoblastic process movement upon the shear stress on the terminal bead, it was assumed here that the odontoblastic process displacement in the fluid flow direction changes linearly with the flow velocity. This assumption is deemed adequate for illustrating the overall behavior of the odontoblastic process in response to the dentinal fluid flow, because a higher rate of fluid flow will lead to a larger odontoblastic process displacement [4]. The CFD model was employed to simulate the τ MSS which will most probably exceed the mechanical threshold of the nociceptors, τ th. For CFD simulation, a physically realistic model representing the inward flow of dentinal fluid is shown in Fig. 1 E. Based on the in vivo structure of the dentinal microtubules innervation system described above and the symmetrical structure of the terminal bead and odontoblastic process in the longitudinally sectioned plane (along their axes), the three-dimensional (3D) structure of fluid flow through the dentinal microtubule innervation system was simplified to a two-dimensional (2D) model. Since the focus of the present research was on the τ MSS, this simplification provides reasonable approximation for the numerical simulation of fluid dynamics. Steady state Navier-Stokes equations for incompressible and laminar flow were employed to model the shear stress experienced by the terminal bead, expressed as:
(1)
(2) where V (m/s), p (Pa), ρ (kg/m3) and µ (Pa·s) are the velocity vector, pressure, density and viscosity of dentinal fluid, respectively. Constant fluid 163 velocity boundary conditions were applied in the simulation and the values of the fluid flow velocities employed were adopted from literature [4]. The experimentally recorded fluid flow velocities (nl s−1 mm−2) were converted into the fluid flow velocities in an individual dentinal microtubule (Text S2). The computational domain was meshed with rectangular elements and the independence of simulated results on mesh size was checked. Since the diameter of local channel (gap between terminal bead and odontoblastic process) is less than 1 µm, the influence of slip boundary (i.e., non-zero flow velocity at a solid wall) on the simulated results should be considered. Therefore, the simulated results were corrected using the following equation, which has been widely accepted [37]:
(3) where τ slip (Pa) and τ non-slip (Pa) are the wall shear stress when slip and non- slip boundary conditions are applied, respectively, δ (µm) is the slip length (the slip length is defined as the distance from the crest of the solid surface to the depth at which the linearly extrapolated velocity reaches zero at the wall ( 0.1 µm) [38], and h (µm) is the distance between two parallel walls (e.g., local channel diameter, 0.12 µm). ∼ Modeling of nociceptor∼ transduction Nociceptors are the receptors for pain sensations [39], mediating the selective passage of specific ions across ion channels of a cell membrane when stimulated by noxious stimulations [40]. The passage of the ions induces an ion current through the cell membrane and generates an action potential [41]. These potentials are conducted from the peripheral sensory site to the synapse in the central nervous system and converted into neurotransmitter release at the presynaptic terminal (frequency modulation) [41]. The ion channels are generally gated by mechanical, thermal and chemical stimulations, with three different currents induced accordingly. Given the parallel distribution of ion channels in the membranes of nociceptors, the total stimulation-induced 2 current, I st (µA/cm ), may be calculated as the sum of the three:
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(4) where I mech, I heat and I chem are separately the currents generated by opening the mechanically-, thermally- and chemically-gated ion channels (all in µA/cm2). Since the intradental nerve terminals are stimulated by shear stress in this study, in what follows only mechanical-gated ion channels were considered for the generation of stimulation-induced current. As the gating of ion channels is a threshold process, the mechanical current (I mech) was taken as a function (f m) of the MSS (τ MSS) on the terminal bead. Consequently, I mech can be determined by:
(5) where τ thr is the mechanical pain threshold. The relationship between the mechanical stimulation and the induced current is still unknown. However, it has been reported that the mechanical current is approximately exponentially proportional to the mechanical stimulation [27], indicating that the mechanically-gated ion channels may behave in a way similar to that of the heat-gated ion channels [28]. The quantitative relationship between the stimulation and current may thence be described as:
(6) where C h1, C h2 and C h3 are the constants; H(x) is the Heaviside function 2 accounting for the threshold process; and I shift (µA/cm ) is the shift current 2 (Text S3). The constants C h1, C h2 and C h3 are set to be 2.0 µA/cm , 2.0 µA/cm2 and −1.0 µA/cm2, respectively. To the authors' best knowledge, the response kinetics of intradental nociceptors has yet been analyzed in the literature. However, all neurons have been found to behave in a quantitatively similar way as that described by the H-H model [42]. In addition, neurons exhibit various types of potassium (K+) conductance. The fast transient K+ current has been observed in a variety of neurons [43], [44]. Hence, a modified H-H model has been proposed to 165 introduce more than one K+ channel to the modeling of the frequency modulation of nociceptors [45]–[47], expressed as:
(7)
Here, V mem is the membrane potential (mV), positive when the membrane is depolarized and negative when the membrane is hyperpolarized; (ms) is the 2 neural discharge time; C mem (µF/cm ) is the membrane capacity per unit + + 2 area; I Na, I K and I L are the sodium (Na ), K and leakage currents (µA/cm ), respectively; and I K2 is an additional current: the fast transient + K current. I Na, I K, I L [42] and I K2 [45] are given by:
(8) where m, n and h are the gating variables; A and B are factors having the same functional significance as factors m and h; V Na, V K, V L and V K2 are the reversal potentials for the Na+, K+, leakage and fast transient K+ currents (all in mV), respectively; and g Na, g K, g L and g A are the maximum ionic conductances of Na+, K+, leakage and the fast transient K+ currents (all in mS/cm2), respectively (see Text S4 for details on the determination of these variables and factors). The modified H-H model was used to model the frequency modulation of intradental nociceptors.
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23.) Bleeding gums and loose teeth can be a sign of mercury poisoning:
A. True B. False www.mercurypoisoned.com/symptoms.html
Symptoms of Chronic Mercury Poisoning
CENTRAL NERVOUS SYSTEM
irritability anxiety/nervousness, often with difficulty in breathing restlessness exaggerated response to stimulation fearfulness emotional instability -lack of self control -fits of anger, with violent, irrational behavior loss of self confidence indecision shyness or timidity, being easily embarrassed loss of memory inability to concentrate lethargy/drowsiness insomnia mental depression, despondency withdrawal suicidal tendencies manic depression
numbness and tingling of hands, feet, fingers, toes, or lips muscle weakness progressing to paralysis ataxia tremors/trembling of hands, feet, lips, eyelids or tongue incoordination myoneural transmission failure resembling Myasthenia Gravis
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Freya Koss (right) was diagnosed with Myasthenia Gravis after being stuck with double vision and ptotis (drooping eyelids) after having amalgam fillings placed.
Freya in 2002 after safe amalgam removal and detoxification. She is now Director of Development for Consumers for Dental Choice. More of her story is on their website at www.toxicteeth.org.
motor neuron disease (ALS) Multiple Sclerosis, see Janie's Story, and Ken Pressner's Speech to the MS Society
HEAD, NECK, ORAL CAVITY DISORDERS
bleeding gums alveolar bone loss loosening of teeth excessive salivation foul breath metallic taste burning sensation, with tingling of lips, face tissue pigmentation (amalgam tattoo of gums) leukoplakia stomatitis (sores in the mouth) ulceration of gingiva, palate, tongue dizziness/acute, chronic vertigo ringing in the ears hearing difficulties speech and visual impairment -glaucoma -restricted, dim vision
GASTROINTESTINAL EFFECTS
food sensitivities, especially to milk and eggs abdominal cramps, colitis, diverticulitis or other G.I. complaint chronic diarrhea/constipation 168
CARDIOVASCULAR EFFECTS
abnormal heart rhythm characteristic findings on EKG -abnormal changes in the S-T segment and/or -lower broadened P wave unexplained elevated serum triglyceride unexplained elevated cholesterol abnormal blood pressure, either high or low
IMMUNOLOGIC
repeated infections -viral and fungal -mycobacteria -candida and other yeast infections cancer autoimmune disorder -arthritis -lupus erythematosus (LE) -multiple sclerosis (MS) -scleroderma -amyolateral sclerosis (ALS) -hypothyroidism
SYSTEMIC EFFECTS
chronic headaches allergies severe dermatitis unexplained reactivity thyroid disturbance subnormal body temperature cold, clammy skin, especially hands and feet excessive perspiration, w/frequent night sweats unexplained sensory symptoms, including pain unexplained numbness or burning sensations unexplained anemia -G-6-PD deficiency Chronic kidney disease -nephrotic syndrome -receiving renal dialysis -kidney infection adrenal disease general fatigue 169
loss of appetite/with or without weight loss loss of weight hypoglycemia
PLEASE REPORT BROKEN LINKS TO marieflow (at) aol.com">marie [email protected].
Copied from the DAMS NEWSLETTER SPRING 1996. Originally from "The IV-C Mercury Detox Program, A Guide for the Patient," a companion handbook to Chronic Mercury Toxicity, New Hope Against and Endemic Disease, by Sam Queen and Betty A. Queen. Call 1-651-644-4572 for more information and a list of biological dentists for your state or province.
A checklist of other symptoms that could be related to mercury toxicity. A Mercury Test by Dr. Hal Huggins:
1. Heart problems _heart/chest pains _angina _tachcardia (heart racing) _heart murmur _low blood pressure _abnormal EKG _endocarditis _partial heart block _high blood pressure _heart attack
2. Skin Problems _unexplained rashes _excessive itching _red flushes of color _rough skin _acne (pimples)
3. Nervous Disorders _bell's Palsy _Multiple Sclerosis _shingles _epilepsy/convulsions _Dr. told you "It's your nerves" _the shakes of hands, feet, head, etc _twitching of face or other muscles
4. Digestion 170
_diverticulitis _ulcers _Crohn's disease _Graves Disease _indigestion _diarrhea _bloated feeling after eating _heartburn _poor appetite
5. Blood Disease _mononucleosis _false positve for venereal disease
6. Cancer _leukemia _Hodgkins disease _any other name
7. Endocrine Problems _diabetes _ovaries _hysterectomy-complete _tipped uterus _overweight _thyroid overactive _testes _pancreas _cervical erosion _underweight _prostate _mensturation-painful, too often or too seldom/ stopping without reason
8. Emotional _sudden anger _depression _wish you were dead _irritability _suicidal tendencies _been divorced
9. Annoying Symptoms _frequent headaches _noises in your ears _ringing in your ears _hissing in your ears _chronic eye inflammation _chronic fatigue _do you tire easily? 171
_swollen lymph nodes _do you sweat excessively or not at all? _hearing problems _cold hands and feet _motion sickness _slow healing _leg cramps _dizziness _get up at night to urinate _urinate frequently during the day _have insomnia _tired when awaken in the morning _have trouble making decisions
10. Allergies _metal _fabrics _soaps and detergents _food _other______
11. Diseases _rheumatoid arthritis _bursitis _tennis elbow _painful joints _Friedreich's ataxia _asthma _osteomyelitis _psoriasis _sickle cell anemia _kidney stones
12. Miscellaneous _Infections take a long time to heal _Do you work around mercury? what capacity?______what medications are you taking that have mercury in them?
13. Dental History _had silver amalgams _had gold fillings _have gold fillings now _removable metal bridge _gold bridge _porcelain caps (crowns) _non-precious crowns _root canal _root canal now 172
_metallic taste in mouth _burning sensation in mouth _increased flow of saliva _have more than half your teeth
Other Symptoms of Mercury Toxicity, compiled by Marie Flowers
heat, burning, tingling, soreness, itching of the the scalp burning muscles in the back and neck, burning ears feeling movement in the brain aching of the bones at the base of the skull sounds of crackling, popping at base of brain headaches right after eating muscular aches in areas of the body where previous injuries have occured double vision crossed eyes (see Carol's story below) chronic bladder infections, see Carol's story legs feeling so heavy like they are weighted down L'hermitte's Sign (electric shock-like sensations throughout the body) burning mouth and tongue, see http://www.flcv.com/galv.html reactions to electricity and oral galvanism of mouth. Story of medical doctor affected.
Signs and Symptoms of Mercury Poisoning from Dental Amalgam1 by Morton Walker, D.P.M. in his book Elements of Danger, Protecting Yourself Against the Hazards of Modern Dentistry
A series of difficulties characteristic of mercury toxicity affecting the eyes
bleeding from the retina of one or both eyes dim vision, expecially after exercise slow and poor accommodation to changes in vision distances Inability to fix one's gaze uncontrollable eye movements eyes drawn to one side imaginary geometric figures appearing in the visual field, which migrate in a few minutes from the periphery toward the center and slowly disappear "film" seeming to appear over the eyes dry eyes a gray ring forming permanently around the cornea (known as Arcus senilis)
One or more heart difficulties:
irregular hearbeat (palpitations), often together with anxiety stong pains in the left part of the chest come on 173
Problems in the upper respiratory tract:
asthmatic breathing troubles, such as a feeling of not being able to inhale A "cracking" sound in the lower part of the pleural sac, forcing one to cough red irritated throat inflammation in the upper airways and pleurisy appearing about a year after the dental treatment with amalgams difficulties in swallowing
Psychological troubles come on such as:
severe amnesia constant feelings of tension and strain anxiety irritability difficulty and even impossiblity to control behavior indecision loss of interest in life mental or emotion depression
Conditions of the brain, including:
tiredness nearly all the time a feeling of being "old" resistance to intellectual work reduced capacity for work, both for intellectual and physical tasks reduced powers of comprehension because information does not come through increased need for sleep headache about once a week. The headache often is migrainelike, especially induced by weather changes and by prolonged sleep in the mornings
Neurological complications can come on like:
vertigo (dizziness) facial paralysis, usually on the right side, that is partly permanent damage to balance and hearing a painful pull a the lower jaw toward the collar bone
Oral discomforts make their appearance such as:
increased salivation often-present sour metallic taste bleeding gums at toothbrushing 174
Numbers of other symptoms gradually showing up, including:
joint pains, especially increasing about a year after receiving the implantation of amalgam fillings pains in the lower back weakness of the muscles with a slowing down of muscular action feelings of pressure, pains, and paresthesis ("pins and needles") in the region of the liver gastrointestinal irritation paresthesis in the region of the lymph nodes under the arms and in the groin exzema or other skin eruptions
1 Sources: Stock, "Die Defaehrlichket des Quecksilberdampfes"; F. Gasser, "Quecksilberbelastung im Menschlichen Korper durch Amalgam," Med.-Biol. Arbeits und Forschungsgemeinsch (Baden-Baden, Germany: Dtsch. Zahnarzt., 1976): K. D. Jorgensen, "The Mechanism of Marginal Fracture of Amalgam fillings," Acta Odont. Scan. 23 (1965): 347.
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24.) What is generally considered the best treatment for NICO is? A. Surgery B. Inject the site with ozone C. Inject the site with homeopathics D. Inject the area with steroids E. all of the above https://www.nihadc.com/library/biological-dentistry/7-integrative-medical- dental-position-paper-nico-cavitations/file.html?accept_license=1
Integrative Medical-Dental position paper: NICO, Cavitations Statement We are dedicated to understanding the clinical significance, assessment and treatment of NICO lesions in the jaw. Furthermore we are involved in clinical outcomes research, effectiveness of assessment and treatment, cost and efficiency of treatment. We recognize the lack of consensus in the patho- physiology, assessment and treatment of NICO lesions and through our empirical observations, clinical achievements, study, networking and researching, we will become a service to our patients, value to our profession and a solution to the clinical and professional understanding of the root causes of health problems. What is a Cavitation (Neurological Inducing Cavitational Osteotis - NICO): Cavitations as the name implies is a hole in the bone – in our case the jaw bone, although this lesion is also found in other bones of the body (although less frequently than the jaw). If a biopsy is taken, it reveals itself as boney tissue that is ischemic (almost dead), often with large fatty globules and other characteristic features of not healthy bone and its marrow. Basically and a hole in the bone, which could be round or any shape sometimes with fingerlike projections extending outward (worm-holes). “Neurological inducing” refers to the potential of this pathology causing neurological disturbance, which originally was understood to be pain in areas away from the NICO site. In fact, these lesions sometimes cause pain with the symptoms manifesting in neurologically “referred’ sites. Now it is widely understood that these neurological inducing lesions (NICO) cause a wide variety of health issues, because they seriously affect the Autonomic Nervous System (ANS). The NICO symptoms where the dysfunction manifests or the general bodily conditions most often referred or not in the immediate vicinity of the NICO lesion, which is the characteristic of neurological inducing lesions.. Controversy: There are three controversies regarding NICO: i. Western school medicine (traditional dental school) while acknowledging NICO lesions for 100 years in its textbooks, minimizes the incidence and the impact on the health of the patient. Those involved in Integrative Medicine (physicians and dentists) disagree. Through testing and empirical observation of the many patients we have treated, we realize that NICO is a major health problem and impediment to many patients healing. ii. NICO lesions have traditionally been treated by surgery only. Most of the clinicians that have historically studied and treated this condition have used a surgical approach to remove the lesion. The 2 non-surgical approach to NICO was developed later and the empirical observation in the thousands of patients appears to indicate that the non-surgical treatment is very helpful for some but not all. iii. Assessment of NICO is another controversial issue. The history is only suggestive. The gold standard for assessing pathological lesions is biopsy and/ or imaging. Traditional imaging (a panorex of the jaw) has been hard for the traditional dental establishment to evaluate and often is not detailed enough to visualize the NICO’s boarders. Other imaging and sonographic (sound) assessments are employed but not well understood by the Medical and Dental specialists at this point in time. Note since NICO is a strong disturbance of the Autonomic Nervous System (ANS) many biofeedback assessment techniques have been successfully employed, with nearly 100% of accuracy in determining NICO as confirmed by pathologic report after surgery. The controversy is that traditional dentistry and medicine often rejects these very useful and inexpensive assessment tools. Our position: We have over 15 years of assessing and treating patients with NICO lesions. We have been present and participated in the beginning of the understanding of this jaw bone issue. We have the ability to assess NICO using the standard biofeedback 176
assessment tools (i.e. meridian stress testing (MST), Autonomic Response Testing (ART) and Contact Regulation Thermography (CRT). Dr. Weiner, a founding member of the Integrative Medical-Dental team has pioneered the advancement of spiral CT scans in assessing NICO with imaging. He also uses MRI and other imaging techniques along with computerized sonography. We have the ability to treat NICO surgically, with 2 dental surgeons with over 20 years of combined surgical experience in NICO surgical treatment. We have also been in the forefront of the non-surgical treatment of these pathological health issues of the jaw. We have observed the dramatic recovery of patient’s health issues over the years from the treatment of NICO (along with other Integrative Medical therapeutics aimed at the root causes of the disease). Some of the health conditions that our patients have had that seemed to have positively responded after the NICO lesions were treated are: pain and TMD dys-function, allergies, autoimmune, cancer, chronic fatigue, heart disease and other generalized and specific health conditions. We at NIHA and the multiple physicians and other informed health professionals that refer to us for this condition have many years of empirical evidence of the great incidence and the importance of NICO treatment in the health and healing of many of our patients. Patho-physiology: what is the causation of NICO and why is it such a problem? There is no consensus in traditional or holistic groups regarding why NICO lesions forms, why it appears to be so prevalent and what are the biological effects and its contribution to the health problems of the patient. We are influences in our opinion by international research, clinical observations regarding assessment and therapeutics, 3 Integrative Medical models, good medical judgment and the clinical outcomes of our patients. The following is our best answer to what is the patho-physiology of NICO: 1. NICO appears to be a dump site for heavy metals (mercury, tin, platinum, palladium, nickel and others) that are stored but cannot be removed (detoxed) from the body. The evidence that influences this statement: a. Research by the German toxicologist Daunderer: in 2000 patient NICO surgery samples, he found a very high concentration of these toxic heavy metals that are found in the metal restorations and crowns in the mouth of the patients and are now known to be slowly released into the body. One patient it was reported in Germany had 20 consecutive surgeries, where high amounts of mercury were recovered. b. MST and ART assessments indicate mercury and other heavy metals in all NICO lesions in patients that had mercury fillings present at one time. Note that the mercury fillings could have been removed for many years, but the dump site (NICO lesion) remains because the body can’t metabolize and detox the NICO lesion. c. When mercury is present we usually use mercury chelating agents to treat the NICO non-surgically, along with other remedies. For this reason, we strongly suggest that the mercury fillings are removed prior to any surgical or non-surgical NICO therapeutics. Get rid of the source first (the toxic metal fillings) then treat the damage (the NICO lesion). d. Principles of Homotoxicology (man’s toxins) state that the body will remove or excrete toxins if it can but if it cannot, the toxins are stored. Mercury and other heavy metals cannot be detoxed easily by the body’s natural processes. Therefore storage sites are used to warehouse the mercury, close to the site of toxification (the fillings of the mouth), and often in an active metabolic site – the area of the wisdom teeth after their extraction. 2. NICO lesions are Toxic Foci or Interference Fields, which are high charged neuro pathological areas that result in a disturbance at a distal site. The concept of toxic foci is not understood by conventional and some holistic Medical and Dental professionals, because it involves a deeper understanding of how the Autonomic Nervous System (ANS) functions and how it appears to protect us from toxic substances that we continually expose ourselves to on a day by day basis, like the presence of mercury fillings in our mouth. Definitions of Interference Fields: chronically altered tissue which encloses organic and inorganic material that cannot be removed or metabolized, which causes remote disturbances of a general and local kind.” Pischinger “An Interference Field is where a pathologically charged tissue or region produces a disturbance via the (SNS) nerves not manifested in a remotely located disease.” W. Huneke The ANS in general and the sympathetic nervous system in particular functions to maintain the best internal milieu or internal environment. The ANS controls every internal extra cellular bodily function – like blood flow, neuropeptide and neurotransmitters, cellular signaling agents, the active transport of all the nutrients and wastes to and from the cells, even the cellular membranes are 4 under the partial control of this very 177
active neurological system that functions “autonomically”, without consciousness. Furthermore, the NICO lesion is an area of scant blood flow and almost no immune system activation, which makes it a great area for chronic infections to ”hide out”, without the immune system to battle The ANS when confronted by a chronically dysfunctional tissue, reacts by creating much sensory neurological activity but on the motor side shuting down the blood flow, immune system and any other healing entities in its arsenal. This is why the NICO lesions can be present for many years (over 40), without healing. So in other words the NICO lesion remains a storage of mercury dump site, with neurological consequences from the toxicity of its contents and the overload of the functional neurological system. All chronic diseases, pain and dys-functions in any tissue, have dys-autonomia, or a dys-regulation in the blood flow and other extra cellular dynamics mentioned above, or else the body- the self healing organism that it is designed to be, would do it job. Since NICO lesions are neurological pathologies, doesn’t it make sense to use neurological testing techniques to determine if NICO is present and if healing is taking place or the neurological disturbance is removed. This is why we utilize Meridian Stress Testing (MST) and Autonomic Response Testing (ART) as very precise tools to assess for NICO. Rule in Integrative Medical testing – if the lesion is primarily physical assess with physical tools – imaging and lab tests; if the lesion is primarily neurological – test with neurological biofeedback tools; if the lesion is primarily mental – test with neuro-psychobiologic, psychological and brain dynamics tools. 3. Some of the effects of NICO on other diseases a. NICO lesions appear to shut down aerobic metabolism, and switch the body’s metabolism to the inefficient anaerobic metabolism. This is a routine finding by Dr. Soloman on her Computron, a MST device. The symptoms of such a condition are chronic fatigue and no energy. When corrected the energy is often restored and the other therapeutic interventions appear to now work. b. The contents of the toxic soup of NICO that have been tested contain potent toxins that poison the Krebs cycle energy producing enzymes. These anti-metabolites can over time overwhelm the detoxifying and transport system to inactivate and carry them out, now adding to general bodily toxicity. This is another reason for the inability to properly utilize oxygen, which is a characteristic in all chronic, degenerative and neoplastic diseases. Dr. Ali, the world famous Integrative Medical physician, refers to this condition as dys-oxygenosis. c. The neurological system is interconnected and linked in a way that is not completely understood. The Chinese have empirically studied this linkage through the meridian system of Traditional Chinese Medicine (TCM), and have linked reflexively the mouth and teeth to meridians, organs, structures and glands. Dead teeth, root canal teeth and NICO all contain these toxic and neurological disturbances, which are linked to these distal structures. The linkage is not well understood at this time , but the result is the shutting down of the blood flow to these structures and / or organs so that the functional capacity is reduced. This chronic condition leaves the 5 organ or structure with less (functional) capacity to work and if injured less capacity to heal. i. Consider that many heart attacks or coronary vasoconstrictions occur with little build up of plaque to cause a physical obstruction, therefore the only explanation is a neurological induced vasoconstriction. The NICO of the 3rd molar of wisdom tooth, the most common site of NICO is on the heart meridian. History: History is very important, but with NICO the history can be allusive because the effects are neurological and toxic overload which have distal and referred symptoms Suspect dys-autonomia Chronic fatigue – cellular energy Allergies Multiple health issues that don’t seem to respond to therapy, especially other integrative medical therpay Tissue/ organ dys-function, especially if non-resistant to other healing therapies – blood flow dys-function, chronic hypo-perfussion; reduces functional capacity – to function and to withstand injury, unable to heal if injured Chronic infections: lyme, herpes, candida, - able to hide away from the Immune system, and blood flow and healing or antibiotic therapy. Chronic pain and dys-function is musculo-skeletal system – lack of blood flow to heal properly. Neoplastic disease – is chronic cellular toxicity, damaging the cellular DNA, lack of immune response – killing the neoplastic cells Degenerative disease – is cellular toxicity and lack of blood flow to heal and regenerate the tissue Suspect NICO if Chronic problems started after 3rd molar extractions, either immediately or a couple years later Difficult 3rd molar extractions, that had a hard time to heal If you had mercury fillings when your 3rd molars were removed If you have degenerative of neoplastic disease If you have energy problems By Mark McClure, DDS, FAGD, 178
ND, Doctor of Integrative Medicine National Integrated Health Associates, 5225 Wisconsin Ave, Suite 401, Washington DC 20015
25.) What percentage of Western Europe has chosen fluoride free water? A. 25% B. 57% C. 78% D. 97% https://sciencebasenutrition.com/fluoride http://fluoridealert.org/content/europe-statements/ At present, 97% of the western European population drinks non-fluoridated water.
26.) Exposure to fluoridated water in babies can cause damage to the developing brain, learning defect and other problems. A. True B. False http://fluoridealert.org/wp-content/uploads/neurath.ppt.feb-10-2020.pdf https://www.hsph.harvard.edu/news/features/fluoridec hildrens- health-grandjean-choi/ F and IQ 33 Very large loss of IQ with increasing tap water F for formula fed infants -9 IQ points (Full Scale IQ) for each 1 mg/L increase in tap water F. The fetal and infant brain is more susceptible than the adult to permanent 188 harm from neurotoxic chemicals. 179
• The complex precisely timed neurodevelopment process offers many opportunities for disruption. • The blood brain barrier is not well developed during the fetal period and the first 6 months of life. • Disruption during even a short window of neurodevelopment can cause life-long permanent harm.
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27.) Risks of ingesting fluoride include: A. Damage to the brain B. Damage to the thyroid and pineal gland C. Risks to bones with an increase in bone cancer D. Renal osteodystrophy E. All of the above.
https://iaomt.org/resources/fluoride-facts/fluoride-exposure-human-health-risks/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3956646/
https://iaomt.org/resources/fluoride-facts/fluoride-exposure-human-health-risks/ https://globalhealing.com/natural-health/9- shockingdangers- of-fluoride/ Acne and other dermatological conditions Arterial calcification and arteriosclerosis Bone weakness and risk of fractures Cancer of the bone, osteosarcoma Cardiac failure Cardiac insufficiency Cognitive deficits Dental fluorosis Diabetes Early puberty in girls Electrocardiogram abnormalities Harm to the fetal brain Hypertension Immune system complications Insomnia Iodine deficiency Lower fertility rates Lower IQ Myocardial damage Neurotoxic effects, including ADHD Osteoarthritis Skeletal fluorosis Temporomandibular joint disorder (TMJ) Thyroid dysfunction
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28.) Added exposure to fluoride can be found in: A. Non-Organic wines and grape juice B. Teflon coated pans C. Green or black tea D. Some prescription medications and general anesthetics E. All of the above
https://www.nap.edu./read/11571/chapter/4#44
Measures of Exposure to Fluoride in the United States The major sources of internal exposure of individuals to fluorides are the diet (food, water, beverages) and fluoride-containing dental products (toothpaste, fluoride supplements). Internal exposure to fluorides also can occur from inhalation (cigarette smoke, industrial emissions), dermal absorption (from chemicals or pharmaceuticals), ingestion or parenteral administration of fluoride-containing drugs, and ingestion of fluoride-containing soil. Information on the pharmacokinetics of fluoride are provided in Chapter 3. The National Research Council’s (NRC’s) 1993 review of the health effects of ingested fluoride reported estimates of average daily fluoride intake from the diet of 0.04-0.07 milligrams per kilogram (mg/kg) of body weight for young children in an area with fluoridated water (fluoride concentration in drinking water, 0.7-1.2 mg per liter [L]; NRC 1993). Dietary intake of fluoride by adults in an area with fluoridated water was variously estimated to be between 1.2 and 2.2 mg/day (0.02-0.03 mg/kg for a 70-kg adult). The fluoride intake from toothpaste or mouth rinse by children with good control of swallowing, assuming twice-a-day use, was estimated to equal the intake from food, water, and beverages. The review acknowledged that “substantially” higher intakes of fluoride from consumption of fluoridated water would result for individuals such as outdoor laborers in warm climates or people with high- urine-output disorders, but these intakes were not quantified. Similarly, children and others with poor control of swallowing could have intakes of fluoride from dental products that exceed the dietary intakes, but these intakes also were not quantified. Other factors cited as affecting individual fluoride intakes include changes in the guidelines for Page 24 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of 182
EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel fluoride supplementation and use of bottled water or home water purification systems rather than fluoridated municipal water. The NRC (1993) recommended further research to “determine and compare the intake of fluoride from all sources, including fluoride-containing dental products, in fluoridated and nonfluoridated communities.” This chapter provides a review of the available information on fluoride exposures in the United States, including sources of fluoride exposure, intakes from various fluoride sources, and factors that could affect individual exposures to fluorides. Population subgroups with especially high exposures are discussed. The major emphasis of this chapter is on chronic exposure rather than acute exposure. The use of biomarkers as alternative approaches to estimation of actual individual exposures is also discussed. In practice, most fluorine added to drinking water is in the form of fluosilicic acid (fluorosilicic acid, H2SiF6) or the sodium salt (sodium fluosilicate, Na2SiF6), collectively referred to as fluorosilicates (CDC 1993); for some smaller water systems, fluoride is added as sodium fluoride (NaF). Fluoride in toothpaste and other dental products is usually present as sodium fluoride (NaF), stannous fluoride (SnF2), or disodium monofluorophosphate (Na2PO3F). Fluorine-containing pesticides and pharmaceuticals also contribute to total fluorine exposures and are considered separately. Fluoride in food and drinking water usually is considered in terms of total fluorine content, assumed to be present entirely as fluoride ion (F−). Information on exposures to fluorosilicates and aluminofluorides is also included. SOURCES OF FLUORIDE EXPOSURE Drinking Water
General Population
The major dietary source of fluoride for most people in the United States is fluoridated municipal (community) drinking water, including water consumed directly, food and beverages prepared at home or in restaurants from 183 municipal drinking water, and commercial beverages and processed foods originating from fluoridated municipalities. On a mean per capita basis, community (public or municipal) water constitutes 75% of the total water ingested in the United States; bottled water constitutes 13%, and other sources (e.g., wells and cisterns) constitute 10% (EPA 2000a). Municipal water sources that are not considered “fluoridated” could contain low concentrations of naturally occurring fluoride, as could bottled water and private wells, depending on the sources. An estimated 162 million people in the United States (65.8% of the population served by public water systems) received “optimally fluori- Page 25 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel dated”1 water in 2000 (CDC 2002a). This represents an increase from 144 million (62.1%) in 1992. The total number of people served by public water systems in the United States is estimated to be 246 million; an estimated 35 million people obtain water from other sources such as private wells (CDC 2002a,b). The U.S. Environmental Protection Agency (EPA) limits the fluoride that can be present in public drinking-water supplies to 4 mg/L (maximum contaminant level, or MCL) to protect against crippling skeletal fluorosis, with a secondary maximum contaminant level (SMCL) of 2 mg/L to protect against objectionable enamel fluorosis (40CFR 141.62(b)[2001], 40CFR 143.3[2001]). Of the 144 million people with fluoridated public water supplies in 1992, approximately 10 million (7%) received naturally fluoridated water, the rest had artificially fluoridated water (CDC 2002c). Of the population with artificially fluoridated water in 1992, more than two-thirds had a water fluoride concentration of 1.0 mg/L, with almost one-quarter having lower 184 concentrations and about 5% having concentrations up to 1.2 mg/L (CDC 1993; see Appendix B). Of the approximately 10 million people with naturally fluoridated public water supplies in 1992, approximately 67% had fluoride concentrations ≤ 1.2 mg/L (CDC 1993; see Appendix B). Approximately 14% had fluoride concentrations between 1.3 and 1.9 mg/L and another 14% had between 2.0 and 3.9 mg/L; 2% (just over 200,000 persons) had natural fluoride concentrations equal to or exceeding 4.0 mg/L.2 Water supplies that exceeded 4.0 mg/L ranged as high as 11.2 mg/L in Colorado, 12.0 mg/L in Oklahoma, 13.0 mg/L in New Mexico, and 15.9 mg/L in Idaho (see Appendix B, Table B-3).3 States with the largest populations receiving water supplies with fluoride at ≥ 4.0 mg/L included Virginia (18,726 persons, up to 6.3 mg/L), Oklahoma (18,895 persons, up to 12.0 mg/L), Texas (36,863 persons, up to 8.8 mg/L), and South Carolina (105,618 persons, up to 5.9 mg/L). Little information is available on the fluoride content of private water sources, but the variability can reasonably be expected to be high and to 1 The term optimally fluoridated water means a fluoride level of 0.7-1.2 mg/L; water fluoride levels are based on the average maximum daily air temperature of the area (see Appendix B). 2 More recently (2000), CDC has estimated that 850,000 people are served by public water supplies containing fluoride in excess of 2 mg/L; of these, 152,000 people receive water containing fluoride in excess of 4 mg/L (unpublished data from CDC as reported in EPA 2003a). Based on analytical data from 16 states, EPA (2003a) estimates that 1.5-3.3 million people nationally are served by public water supplies with fluoride concentrations exceeding 2 mg/L; of these 118,000-301,000 people receive water with fluoride concentrations greater than 4 mg/L. 3 High-fluoride municipal waters are generally found in regions that have high fluoride concentrations in the groundwater or in surface waters. ATSDR (2003) has reviewed fluoride concentrations in environmental media, including groundwater and surface water. Fleischer (1962) and Fleischer et al. (1974) reported fluoride concentrations in groundwater by county for the coterminous United States. Page 26 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. × 185
Save Cancel depend on the region of the country. Fluoride measured in well water in one study in Iowa ranged from 0.06 to 7.22 mg/L (mean, 0.45 mg/L); home-filtered well water contained 0.02-1.00 mg/L (mean, 0.32 mg/L; Van Winkle et al. 1995). Hudak (1999) determined median fluoride concentrations for 237 of 254 Texas counties (values were not determined for counties with fewer than five observations). Of the 237 counties, 84 have median groundwater fluoride concentrations exceeding 1 mg/L; of these, 25 counties exceed 2 mg/L and five exceed 4 mg/L. Residents in these areas (or similar areas in other states) who use groundwater from private wells are likely to exceed current guidelines for fluoride intake. Duperon et al. (1995) pointed out that fluoride concentrations reported by local water suppliers can be substantially different from concentrations measured in water samples obtained in homes. Use of home water filtration or purification systems can reduce the fluoride concentration in community water by 13% to 99%, depending on the type of system (Duperon et al. 1995; Van Winkle et al. 1995; Jobson et al. 2000). Distillation or reverse osmosis can remove nearly all the fluoride. The extent of use of home water filtration or purification systems nationally is not known but obviously would affect the fluoride intake for people using such systems. Van Winkle et al. (1995) reported that 11% of their study population (in Iowa) used some type of home filtration either for well water or for public water. Fluoride concentrations in bottled water4 are regulated by law to a maximum of 1.4-2.4 mg/L if no fluoride is added and a maximum of 0.8-1.7 mg/L if fluoride is added (the applicable value within the range depends on the annual average of maximum daily air temperatures at the location of retail sale; 21CFR 165.110[2003]). Maximum fluoride concentrations for imported bottled water are 1.4 mg/L if no fluoride is added and 0.8 mg/L if fluoride is added (21CFR 165.110[2003]). Fluoride concentrations are required on labels in the United States only if fluoride is added. Fluoride concentrations listed on labels or in chemical analyses available on the Internet for various brands range from 0 to 3.6 mg/L (Bartels et al. 2000; Johnson and DeBiase 2003; Bottled Water Web 2004); of those without added fluoride, most are below 0.6 mg/L. Most brands appear to list fluoride content only if they are specifically advertising the fact that their water is fluoridated; fluoride concentrations of 186 these brands range from 0.5 to 0.8 mg/L (for “nursery” or “infant” water) up to 1.0 mg/L. Several reports indicate 4 The term “bottled water” applies to water intended for human consumption, containing no added ingredients besides fluoride or appropriate antimicrobial agents; the regulations apply to bottled water, drinking water, artesian water, artesian well water, groundwater, mineral water, purified water, demineralized water, deionized water, distilled water, reverse osmosis water, purified drinking water, demineralized drinking water, deionized drinking water, distilled drinking water, reverse osmosis drinking water, sparkling water, spring water, and well water (21CFR 165.110[2003]). Page 27 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel that fluoride concentrations obtained from the manufacturer or stated on labels for bottled waters might not be accurate (Weinberger 1991; Toumba et al. 1994; Bartels et al. 2000; Lalumandier and Ayers 2000; Johnson and DeBiase 2003; Zohouri et al. 2003). Measured fluoride concentrations in bottled water sold in the United States have varied from 0 to 1.36 mg/L (Nowak and Nowak 1989; Chan et al. 1990; Stannard et al. 1990; Van Winkle et al. 1995; Bartels et al. 2000; Lalumandier and Ayers 2000; Johnson and DeBiase 2003). Van Winkle et al. (1995) reported a mean of 0.18 mg/L for 78 commercial bottled waters in Iowa. Johnson and DeBiase (2003) more recently reported values ranging from 0 to 1.2 mg/L for 65 bottled waters purchased in West Virginia, with 57 brands having values below 0.6 mg/L. Measured fluoride concentrations in bottled waters in other countries have similar ranges: 0.05-4.8 mg/L in Canada (Weinberger 1991), 0.10-0.80 mg/L in the United Kingdom (Toumba et al. 1994), and 0.01-0.37 mg/L more recently in the United Kingdom (Zohouri et 187 al. 2003).5 Bartels et al. (2000) found significant variation in fluoride concentrations among samples of the same brand with different bottling dates purchased in the same city. In general, distilled and purified (reverse osmosis) waters contain very low concentrations of fluoride; drinking water (often from a municipal tap) and spring water vary with their source, as do mineral waters, which can be very low or very high in fluoride. Most spring water sold in the United States probably has a low fluoride content (<0.3 mg/L). Typical fluoride concentrations in various types of drinking water in the United States are summarized in Table 2-1. Average per capita ingestion of community or municipal water is estimated to be 927 mL/day (EPA 2000a; see Appendix B6). The estimated 90th percentile of the per capita ingestion of community water from that survey is 2.016 L/day. Estimated intakes by those actually consuming community water (excluding people with zero ingestion of community water) are higher, with a mean of 1.0 L/day and a 90th percentile of 2.069 L/day (EPA 2000a). Thus, if national estimates of water intake (see Appendix B) 5 The European Commission has set a maximum limit of 5.0 mg/L for fluoride in natural mineral waters, effective January 1, 2008 (EC 2003). In addition, natural mineral waters with a fluoride concentration exceeding 1.5 mg/L must be labeled with the words “contains more than 1.5 mg/L of fluoride: not suitable for regular consumption by infants and children under 7 years of age,” and for all natural mineral waters, the actual fluoride content is to be listed on the label. England has essentially the same requirements (TSO 2004), applicable to all bottled waters (natural mineral waters, spring water, and bottled drinking water). 6 As described more fully in Appendix B, the values from EPA (2000a) are from a short-term survey of more than 15,000 individuals in the United States. Although these values are considered reasonable indicators both of typical water consumption and of the likely range of water consumption on a long-term basis, they should not be used by themselves to predict the number of individuals or percentage of the population that consumes a given amount of water on a long-term basis. Page 28 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
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Save Cancel TABLE 2-1 Typical Fluoride Concentrations of Major Types of Drinking Water in the United States Source Range, mg/La Municipal water (fluoridated) 0.7-1.2 Municipal water (naturally fluoridated) 0.7-4.0+ Municipal water (nonfluoridated) <0.7 Well water 0-7+ Bottled water from municipal source 0-1.2 Spring water 0-1.4 (usually <0.3) Bottled “infant” or “nursery” water 0.5-0.8 Bottled water with added fluorideb 0.8-1.0 Distilled or purified water <0.15 aSee text for relevant references. bOther than “infant” or “nursery” water. are assumed to be valid for the part of the population with fluoridated water supplies, the intake of fluoride for a person with average consumption of community water (1 L/day) in a fluoridated area ranges from 0.7 to 1.2 mg/day, depending on the area. A person with consumption of community water equivalent to the 90th percentile in that survey (2.069 L/day) would have a fluoride intake between 1.4 and 2.5 mg/day, from community water alone. Table 2-2 provides examples of fluoride intake by typical and high consumers of municipal water by age group. The estimates of water consumption described in Appendix B are in keeping with recently published “adequate intake” values for total water consumption (including drinking water, all beverages, and moisture in food; IOM 2004; see Appendix B, Table B-10). Note that these estimates are national values; the range of values for optimal fluoridation was intended to account for expected regional differences in water consumption due to regional temperature differences (see Appendix B). A separate study based on the same data used by EPA (2000a) found no strong or consistent association between water intake and month or season (Heller et al. 1999). Another recent study of American children aged 1-10 years also found no significant relationship between water consumption and mean temperature in modern conditions (perhaps due to artificial temperature regulation) and suggested that the temperature-related guidelines for fluoride concentrations in drinking water be reevaluated (Sohn et al. 2001). 189
Actual intakes of fluoride from drinking water by individuals depend on their individual water intakes, the source or sources of that water, and the use of home water purification or filtration systems. As described earlier, fluoride concentrations in community water might vary from their reported concentrations; fluoride content of bottled water also varies considerably with brand or source, with packaging date for a given brand, and from Page 29 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel TABLE 2-2 Examples of Fluoride Intake from Consumption of Community (Municipal) Water by People Living in Fluoridated Areasa Typical Consumersb High Consumersc Water Consumption Fluoride Intaked Water Consumption Fluoride Intaked mL/day mL/kg/day mg/day mg/kg/day mL/day mL/kg/day mg/day mg/kg/day U.S. population 1,000 17 0.7-1.2 0.012-0.020 2,100 33 1.5-2.5 0.023-0.040 (total) All infants (<1 500 60 0.35-0.6 0.042-0.072 950 120 0.67-1.1 0.084-0.14 year)e Children 1-2 years 350 26 0.25-0.42 0.018-0.031 700 53 0.49-0.84 0.037-0.064 Children 3-5 years 450 23 0.32-0.54 0.016-0.028 940 45 0.66-1.1 0.032-0.054 Children 6-12 years 500 16 0.35-0.6 0.011-0.019 1,000 33 0.7-1.2 0.023-0.040 Youths 13-19 years 800 12 0.56-0.96 0.0084-0.014 1,700 26 1.2-2.0 0.018-0.031 Adults 20-49 years 1,100 16 0.77-1.3 0.011-0.019 2,200 32 1.5-2.6 0.022-0.038 Adults 50+ years 1,200 17 0.84-1.4 0.012-0.020 2,300 32 1.6-2.8 0.022-0.038 Females 13-49 980 15 0.69-1.2 0.011-0.018 2,050 32 1.4-2.5 0.022-0.038 yearsf aBased on consumption data described in Appendix B for people actually consuming community (municipal) water. bBased on a typical consumption rate of community (municipal) water for the age group. cBased on a reasonably high (but not upper bound) consumption rate of community (municipal) water for the age group; some individual exposures could be higher. dBased on fluoride concentrations of 0.7-1.2 mg/L. 190
eIncludes any infant, nursing or nonnursing, who consumes at least some community water; these infants may be fed primarily breast milk, ready-to-feed formula (to which no water is normally added), or formula prepared from concentrate (which requires addition of water). fWomen of childbearing age. Page 30 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel information (if any) given on the labels or provided by the manufacturer. Private water sources (e.g., wells and cisterns) probably are even more variable in fluoride content, with some regions of the country being especially high and others very low. A number of authors have pointed out the difficulty doctors and dentists face in ascertaining individual fluoride intakes, just from drinking water (from all sources), for the purpose of prescribing appropriate fluoride supplementation (Nowak and Nowak 1989; Chan et al. 1990; Stannard et al. 1990; Levy and Shavlick 1991; Weinberger 1991; Dillenberg et al. 1992; Jones and Berg 1992; Levy and Muchow 1992; Toumba et al. 1994; Duperon et al. 1995; Van Winkle et al. 1995; Heller et al. 1999; Bartels et al. 2000; Lalumandier and Ayers 2000; Johnson and DeBiase 2003; Zohouri et al. 2003).
High Intake Population Subgroups
EPA, in its report to Congress on sensitive subpopulations (EPA 2000b), defines sensitive subpopulations in terms of either their response (more severe response or a response to a lower dose) or their exposure (greater exposure than the general population). Hence, it is appropriate to consider those population subgroups whose water intake is likely to be substantially above the national average for the corresponding sex and age group. These 191 subgroups include people with high activity levels (e.g., athletes, workers with physically demanding duties, military personnel); people living in very hot or dry climates, especially outdoor workers; pregnant or lactating women; and people with health conditions that affect water intake. Such health conditions include diabetes mellitus, especially if untreated or poorly controlled; disorders of water and sodium metabolism, such as diabetes insipidus; renal problems resulting in reduced clearance of fluoride; and short-term conditions requiring rapid rehydration, such as gastrointestinal upsets or food poisoning (EPA 2000a). (While the population sample described in Appendix B [Water Ingestion and Fluoride Intakes] included some of these individuals, the study did not attempt to estimate means or distributions of intake for these specific subgroups.) As shown in Appendix B (Tables B-4 to B-9), some members of the U.S. population could have intakes from community water sources of as much as 4.5-5 L/day (as high as 80 mL/kg/day for adults). Some infants have intakes of community water exceeding 200 mL/kg/day. Heller et al. (1999), using the same data set as EPA (2000a), reported that 21 of 14,640 people (of all ages) had water intakes over 6 standard deviations from the mean (greater than 249 mL/kg/day). Whyte et al. (2005) describe an adult woman who consistently consumed 1-2 gallons (3.8-7.6 L) of fluid per day (instant tea made with well water); no specific reason for her high fluid consumption is given. Page 31 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel Fluid requirements of athletes, workers, and military personnel depend on the nature and intensity of the activity, the duration of the activity, and the ambient temperature and humidity. Total sweat losses for athletes in various sports 192 can range from 200 to 300 mL/hour to 2,000 mL/hour or more (Convertino et al. 1996; Horswill 1998; Cox et al. 2002; Coyle 2004). Most recommendations on fluid consumption for athletes are concerned with matching fluid replacement to fluid losses during the training session or competition to minimize the detrimental effects of dehydration on athletic performance (Convertino et al. 1996; Horswill 1998; Coris et al. 2004; Coyle 2004). Depending on the nature of the sport or training session, the ease of providing fluid, and the comfort of the athlete with respect to content of the gastrointestinal tract, fluid intake during exercise is often only a fraction (e.g., one-half) of the volume lost, and losses of 2% of body weight or more might occur during an exercise session in spite of fluid consumption during the session (Convertino et al. 1996; Cox et al. 2002; Coris et al. 2004; Coyle 2004). Total daily fluid consumption by athletes generally is not reported; for many athletes, it is probably on the order of 5% of body weight (50 mL/ kg/day) or more to compensate for urinary and respiratory losses as well as sweat losses. For example, Crossman (2003) described a professionally prepared diet plan for a major league baseball player that includes 26 cups (6.2 L) of water or sports drink on a workout day and 19 cups (4.5 L) on an off-day; this is in addition to 9-11 cups (2.1-2.6 L) of milk, fruit juice, and sports drink with meals and scheduled snacks (total fluid intake of 6.8-8.8 L/day, or 52-67 mL/kg/day for a 132-kg player7). While some players and teams probably use bottled or distilled water, most (especially at the amateur and interscholastic levels) probably use local tap water; also, sports drinks might be prepared (commercially or by individuals) with tap water. The U.S. Army’s policy on fluid replacement for warm-weather training calls for 0.5-1 quart/hour (0.47-0.95 L/hour), depending on the temperature, humidity, and type of work (Kolka et al. 2003; USASMA 2003). In addition, fluid intake is not to exceed 1.5 quarts/hour (1.4 liter/hour) or 12 quarts/day (11.4 L/day). The Army’s planning factor for individual tap water consumption ranges from 1.5 gallons/day (5.7 L/day) for temperate conditions to 3.0 gallons/day (11.4 L/day) for hot conditions (U.S. Army 1983). Hourly intake can range from 0.21 to 0.65 L depending on the temperature (McNall and Schlegel 1968), and daily intake among physically active individuals can range from 6 to 11 L (U.S. Army 1983, cited by EPA 1997). Nonmilitary outdoor workers in hot or dry climates probably would have similar needs. 7 The player’s weight was obtained from the 2003 roster of the Cleveland Indians baseball team (http://cleveland.indians.mlb.com). Page 32 193
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Save Cancel Water intakes for pregnant and lactating women are listed separately in Appendix B (Tables B-4 to B-9). Total water intake for pregnant women does not differ greatly from that for all adult females (Table B-9), while total water consumption by lactating women is generally higher. For the highest consumers among lactating women, consumption rates approximate those for athletes and workers (50-70 mL/kg/day). Diabetes mellitus and diabetes insipidus are both characterized by high water intakes and urine volumes, among other things (Beers and Berkow 1999; Eisenbarth et al. 2002; Robinson and Verbalis 2002; Belchetz and Hammond 2003). People with untreated or poorly controlled diabetes mellitus would be expected to have substantially higher fluid intakes than nondiabetic members of the population. The American Diabetes Association (2004) estimates that 18.2 million people in the United States (6.3% of the population) have diabetes mellitus and that 5.2 million of these are not aware they have the disease. Other estimates range from 16 to 20 million people in the United States, with up to 50% undiagnosed (Brownlee et al. 2002; Buse et al. 2002). Diabetes insipidus, or polyuria, is defined as passage of large volumes of urine, in excess of about 2 L/m2/day (approximately 150 mL/kg/day at birth, 110 mL/kg/day at 2 years, and 40 mL/kg/day in older children and adults) (Baylis and Cheetham 1998; Cheetham and Baylis 2002). Diabetes insipidus includes several types of disease distinguished by cause, including both familial and acquired disorders (Baylis and Cheetham 1998; Cheetham and Baylis 2002; Robinson and Verbalis 2002). Water is considered a therapeutic agent for diabetes insipidus (Beers and Berkow 1999; Robinson and Verbalis 2002); in addition, some kinds of diabetes insipidus can be treated by 194 addressing an underlying cause or by administering vasopressin (antidiuretic hormone) or other agents to reduce polyuria to a tolerable level. The Diabetes Insipidus Foundation (2004) estimates the number of diabetes insipidus patients in the United States at between 40,000 and 80,000. Someone initially presenting with central or vasopressin-sensitive diabetes insipidus might ingest “enormous” quantities of fluid and may produce 3-30 L of very dilute urine per day (Beers and Berkow 1999) or up to 400 mL/kg/day (Baylis and Cheetham 1998). Most patients with central diabetes insipidus have urine volumes of 6-12 L/day (Robinson and Verbalis 2002). Patients with primary polydipsia might ingest and excrete up to 6 L of fluid per day (Beers and Berkow 1999). Pivonello et al. (1998) listed water intakes of 5.5-8.6 L/day for six adults with diabetes insipidus who did not take vasopressin and 1.4-2.5 L/day for 12 adults who used a vasopressin analogue. An estimated 20% to 40% of patients on lithium therapy have a urine volume > 2.5 L/day, and up to 12% have frank nephrogenic diabetes insipidus characterized by a urine volume > 3 L/day (Mukhopadhyay et al. 2001). Page 33 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel Five papers described enamel fluorosis in association with diabetes insipidus or polydipsia (Table 2-3). Two of the papers described cases of enamel fluorosis in the United States resulting from fluoride concentrations of 1, 1.7, or 2.6 mg/L in drinking water (Juncos and Donadio 1972; Greenberg et al. 1974). The two individuals drinking water with fluoride at 1.7 and 2.6 mg/L also had roentgenographic bone changes consistent with “systemic fluorosis”8 (Juncos and Donadio 1972). These patients and four other renal patients in the U.S. “in whom fluoride may have been the cause of detectable 195 clinical and roentgenographic effects” were also reported by Johnson et al. (1979); most of the patients had urine volumes exceeding 3 L/day and drinking water with fluoride concentrations around 1.7-3 mg/L. Moderate and severe enamel fluorosis have been reported in diabetes insipidus patients in other countries with drinking water containing fluoride at 0.5 mg/L (Klein 1975) or 1 mg/L (Seow and Thomsett 1994), and severe enamel fluorosis with skeletal fluorosis has been reported with fluoride at 3.4 mg/L (Mehta et al. 1998). Greenberg et al. (1974) recommended that children with any disorder that gives rise to polydipsia and polyuria9 be supplied a portion of their water from a nonfluoridated source. Table 2-4 provides examples of fluoride intake by members of several population subgroups characterized by above-average water consumption (athletes and workers, patients with diabetes mellitus or diabetes insipidus). It should be recognized that, for some groups of people with high water intakes (e.g., those with a disease condition or those playing indoor sports such as basketball or hockey), there probably will be little correlation of water intake with outdoor temperature—such individuals in northern states would consume approximately the same amounts of water as their counterparts in southern states. However, fluoridation still varies from state to state (Appendix B), so that some individuals could consume up to 1.7 times as much as others for the same water intake (1.2 versus 0.7 mg/L). Background Food Measured fluoride in samples of human breast milk is very low. Dabeka et al. (1986) found detectable concentrations in only 92 of 210 samples (44%) obtained in Canada, with fluoride ranging from <0.004 to 0.097 mg/L. The mean concentration in milk from mothers in fluoridated 8 These two individuals also had impaired renal function, which could have increased their retention of fluoride (see Chapter 3). 9 Greenberg et al. (1974) listed “central diabetes insipidus, psychogenic water ingestion, renal medullary disease, including hypercalemic nephropathy, hypokalemic nephropathy and anatomic and vascular disturbances and those diseases causing solute diuresis” as disorders associated with “excessive” consumption of water and therefore the possibility of “fluoride toxicity in a community with acceptable fluoride concentration.” Page 34 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. 196
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Save Cancel TABLE 2-3 Case Reports of Fluorosis in Association with Diabetes Insipidus or Polydipsia Study Subjects Exposure Conditions Comments Reference (a) 18-year-old (a) “high” intake of well water Enamel fluorosis and Juncos and boy, 57.4 kg containing fluoride at 2.6 mg/L roentgenographic bone changes Donadio (b) 17-year-old since early childhood; current consistent with “systemic 1972 girl, 45.65 kg intake, 7.6 L/day (0.34 fluorosis,” attributed to the (United States) mg/kg/day) combination of renal (b) “high” intake of water insufficiency and polydipsia (the containing fluoride at 1.7 mg/L latter resulting from the renal since infancy; current intake, 4 disease); reported by the Mayo L/day (0.15 mg/kg/day) Clinic 2 boys (ages 10 Fluoridated communities in the Enamel fluorosis; fluoride Greenberg and 11) with U.S. (1 mg/L); one child since concentrations in deciduous teeth et al. 1974 familial birth, one since age 4; fluid (enamel layer 50-100 µm from nephrogenic intake ranged from 2.6 to 6 surface) 3-6 times those in diabetes times normal daily intake for controls (normal boys aged 10-14 insipidus age (approximately 1.25-3 residing in an area with fluoride (United States) L/day at time of study) at 1 mg/L) Mother and four Water had “lower than Enamel fluorosis in all four Klein 1975 children with accepted” fluoride content (0.5 children: severe in the older two familial mg/L); water consumption by who were not treated for diabetes pituitary mother and two teenage insipidus, milder in the two diabetes daughters (none used younger children who were insipidus vasopressin) was 10-15 L/day treated for diabetes insipidus. (Israel) each; two younger children Mother also had diabetes treated for diabetes insipidus insipidus and fluorosis; she had from ages 3 and 5 grown up in Kurdistan with an unknown water fluoride content Six cases of Children had average water Moderate (one child) or severe Seow and familial intake of 8-10 L/day; two of the (one child) enamel fluorosis in Thomsett pituitary children lived in fluoridated the two children who lived in 1994 diabetes areas (1 mg/L) fluoridated areas insipidus (Australia) 197
Two brothers Well water with fluoride at 3.4 Severe enamel fluorosis, skeletal Mehta et with pituitary mg/L deformities, and radiological al. 1998 diabetes evidence of skeletal fluorosis insipidus (ages 17 and 7) (India) Page 35 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel TABLE 2-4 Examples of Fluoride Intake from Drinking Water by Members of Selected Population Subgroups Living in Fluoridated Areasa Typical Consumersb High Consumersc Water Consumption Fluoride Intaked Water Consumption Fluoride Intaked Population Subgroup (Weight) mL/day mL/kg/day mg/day mg/kg/day mL/day mL/kg/day mg/day mg/kg/day Athletes, workers, military (50 kg) 2,500 50 1.8-3.0 0.035-0.06 3,500 70 2.5-4.2 0.049-0.084 Athletes, workers, military (70 kg) 3,500 50 2.5-4.2 0.035-0.06 4,900 70 3.4-5.9 0.049-0.084 Athletes, workers, military (100 5,000 50 3.5-6.0 0.035-0.06 7,000 70 4.9-8.4 0.049-0.084 kg) Athletes and workers (120 kg) 6,000 50 4.2-7.2 0.035-0.06 8,400 70 5.9-10 0.049-0.084 DM patients (20 kg) 1,000 50 0.7-1.2 0.035-0.06 2,000 100 1.4-2.4 0.07-0.12 DM patients (70 kg) 3,500 50 2.5-4.2 0.035-0.06 4,900 70 3.4-5.9 0.049-0.084 NDI patients (20 kg) 1,000 50 0.7-1.2 0.035-0.06 3,000 150 2.1-3.6 0.11-0.18 NDI patients (70 kg) 3,500 50 2.5-4.2 0.035-0.06 10,500 150 7.4-13 0.11-0.18 aAssumes all drinking water is from fluoridated community (municipal) sources. bBased on a typical consumption rate for the population subgroup. cBased on a reasonably high (but not upper bound) consumption rate for the population subgroup; some individual exposures could be higher. dBased on fluoride concentrations of 0.7-1.2 mg/L. ABBREVIATIONS: DM, diabetes mellitus; NDI, nephrogenic diabetes insipidus. Page 36 198
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Save Cancel communities (1 mg/L in the water) was 0.0098 mg/L; in nonfluoridated communities, the mean was 0.0044 mg/L). Fluoride concentrations were correlated with the presence of fluoride in the mother’s drinking water. Spak et al. (1983) reported mean fluoride concentrations in colostrum of 0.0053 mg/L (0.28 µM/L) in an area in Sweden with fluoride at 0.2 mg/L in drinking water and 0.0068 mg/L (0.36 µM/L) in an area with fluoride at 1.0 mg/L in the drinking water; in the fluoridated area, the mean fluoride concentration in mature milk was 0.007 mg/L (0.37 µM/L). No statistically significant difference in milk fluoride concentration between the two areas was found. Hossny et al. (2003) reported fluoride concentrations in breast milk of 60 mothers in Cairo, Egypt, ranging from 0.002 to 0.01 mg/L [0.1-0.6 µM/L; median, 0.0032 mg/L (0.17 µM/L); mean, 0.0046 mg/L (0.24 µM/L)]. Cairo is considered nonfluoridated, with a reported water fluoride concentration of 0.3 mg/L (Hossny et al. 2003). Opinya et al. (1991) found higher fluoride concentrations in mothers’ milk (mean, 0.033 mg/L; range, 0.011-0.073 mg/L), but her study population was made up of mothers in Kenya with an average daily fluoride intake of 22.1 mg. However, even at very high fluoride intakes by mothers, breast milk still contains very low concentrations of fluoride compared with other dietary fluoride sources. No significant correlation was established between the fluoride in milk and the intake of fluoride in the Kenyan study (Opinya et al. 1991). Cows’ milk likewise contains very low fluoride concentrations, compared with other dietary sources such as drinking water. Dairy milk samples measured in Houston contained fluoride at 0.007 to 0.068 mg/L (average, 0.03 mg/L) (Liu et al. 1995). Milk samples in 11 Canadian cities contained 0.007-0.086 mg/L (average, 0.041 mg/L) (Dabeka and McKenzie 1987). A 199 sample of soy milk contained much more fluoride than a sample of dairy milk, with a measured concentration of 0.491 mg/L (Liu et al. 1995). Infant formulas vary in fluoride content, depending on the type of formula and the water with which it is prepared. Dabeka and McKenzie (1987) reported mean fluoride concentrations in ready-to-use formulas of 0.23 mg/L for formulas manufactured in the United States and 0.90 mg/L for formulas manufactured in Canada. Van Winkle et al. (1995) analyzed 64 infant formulas, 47 milk-based and 17 soy-based. For milk-based formulas, mean fluoride concentrations were 0.17 mg/L for ready-to-feed, 0.12 mg/L for liquid concentrates reconstituted with distilled water, and 0.14 mg/L for powdered concentrates reconstituted with distilled water. Mean fluoride concentrations for soy-based formulas were 0.30, 0.24, and 0.24 mg/L for ready-to-feed, liquid concentrates, and powdered concentrates, respectively (the latter two were reconstituted with distilled water). Obviously, the fluoride concentration in home-prepared formula depends on the fluoride concentrations in both the formula concentrate and the home Page 37 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel drinking water. Fomon et al. (2000) have recommended using low-fluoride water to dilute infant formulas. Heilman et al. (1997) found 0.01 to 8.38 µg of fluoride per g of prepared infant foods. The highest concentrations were found in chicken (1.05-8.38 µg/g); other meats varied from 0.01 µg/g (veal) to 0.66 µg/g (turkey). Other foods—fruits, desserts, vegetables, mixed foods, and cereals—ranged from 0.01 to 0.63 µg/g. The fluoride concentrations in most foods are attributable primarily to the water used in processing (Heilman et al. 1997); fluoride in 200 chicken is due to processing methods (mechanical deboning) that leave skin and residual bone particles in the meat (Heilman et al. 1997; Fein and Cerklewski 2001). An infant consuming 2 oz (about 60 g) of chicken daily at 8 µg of fluoride per g would have an intake of about 0.48 mg (Heilman et al. 1997). Tea can contain considerable amounts of fluoride, depending on the type of tea and its source. Tea plants take up fluoride from soil along with aluminum (Shu et al. 2003; Wong et al. 2003). Leaf tea, including black tea and green tea, is made from the buds and young leaves of the tea plant, the black tea with a fermentation process, and the green tea without. Oolong tea is intermediate between black and green tea. Brick tea, considered a low-quality tea, is made from old (mature) leaves and sometimes branches and fruits of the tea plant (Shu et al. 2003; Wong et al. 2003). Fluoride accumulates mostly in the leaves of the tea plant, especially the mature or fallen leaves. Measured fluoride concentrations in tea leaves range from 170 to 878 mg/kg in different types of tea, with brick tea generally having 2-4 times as much fluoride as leaf tea (Wong et al. 2003). Commercial tea brands in Sichuan Province of China ranged from 49 to 105 mg/kg dry weight for green teas and 590 to 708 mg/kg dry weight for brick teas (Shu et al. 2003). Infusions of Chinese leaf tea (15 kinds) made with distilled water have been shown to have fluoride at 0.6-1.9 mg/L (Wong et al. 2003). Brick teas, which are not common in the United States, contain 4.8-7.3 mg/L; consumption of brick teas has been associated with fluorosis in some countries (Wong et al. 2003). Chan and Koh (1996) measured fluoride contents of 0.34-3.71 mg/L (mean, 1.50 mg/L) in caffeinated tea infusions (made with distilled, deionized water), 1.01-5.20 mg/L (mean, 3.19 mg/L) in decaffeinated tea infusions, and 0.02- 0.15 mg/L (mean, 0.05 mg/L) in herbal tea infusions, based on 44 brands of tea available in the United States (Houston area). Whyte et al. (2005) reported fluoride concentrations of 1.0-6.5 mg/L in commercial teas (caffeinated and decaffeinated) obtained in St. Louis (prepared with distilled water according to label directions). Warren et al. (1996) found fluoride contents of 0.10-0.58 mg/L in various kinds and brands of coffee sold in the United States (Houston area), with a slightly lower mean for decaffeinated (0.14 mg/L) than for caffeinated (0.17 mg/L) coffee. Instant Page 38 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of 201
EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel coffee had a mean fluoride content of 0.30 mg/L (all coffees tested were prepared with deionized distilled water). Fluoride concentrations of 0.03 mg/L (fruit tea) to 3.35 mg/L (black tea) were reported for iced-tea products sold in Germany primarily by international companies (Behrendt et al. 2002). In practice, fluoride content in tea or coffee as consumed will be higher if the beverage is made with fluoridated water; however, for the present purposes, the contribution from water for beverages prepared at home is included in the estimated intakes from drinking water, discussed earlier. Those estimates did not include commercially available beverages such as fruit juices (not including water used to reconstitute frozen juices), juice-flavored drinks, iced- tea beverages, carbonated soft drinks, and alcoholic beverages. Kiritsy et al. (1996) reported fluoride concentrations in juices and juice-flavored drinks of 0.02-2.8 mg/L (mean, 0.56 mg/L) for 532 different drinks (including five teas) purchased in Iowa City (although many drinks represented national or international distribution); frozen-concentrated beverages were reconstituted with distilled water before analysis. White grape juices had the highest mean fluoride concentration (1.45 mg/L); upper limits on most kinds of juices exceeded 1.50 mg/L. Stannard et al. (1991) previously reported fluoride concentrations from 0.15 to 6.80 mg/L in a variety of juices originating from a number of locations in the United States. The variability in fluoride concentrations is due primarily to variability in fluoride concentrations in the water used in manufacturing the product (Kiritsy et al. 1996). The high fluoride content of grape juices (and grapes, raisins, and wines), even when little or no manufacturing water is involved, is thought to be due to a pesticide (cryolite) used in grape growing (Stannard et al. 1991; Kiritsy et al. 1996; Burgstahler and Robinson 1997). Heilman et al. (1999) found fluoride concentrations from 0.02 to 1.28 mg/L (mean, 0.72 mg/L) in 332 carbonated beverages from 17 production sites, all purchased in Iowa. In general, these concentrations reflect that of the water used in manufacturing. Estimated mean intakes from the analyzed beverages 202 were 0.36 mg/day for 2- to 3-year-old children and 0.60 mg/day for 7- to 10- year-olds (Heilman et al. 1999). Pang et al. (1992) estimated mean daily fluoride intakes from beverages (excluding milk and water) for children of 0.36, 0.54, and 0.60 mg, for ages 2-3, 4-6, and 7-10, respectively; daily total fluid intake ranged from 970 to 1,240 mL, and daily beverage consumption ranged from 585 to 756 mL. Burgstahler and Robinson (1997) reported fluoride contents of 0.23-2.80 mg/L in California wines, with 7 of 19 samples testing above 1 mg/L; the fluoride in wine and in California grapes (0.83-5.20 mg/kg; mean, 2.71 mg/kg) was attributed to the use of cryolite (Na3AlF6) as a pesticide in the vineyards. Martínez et al. (1998) reported fluoride concentrations from 0.03 to 0.68 mg/L in wines from the Canary Islands; most fluoride concentrations in the wines were in the range of 0.10-0.35 mg/L. A maximum legal thresh- Page 39 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel old of 1 mg/L for the fluoride concentration in wine has been established by the Office International de la Vigne et du Vin (OIV 1990; cited by Martínez et al. 1998). Warnakulasuriya et al. (2002) reported mean fluoride concentrations of 0.08-0.71 mg/L in beers available in Great Britain; one Irish beer contained fluoride at 1.12 mg/L. Examples of fluoride intakes that could be expected in heavy drinkers (8-12 drinks per day) are given in Table 2-5. R.D. Jackson et al. (2002) reported mean fluoride contents from 0.12 µg/g (fruits) to 0.49 µg/g (grain products) in a variety of noncooked, nonreconstituted foods (excluding foods prepared with water). Fluoride contents in commercial beverages (excluding reconstituted and fountain beverages) averaged 0.55 µg/g; those in milk and milk products averaged 203
0.31 µg/g. In the same study, fluoride contents in water, reconstituted beverages, and cooked vegetables and grain products (cereals, pastas, soups) differed significantly between two towns in Indiana, one with a water fluoride content of 0.2 mg/L and one with an optimally fluoridated water supply (1.0 mg/L). Bottled fruit drinks, water, and carbonated beverages purchased in the two towns did not differ significantly. The mean daily fluoride ingestion for children 3-5 years old from food and beverages (including those prepared with community water) was estimated to be 0.454 mg in the low-fluoride town and 0.536 mg in the fluoridated town. Dabeka and McKenzie (1995) reported mean fluoride contents in various food categories in Winnipeg, ranging up to 2.1 µg/g for fish, 0.61 µg/g for soup, and 1.15 µg/g for beverages; the highest single items were cooked veal (1.2 µg/g), canned fish (4.6 µg/g), shellfish (3.4 µg/g), cooked wheat cereal (1.0 µg/g), and tea (5.0 µg/g). Estimated dietary intakes (including fluoridated tap water) varied from 0.35 mg/day for children aged 1-4 to 3.0 mg/day for 40- to 64-year-old males. Over all ages and both sexes, the esti- TABLE 2-5 Examples of Fluoride Intakes by Heavy Drinkers from Alcoholic Beverages Alone Fluoride Intake, mg/day Fluoride Concentration, 8 drinks per 12 drinks per Beverage mg/L day day Beer (12-oz. cans or bottles) 0.5 1.4 2.1 1.0 2.8 4.3 Wine (5-oz. glasses) 0.3 0.35 0.53 1.0 1.2 1.8 Mixed drinks (1.5 oz. liquor + 6.5 oz. 0.7a 1.1 1.6 mixer and ice) 1.0a 1.5 2.3 aIn carbonated soda and ice. Page 40 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
204
Save Cancel mated average dietary intake of fluoride was 1.76 mg/day; the food category contributing most to the estimated intake was beverages (80%). Rojas-Sanchez et al. (1999) estimated fluoride intakes for children (aged 16-40 months) in three communities in Indiana, including a low-fluoride community, a “halo” community (not fluoridated, but in the distribution area of a fluoridated community), and a fluoridated community. For fluoride in food, the mean intakes were 0.116-0.146 mg/day, with no significant difference between communities. Intake from beverages was estimated to be 0.103, 0.257, and 0.396 mg/day for the low-, halo, and high-fluoride communities; differences between the towns were statistically significant. Apart from drinking water (direct and indirect consumption, as described earlier), the most important foods in terms of potential contribution to individual fluoride exposures are infant formula, commercial beverages such as juice and soft drinks, grapes and grape products, teas, and processed chicken (Table 2-6). Grapes and grape products, teas, and processed chicken can be high in fluoride apart from any contribution from preparation or process water. Commercial beverages and infant formulas, however, greatly depend on the fluoride content of the water used in their preparation or manufacture (apart from water used in their in-home preparation); due to widespread distribution, such items could have similar fluoride concentrations in most communities, on average. TABLE 2-6 Summary of Typical Fluoride Concentrations of Selected Food and Beverages in the United States Source Range, mg/L Range, mg/kg Human breast milk Fluoridated area (1 mg/L) 0.007-0.01 — Nonfluoridated area 0.004 — Cow’s milk ≤0.07 — Soy milk 0.5 — Milk-based infant formulaa ≤0.2 — Soy-based infant formulaa 0.2-0.3 — Infant food—chicken — 1-8 Infant food—other — 0.01-0.7 Teaa 0.3-5 — Herbal teaa 0.02-0.15 — Coffeea 0.1-0.6 — 205
Grape juicea ≤3 — Other juices and juice drinksa ≤1.5 — Grapes — 0.8-5 Carbonated beverages 0.02-1.3 — Wine 0.2-3 — Beer 0.08-1 — aNot including contribution from local tap water. Page 41 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel Because of the wide variability in fluoride content in items such as tea, commercial beverages and juices, infant formula, and processed chicken, and the possibility of a substantial contribution to an individual’s total fluoride intake, a number of authors have suggested that such fluoride sources be considered in evaluating an individual’s need for fluoride supplementation (Clovis and Hargreaves 1988; Stannard et al. 1991; Chan and Koh 1996; Kiritsy et al. 1996; Warren et al. 1996; Heilman et al. 1997, 1999; Levy and Guha-Chowdhury 1999), especially for individuals who regularly consume large amounts of a single product (Stannard et al. 1991; Kiritsy et al. 1996). Several authors also point out the difficulty in evaluating individual fluoride intake, given the wide variability of fluoride content among similar items (depending on point of origin, etc.), the wide distribution of many products, and the lack of label or package information about fluoride content for most products (Stannard et al. 1991; Chan and Koh 1996; Behrendt et al. 2002). Dental Products and Supplements 206
Fluoridated dental products include dentifrices (toothpastes, powders, liquids, and other preparations for cleaning teeth) for home use and various gels and other topical applications for use in dental offices. More than 90% of children ages 2-16 years surveyed in 1983 or 1986 used fluoride toothpaste (Wagener et al. 1992). Of these children, as many as 15% to 20% in some age groups also used fluoride supplements or mouth rinses (Wagener et al. 1992). Using the same 1986 survey data, Nourjah et al. (1994) reported that most children younger than 2 years of age used fluoride dentifrices. Most toothpaste sold in the United States contains fluoride (Newbrun 1992), usually 1,000-1,100 parts per million (ppm) (0.1-0.11%).10 The amount of fluoride actually swallowed by an individual depends on the amount of toothpaste used, the swallowing control of the person (especially for young children), and the frequency of toothpaste use. Ophaug et al. (1980, 1985) estimated the intake of fluoride by small children (2-4 years) to be 0.125-0.3 mg per brushing; a 2-year-old child brushing twice daily would ingest nearly as much fluoride from the toothpaste as from food and fluoridated drinking water combined (Ophaug et al. 1985). Levy and Zarei-M (1991) reported estimates of 0.12-0.38 mg of fluoride ingested per brushing. Burt (1992) and Newbrun (1992) reported estimates of 0.27 10 Equivalent to 1-1.1 mg fluoride ion per gram of toothpaste. This may be expressed in various ways on the package, e.g., as 0.24% or 0.243% sodium fluoride (NaF), 0.76% or 0.8% monofluorophosphate (Na2PO3F), or 0.15% w/v fluoride (1.5 mg fluoride ion per cubic centimeter of toothpaste). Page 42 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel 207 mg/day for a preschool child brushing twice daily with standard-strength (1,000 ppm) toothpaste. Levy (1993, 1994) and Levy et al. (1995a) reviewed a number of studies of the amount of toothpaste people of various ages ingest. Amounts of toothpaste used per brushing range from 0.2 to 5 g, with means around 0.4-2 g, depending on the age of the person. The estimated mean percentage of toothpaste ingested ranges from 3% in adults to 65% in 2-year-olds. Children who did not rinse after toothbrushing ingested 75% more toothpaste than those who rinsed. Perhaps 20% of children have fluoride intakes from toothpaste several times greater than the mean values, and some children probably get more than the recommended amount of fluoride from toothpaste alone, apart from food and beverages (Levy 1993, 1994). Mean intakes of toothpaste by adults were measured at 0.04 g per brushing (0.04 mg of fluoride per brushing for toothpaste with 0.1% fluoride), with the 90th percentile at 0.12 g of toothpaste (0.12 mg of fluoride) per brushing (Barnhart et al. 1974). Lewis and Limeback (1996) estimated the daily intake of fluoride from dentifrice (products for home use) to be 0.02-0.06, 0.008-0.02, 0.0025, and 0.001 mg/kg, for ages 7 months to 4 years, 5-11 years, 12-19 years, and 20+ years, respectively. Rojas-Sanchez et al. (1999) estimated fluoride intake from dentifrice at between 0.42 and 0.58 mg/day in children aged 16-40 months in three communities in Indiana. Children tend to use more toothpaste when provided special “children’s” toothpaste than when given adult toothpaste (Levy et al. 1992; Adair et al. 1997), and many children do not rinse or spit after brushing (Naccache et al. 1992; Adair et al. 1997). Estimates of typical fluoride ingestion from toothpaste are given by age group in Table 2-7; these estimates are for typical rather than high or upper- bound intakes, and many individuals could have substantially higher intakes. A number of papers have suggested approaches to decreasing children’s intake of fluoride from toothpaste, including decreasing the fluoride content in TABLE 2-7 Estimated Typical Fluoride Intakes from Toothpastea Age Group, years Fluoride Intake, mg/day Age Group, years Fluoride Intake, mg/day Infants < 0.5b 0 Youth 13-19 0.2 Infants 0.5-1 0.1 Adults 20-49 0.1 Children 1-2 0.15 Adults 50+ 0.1 Children 3-5 0.25 Females 13-49c 0.1 Children 6-12 0.3 aBased on information reviewed by Levy et al. (1995a). Estimates assume two brushings per day with fluoride toothpaste (0.1% fluoride) and moderate rinsing. bAssumes no brushing before 6 months of age. cWomen of childbearing age. 208
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Save Cancel children’s toothpaste, discouraging the use of fluoride toothpaste by children less than 2 years old, avoiding flavored children’s toothpastes, encouraging the use of very small amounts of toothpaste, encouraging rinsing and expectorating (rather than swallowing) after brushing, and recommending careful parental supervision (e.g., Szpunar and Burt 1990; Levy and Zarei-M 1991; Simard et al. 1991; Burt 1992; Levy et al. 1992, 1993, 1997, 2000; Naccache et al. 1992; Newbrun 1992; Levy 1993, 1994; Bentley et al. 1999; Rojas-Sanchez et al. 1999; Warren and Levy 1999; Fomon et al. 2000). Topical applications of fluoride in a professional setting can lead to ingestion of 1.3-31.2 mg (Levy and Zarei-M 1991). Substantial ingestion of fluoride also has been demonstrated from the use of fluoride mouth rinse and self-applied topical fluoride gel (Levy and Zarei-M 1991). Heath et al. (2001) reported that 0.3-6.1 mg of fluoride (5-29% of total applied) was ingested by young adults who used gels containing 0.62-62.5 mg of fluoride. Levy et al. (2003a) found that two-thirds of children had at least one fluoride treatment by age 6 and that children with dental caries were more likely to have had such a treatment. Their explanation is that professional application of topical fluoride is used mostly for children with moderate to high risk for caries. In contrast, Eklund et al. (2000), in a survey of insurance claims for more than 15,000 Michigan children treated by 1,556 different dentists, found no association between the frequency of use of topical fluoride (professionally applied) and restorative care. Although these were largely low-risk children, for whom routine use of professionally applied fluoride is not recommended, two-thirds received topical fluoride at nearly every office visit. The authors 209 recommended that the effectiveness of professionally applied topical fluoride products in modern clinical practice be evaluated. Exposures from topical fluorides during professional treatment are unlikely to be significant contributors to chronic fluoride exposures because they are used only a few times per year. However, they could be important with respect to short-term or peak exposures. Heath et al. (2001) found that retention of fluoride ion in saliva after the use of dentifrice (toothpaste, mouthrinse, or gel) was proportional to the quantity used, at least for young adults. They were concerned with maximizing the retention in saliva to maximize the topical benefit of the fluoride. Sjögren and Melin (2001) were also concerned about enhancing the retention of fluoride in saliva and recommend minimal rinsing after toothbrushing. However, fluoride in saliva eventually will be ingested, so enhancing the retention of fluoride in saliva after dentifrice use also enhances the ingestion of fluoride from the dentifrice. Fluoride supplements (NaF tablets, drops, lozenges, and rinses) are intended for prescriptions for children in low-fluoride areas; dosages generally range from 0.25 to 1.0 mg of fluoride/day (Levy 1994; Warren and Levy Page 44 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel 1999). Appropriate dosages should be based on age, risk factors (e.g., high risk for caries), and ingestion of fluoride from other sources (Dillenberg et al. 1992; Jones and Berg 1992; Levy and Muchow 1992; Levy 1994; Warren and Levy 1999). Although compliance is often considered to be a problem, inappropriate use of fluoride supplements has also been identified as a risk 210 factor for enamel fluorosis (Dillenberg et al. 1992; Levy and Muchow 1992; Levy 1994; Pendrys and Morse 1995; Warren and Levy 1999). The dietary fluoride supplement schedule in the United States, as revised in 1994 by the American Dental Association, now calls for no supplements for children less than 6 months old and none for any child whose water contains at least 0.6 mg/L (Record et al. 2000; ADA 2005; Table 2-8). Further changes in recommendations for fluoride supplements have been suggested (Fomon and Ekstrand 1999; Newbrun 1999; Fomon et al. 2000), including dosages based on individual body weight rather than age (Adair 1999) and the use of lozenges to be sucked rather than tablets to be swallowed (Newbrun 1999), although others disagree (Moss 1999). The Canadian recommendations for fluoride supplementation include an algorithm for determining the appropriateness for a given child and then a schedule of doses; no supplementation is recommended for children whose water contains at least 0.3 mg/L or who are less than 6 months old (Limeback et al. 1998; Limeback 1999b). Fluoride in Air Fluoride (either as hydrogen fluoride, particulate fluorides, or fluorine gas) is released to the atmosphere by natural sources such as volcanoes11 and by a number of anthropogenic sources. In North America, anthropogenic sources of airborne fluoride include coal combustion by electrical utilities and other entities, aluminum production plants, phosphate fertilizer plants, chemical production facilities, steel mills, magnesium plants, and manufacturers of brick and structural clay (reviewed by ATSDR 2003). Estimated airborne releases of hydrogen fluoride in the United States in 2001 were 67.4 million pounds (30.6 million kg; TRI 2003), of which at least 80% was attributed to electrical utilities (ATSDR 2003). Airborne releases of fluorine gas totaled about 9,000 pounds or 4,100 kg (TRI 2003). Anthropogenic hydrogen fluoride emissions in Canada in the mid-1990s were estimated at 5,400 metric tons (5.4 million kg or 11.9 million pounds), of which 75% was attributed to primary aluminum producers (CEPA 1996). 11 Volcanic activity historically has been a major contributor of HF and other contaminants to the atmosphere in some parts of the world, with some volcanoes emitting 5 tons of HF per day (Nicaragua) or as much as 15 million tons during a several month eruption (Iceland) (Durand and Grattan 2001; Grattan et al. 2003; Stone 2004). Page 45 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of 211
EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel TABLE 2-8 Dietary Fluoride Supplement Schedule of 1994 Fluoride Concentration in Drinking Water, mg/L Age < 0.3 0.3-0.6 > 0.6 Birth to 6 months None None None 6 months to 3 years 0.25 mg/day None None 3-6 years 0.50 mg/day 0.25 mg/day None 6-16 years 1.0 mg/day 0.50 mg/day None SOURCE: ADA 2005. Reprinted with permission; copyright 2005, American Dental Association. Measured fluoride concentrations in air in the United States and Canada typically range from 0.01 to 1.65 µg/m3, with most of it (75%) present as hydrogen fluoride (CEPA 1996). The highest concentrations (>1 µg/m3) correspond to urban locations or areas in the vicinity of industrial operations. Historically, concentrations ranging from 2.5 to 14,000 µg/m3 have been reported near industrial operations in various countries (reviewed by EPA 1988). Ernst et al. (1986) reported an average concentration of airborne fluoride of about 600 µg/m3 during the 1981 growing season in a rural inhabited area (Cornwall Island) on the U.S.-Canadian border directly downwind from an aluminum smelter. Hydrogen fluoride is listed as a hazardous air pollutant in the Clean Air Act Amendments of 1990 (reviewed by ATSDR 2003), and as such, its emissions are subject to control based on “maximum achievable control technology” emission standards. Such standards are already in effect for fluoride emissions from primary and secondary aluminum production, phosphoric acid manufacture and phosphate fertilizer production, and hydrogen fluoride production (ATSDR 2003). For most individuals in the United States, exposure to airborne fluoride is expected to be low compared with ingested fluoride (EPA 1988); exceptions include people in heavily industrialized areas or having occupational exposure. Assuming inhalation rates of 10 m3/day for children and 20 m3/day for adults, fluoride exposures from inhalation in rural areas (<0.2 212
µg/m3 fluoride) would be less than 2 µg/day (0.0001-0.0002 mg/kg/day) for a child and 4 µg/day (0.00006 mg/kg/day) for an adult. In urban areas (<2 µg/m3), fluoride exposures would be less than 20 µg/day (0.0001-0.002 mg/kg/day) for a child and 40 µg/day (0.0006 mg/kg/day) for an adult. Lewis and Limeback (1996) used an estimate of 0.01 µg/kg/day (0.00001 mg/kg/day) for inhaled fluoride for Canadians; this would equal 0.1 µg/day for a 10-kg child or 0.7 µg/day for a 70-kg adult. Occupational exposure at the Occupational Safety and Health Administration (OSHA) exposure limit of 2.5 mg/m3 would result in a fluoride intake of 16.8 mg/day for an 8-hour working day (0.24 mg/kg/day for a Page 46 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel 70-kg person) (ATSDR 2003). Heavy cigarette smoking could contribute as much as 0.8 mg of fluoride per day to an individual (0.01 mg/kg/day for a 70- kg person) (EPA 1988). Fluoride in Soil Fluoride in soil could be a source of inadvertent ingestion exposure, primarily for children. Typical fluoride concentrations in soil in the United States range from very low (<10 ppm) to as high as 3% to 7% in areas with high concentrations of fluorine-containing minerals (reviewed by ATSDR 2003). Mean or typical concentrations in the United States are on the order of 300- 430 ppm. Soil fluoride content may be higher in some areas due to use of fluoride-containing phosphate fertilizers or to deposition of airborne fluoride released from industrial operations. Estimated values for inadvertent soil ingestion by children (excluding those with pica) are 100 mg/day (mean) and 400 mg/day (upper bound) (EPA 1997); 213 the estimated mean value for soil ingestion by adults is 50 mg/ day (EPA (1997). For a typical fluoride concentration in soil of 400 ppm, therefore, estimated intakes of fluoride by children would be 0.04 (mean) to 0.16 mg/day (upper bound) and by adults, 0.02 mg/day. For a 20-kg child, the mass- normalized intake would be 0.002-0.008 mg/kg/day; for a 70-kg adult, the corresponding value would be 0.0003 mg/kg/day. Erdal and Buchanan (2005) estimated intakes of 0.0025 and 0.01 mg/kg/day for children (3-5 years), for mean and reasonable maximum exposures, respectively, based on a fluoride concentration in soil of 430 ppm. In their estimates, fluoride intake from soil was 5-9 times lower than that from fluoridated drinking water. For children with pica (a condition characterized by consumption of nonfood items such as dirt or clay), an estimated value for soil ingestion is 10 g/day (EPA 1997). For a 20-kg child with pica, the fluoride intake from soil containing fluoride at 400 ppm would be 4 mg/day or 0.2 mg/kg/day. Although pica in general is not uncommon among children, the prevalence is not known (EPA 1997). Pica behavior specifically with respect to soil or dirt appears to be relatively rare but is known to occur (EPA 1997); however, fluoride intake from soil for a child with pica could be a significant contributor to total fluoride intake. For most children and for adults, fluoride intake from soil probably would be important only in situations in which the soil fluoride content is high, whether naturally or due to industrial pollution. Pesticides Cryolite and sulfuryl fluoride are the two pesticides that are regulated for their contribution to the residue of inorganic fluoride in foods. For food Page 47 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel 214 use pesticides, EPA establishes a tolerance for each commodity to which a pesticide is allowed to be applied. Tolerance is the maximum amount of pesticide allowed to be present in or on foods. In the environment, cryolite breaks down to fluoride, which is the basis for the safety evaluation of cryolite and synthetic cryolite pesticides (EPA 1996a). Fluoride ions are also degradation products of sulfuryl fluoride (EPA 1992). Thus, the recent evaluation of the dietary risk of sulfuryl fluoride use on food takes into account the additional exposure to fluoride from cryolite (EPA 2004). Sulfuryl fluoride is also regulated as a compound with its own toxicologic characteristics. Cryolite, sodium hexafluoroaluminate (Na3AlF6), is a broad spectrum insecticide that has been registered for use in the United States since 1957. Currently, it is used on many food (tree fruits, berries, and vegetables) and feed crops, and on nonfood ornamental plants (EPA 1996a). The respective fluoride ion concentrations from a 200 ppm aqueous synthetic cryolite (97.3% pure) at pH 5, 7, and 9 are estimated at 16.8, 40.0, and 47.0 ppm (approximately 15.5%, 37%, and 43% of the total available fluorine) (EPA 1996a). A list of tolerances for the insecticidal fluorine compounds cryolite and synthetic cryolite is published in the Code of Federal Regulations (40 CFR § 180.145(a, b, c) [2004]). Current tolerances for all commodities are at 7 ppm. Sulfuryl fluoride (SO2F2), is a structural fumigant registered for use in the United States since 1959 for the control of insects and vertebrate pests. As of January 2004, EPA published a list of tolerances for sulfuryl fluoride use as a post-harvest fumigant for grains, field corn, nuts, and dried fruits (69 Fed. Reg. 3240 [2004]; 40 CFR 180.575(a) [2004]). The calculated exposure threshold at the drinking-water MCL of 4 mg/L was used as the basis for assessing the human health risk associated with these decisions (EPA 2004). Concerns were raised that foods stored in the freezer during sulfuryl fluoride residential fumigation might retain significant amounts of fluoride residue. Scheffrahn et al. (1989) reported that unsealed freezer foods contained fluoride at as high as 89.7 ppm (flour, at 6,803 mg-hour/L rate of sulfuryl fluoride application) while no fluoride residue was detected (0.8 ppm limit of detection) in foods that were sealed with polyethylene film. A later study reported fluoride residue above 1 ppm in food with higher fat contents (e.g., 5.643 ppm in margarine) or that was improperly sealed (e.g., 7.66 ppm in a reclosed peanut butter PETE [polyethylene terephthalate] jar) (Scheffrahn et al. 1992). Dietary exposure for a food item is calculated as the product of its consumption multiplied by the concentration of the residue of concern. The total daily dietary exposure for an individual is the sum of exposure from all food items consumed in a day. A chronic dietary exposure assessment of Page 48 215
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Save Cancel fluoride was recently conducted for supporting the establishment of tolerances for the post-harvest use of sulfuryl fluoride. EPA (2004) used the Dietary Exposure Evaluation Model (DEEM-FCID), a computation program, to estimate the inorganic fluoride exposure from cryolite, sulfuryl fluoride, and the background concentration of fluoride in foods. DEEM-FCID (Exponent, Inc) uses the food consumption data from the 1994-1996 and 1998 Continuing Survey of Food Intakes by Individuals (CSFII) conducted by the U.S. Department of Agriculture (USDA). The 1994-1996 database consists of food intake diaries of more than 15,000 individuals nationwide on two nonconsecutive days. A total of 4,253 children from birth to 9 years of age are included in the survey. To ensure that the eating pattern of young children is adequately represented in the database, an additional survey was conducted in 1998 of 5,559 children 0-9 years of age. The latter survey was designed to be compatible with the CSFII 1994-1996 data so that the two sets of data can be pooled to increase the sample size for children. The Food Commodity Intake Database (FCID) is jointly developed by EPA and USDA for the purpose of estimating dietary exposure from pesticide residues in foods. It is a translated version of the CSFII data that expresses the intake of consumed foods in terms of food commodities (e.g., translating apple pie into its ingredients, such as apples, flour, sugar, etc.) (EPA 2000c). All foods and food forms (e.g., grapes—fresh, cooked, juice, canned, raisins, wine) with existing tolerances for cryolite and sulfuryl fluoride were included in the recent EPA fluoride dietary exposure analysis (EPA 2004). For the analysis of fluoride exposure from cryolite, residue data taken from monitoring surveys, field studies, and at tolerance were adjusted to reflect changes in concentration during food processing (e.g., mixing in milling, 216 dehydration, and food preparation). For the fluoride exposure from post- harvest treatment with sulfuryl fluoride, the measured residues are used without further adjustment except for applying drawdown factors in grain mixing (EPA 2004). In estimating fluoride exposure from both cryolite- and sulfuryl fluoride-treated foods, residue concentrations were adjusted for the percentage of crop treated with these pesticides based on the information from market share and agricultural statistics on pesticide use. Fluoride exposures from a total of 543 forms of foods (e.g., plant-based, bovine, poultry, egg, tea) containing fluoride were also estimated as the background food exposure. Residue data were taken from surveys and residue trials (EPA 2004). No adjustments were made to account for residue concentration through processing or dehydration. Theoretically, the exposure from some processed foods (e.g., dried fruits) could potentially be higher than if their residue concentrations were assumed to be the same as in the fresh commodities (e.g., higher exposure from higher residue in dried fruits than assuming same residue concentration for both dried and fresh fruits.) However, these considerations are apparently offset by the Page 49 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel use of higher residue concentrations for many commodities (e.g., using the highest values from a range of survey data, the highest value as surrogate for when data are not available, assuming residue in dried fruits and tree nuts at one-half the limit of quantification when residue is not detected) such that the overall dietary exposure was considered overestimated (EPA 2004). The dietary fluoride exposure thus estimated ranged from 0.0003 to 0.0031 mg/kg/day from cryolite, 0.0003 to 0.0013 mg/kg/day from sulfuryl fluoride, 217 and 0.005 to 0.0175 mg/kg/day from background concentration in foods (EPA 2004). Fine-tuning the dietary exposure analysis using the comprehensive National Fluoride Database recently published by USDA (2004) for many foods also indicates that the total background food exposure would not be significantly different from the analysis by EPA, except for the fluoride intake from tea. A closer examination of the residue profile used by EPA (2004) for background food exposure analysis reveals that 5 ppm, presumably a high- end fluoride concentration in brewed tea, was entered in the residue profile that called for fluoride concentration in powdered or dried tea. According to the USDA survey database (2004), the highest detected fluoride residue in instant tea powder is 898.72 ppm. The corrected exposure estimate is presented in the section “Total Exposure to Fluoride” later in this chapter. Fluorinated Organic Chemicals Many pharmaceuticals, consumer products, and pesticides contain organic fluorine (e.g., −CF3, −SCF3, −OCF3). Unlike chlorine, bromine, and iodine, organic fluorine is not as easily displaced from the alkyl carbon and is much more lipophilic than the hydrogen substitutes (Daniels and Jorgensen 1977; PHS 1991). The lipophilic nature of the trifluoromethyl group contribute to the enhanced biological activity of some pharmaceutical chemicals. The toxicity of fluorinated organic chemicals usually is related to their molecular characteristics rather than to the fluoride ions metabolically displaced. Fluorinated organic chemicals go through various degrees of bio- transformation before elimination. The metabolic transformation is minimal for some chemicals. For example, the urinary excretion of ciprofloxacin (fluoroquinolone antibacterial agent) consists mainly of the unchanged parent compound or its fluorine-containing metabolites (desethylene-, sulfo-, oxo-, and N-formyl ciprofloxacin) (Bergan 1989). Nevertheless, Pradhan et al. (1995) reported an increased serum fluoride concentration from 4 µM (0.076 ppm) to 11 µM (0.21 ppm) in 19 children from India (8 months to 13 years old) within 12 hours after the initial oral dose of ciprofloxacin at 15-25 mg/kg. The presumed steady state (day 7 of repeated dosing) 24-hour urinary fluoride concentration was 15.5% higher than the predosing Page 50 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. 218
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Save Cancel concentration (59 µM versus 51 µM; or, 1.12 ppm versus 0.97 ppm). Another example of limited contribution to serum fluoride concentration from pharmaceuticals was reported for flecainide, an antiarrhythmic drug. The peak serum fluoride concentration ranged from 0.0248 to 0.0517 ppm (1.3 to 2.7 µM) in six healthy subjects (26-54 years old, three males, and three females) 4.5 hours after receiving a single oral dose of 100 mg of flecainide acetate (Rimoli et al. 1991). One to two weeks before the study, the subjects were given a poor fluoride diet, used toothpaste without fluoride, and had low fluoride (0.08 mg/L) in their drinking water. Other fluoride-containing organic chemicals go through more extensive metabolism that results in greater increased bioavailability of fluoride ion. Elevated serum fluoride concentrations from fluorinated anesthetics have been extensively studied because of the potential nephrotoxicity of methoxyflurane in association with elevated serum fluoride concentrations beyond a presumed toxicity benchmark of 50 µM (Cousins and Mazze 1973; Mazze et al. 1977). A collection of data on peak serum fluoride ion concentrations from exposures to halothane, enflurane, isoflurane, and sevoflurane is given in Appendix B. These data serve to illustrate a wide range of peak concentrations associated with various use conditions (e.g., length of use, minimum alveolar concentration per hour), biological variations (e.g., age, gender, obesity, smoking), and chemical-specific characteristics (e.g., biotransformation pattern and rates). It is not clear how these episodically elevated serum fluoride ion concentrations contribute to potential adverse effects of long-term sustained exposure to inorganic fluoride from other media, such as drinking water, foods, and dental-care products. Elevated free fluoride ion (< 2% of administered dose) also was detected in the plasma and urine of some patients after intravenous administration of fluorouracil (Hull et al. 1988). Nevertheless, the major forms of urinary excretion were still the unchanged parent compound and its fluorine- containing metabolites (dihydrofluorouracil, α-fluoro-β-ureidopropanoic acid, α-fluoro-β-alanine). The extent of dermal absorption of topical fluorouracil cream varies with skin condition, product formulation, and the conditions of 219 use. Levy et al. (2001a) reported less than 3% systemic fluorouracil absorption in patients treated with 0.5% or 5% cream for actinic keratosis. A group of widely used consumer products is the fluorinated telomers and polytetrafluoroethylene, or Teflon. EPA is in the process of evaluating the environmental exposure to low concentrations of perfluorooctanoic acid (PFOA) and its principal salts that are used in manufacturing fluoropolymers or as their breakdown products (EPA 2003b). PFOA is persistent in the environment. It is readily absorbed through oral and inhalation exposure and is eliminated in urine and feces without apparent biotransformation (EPA 2003b; Kudo and Kawashima 2003). Unchanged plasma and urine fluoride concentrations in rats that received intraperitoneal injections of Page 51 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel PFOA also indicated a lack of defluorination (Vanden Heuvel et al. 1991). (See Chapter 3 for more discussion of PFOA.) Aluminofluorides, Beryllofluorides, and Fluorosilicates
Aluminofluorides and Beryllofluorides
Complexes of aluminum and fluoride (aluminofluorides, most often AlF3 or − − AlF4 ) or beryllium and fluoride (beryllofluorides, usually as BeF3 ) occur when the two elements are present in the same environment (Strunecka and Patocka 2002). Fluoroaluminate complexes are the most common forms in which fluoride can enter the environment. Eight percent of the earth’s crust is composed of aluminum; it is the most abundant metal and the third most abundant element on earth (Liptrot 1974). The most common form for the 220
inorganic salt of aluminum and fluoride is cryolite (Na3AlF6). In fact, of the more than 60 metals on the periodic chart, Al3+ binds fluoride most strongly (Martin 1988). With the increasing prevalence of acid rain, metal ions such as aluminum become more soluble and enter our day-to-day environment; the opportunity for bioactive forms of AlF to exist has increased in the past 100 years. Human exposure to aluminofluorides can occur when a person ingests both a fluoride source (e.g., fluoride in drinking water) and an aluminum source; sources of human exposure to aluminum include drinking water, tea, food residues, infant formula, aluminum-containing antacids or medications, deodorants, cosmetics, and glassware (ATSDR 1999; Strunecka and Patocka 2002; Li 2003; Shu et al. 2003; Wong et al. 2003). Aluminum in drinking water comes both from the alum used as a flocculant or coagulant in water treatment and from leaching of aluminum into natural water by acid rain (ATSDR 1999; Li 2003). Exposure specifically to aluminofluoride complexes is not the issue so much as the fact that humans are routinely exposed to both elements. Human exposure to beryllium occurs primarily in occupational settings, in the vicinity of industrial operations that process or use beryllium, and near sites of beryllium disposal (ATSDR 2002). Aluminofluoride and beryllofluoride complexes appear to act as analogues of phosphate groups—for example, the terminal phosphate of guanidine triphosphate (GTP) or adenosine triphosphate (ATP) (Chabre 1990; Antonny and Chabre 1992; Caverzasio et al. 1998; Façanha and Okorokova-Façanha 2002; Strunecka and Patocka 2002; Li 2003). Thus, aluminofluorides might influence the activity of a variety of phosphatases, phosphorylases, and kinases, as well as the G proteins involved in biological signaling systems, by inappropriately stimulating or inhibiting normal function of the protein (Yatani and Brown 1991; Caverzasio et al. 1998; Façanha and Okorokova-Façanha 2002; Strunecka and Patocka 2002; Li Page 52 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
221
Save Cancel 2003). Aluminofluoride complexes have been reported to increase the concentrations of second messenger molecules (e.g., free cytosolic Ca2+, inositol 1,4,5-trisphosphate, and cyclic AMP) for many bodily systems (Sternweis and Gilman 1982; Strunecka et al. 2002; Li 2003). The increased toxicity of beryllium in the presence of fluoride and vice versa was noted as early as 1949 (Stokinger et al. 1949). For further discussion of aluminofluorides, see Chapters 5 and 7. Further research should include characterization of both the exposure conditions and the physiological conditions (for fluoride and for aluminum or beryllium) under which aluminofluoride and beryllofluoride complexes can be expected to occur in humans as well as the biological effects that could result.
Fluorosilicates
Most fluoride in drinking water is added in the form of fluosilicic acid (fluorosilicic acid, H2SiF6) or the sodium salt (sodium fluosilicate, Na2SiF6), collectively referred to as fluorosilicates (CDC 1993). Of approximately 10,000 fluoridated water systems included in the CDC’s 1992 fluoridation census, 75% of them (accounting for 90% of the people served) used fluorosilicates. This widespread use of silicofluorides has raised concerns on at least two levels. First, some authors have reported an association between the use of silicofluorides in community water and elevated blood concentrations of lead in children (Masters and Coplan 1999; Masters et al. 2000); this association is attributed to increased uptake of lead (from whatever source) due to incompletely dissociated silicofluorides remaining in the drinking water (Masters and Coplan 1999; Masters et al. 2000) or to increased leaching of lead into drinking water in systems that use chloramines (instead of chlorine as a disinfectant) and silicofluorides (Allegood 2005; Clabby 2005; Maas et al. 2005).12,13 Macek et al. (2006) have also compared blood lead concentrations in children by method of water fluoridation; they stated that their analysis did not support an association between blood lead concentrations and silicofluorides, but also could not refute it, 12 In common practice, chloramines are produced with an excess of ammonia, which appears to react with silicofluorides to produce an ammonium-fluorosilicate intermediate which facilitates lead dissolution from plumbing components (Maas et al. 2005). 13 Another possible explanation for increased blood lead concentrations which has not been examined is the effect of fluoride intake on calcium metabolism; a review by Goyer (1995) indicates that higher blood and tissue concentrations of lead occur when the diet is low in 222
calcium. Increased fluoride exposure appears to increase the dietary requirement for calcium (see Chapter 8); in addition, the substitution of tap-water based beverages (e.g., soft drinks or reconstituted juices) for dairy products would result in both increased fluoride intake and decreased calcium intake. Page 53 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel especially for children living in older housing. Second, essentially no studies have compared the toxicity of silicofluorides with that of sodium fluoride, based on the assumption that the silicofluorides will have dissociated to free fluoride before consumption (see also Chapter 7). Use of more sophisticated analytical techniques such as nuclear magnetic resonance has failed to detect any silicon- and fluorine-containing species 2− other than hexafluorosilicate ion (SiF6 ) (Urbansky 2002; Morris 2004). In drinking water at approximately neutral pH and typical fluoride concentrations, all the silicofluoride appears to be dissociated entirely to silicic acid [Si(OH)4], fluoride ion, and HF (Urbansky 2002; Morris 2004); any intermediate species either exist at extremely low concentrations or are highly transient. 2− SiF6 would be present only under conditions of low pH (pH < 5; Urbansky 2002; Morris 2004) and high fluoride concentration (above 16 mg/L according 2− to Urbansky [2002]; at least 1 g/L to reach detectable levels of SiF6 , according to Morris [2004]). Urbansky (2002) also stated that the silica contribution from the fluoridating agent is usually trivial compared with native silica in the water; therefore, addition of any fluoridating agent (or the 2− presence of natural fluoride) could result in the presence of SiF6 in any water if other conditions (low pH and high total fluoride concentration) are met. Both Urbansky (2002) and Morris (2004) indicate that other substances in the 223 water, especially metal cations, might form complexes with fluoride, which, depending on pH and other factors, could influence the amount of fluoride actually present as free fluoride ion. For example, P.J. Jackson et al. (2002) have calculated that at pH 7, in the presence of aluminum, 97.46% of a total fluoride concentration of 1 mg/L is present as fluoride ion, but at pH 6, only 21.35% of the total fluoride is present as fluoride ion, the rest being present in + various aluminum fluoride species (primarily AlF2 and AlF3). Calculations were not reported for pH < 6. Further research should include analysis of the concentrations of fluoride and various fluoride species or complexes present in tap water, using a range of water samples (e.g., of different hardness and mineral content). In addition, given the expected presence of fluoride ion (from any fluoridation source) and silica (native to the water) in any fluoridated tap water, it would be useful to examine what happens when that tap water is used to make acidic beverages or products (commercially or in homes), especially fruit juice from concentrate, tea, and soft drinks. Although neither Urbansky (2002) nor Morris (2004) 2− discusses such beverages, both indicate that at pH < 5, SiF6 would be 2− present, so it seems reasonable to expect that some SiF6 would be present in acidic beverages but not in the tap water used to prepare the beverages. Consumption rates of these beverages are high for many people, and 2− therefore the possibility of biological effects of SiF6 , as opposed to free fluoride ion, should be examined. Page 54 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel RECENT ESTIMATES OF TOTAL FLUORIDE EXPOSURE 224
A number of authors have reviewed fluoride intake from water, food and beverages, and dental products, especially for children (NRC 1993; Levy 1994; Levy et al. 1995a,b,c; Lewis and Limeback 1996; Levy et al. 2001b). Heller et al. (1999, 2000) estimated that a typical infant less than 1 year old who drinks fluoridated water containing fluoride at 1 mg/L would ingest approximately 0.08 mg/kg/day from water alone. Shulman et al. (1995) also calculated fluoride intake from water, obtaining an estimate of 0.08 mg/kg/day for infants (7-9 months of age), with a linearly declining intake with age to 0.034 mg/kg/day for ages 12.5-13 years. Levy et al. (1995b,c; 2001b) have estimated the intake of fluoride by infants and children at various ages based on questionnaires completed by the parents in a longitudinal study. For water from all sources (direct, mixed with formula, etc.), the intake of fluoride by infants (Levy et al. 1995b) ranged from 0 (all ages examined) to as high as 1.73 mg/day (9 months old). Infants fed formula prepared from powdered or liquid concentrate had fluoride intakes just from water in the formula of up to 1.57 mg/day. The sample included 124 infants at 6 weeks old and 77 by 9 months old. Thirty-two percent of the infants at 6 weeks and 23% at age 3 months reportedly had no water consumption (being fed either breast milk or ready-to-feed formula without added water). Mean fluoride intakes for the various age groups ranged from 0.29 to 0.38 mg/day; however, these values include the children who consumed no water, and so are not necessarily applicable for other populations. For the same children, mean fluoride intakes from water, fluoride supplement (if used), and dentifrice (if used) ranged from 0.32 to 0.38 mg/day (Levy et al. 1995c); the maximum fluoride intakes ranged from 1.24 (6 weeks old) to 1.73 mg/day (9 months old). Ten percent of the infants at 3 months old exceeded an intake of 1.06 mg/day. For a larger group of children (about 12,000 at 3 months and 500 by 36 months of age; Levy et al. 2001b), mean fluoride intakes from water, supplements, and dentifrice combined ranged from 0.360 mg/day (12 months old) to 0.634 mg/day (36 months old). The 90th percentiles ranged from 0.775 mg/day (16 months old) to 1.180 mg/day (32 months old). Maximum intakes ranged from 1.894 mg/day (16 months old) to 7.904 mg/day (9 months old) and were attributable only to water (consumption of well water with 5-6 mg/L fluoride; about 1% of the children had water sources containing more than 2 mg/L fluoride). For ages 1.5-9 months, approximately 40% of the infants exceeded a mass-normalized intake level for fluoride of 0.07 mg/kg/day; for ages 12-36 months, about 10-17% exceeded that level (Levy et al. 2001b). Levy et al. (2003b) reported substantial variation in total fluoride intake among children aged 36-72 months, with some individual intakes greatly Page 55 225
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Save Cancel exceeding the means. The mean intake per unit of body weight declined with age from 0.05 to 0.06 mg/kg/day at 36 months to 0.03-0.04 mg/kg/day at 72 months; 90th percentile values declined from about 0.10 mg/kg/day to about 0.06 mg/kg/day (Levy et al. 2003b). Singer et al. (1985) reported mean estimated total fluoride intakes of 1.85 mg/day for 15- to 19-year-old males (based on a market-basket survey and a diet of 2,800 calories per day) in a fluoridated area (>0.7 mg/L) and 0.86 mg/day in nonfluoridated areas (<0.3 mg/L). Beverages and drinking water contributed approximately 75% of the total fluoride intake. Lewis and Limeback (1996) estimated total daily fluoride intakes of 0.014- 0.093 mg/kg for formula-fed infants and 0.0005-0.0026 mg/kg for breast-fed infants (up to 6 months). For children aged 7 months to 4 years, the estimated daily intakes from food, water, and household products (primarily dentifrice) were 0.087-0.160 mg/kg in fluoridated areas and 0.045-0.096 mg/kg in nonfluoridated areas. Daily intakes for other age groups were 0.049-0.079, 0.033-0.045, and 0.047-0.058 mg/kg for ages 5-11, 12-19, and 20+ in fluoridated areas, and 0.026-0.044, 0.017-0.021, and 0.032-0.036 mg/kg for the same age groups in nonfluoridated areas. Rojas-Sanchez et al. (1999) estimated mean total daily fluoride intakes from foods, beverages, and dentifrice by 16- to 40-month-old children to be 0.767 mg (0.056 mg/kg) in a nonfluoridated community and 0.965 mg (0.070-0.073 mg/kg) in both a fluoridated community and a “halo” community. The higher mean dentifrice intake in the halo community than in the fluoridated community compensated for the lower dietary intake of fluoride in the halo community. Between 45% and 57% of children in the communities with higher daily fluoride intake exceeded the “upper estimated threshold limit” of 0.07 226 mg/kg, even without including any fluoride intake from supplements, mouth rinses, or gels in the study. Erdal and Buchanan (2005), using a risk assessment approach based on EPA practices, estimated the cumulative (all sources combined) daily fluoride intake by infants (<1-year-old) in fluoridated areas to be 0.11 and 0.20 mg/kg for “central tendency” and “reasonable maximum exposure” conditions, respectively. For infants in nonfluoridated areas, the corresponding intakes were 0.08 and 0.11 mg/kg. For children aged 3-5, the estimated intakes were 0.06 and 0.23 mg/kg in fluoridated areas and 0.06 and 0.21 in nonfluoridated areas. TOTAL EXPOSURE TO FLUORIDE A systematic estimation of fluoride exposure from pesticides, background food, air, toothpaste, fluoride supplement, and drinking water is presented in this section. The estimated typical or average chronic exposures to inorganic fluoride from nonwater sources are presented in Table 2-9. Page 56 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel TABLE 2-9 Total Estimated Chronic Inorganic Fluoride Exposure from Nonwater Sources Average Inorganic Fluoride Exposure, mg/kg/day Population Sulfuryl Background Total Subgroups Fluoridea Cryolitea Fooda Toothpasteb Aira Nonwater Supplementc All infants (<1 0.0005 0.0009 0.0096 0 0.0019 0.0129 0.0357 year) Nursing 0.0003 0.0004 0.0046 0 0.0019 0.0078d 0.0357 Nonnursing 0.0006 0.0012 0.0114 0 0.0019 0.0151 0.0357 Children 1-2 years 0.0013 0.0031 0.0210 0.0115 0.0020 0.0389 0.0192 227
Children 3-5 years 0.0012 0.0020 0.0181 0.0114 0.0012 0.0339 0.0227 Children 6-12 0.0007 0.0008 0.0123 0.0075 0.0007 0.0219 0.0250 years Youth 13-19 years 0.0004 0.0003 0.0097 0.0033 0.0007 0.0144 0.0167 Adults 20-49 years 0.0003 0.0004 0.0114 0.0014 0.0006 0.0141 0 Adults 50+ years 0.0003 0.0005 0.0102 0.0014 0.0006 0.0130 0 Females 13-49 0.0003 0.0005 0.0107 0.0016 0.0006 0.0137 0 yearse aBased on the exposure assessment by EPA (2004). Background food exposures are corrected for the contribution from powdered or dried tea at 987.72 ppm instead of 5 ppm used in EPA analysis. bBased on Levy et al. (1995a), assuming two brushings per day with fluoride toothpaste (0.1% F) and moderate rinsing. The estimated exposures are: 0 mg/day for infants; 0.15 mg/day for 1-2 years; 0.25 mg/day for 3-5 years; 0.3 mg/day for 6-12 years; 0.2 mg/day for 13-19 years; 0.1 mg/day for all adults and females 13-49 years. The calculated exposure in mg/kg/day is based on the body weights from EPA (2004). For most age groups, these doses are lower than the purported maximum of 0.3 mg/day used for all age groups by EPA (2004). cBased on ADA (2005) schedule (Table 2-8) and body weights from EPA (2004). Note that the age groups here do not correspond exactly to those listed by ADA (2005). The estimated exposures are: 0.25 mg/day for infant and 1-2 years; 0.5 mg/day for 3-5 years, and 1 mg/day for 6-12 years and 13-19 years. dIncludes the estimated 0.0006 mg/kg/day from breast milk. Using the higher estimated breast-milk exposure from a fluoridated area (approximately 0.0014 mg/kg/day) results in 0.0086 mg/kg/day for total nonwater exposure. eWomen of childbearing age. The exposures from pesticides (sulfuryl fluoride and cryolite), background food, and air are from a recent exposure assessment by EPA (2004). The background food exposure is corrected for the contribution from powdered or dried tea by using the appropriate residue concentration of 897.72 ppm Page 57 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel for instant tea powder instead of the 5 ppm for brewed tea used in the EPA (2004) analysis. It should be noted that the exposure from foods treated with sulfuryl fluoride is not applicable before its registration for post-harvest fumigation in 2004. The exposure from toothpaste is based on Levy et al. 228
(1995a; see Table 2-7). The use of fluoride-containing toothpaste is assumed not to occur during the first year of life. Fluoride supplements are considered separately in Table 2-9 and are not included in the “total nonwater” column. Children 1-2 years old have the highest exposures from all nonwater source components. The two highest nonwater exposure groups are children 1-2 and 3-5 years old, at 0.0389 and 0.0339 mg/kg/day, respectively (Table 2-9). These doses are approximately 2.5-3 times those of adult exposures. The estimated exposures from drinking water are presented in Table 2-10, using the DEEM-FCID model (version 2.03, Exponent Inc.). The water consumption data are based on the FCID translated from the CSFII 1994- 1996 and 1998 surveys and represent an update to the information presented in Appendix B. The food forms for water coded as “direct, tap”; “direct, source nonspecified”; “indirect, tap”; and “indirect, source nonspecified” are assumed to be from local tap water sources. The sum of these four categories constitutes 66-77% of the total daily water intake. The remaining 23-34% is designated as nontap, which includes four food forms coded as “direct, bottled”; “direct, others”; “indirect, bottled”; and TABLE 2-10 Estimated Chronic (Average) Inorganic Fluoride Exposure (mg/kg/day) from Drinking Water (All Sources)a Fluoride Concentrations in Tap Water (fixed nontap water at 0.5 mg/L) Population Subgroups 0 mg/L 0.5 mg/L 1.0 mg/L 2.0 mg/L 4.0 mg/L All infants (<1 year) 0.0120 0.0345 0.0576 0.1040 0.1958 Nursing 0.0050 0.0130 0.0210 0.0370 0.0700 Nonnursing 0.0140 0.0430 0.0714 0.1290 0.2430 Children 1-2 years 0.0039 0.0157 0.0274 0.0510 0.0982 Children 3-5 years 0.0036 0.0146 0.0257 0.0480 0.0920 Children 6-12 years 0.0024 0.0101 0.0178 0.0330 0.0639 Youth 13-19 years 0.0018 0.0076 0.0134 0.0250 0.0484 Adults 20-49 years 0.0024 0.0098 0.0173 0.0320 0.0620 Adults 50+ years 0.0023 0.0104 0.0184 0.0340 0.0664 Females 13-49 yearsb 0.0025 0.0098 0.0171 0.0320 0.0609 aEstimated from DEEM-FCID model (version 2.03, Exponent Inc.). The water consumption data are based on diaries from the CSFII 1994-1996 and 1998 surveys that are transformed into food forms by the Food Commodity Intake Database (FCID). The food forms coded as “direct, tap”; “direct, source nonspecified”; “indirect, tap”; and “indirect, source nonspecified” are assumed to be from tap water sources. bWomen of childbearing age. Page 58 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of 229
EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel “indirect, others”. Fluoride exposures from drinking water (Table 2-10) are estimated for different concentrations of fluoride in the local tap water (0, 0.5, 1.0, 2.0, or 4.0 mg/L), while assuming a fixed 0.5 mg/L for all nontap sources (e.g., bottled water). The assumption for nontap water concentration is based on the most recent 6-year national public water system compliance monitoring from a 16-state cross section that represents approximately 41,000 public water systems, showing average fluoride concentrations of 0.482 mg/L in groundwater and 0.506 mg/L in surface water (EPA 2003a). The reported best estimates for exceeding 1.2, 2, and 4 mg/L in surface-water source systems are 9.37%, 1.11%, and 0.0491%, respectively; for groundwater source systems, the respective estimates are 8.54%, 3.05%, and 0.55%. Table 2- 10 shows that nonnursing infants have the highest exposure from drinking water. The estimated daily drinking-water exposures at tap-water concentrations of 1, 2, and 4 mg/L are 0.0714, 0.129, and 0.243 mg/kg, respectively. These values are approximately 2.6 times those for children 1-2 and 3-5 years old and 4 times the exposure of adults. The estimated total fluoride exposures aggregated from all sources are presented in Table 2-11. These values represent the sum of exposures from Table 2-9 and 2-10, assuming fluoride supplements might be given to infants and children up to 19 years old in low-fluoride tap-water scenarios (0 and 0.5 mg/L). Table 2-11 shows that, when tap water contains fluoride, nonnursing infants have the highest total exposure. They are 0.087, 0.144, and 0.258 mg/kg/day in tap water at 1, 2, and 4 mg/L, respectively. At 4 mg/L, the total exposure for nonnursing infants is approximately twice the exposure for children 1-2 and 3-5 years old and 3.4 times the exposure for adults. The relative source contributions to the total exposure in Table 2-11 for scenarios with 1, 2, and 4 mg/L in tap water are illustrated in Figures 2-1, 2-2, and 2-3, respectively. Numerical values for the 1-, 2-, and 4-mg/L scenarios are given later in the summary tables (Tables 2-13, 2-14, and 2-15). Under the assumptions for estimating the exposure, the contribution from pesticides plus 230 fluoride in the air is within 4% to 10% for all population subgroups at 1 mg/L in tap water, 3-7% at 2 mg/L in tap water, and 1-5% at 4 mg/L in tap water. The contributions from the remaining sources also vary with different tap-water concentrations. For nonnursing infants, who represent the highest total exposure group even without any exposure from toothpaste, the contribution from drinking water is 83% for 1 mg/L in tap water (Figure 2-1). As the tap- water concentration increases to 2 and 4 mg/L, the relative drinking-water contribution increases to 90% and 94%, respectively (Figures 2-2 and 2-3). The proportion of the contribution from all sources also varies in children 1-2 and 3-5 years old. At 1 mg/L, the drinking-water contribution is approximately 42%, while the contributions from toothpaste and background food are sizable, approximately 18% and Page 59 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel TABLE 2-11 Total Estimated (Average) Chronic Inorganic Fluoride Exposure (mg/kg/day) from All Sources, Assuming Nontap Water at a Fixed Concentrationa Concentration in Tap Water (fixed nontap water at 0.5 mg/L) With Fluoride Supplement Without Fluoride Supplement Population Subgroups 0 mg/L 0.5 mg/L 0 mg/L 0.5 mg/L 1 mg/L 2 mg/L 4 mg/L All infants (<1 year) 0.061 0.083 0.025 0.047 0.070 0.117 0.209 Nursingb 0.049 0.057 0.013 0.021 0.030 0.046 0.079 Nonnursing 0.065 0.094 0.029 0.058 0.087 0.144 0.258 Children 1-2 years 0.062 0.074 0.043 0.055 0.066 0.090 0.137 Children 3-5 years 0.060 0.071 0.038 0.049 0.060 0.082 0.126 Children 6-12 years 0.049 0.057 0.024 0.032 0.040 0.055 0.086 Youth 13-19 years 0.033 0.039 0.016 0.022 0.028 0.039 0.063 231
Adults 20-49 years 0.017 0.024 0.017 0.024 0.031 0.046 0.076 Adults 50+ years 0.015 0.023 0.015 0.023 0.031 0.047 0.079 Females 13-49 yearsc 0.016 0.024 0.016 0.024 0.031 0.046 0.075 aThe estimated exposures from fluoride supplements and total nonwater sources (including pesticides, background food, air, and toothpaste) are from Table 2-9. The estimated exposures from drinking water are from Table 2-10. For nonfluoridated areas (tap water at 0 and 0.5 mg/L), the total exposures are calculated both with and without fluoride supplements. bThe higher total nonwater exposure of 0.0086 mg/kg/day that includes breast milk from a fluoridated area (footnote in Table 2- 9) is used to calculate the exposure estimates for the “without supplement” groups that are exposed to fluoride in water at 1, 2, and 4 mg/L. cWomen of childbearing age. 31%, respectively (Figure 2-1). At 2 mg/L, the drinking-water contribution is raised to approximately 57%, while the contributions from toothpaste and background food are reduced to 13% and 23%, respectively (Figure 2-2). At 4 mg/L, the relative contribution of drinking water continues to increase to approximately 72%, while the contribution from toothpaste and background food are further reduced to approximately 9% and 15%, respectively (Figure 2-3). As age increases toward adulthood (20+ years), the contribution from toothpaste is reduced to approximately 5% at 1 mg/ L, 3-4% at 2 mg/L, and 2% at 4 mg/L. Correspondingly, the contribution from drinking water increases to approximately 57% at 1 mg/L, 70% at 2 mg/L, and 82% at 4 mg/L. Data presented in Tables 2-9 to 2-11 are estimates of typical exposures, while the actual exposure for an individual could be lower or higher. There are inherent uncertainties in estimating chronic exposure based on the 2-day CSFII surveys. The DEEM-FCID model assumes that the average Page 60 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
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FIGURE 2-1 Source contribution to total inorganic fluoride exposure, including fluoride at 1 mg/L in tap water. The estimated chronic inorganic fluoride exposures from the various routes are presented in Tables 2-9 and 2-10. No fluoride supplement is included for any population subgroup. The total exposures as presented in Table 2-11 for the population subgroups are: 0.030 mg/kg/day (nursing infants), 0.087 mg/kg/day (non-nursing infants), 0.066 mg/kg/day (1-2 years old), 0.060 mg/kg/day (3-5 years old), 0.040 mg/kg/day (6-12 years old), 0.028 mg/kg/day (13-19 years old), and 0.031 mg/kg/day for adults (20 to 50+ years old) and women of childbearing age (13-49 years old). intake from the cross-sectional survey represents the longitudinal average for a given population. Thus, the chronic exposures of those who have persistently high intake rates, especially for food items that contain high concentrations of fluoride (e.g., tea), are likely to be underestimated. For example, at an average fluoride concentration of 3.3 mg/L for brewed tea and 0.86 mg/L for iced tea (USDA 2004), the tea component in the background food presented in Table 2-9 represents an average daily consumption of one- half cup of brewed tea or 2 cups of iced tea. A habitual tea drinker, especially for brewed tea, can be expected to significantly exceed these con- Page 61 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 233
2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
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FIGURE 2-2 Source contribution to total inorganic fluoride exposure, including fluoride at 2 mg/L fluoride in tap water. The estimated chronic inorganic fluoride exposures from the various routes are presented in Tables 2-9 and 2- 10. No fluoride supplement is included for any population subgroup. The total exposures as presented in Table 2-11 for the population subgroups are: 0.046 mg/kg/day (nursing infants), 0.144 mg/kg/day (non-nursing infants), 0.090 mg/kg/day (1-2 years old), 0.082 mg/kg/day (3-5 years old), 0.055 mg/kg/day (6-12 years old), 0.039 mg/kg/day (13-19 years old), and 0.046-0.047 mg/kg/day for adults (20-50+ years old) and women of childbearing age (13- 49 years old). 234 sumption rates. Other groups of people who are expected to have exposures higher than those calculated here include infants given fluoride toothpaste before age 1, anyone who uses toothpaste more than twice per day or who swallows excessive amounts of toothpaste, children inappropriately given fluoride supplements in a fluoridated area, children in an area with high fluoride concentrations in soil, and children with pica who consume large amounts of soil. The exposure estimates presented in this chapter for non-drinking-water routes are based on the potential profile of fluoride residue concentrations Page 62 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
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FIGURE 2-3 Source contribution to total inorganic fluoride exposure, including fluoride at 4 mg/L in tap water. The estimated chronic inorganic fluoride exposures from the various routes are presented in Tables 2-9 and 2-10. No fluoride supplement is included for any population subgroup. The total exposures as presented in Table 2-11 for the population subgroups are: 0.079 mg/kg/day (nursing infants), 0.258 mg/kg/day (nonnursing infants), 0.137 mg/kg/day (1-2 years old), 0.126 mg/kg/day (3-5 years old), 0.086 mg/kg/day (6-12 years old), 0.063 mg/kg/day (13-19 years old), 0.075-0.079 mg/kg/day for adults (20-50+ years old) and women of childbearing age (13-49 years old). in the current exposure media. They likely do not reflect the concentration of past exposure scenarios, particularly for routes that show changes in time (e.g., pesticide use practices). Any new and significant source of fluoride exposure, such as commodities approved for sulfuryl fluoride fumigation application beyond April 2005, is expected to alter the percentage of drinking water contribution as presented in this chapter. Different assumptions for the drinking-water concentration alone also can result in slightly different estimates. For example, values in Table 2-11 are derived from assuming that the nontap water has a fixed fluoride concentration of 0.5 mg/L, while tap-water concentration varies up to 4 mg/L. Table 2-12 provides alternative calculations of total exposure by assuming 236
Page 63 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel TABLE 2-12 Total Estimated (Average) Chronic Inorganic Fluoride Exposure (mg/kg/day) from All Sources, Assuming the Same Specified Fluoride Concentration for Both Tap and Nontap Watersa Concentration in All Water 1 mg/L 2 mg/L 4 mg/L 1 mg/L 2 mg/L 4 mg/L Population Subgroups Modeled water intakeb EPA default water intakec All infants (<1 year) 0.082 0.151 0.289 0.113 0.213 0.413 Nursing 0.034 0.060 0.111 0.109 0.209 0.409 Nonnursing 0.100 0.186 0.357 0.115 0.215 0.415 Children 1-2 years 0.070 0.102 0.164 0.139 0.239 0.439 Children 3-5 years 0.063 0.093 0.151 NA NA NA Children 6-12 years 0.042 0.062 0.103 NA NA NA Youth 13-19 years 0.030 0.045 0.075 NA NA NA Adults 20-49 years 0.034 0.053 0.093 0.043 0.071 0.128 Adults 50+ years 0.034 0.054 0.096 0.042 0.070 0.127 Females 13-49 yearsd 0.033 0.053 0.092 0.042 0.071 0.128 aThe estimated exposures from nonwater sources (including pesticides, background food, air, and toothpaste) are from Table 2- 9. No fluoride supplement is included in the total fluoride exposure estimates. bThe component of drinking-water exposure is estimated from DEEM-FCID. cThe EPA default daily water intake rate is 1 L for a 10-kg child and 2 L for a 70-kg adult. NA: not applicable based on EPA’s default body weight. dWomen of childbearing age. that all sources of drinking water (both tap and nontap water) contain the same specified fluoride concentration. Within this assumption, the drinking- water component can be estimated from either the DEEM-FCID model or the default drinking-water intake rate currently used by EPA for establishing the MCL (1 L/day for a 10-kg child and 2 L/day for a 70-kg adult). 237
Some uncertainties exist regarding the extent the FCID database may include all processed waters (e.g., soft drinks and soups). Thus, the exposure using EPA’s defaults as presented in Table 2-12 can serve as a bounding estimate from the water contribution. The difference in the total fluoride exposure calculated from the two water intake methods (i.e., EPA defaults versus FCID modeled) varies with different population subgroups shown in Table 2-12. In general, as the drinking-water contribution to the total exposure becomes more prominent at higher drinking-water concentration, the differences in total exposure approach the differences in drinking-water intake rates of the two methods. Using EPA’s default adult water intake rate of 28.6 mL/kg/day (based on 2 L/day for a 70 kg adult) results in approximately 32-39% higher total exposure than the model estimates. This approximates the 38-45% lower model estimate of total water intake rate Page 64 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel (i.e., 19.7 mL/kg/day for 20-49 year olds, 20.7 mL/kg/day for 50+ year olds). Using EPA’s default water intake rate for a child results in approximately 16% higher total exposure than the model estimates for nonnursing infants at 4 mg/L drinking water. This reflects closely the difference in the total water intake between the default 100 mL/kg/day (based on 1 L/day for a 10 kg child) and the DEEM-FCID estimate of 85.5 mL/kg/day for this population group. Similarly, for nursing infants, the 3.7-fold higher total exposure at 4 mg/L from using the EPA’s default of 100 mL/kg/day also reflects their significantly lower model estimate of total water intake (i.e., 25.6 mL/kg/day). Two additional simple conceptual observations can be made to relate data presented in Table 2-12 to those in Tables 2-9 and 2-11. By using a fixed rate of water 238 intake for infants and children 1-2 years old, the difference in their total exposure is due to the contribution from all nonwater sources as presented in Table 2-9. The difference between model estimates presented in Table 2- 11 (last 3 columns) by varying concentrations for tap water alone (with fixed nontap water at 0.5 mg/L) and estimates using one fluoride concentration for both tap and nontap waters in Table 2-12 (first 3 columns) reflects the contribution from the nontap-water component. The fluoride exposure estimates presented thus far, regardless of the various assumptions (e.g., the same versus different fluoride concentrations in tap and nontap water) and different water intake rates (e.g., EPA default versus estimates from FCID database of the CSFII surveys), do not include those who have sustained high water intake rates as noted previously (athletes, workers, and individuals with diabetes mellitus or nephrogenic diabetes insipidus (see Table 2-4). The high-end exposures for these high- water-consumption population subgroups are included in the summaries below. SUMMARY OF EXPOSURE ASSESSMENT The estimated aggregated total fluoride exposures from pesticides, background food, air, toothpaste, and drinking water are summarized for drinking water fluoride concentrations of 1 mg/L (Table 2-13), 2 mg/L (Table 2- 14), and 4 mg/L (Table 2-15). Two sets of exposures are presented using different approaches to estimate the exposure from drinking water. One is estimated by modeling water intakes based on FCID data and assuming a fixed nontap water concentration of 0.5 mg/L. The other is estimated using EPA default drinking-water intake rates (i.e., 1 L/day for a 10 kg child, 2 L/day for a 70 kg adult) and assuming the same concentration for tap and nontap waters. Both sets of estimates include the same fluoride exposure from nonwater sources. The total exposure from the latter approach is higher than the model estimates due to the higher default drinking water intake rates and the assumption that nontap waters contain the same concentration of fluoride residue as the tap water. Page 65 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. 239
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Save Cancel TABLE 2-13 Contributions to Total Fluoride Chronic Exposure at 1 mg/L in Drinking Water % Contribution to Total Exposure Population Subgroups Total Exposure, mg/kg/day Pesticides and Air Background Food Toothpaste Drinking Water Modeled average water consumer (Tap water at 1 mg/L, nontap water at 0.5 mg/L; Table 2-11) All infants (<1 year) 0.070 4.7 13.6 0 81.7 Nursing 0.030 8.9 15.6 0 70.8 Nonnursing 0.087 4.3 13.2 0 82.5 Children 1-2 years 0.066 9.7 31.7 17.4 41.3 Children 3-5 years 0.060 7.4 30.4 19.1 43.1 Children 6-12 years 0.040 5.4 30.9 18.9 44.8 Youth 13-19 years 0.028 4.9 34.8 12.0 48.3 Adults 20-49 years 0.031 4.0 36.3 4.6 55.1 Adults 50+ years 0.031 4.4 32.4 4.6 58.7 Females 13-49 yearsa 0.031 4.4 34.7 5.3 55.6 EPA default water intake, all water at 1 mg/L (1 L/day for 10-kg child; 2 L/day for 70-kg adult; Table 2-12) All infants (<1 year) 0.113 2.9 8.5 0 88.6 Nursing 0.109 2.4 4.3 0 92.0 Nonnursing 0.115 3.2 9.9 0 86.9 Children 1-2 years 0.139 4.6 15.1 8.3 72.0 Adults 20-49 years 0.043 3.0 26.7 3.3 67.0 High end of high water intake individuals all water at 1 mg/L (based on intake rates in Table 2-4) Athletes and workers 0.084 1.5 13.5 1.7 83.3 DM patients (3-5 years) 0.134 3.3 13.5 8.5 74.7 DM patients (adults) 0.084 1.5 13.5 1.7 83.3 NDI patients (3-5 years) 0.184 2.4 9.9 6.2 81.6 NDI patients (adults) 0.164 0.8 6.9 0.9 91.4 aWomen of childbearing age. ABBREVIATIONS: DM, diabetes mellitus; NDI, nephrogenic diabetes insipidus. Although each of these exposure estimates have areas of uncertainty, the average total daily fluoride exposure is expected to fall between them. For the modeling estimates, there are inherent uncertainties in modeling long-term intake rates based on the cross-sectional CSFII dietary survey data. Thus, the exposure from any dietary component, water or other foods, could be underestimated for individuals who have habitually higher intake rates (e.g., 240 water, tea). Specific to the water component, there are also uncertainties regarding the extent the FCID database may include all processed waters (e.g., soft drinks and soups). On the other hand, the EPA Page 66 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel TABLE 2-14 Contributions to Total Fluoride Chronic Exposure at 2 mg/L in Drinking Water % Contribution to Total Exposure Population Subgroups Total Exposure, mg/kg/day Pesticides and Air Background Food Toothpaste Drinking Water Modeled average water consumer (Tap water at 2 mg/L, nontap water at 0.5 mg/L; Table 2-11) All infants (<1 year) 0.117 2.8 8.2 0 89.0 Nursing 0.046 5.8 10.1 0 81.0 Nonnursing 0.144 2.6 7.9 0 89.5 Children 1-2 years 0.090 7.1 23.3 12.8 56.7 Children 3-5 years 0.082 5.4 22.1 13.9 58.6 Children 6-12 years 0.055 3.9 22.4 13.7 60.1 Youth 13-19 years 0.039 3.5 24.5 8.5 63.5 Adults 20-49 years 0.046 2.8 24.7 3.1 69.4 Adults 50+ years 0.047 2.9 21.7 3.0 72.4 Females 13-49 yearsa 0.046 3.0 23.4 3.6 70.1 EPA default water intake, all water at 1 mg/L (2 L/day for 10-kg child; 2 L/day for 70-kg adult; Table 2-12) All infants (<1 year) 0.213 1.6 4.5 0 93.9 Nursing 0.209 1.3 2.2 0 95.8 Nonnursing 0.215 1.7 5.3 0 93.0 Children 1-2 years 0.239 2.7 8.8 4.8 83.7 Adults 20-49 years 0.071 1.8 16.0 2.0 80.2 High end of high water intake individuals all water at 2 mg/L (based on intake rates in Table 2-4) 241
Athletes and workers 0.154 0.8 7.4 0.9 90.9 DM patients (3-5 years) 0.234 1.9 7.7 4.9 85.5 DM patients (adults) 0.154 0.8 7.4 0.9 90.9 NDI patients (3-5 years) 0.334 1.3 5.4 3.4 89.9 NDI patients (adults) 0.314 0.4 3.6 0.5 95.5 aWomen of childbearing age. ABBREVIATIONS: DM, diabetes mellitus; NDI, nephrogenic diabetes insipidus. default water intake rate is likely higher than the average rate for certain population subgroups (e.g., nursing infants). The estimates presented in Tables 2-13, 2-14, and 2-15 show that on a per body weight basis, the exposures are generally higher for young children than for the adults. By assuming that the nontap water concentration is fixed at 0.5 mg/L, nonnursing infants have the highest model-estimated average total daily fluoride exposure: 0.087, 0.144, and 0.258 mg/kg/day when tap-water concentrations of fluoride are 1, 2, and 4 mg/L, respectively (Table 2-11, Page 67 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel TABLE 2-15 Contributions to Total Fluoride Chronic Exposure at 4 mg/L in Drinking Water % Contribution to Total Exposure Population Subgroups Total Exposure, mg/kg/day Pesticides and Air Background Food Toothpaste Drinking Water Modeled average water consumer (Tap water at 4 mg/L, nontap water at 0.5 mg/L; Table 2-11) All infants (<1 year) 0.209 1.6 4.6 0 93.9 Nursing 0.079 3.3 5.9 0 89.0 Nonnursing 0.258 1.4 4.4 0 94.1 Children 1-2 years 0.137 4.7 15.3 8.4 71.6 Children 3-5 years 0.126 3.5 14.4 9.0 73.1 Children 6-12 years 0.086 2.5 14.3 8.7 74.5 242
Youth 13-19 years 0.063 2.2 15.4 5.3 77.1 Adults 20-49 years 0.076 1.7 15.0 1.9 81.5 Adults 50+ years 0.079 1.7 12.8 1.8 83.7 Females 13-49 yearsa 0.075 1.8 14.3 2.2 81.7 EPA default water intake all water at 4 mg/L (1 L/day for 10-kg child; 2 L/day for 70-kg adult; Table 2-12) All infants (<1 year) 0.413 0.8 2.3 0 96.9 Nursing 0.409 0.6 1.1 0 97.9 Nonnursing 0.415 0.9 2.8 0 96.4 Children 1-2 years 0.439 1.5 4.8 2.6 91.1 Adults 20-49 years 0.128 1.0 8.9 1.1 89.0 High end of high water intake individuals, all water at 4 mg/L (based on intake rates in Table 2-4) Athletes and workers 0.294 0.4 3.9 0.5 95.2 DM patients (3-5 years) 0.434 1.0 4.2 2.6 92.2 DM patients (adults) 0.294 0.4 3.9 0.5 95.2 NDI patients (3-5 years) 0.634 0.7 2.9 1.8 94.7 NDI patients (adults) 0.614 0.2 1.9 0.2 97.7 aWomen of childbearing age. ABBREVIATIONS: DM, diabetes mellitus; NDI, nephrogenic diabetes insipidus and Tables 2-13, 2-14, and 2-15). The major contributing factor is their much higher model-estimated drinking-water exposure than other age groups (Table 2-10). The total exposures of nonnursing infants are approximately 2.8-3.4 times that of adults. By holding the exposure from drinking water at a constant with the EPA default water intake rates, children 1-2 years old have slightly higher total exposure than the nonnursing infants, reflecting the higher exposure from nonwater sources (Table 2-9). The estimated total fluoride exposures for children 1-2 years old are 0.139, 0.239, Page 68 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel 243 and 0.439 mg/kg/day for 1, 2, and 4 mg/L of fluoride in drinking water, respectively (Tables 2-13, 2-14, 2-15). These exposures are approximately 3.4 times that of adults. The estimated total exposure for children 1-2 years old and adults at 4 mg/L fluoride in drinking water is approximately two times the exposure at 2 mg/L and three times the exposure at 1 mg/L. The estimated total daily fluoride exposures for three population subgroups with significantly high water intake rates are included in Tables 2-13, 2-14, and 2-15. The matching age groups for data presented in Table 2-4 are: adults ≥ 20 years old for the athletes and workers, and both children 3-5 years old (default body weight of 22 kg) and adults for individuals with diabetes mellitus and nephrogenic diabetes insipidus. In estimating the total exposure, the high-end water intake rates from Table 2-4 are used to calculate the exposure from drinking water. The total exposures for adult athletes and workers are 0.084, 0.154, and 0.294 mg/kg/day at 1, 2, and 4 mg/L of fluoride in water, respectively. These doses are approximately two times those of the adults with a default water intake rate of 2 L/day. For individuals with nephrogenic diabetes insipidus, the respective total fluoride exposures for children (3-5 years old) and adults are 0.184 and 0.164 mg/kg/ day at 1 mg/L, 0.334 and 0.314 mg/kg/day at 2 mg/L, and 0.634 and 0.614 mg/kg/day at 4 mg/L. Compared to the exposure of children 1-2 years old, who have the highest total exposure among all age groups of the general population (i.e., 0.139-0.439 mg/kg/day at 1-4 mg/L, assuming EPA’s 100 mL/kg/day default water intake rate for children), the highest estimated total exposure among these high water intake individuals (i.e., 0.184-0.634 mg/kg/day for children 3- 5 years old with nephrogenic diabetes insipidus, assuming 150 mL/kg/day high-end water intake rate) are 32-44% higher. The relative contributions from each source of exposure are also presented in Tables 2-13, 2-14, and 2-15. For an average individual, the model- estimated drinking-water contribution to the total fluoride exposure is 41-83% at 1 mg/L in tap water, 57-90% at 2 mg/L, and 72-94% at 4mg/L in tap water (see also Figures 2-1, 2-2, and 2-3). Assuming that all drinking-water sources (tap and nontap) contain the same fluoride concentration and using the EPA default drinking-water intake rates, the drinking-water contribution is 67-92% at 1 mg/L, 80-96% at 2 mg/L, and 89-98% at 4 mg/L. The drinking-water contributions for the high water intake individuals among adult athletes and workers, and individuals with diabetes mellitus and nephrogenic diabetes insipidus, are 75-91% at 1 mg/L, 86-96% at 2 mg/L, and 92-98% at 4 mg/L. As noted earlier, these estimates were based on the information that was available to the committee as of April 2005. Any new and significant sources of fluoride exposure are expected to alter the percentage of drinking-water 244 contribution as presented in this chapter. However, water will still be the most significant source of exposure. Page 69 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel BIOMARKERS OF EXPOSURE, EFFECT, AND SUSCEPTIBILITY Biological markers, or biomarkers, are broadly defined as indicators of variation in cellular or biochemical components or processes, structure, or function that are measurable in biological systems or samples (NRC 1989a). Biomarkers often are categorized by whether they indicate exposure to an agent, an effect of exposure, or susceptibility to the effects of exposure (NRC 1989a). Vine (1994) described categories of biological markers in terms of internal dose, biologically effective dose, early response, and disease, plus susceptibility factors that modify the effects of the exposure. Factors that must be considered in selecting a biomarker for a given study include the objectives of the study, the availability and specificity of potential markers, the feasibility of measuring the markers (including the invasiveness of the necessary techniques and the amount of biological specimen needed), the time to appearance and the persistence of the markers in biological media, the variability of marker concentrations within and between individuals, and aspects (e.g., cost, sensitivity, reliability) related to storage and analysis of the samples (Vine 1994). ATSDR (2003) recently reviewed biomarkers of exposure and effect for fluoride. Biomarkers of exposure to fluoride consist of measured fluoride concentrations in biological tissues or fluids that can be used as indices of an individual’s exposure to fluoride. For fluoride, concentrations in a number of tissues and fluids, including teeth, bones, nails, hair, urine, blood or plasma, 245 saliva, and breast milk, have been used to estimate exposures (Vine 1994; Whitford et al. 1994; ATSDR 2003). Table 2-16 gives examples of measurements in humans together with the associated estimates of exposure. The Centers for Disease Control and Prevention (CDC 2003, 2005) has measured a number of chemicals in blood or urine of members of the U.S. population, but thus far fluoride has not been included in their survey. Fluoride concentrations in bodily fluids (e.g., urine, plasma, serum, saliva) are probably most suitable for evaluating recent or current fluoride exposures or fluoride balance (intake minus excretion), although some sources indicate that samples obtained from fasting persons may be useful for estimating chronic fluoride intake or bone fluoride concentrations (e.g., Ericsson et al. 1973; Waterhouse et al. 1980). Examples of the association between estimated fluoride intakes (or mass-normalized intakes) and measured fluoride concentrations in urine, plasma, and serum for individuals and groups are shown in Figures 2-4, 2-5, 2-6, and 2-7. Note that in most cases, the variation in fluoride intake is not sufficient to explain the variation in the measured fluoride concentrations. A number of parameters affect individual fluoride uptake, retention, and excretion (Chapter 3) (Whitford 1996). In addition, a significant decrease in fluoride exposure might not be Page 70 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel TABLE 2-16 Summary of Selected Biomarkers for Fluoride Exposure in Humans Number of Fluoride Fluoride Exposure Persons Concentration Reference Urine 246
1.2-2.2 mg/day 5 0.8-1.2 mg/day Teotia et al. 1978 (Figure 2-4) 2.5-3.8 mg/daya 2 1.2-2.2 mg/day 8.7-9.2 mg/day 3 3.2-5.8 mg/day 21.0-28.0 mg/day 2 10.0-11.0 mg/day 48.0-52.0 mg/day 2 15.0-18.5 mg/day 1.0 mg/L in drinking water 17 1.5 (0.2) mg/L Bachinskii et al. 1985 (Figure 2-6) 1.9 (0.3) mg/day 2.3 mg/L in drinking water 30 2.4 (0.2) mg/L 2.7 (0.2) mg/day 0.09 (range, 0.06-0.11) mg/L in 45 0.15 (0.07) mg/Lb Schamschula et al. 1985 drinking water (Figure 2-6) 0.82 (range, 0.5-1.1) mg/L in 53 0.62 (0.26) mg/Lb drinking water 1.91 (range, 1.6-3.1) mg/L in 41 1.24 (0.52) mg/Lb drinking water 0.32 mg/L in drinking water 100 0.77 (0.49) mg/Lb Czarnowski et al. 1999 (Figure 2-6) 1.69 mg/L in drinking water 111 1.93 (0.82) mg/Lb 2.74 mg/L in drinking water 89 2.89 (1.39) mg/Lb About 3 mg/day 1 2.30-2.87 mg/day Whitford et al. 1999a About 6 mg/day 1 4.40-5.13 mg/day 7.35 (1.72) mg/dayb 50 9.45 (4.11) mg/Lb Gupta et al. 2001 (Figure 2-7) 11.97 (1.8) mg/dayb 50 15.9 (9.98) mg/Lb 14.45 (3.19) mg/daya 50 17.78 (7.77) mg/La 32.56 (9.33) mg/daya 50 14.56 (7.88) mg/La 0.93 (0.39) mg/dayb [0.053 11 0.91 (0.45) mg/Lb Haftenberger et al. 2001 (0.021) mg/kg/dayb] (Figure 2-5) 1.190 (0.772) mg/day from all 20 0.481 (0.241) Pessan et al. 2005 sourcesb mg/dayb Plasma 1.2-2.2 mg/day 5 0.020-0.038 mg/L Teotia et al. 1978 (Figure 2-4) 2.5-3.8 mg/day 2 0.036-0.12 mg/L 8.7-9.2 mg/day 3 0.15-0.18 mg/L 21.0-28.0 mg/day 2 0.11-0.17 mg/L 48.0-52.0 mg/day 2 0.14-0.26 mg/L Serum 247
1.0 mg/L in drinking water 17 0.21 (0.01) mg/L Bachinskii et al. 1985 (Figure 2-6) 2.3 mg/L in drinking water 30 0.25 (0.01) mg/L 7.35 (1.72) mg/dayb 50 0.79 (0.21) mg/Lb Gupta et al. 2001 (Figure 2-7) 11.97 (1.8) mg/dayb 50 1.10 (0.58) mg/Lb 14.45 (3.19) mg/dayb 50 1.10 (0.17) mg/Lb 32.56 (9.33) mg/dayb 50 1.07 (0.17) mg/Lb Page 71 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel Number of Fluoride Fluoride Exposure Persons Concentration Reference 0.3 mg/L in drinking water: 48 0.0042 (0.0027) Hossny et al. 2003 Breastfed infants mg/Lb All infants (4 weeks-2 years) 97 0.0051 (0.0030) mg/Lb Preschoolers (2-6 years) 100 0.011 (0.0049) mg/Lb Primary schoolers (6-12 years) 99 0.010 (0.0042) mg/Lb Saliva 0.09 (range, 0.06-0.11) mg/L in 45 6.25 (2.44) µg/Lb Schamschula et al. drinking water 1985 0.82 (range, 0.5-1.1) mg/L in 53 11.23 (4.29) µg/Lb drinking water 248
1.91 (range, 1.6-3.1) mg/L in 41 15.87 (6.01) µg/Lb drinking water 0.1 mg/L in drinking water 27 1.9-55.1 µg/L Oliveby et al. 1990 1.2 mg/L in drinking water 27 1.9-144 µg/L Oliveby et al. 1990 Plaque 0.09 (range, 0.06-0.11) mg/L in 45 5.04 (4.60) ppmb Schamschula et al. drinking water 1985 0.82 (range, 0.5-1.1) mg/L in 53 8.47 (9.69) ppmb drinking water 1.91 (range, 1.6-3.1) mg/L in 41 19.6 (19.3) ppmb drinking water Hair 0.09 (range, 0.06-0.11) mg/L in 45 0.18 (0.07) µg/gb Schamschula et al. drinking water 1985 0.82 (range, 0.5-1.1) mg/L in 53 0.23 (0.11) µg/gb drinking water 1.91 (range, 1.6-3.1) mg/L in 41 0.40 (0.25) µg/gb drinking water 0.27 mg/L in drinking water and 2.8 59 1.35 (0.95) µg/gb Hac et al. 1997 µg/m3 in air 0.32 mg/L in drinking water 53 4.13 (2.24) µg/gb Czarnowski et al. 1999 1.69 mg/L in drinking water 111 10.25 (6.63) µg/gb 2.74 mg/L in drinking water 84 14.51 (6.29) µg/gb Breast milk 0.2 mg/L in drinking water 47 0.0053 mg/L Spak et al. 1983 (colostrum) Page 72 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
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Save Cancel Number of Fluoride Fluoride Exposure Persons Concentration Reference 1.0 mg/L in drinking water 79 0.0068 mg/L (colostrum) 1.0 mg/L in drinking water 17 0.007 mg/L (mature milk) Nonfluoridated community 32 0.0044 mg/L Dabeka et al. 1986 1 mg/L in drinking water 112 0.0098 mg/L 22.1 mg/day (mean) 27 0.011-0.073 mg/L Opinya et al. 1991 0.3 mg/L in drinking water 60 0.0046 (0.0025) Hossny et al. 2003 mg/Lb Fingernails 0.09 (range, 0.06-0.11) mg/L in drinking 45 0.79 (0.26) ppmb Schamschula et al. water 1985 0.82 (range, 0.5-1.1) mg/L in drinking 53 1.31 (0.49) ppmb water 1.91 (range, 1.6-3.1) mg/L in drinking 41 2.31 (1.14) ppmb water About 3 mg/day 1 1.94-3.05 mg/kg Whitford et al. 1999a About 6 mg/day (after 3.5 months) 1 4.52-5.38 mg/kg 0.1 mg/L in drinking water 10 0.75-3.53 mg/kg 1.6 mg/L in drinking water 6 2.28-7.53 mg/kg 2.3 mg/L in drinking water 9 4.00-13.18 mg/kg 0.7-1.0 mg/L in drinking water, without 10 2.3-7.3 mg/kg Corrêa Rodrigues et fluoride dentifrice al. 2004 0.7-1.0 mg/L in drinking water, with 10 10.1 mg/kg (peak) fluoride dentifrice (after 4 months) 0.004 ± 0.003 mg/kg/day 15 0.42-6.11 µg/g Levy et al. 2004 0.029 ± 0.029 mg/kg/day 15 0.87-7.06 µg/g Toenails 0.09 mg/L in drinking water 4.2 ppm Feskanich et al. 1998 1.0 mg/L in drinking water 6.4 ppm 3 mg/day 1 1.41-1.60 mg/kg Whitford et al. 1999a 250
0.7-1.0 mg/L in drinking water, without 10 2.5-5.6 mg/kg Corrêa Rodrigues et fluoride dentifrice al. 2004 0.7-1.0 mg/L in drinking water, with 10 9.2 mg/kg (peak) fluoride dentifrice (after 4 months) 0.004 ± 0.003 mg/kg/day 15 0.08-3.89 µg/g Levy et al. 2004 0.029 ± 0.029 mg/kg/day 15 0.81-6.38 µg/g Teeth Normal NA 190-300 ppm (total Roholm 1937 ash) Page 73 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel Number of Fluoride Concentration Fluoride Exposure Persons Reference Cryolite workers 5 1,100-5,300 ppm (total ash) Enamel (0.44-0.48 µm depth) 0.09 (range, 0.06-0.11) 45 1,549 (728) ppmb Schamschula et mg/L in drinking al. 1985 water 0.82 (range, 0.5-1.1) 53 2,511 (1,044) ppmb mg/L in drinking water 1.91 (range, 1.6-3.1) 41 3,792 (1,362) ppmb mg/L in drinking water Enamel (2.44-2.55 µm depth) 251
0.09 (range, 0.06-0.11) 45 641 (336) ppmb Schamschula et mg/L in drinking al. 1985 water 0.82 (range, 0.5-1.1) 53 1,435 (502) ppmb mg/L in drinking water 1.91 (range, 1.6-3.1) 41 2,107 (741) ppmb mg/L in drinking water Enamel 0.7 or 1.0 mg/L in 30 0-192 µg/g Vieira et al. drinking water 2005 Dentin 0.7 or 1.0 mg/L in 30 59-374 µg/g Vieira et al. drinking water 2005 Bones Normal NA 480-2,100 ppm in bone ash (ribs) Roholm 1937 Cryolite workers 2 9,900 and 11,200 ppm in bone ash (ribs) ranges (ppm in bone ash, various bone types, 3,100-9,900 and 8,100-13,100 in the 2 individuals 0.1-0.4 mg/L in 33 326-2,390 ppm in bone ashc Zipkin et al. drinking water 1958 1.0 mg/L in drinking 5 1,610-4,920 ppm in bone ashd water 2.6 mg/L in drinking 27 1,560-10,800 ppm in bone ashe water 4.0 mg/L in drinking 4 4,780-11,000 ppm in bone ashf water Page 74 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
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Save Cancel Fluoride Exposure Number of Fluoride Concentration Reference Persons < 0.2 mg/L in drinking water since 8 1,379 (179) ppm in Eble et al. infancy bone ashg 1992 1 mg/L in drinking water at least 23 9 1,775 (313) ppm in years or since infancy bone ashg 0.27 mg/L in drinking water and 2.8 59 625.7 (346.5) ppmb,h Hac et al. µg/m3 in air 1997 0.7 or 1.0 mg/L in drinking water 30 0-396 ppmi Vieira et al. 2005 aPrevious exposure of 30-38 mg/day, 2-5 years before study. bMean and standard deviation. cReported as 0.019-0.119% in bone, with ash content of 43.2-68.4%. dReported as 0.100-0.238% in bone, with ash content of 45.9-62.2%. eReported as 0.092-0.548% in bone, with ash content of 32.7-66.7%. fReported as 0.261-0.564% in bone, with ash content of 44.3-62.8%. gMean and standard error of the mean. hReported as µg fluoride per gram bone; appears to be dry weight of bone, not bone ash. iMeasured by Instrumental Neutron Activation Analysis; appears to be wet weight of bone. ABBREVIATION: NA, not available. reflected immediately in urine or plasma, presumably because of remobilization of fluoride from resorbed bone.14 Concentrations of salivary fluoride (as excreted by the glands) are typically about two-thirds of the plasma fluoride concentration and independent of the salivary flow rate (Rölla and Ekstrand 1996); fluoride in the mouth from dietary intake or dentifrices also affects the concentrations measured in whole saliva. Significantly higher concentrations of fluoride were found in whole saliva and plaque following use of a fluoridated dentifrice versus a nonfluoridated dentifrice by children residing in an area with low fluoride (<0.1 mg/L) in drinking water. Concentrations were 15 times higher in whole saliva and 3 times higher in plaque, on average, 1 hour after use of the dentifrice (Whitford et al. 2005). Whitford et al. (1999b) found that whole-saliva fluoride concentrations in 5- to 10-year-old children were not signifi- 14 For example, following defluoridation of a town’s water supply from 8 mg/L to around 1.3 mg/L (mean daily fluoride content over 113 weeks), urinary fluoride concentrations in males fell from means of 6.5 (children) and 7.7 (adults) mg/L before defluoridation to 4.9 and 5.1 mg/L, respectively, after 1 week, 3.5 and 3.4 mg/L, respectively, after 39 weeks, and 2.2 and 2.5 mg/L, respectively, after 113 weeks (Likins et al. 1956). An estimate of current fluoride 253
intake (as opposed to fluoride balance) from a urine sample during this period would probably have been an overestimate. Page 75 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
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FIGURE 2-4 Urinary fluoride excretion (left) and fasting plasma fluoride concentration (right) as functions of current daily fluoride intake for individual adults (nine males, five females) aged 18-58 years. Data from Teotia et al. 1978. cantly related to those in either plasma or parotid ductal saliva. However, fluoride concentrations in parotid ductal saliva were strongly correlated to the plasma fluoride concentrations (r = 0.916), with a saliva-to-plasma fluoride concentration ratio of 0.80 (SE = 0.03, range from 0.61 to 1.07). For three- quarters of the study population (13 of 17), the fluoride concentration in 254 parotid ductal saliva could be used to estimate plasma fluoride concentrations within 20% or less, and the largest difference was 32%. Measured fluoride concentrations in human breast milk have been correlated with the mother’s fluoride intake in some studies (Dabeka et al. 1986) and not well correlated in other studies (Spak et al. 1983; Opinya et al. 1991). In general, measurements of fluoride in breast milk would be of limited use in exposure estimation because of the very low concentrations even in cases of high fluoride intake, lack of a consistent correlation with the mother’s fluoride intake, and limitation of use to those members of a population who are lactating at the time of sampling. Schamschula et al. (1985) found increasing concentrations of fluoride in urine, nails, hair, and saliva with increasing water fluoride concentration in a sample of Hungarian children, but fluoride contents were not directly proportional to the water fluoride content. Although means were significantly different between groups, there was sufficient variability among individuals within groups that individual values between groups overlapped. Feskanich et al. (1998) used toenail fluoride as an indicator of long-term Page 76 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
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FIGURE 2-5 Urinary fluoride excretion (left) and concentration (right) as functions of current daily fluoride intake (top) or body-weight normalized intake (bottom) for individual children (six boys, five girls) aged 3-6 years. Data from Haftenberger et al. 2001. fluoride intake and considered it to be a better long-term marker than plasma concentrations. Whitford et al. (1999a) found a direct relationship between fluoride concentrations in drinking water and fluoride concentrations in fingernail clippings from 6- to 7-year-old children with no known fluoride exposure other than from drinking water. In nail samples from one adult, Whitford et al. (1999a) also found that an increase in fluoride intake was reflected in fingernail fluoride concentrations approximately 3.5 months later and that toenails had significantly lower fluoride concentrations than fingernails. Levy et al. (2004) also found higher fluoride concentrations in fingernails Page 77 256
Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
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FIGURE 2-6 Urinary (left) and serum (right) fluoride concentrations as functions of fluoride concentration in drinking water. Dark symbols indicate means of groups; vertical lines indicate 1 standard deviation from the mean. Data from Bachinskii et al. (1985; circles), Schamschula et al. (1985; diamonds), and Czarnowski et al. (1999; triangles). Data from Bachinskii et al. represent 47 adults (ages 19-59); data from Schamschula et al. represent children aged 14 years; and data from Czarnowski et al. represent adults (ages 24-77, mean age 50). 257
FIGURE 2-7 Urinary (left) and serum (right) fluoride concentrations as functions of estimated daily fluoride intake (data from Gupta et al. 2001). Dark circles indicate means of groups of 50 children (ages 6-12); vertical lines indicate 1 standard deviation from the mean. Page 78 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel than in toenails in 2- to 6-year old children and showed a correlation between nail concentrations and dietary fluoride intake (exclusive of fluoride in toothpaste). Plasma fluoride in these children was not correlated with fluoride in fingernails, toenails, diet, or drinking water. In contrast, Corrêa Rodrigues et al. (2004), in samples from 2- to 3-year-old children, found no significant differences in fluoride concentrations between fingernails and toenails collected at the same time. An increase in fluoride intake in these children was reflected in nail samples approximately 4 months 258 later (Corrêa Rodrigues et al. 2004). Most likely, differences in “lag times” and differences between fingernails and toenails in the same individual reflect differences in growth rates of the nails due to factors such as age or differences in blood flow. McDonnell et al. (2004) found a wide variation in growth rates of thumbnails of 2- and 3-year-old children; age, gender, and fluoride exposure had no effect on the growth rates. However, it was emphasized that, for any study in which it is of interest to estimate the timing of a fluoride exposure based on measurements of fluoride in nails, the growth rate of the nails should be measured for each individual. Czarnowski et al. (1999) found correlations between water fluoride concentrations and urinary fluoride, fluoride in hair, and bone mineral density measured in 300 people in the Gdánsk region of Poland. For workers with occupational exposure to airborne fluoride (largely HF), Czarnowski and Krechniak (1990) found good correlation among groups of workers between fluoride concentrations in urine and nails (r = 0.99); correlation between concentrations in urine and hair or hair and nails was also positive but not as good (r = 0.77 and 0.70, respectively). For individual values, positive correlation was found only between concentrations in urine and nails (r = 0.73). It was not possible to establish correlations between fluoride concentrations in biological media and air (Czarnowski and Krechniak 1990). Measuring the fluoride content of teeth and bones can give an indication of chronic or cumulative fluoride exposure, although after cessation of fluoride exposure, bone fluoride concentrations slowly decrease because of resorption of bone. In addition, bone turnover results in the accumulation of various concentrations of fluoride in different bone types and sites (Selwitz 1994). Dentin has also been suggested as a reasonably accurate marker for long- term exposure (Selwitz 1994), although Vieira et al. (2005) found no correlation between bone fluoride and either enamel or dentin fluoride in persons with exposure to 0.07 or 1.0 mg/L fluoride in drinking water. Roholm (1937) reported that the fluoride content in normal teeth varied from 190 to 300 ppm (0.19 to 0.30 mg/g) in the total ash, with 5-7 times as much fluoride in the dentin as in the enamel. Fluoride content in the total ash of teeth from five cryolite workers (employed 8-10 years; three with osteosclerosis) contained 1,100-5,300 ppm (1.1-5.3 mg/g), with the most carious teeth containing the most fluoride. Roholm (1937) also reported Page 79 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of 259
EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel normal bone fluoride concentrations of 480-2,100 ppm in bone ash (0.48-2.1 mg/g bone ash in ribs), with concentrations between 3,100 and 13,100 ppm in bone ash (3.1 and 13.1 mg/g bone ash; varying with type of bone) in two cryolite workers. Hodge and Smith (1965), summarizing several reports, listed mean concentrations of bone fluoride in normal individuals between 450 and 1,200 ppm in bone ash and in people “suffering excessive exposure” to fluorides between 7,500 and 20,830 ppm in bone ash. More recently, Eble et al. (1992) have reported fluoride concentrations in bone ash ranging from 378 ppm (16-year old with <0.2 mg/L fluoride in drinking water since infancy) to 3,708 ppm (79-year old with fluoridated water). A 46-year old female with chronic renal failure had a fluoride concentration in bone ash of 3,253 ppm (Eble et al. 1992). The data of Zipkin et al. (1958) shows a good relationship between drinking- water fluoride and the mean percentage of fluoride in bone (iliac crest, rib, and vertebra) for adults in areas of various fluoride concentrations in drinking water. However, the ranges (Table 2-16; see also Chapter 3, Figure 3-1) suggest that variability among individuals within groups could be large, probably reflecting variability in individual fluoride intakes, duration of exposure, and age. A major disadvantage of measuring bone fluoride is the invasiveness of bone sampling in live individuals. Although easier to do, x-ray screening for increased bone density should be done only when the need for information justifies the radiation dose involved; in addition, bone density might not be related solely to fluoride exposure or to bone fluoride content. The two most important biomarkers of effect for fluoride are considered to be enamel fluorosis and skeletal fluorosis (ATSDR 2003); these are discussed more fully in Chapters 4 and 5. Enamel fluorosis is characterized by mottling and erosion of the enamel of the teeth and is associated with elevated fluoride intakes during the childhood years when the teeth are developing. According to the U.S. Public Health Service (PHS 1991), both the percent prevalence and the increasing severity of enamel fluorosis are associated with increasing 260 fluoride concentration in drinking water (and presumably actual fluoride intake). For “optimally” fluoridated water (0.7-1.2 mg/L), 22% of children examined in the 1980s showed some fluorosis (mostly very mild or mild); at water fluoride concentrations above 2.3 mg/L, more than 70% of children showed fluorosis (PHS 1991; NRC 1993). Some children developed fluorosis even at the lowest fluoride concentrations (<0.4 mg/L), suggesting that either fluoride intakes are variable within a population with the same water supply or there is variability in the susceptibility to fluorosis within populations (or both). Baelum et al. (1987) indicated that 0.03 mg/kg/day might not be protective against enamel fluorosis, and Fejerskov et al. (1987) stated that the borderline dose above which enamel fluorosis might develop could be as low as 0.03 mg/kg/day. Page 80 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel DenBesten (1994) described the limitations of using enamel fluorosis as a biomarker of exposure: enamel fluorosis is useful only for children less than about 7 years old when the exposure occurred; the incidence and degree of fluorosis vary with the timing, duration, and concentration; and there appear to be variations in individual response. Selwitz (1994), summarizing a workshop on the assessment of fluoride accumulation, also indicated that variability in response (incidence and severity of enamel fluorosis) to fluoride exposure may result from physiological differences among individuals and that enamel fluorosis is not an adequate biomarker for fluoride accumulation or potentially adverse health effects beyond the period of tooth formation. Selwitz (1994) did suggest that enamel fluorosis could be used as a biomarker of fluoride exposure in young children within a community over time. 261
Skeletal fluorosis (see also Chapter 5) is characterized by increased bone mass, increased radiographic density of the bones, and a range of skeletal and joint symptoms; preclinical skeletal fluorosis is associated with fluoride concentrations of 3,500-5,500 ppm in bone ash and clinical stages I, II, and III with concentrations of 6,000-7,000, 7,500-9,000, and >8,400, respectively (PHS 1991), although other sources indicate lower concentrations of bone fluoride in some cases of skeletal fluoride (see Chapter 5). According to the Institute of Medicine, “Most epidemiological research has indicated that an intake of at least 10 mg/day [of fluoride] for 10 or more years is needed to produce clinical signs of the milder forms of [skeletal fluorosis]” (IOM 1997). However, the National Research Council (NRC 1993) indicated that crippling (as opposed to mild) skeletal fluorosis “might occur in people who have ingested 10-20 mg of fluoride per day for 10-20 years.” A previous NRC report (NRC 1977) stated that a retention of 2 mg of fluoride per day (corresponding approximately to a daily intake of 4-5 mg) “would mean that an average individual would experience skeletal fluorosis after 40 yr, based on an accumulation of 10,000 ppm fluoride in bone ash.” Studies in other countries indicate that skeletal fluorosis might be in part a marker of susceptibility as well as exposure, with factors such as dietary calcium deficiency involved in addition to fluoride intake (Pettifor et al. 1989; Teotia et al. 1998). Hodge and Smith (1965) summarized a number of studies of skeletal fluorosis, including two that indicated affected individuals in the United States with water supplies containing fluoride at 4.8 or 8 mg/L. They also stated categorically that “crippling fluorosis has never been seen in the United States.” The individuals with endemic fluorosis at 4.8 mg/L are referred to elsewhere as having “radiographic osteosclerosis, but no evidence of skeletal fluorosis” (PHS 1991). In combination with high fluid intake and large amounts of tea, “the lowest drinking-water concentration of fluoride Page 81 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
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Save Cancel associated with symptomatic skeletal fluorosis that has been reported to date is 3 ppm, outside of countries such as India” (NRC 1977). Both the PHS (1991) and the NRC (1993) indicated that only five cases of crippling skeletal fluorosis have been reported in the literature in the United States (including one case in a recent immigrant from an area with fluoride in the drinking water at 3.9 mg/L) (PHS 1991). These individuals were said to have water supplies ranging from 3.9 to 8.0 mg/L (water fluoride content given for one of the individuals is actually less than 3.9 mg/L) (PHS 1991). Two of the individuals had intakes of up to 6 L/day of water containing fluoride at 2.4- 3.5 or 4.0-7.8 mg/L (PHS 1991; NRC 1993); this corresponds to fluoride intakes of up to 14.4-21 or 24-47 mg/day. Several cases of skeletal fluorosis reported in the United States are summarized in Table 2-17. These reports indicate that a fluoride concentration of 7-8 mg/L for 7 years is sufficient to bring about skeletal fluorosis (Felsenfeld and Roberts 1991), but skeletal fluorosis may occur at much lower fluoride concentrations in cases of renal insufficiency (Juncos and Donadio 1972; Johnson et al. 1979). People who consume instant tea are at increased risk of developing skeletal fluorosis, especially if they drink large volumes, use extra- strength preparations, or use fluoridated or fluoride-contaminated water (Whyte et al. 2005). In summary, selecting appropriate biomarkers for a given fluoride study depends on a number of factors, as listed above. A major consideration is the time period of interest for the study (e.g., current or recent exposures versus exposures in childhood versus cumulative exposures) and whether the intent is to demonstrate differences among groups or to characterize exposures of specific individuals. Many of the areas for further research identified by a 1994 workshop (Whitford et al. 1994) are still relevant for improving the assessment of fluoride exposures. FINDINGS Table 2-18 summarizes various published perspectives on the significance of given concentrations of fluoride exposure. Historically, a daily intake of 4-5 mg by an adult (0.057-0.071 mg/kg for a 70-kg adult) was considered a “health hazard” (McClure et al. 1945, cited by Singer et al. 1985). However, the Institute of Medicine (IOM 1997) now lists 10 mg/day as a “tolerable upper intake” for children > 8 years old and adults, although that intake has also been associated with the possibility of mild (IOM 1997) or even crippling (NRC 1993) skeletal fluorosis. 263
The recommended optimal fluoride intake for children to maximize caries prevention and minimize the occurrence of enamel fluorosis is often stated as being 0.05-0.07 mg/kg/day (Levy 1994; Heller et al. 1999, 2000). Burt (1992) attempted to track down the origin of the estimate of 0.05-0.07 Page 82 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel TABLE 2-17 Case Reports of Skeletal Fluorosis in the United States Study Subjects Exposure Conditions Comments Reference (a) 18-year-old (a) “high” intake of well water Enamel fluorosis and Juncos and boy, 57.4 kg containing fluoride at 2.6 mg/L roentgenographic bone changes Donadio (b) 17-year-old since early childhood; current consistent with “systemic 1972 girl, 45.65 kg intake, 7.6 L/day (0.34 fluorosis,” attributed to the mg/kg/day) combination of renal (b) “high” intake of water insufficiency and polydipsia containing fluoride at 1.7 mg/L (the latter resulting from the since infancy; current intake, 4 renal disease); reported by the L/day (0.15 mg/kg/day) Mayo Clinic Six renal patients Drinking water with 1.7-3 mg/L Fluoride “may have been the Johnson et seen at the Mayo fluoride; water consumption not cause of detectable clinical and al. 1979 Clinic over a stated, but urine volumes of roentgenographic effects” several year “most” of the patients exceeded Five of the patients had renal period (includes 3 L/day disease of at least 15 years the two patients duration before skeletal reported by symptoms developed Juncos and Donadio) 264
54-year-old Well water with fluoride Osteosclerosis, elevated serum Felsenfeld woman in concentration of 7.3-8.2mg/L alkaline phosphatase, stiffness and Oklahoma (382-429 µmol/L); duration of of knees and hips (2 years Roberts residence at that location, 7 duration), kyphosis 1991 years; prior to that she had used Renal insufficiency was not a municipal water at less than 2 factor mg/L fluoride; water consumption not reported, but considered likely to be “increased” due to hot summers 52-year-old Daily consumption of 1-2 Osteosclerosis, increased bone Whyte et woman in gallons (3.8-7.6 L) per day of mineral density, bone and joint al. 2005 Missouri double-strength instant tea pains made with unfiltered well water Intake of fluoride from well (2.8 mg/L fluoride in the well water alone was considered water) for close to 10 years; sufficient to cause mild skeletal estimated fluoride intake of 37- fluorosis 74 mg/day (11-22 mg/day from No mention of any renal well water and 26-52 mg/day disease from tea) Page 83 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel TABLE 2-18 Summary of Current and Historical Perspectives on Fluoride Exposure Exposure, mg/kg/day Description Reference 0.0014 “Adequate intake” for children < 6 months olda (0.01 IOM 1997; ADA 2005 mg/day) 265
0.01-0.04 Average daily dietary fluoride intake for children 0-2 IOM 1997b years old residing in nonfluoridated areas (< 0.4 mg/L) 0.017-0.031 Average daily intake by adults in a fluoridated area NRC 1993 (1.2-2.2 mg/day)c 0.017-0.054 Lower end of “safe and adequate daily dietary intake” NRC 1989b for children ≥ 0-10 yearsd (0.1-1.5 mg/day) 0.019-0.033 Lower end of “safe and adequate daily dietary intake” NRC 1989b for children 10 years and adultsd (1.5 mg/day) 0.02-0.10 Average daily dietary fluoride intake for children 1-9 McClure 1943e years residing in fluoridated areas (0.7-1.1 mg/L) 0.038-0.069 Upper end of “safe and adequate daily dietary intake” NRC 1989b for children ≥ 10 years and adultsd (2.5-4.0 mg/day) 0.04-0.07 Average daily intake by children in a fluoridated area NRC 1993 0.05 “Adequate intake” for all ages above 6 months olda,f IOM 1997; ADA 2005 0.05 ATSDR’s minimal risk levelg (chronic duration, based ATSDR 2003 on increased rate of bone fractures)h 0.05-0.13 Average daily dietary fluoride intake for children 0-2 IOM 1997b years old residing in fluoridated areas (0.7-1.1 mg/L) 0.05-0.07 “Optimal” intake to maximize caries prevention and Levy 1994; Heller et al. minimize the occurrence of enamel fluorosis 1999, 2000 0.05-0.07 “Useful upper limit for fluoride intake in children” Burt 1992 0.057-0.071 “Health hazard” for adults (4-5 mg/day)c McClure et al. 1945 0.057 EPA’s SMCL (2 mg/l; adult intake)i 40CFR 143.3[2001] 0.06 EPA’s reference dosej (based on protection of children EPA 1989 from objectionable enamel fluorosis)k 0.083-0.13 Upper end of “safe and adequate daily dietary intake” NRC 1989b for children 0-10 years oldd (0.5-2.5 mg/day) 0.10 “Tolerable upper intake”l for ages 0-8a (0.7-2.2 IOM 1997; ADA 2005 mg/day) 0.10 EPA’s SMCL (2 mg/L; child intake)m 40CFR 143.3 [2001] 0.11 EPA’s MCLG and MCL (4 mg/L; adult intake)n 40CFR 141.62(b)[2001] 0.13-0.18 “Tolerable upper intake”o for ages ≥ 14a (10 mg/day) IOM 1997; ADA 2005 0.2 EPA’s MCLG and MCL (4 mg/L; child intake)p 40CFR 141.62(b)[2001] Page 84 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of 266
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Exposure, mg/kg/day Description Reference 0.25 “Tolerable upper intake”o for ages 9-13a (10 IOM 1997; ADA 2005 mg/day) aBased on intakes and average body weights listed by IOM (1997) and ADA (2005); see Table B-17 in Appendix B. bSummaries of papers published between 1979 and 1988 (IOM 1997). cBased on a 70-kg adult. dBased on intakes and median weights listed by NRC (1989b); see Table B-16 in Appendix B. eSummarized by IOM (1997). fRange, 0.045-0.056 mg/kg/day. gA minimal risk level (MRL) is an estimate of the daily human exposure to a hazardous substance that is likely to be without appreciable risk of adverse noncancer health effects over a specified duration of exposure (ATSDR 2003). hThe ATSDR (2003) states that an intermediate-duration MRL derived from a study of thyroid effects in rats would have been lower (more protective) than the chronic-duration MRL of 0.05, but the value of that MRL is not given. iBased on intake of 2 L/day by a 70-kg adult of water containing fluoride at 2 mg/L. jReference dose (RfD) is an estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime (EPA 1989). kBased on a fluoride concentration of 1 mg/L in drinking water; the RfD for fluoride contains no uncertainty factor or modifying factor, although RfDs for other substances contain uncertainty factors to account for things such as variability within the human population (EPA 2003b). lBased on moderate enamel fluorosis (IOM 1997). mBased on intake of 1 L/day by a 20-kg child of water containing fluoride at 2 mg/L. nBased on intake of 2 L/day by a 70-kg adult of water containing fluoride at 4 mg/L. oBased on skeletal fluorosis for adults and children ≥ age 9 (IOM 1997). pBased on intake of 1 L/day by a 20-kg child of water containing fluoride at 4 mg/L. mg/kg/day as an optimum intake of fluoride but was unable to find it. He interpreted the available evidence as suggesting that 0.05-0.07 mg/kg/day (from all sources) “remains a useful upper limit for fluoride intake in children” (see also NRC 1993). 267
Figure 2-8 shows the average intake of fluoride from all sources estimated in this report (Table 2-11), with 1 mg/L in drinking water; Figure 2-9 shows the average intake of fluoride from drinking water alone (Table 2-10), given a fluoride concentration at the MCLG/MCL (4 mg/L). For comparison purposes, an intake of 0.05-0.07 mg/kg/day is indicated on the graphs. Based on EPA’s estimates of community water consumption by consumers with an average intake (EPA 2000a), if that water is fluoridated, children Page 85 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
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FIGURE 2-8 Estimated average intake of fluoride from all sources, at 1 mg/L in drinking water (based on Table 2-11). Horizontal lines indicate an intake of 0.05-0.07 mg/kg/day. less than 6 months old have an intake at or above 0.05-0.07 mg/kg/day (see Appendix B, Table B-10). Children from 6 months to 1 year old have similar intakes if their water is fluoridated at 1 or 1.2 mg/L. No other age groups have that intake at ordinary fluoride concentrations; all age groups reach or exceed that intake with water at 4 mg/L. For individuals with higher- than-average intake of community water, intakes for the youngest children (<1 year) might exceed 0.05-0.07 mg/kg/day at all concentrations of water fluoridation (see Appendix B, Tables B-11, B-12, and B-13); for fluoride concentrations corresponding to the SMCL (2 mg/L) or MCL (4 mg/L), an intake of 0.05-0.07 mg/kg/day is reached or exceeded by all age groups. Note that the estimates in Appendix B include only the fluoride contribution from Page 86 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 269
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FIGURE 2-9 Estimated average intake of fluoride from drinking water alone, based on a fluoride concentration of 4 mg/L (MCLGl/MCL; based on Table 2- 10). Horizontal lines indicate an intake of 0.05-0.07 mg/kg/day. community water (drinking water, plus beverages and foods prepared with community water at home or in local eating establishments); if contributions 270 from food, tea, commercial beverages, toothpastes, and other sources are added, total intakes by individuals will increase accordingly. Estimates of total exposure (typical or average) shown in Table 2- 11 indicate that all children through age 12 who take fluoride supplements (assuming low water fluoride) will reach or exceed 0.05-0.07 mg/kg/day. For children not on supplements, nonnursing infants with fluoride in tap water at ≥0.5 mg/L will exceed 0.05-0.07 mg/kg/day for typical exposures. Also, children through 5 years old (≥0.5 mg/L in tap water), children 6-12 years old (≥2 mg/L in tap water), and teenagers and adults (≥4 mg/L in tap water) will exceed 0.05-0.07 mg/kg/day with typical or average fluoride exposures in terms of water consumption and toothpaste ingestion. Page 87 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. ×
Save Cancel A number of researchers have pointed out both the importance of evaluating individual fluoride intake from all sources and the difficulties associated with doing so, given the variability of fluoride content in various foods and beverages and the variability of individual intakes of the specific items (Clovis and Hargreaves 1988; Nowak and Nowak 1989; Chan et al. 1990; Stannard et al. 1990, 1991; Weinberger 1991; Toumba et al. 1994; Duperon et al. 1995; Van Winkle et al. 1995; Chan and Koh 1996; Kiritsy et al. 1996; Warren et al. 1996; Heilman et al. 1997, 1999; Heller et al. 1999; Levy and Guha- Chowdhury 1999; Lalumandier and Ayers 2000). However, as shown in Figure 2-1, for typical individuals, the single most important contributor to fluoride exposures (approaching 50% or more) is fluoridated water and other beverages and foods prepared or manufactured with fluoridated water. RECOMMENDATIONS 271
Fluoride should be included in nationwide biomonitoring surveys and nutritional studies (e.g., CDC’s National Health and Nutrition Examination Survey and affiliated studies). In particular, analysis of fluoride in blood and urine samples taken in these surveys would be valuable. National data on fluoridation (e.g., CDC 1993) should be updated on a regular basis. Probabilistic analysis should be performed for the uncertainty in estimates of individual and group exposures and for population distributions of exposure (e.g., variability with respect to long-term water consumption). This would permit estimation of the number of people exposed at various concentrations, identification of population subgroups at unusual risk for high exposures, identification or confirmation of those fluoride sources with the greatest impact on individual or population exposures, and identification or characterization of fluoride sources that are significant contributors to total exposure for certain population subgroups. To assist in estimating individual fluoride exposure from ingestion, manufacturers and producers should provide information on the fluoride content of commercial foods and beverages. To permit better characterization of current exposures from airborne fluorides, ambient concentrations of airborne hydrogen fluoride and particulates should be reported on national and regional scales, especially for areas of known air pollution or known sources of airborne fluorides. Additional information on fluoride concentrations in soils in residential and recreational areas near industrial fluoride sources also should be obtained. Additional studies on the relationship between individual fluoride exposures and measurements of fluoride in tissues (especially bone and nails) and bodily fluids (especially serum and urine) should be conducted. Such Page 88 Suggested Citation:"2 Measures of Exposure to Fluoride in the United States." National Research Council. 2006. Fluoride in Drinking Water: A Scientific Review of EPA's Standards. Washington, DC: The National Academies Press. doi: 10.17226/11571. 272
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Save Cancel studies should determine both absolute intakes (mg/day) and body- weight normalized intakes (mg/kg/day). Assumptions about the influence of environmental factors, particularly temperature, on water consumption should be reevaluated in light of current lifestyle practices (e.g., greater availability of air conditioning, participation in indoor sports). Better characterization of exposure to fluoride is needed in epidemiology studies investigating potential effects. Important exposure aspects of such studies would include the following: o collecting data on general dietary status and dietary factors that could influence exposure or effects, such as calcium, iodine, and aluminum intakes o characterizing and grouping individuals by estimated (total) exposure, rather than by source of exposure, location of residence, fluoride concentration in drinking water, or other surrogates o reporting intakes or exposures with and without normalization for body weight (e.g., mg/day and mg/kg/day) o addressing uncertainties associated with exposure, including uncertainties in measurements of fluoride concentrations in bodily fluids and tissues o reporting data in terms of individual correlations between intake and effect, differences in subgroups, and differences in percentages of individuals showing an effect and not just differences in group or population means. Further analysis should be done of the concentrations of fluoride and various fluoride species or complexes (especially fluorosilicates and aluminofluorides) present in tap water, using a range of water samples (e.g., of different hardness and mineral content). Research also should include characterizing any changes in speciation that occur when tap water is used for various purposes—for example, to make acidic beverages. 273
2− The possibility of biological effects of SiF6 , as opposed to free fluoride ion, should be examined. The biological effects of aluminofluoride complexes should be researched further, including the conditions (exposure conditions and physiological conditions) under which the complexes can be expected to occur and to have biological effects.
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29.) Most common home water filters, such as Brita, effectively remove fluoride from the water. A. True B. False https://fluoridealert.org/content/top_ten/
TOP 10 WAYS TO REDUCE FLUORIDE EXPOSURE Fluoride Action Network
The following 10 tips will allow you to significantly reduce your daily exposure to fluoride.
1) Stop Drinking Fluoridated Water:
Tap water consumption is, on average, the largest daily source of fluoride exposure for people who live in areas that add fluoride to the water. Avoiding consumption of fluoridated water is especially critical for infants. If you live in area which fluoridates its water, you can avoid drinking the fluoride in one of three ways: 1. Water Filters: One way of avoiding the fluoride from tap water is to purchase a water filter. Not all water filters, however, remove fluoride. The three types of filters that can remove fluoride are reverse osmosis, deionizers (which use ion- exchange resins), and activated alumina. Each of these filters should be able to remove about 90% of the fluoride. By contrast, “activated carbon” filters (e.g., Brita & Pur) do not remove fluoride. For more information on water filters, click here. 2. Spring Water: Another way to avoid fluoride from tap water is to purchase spring water. Most brands of spring water contain very low levels of fluoride. Some brands, however, do contain high levels (e.g., Trinity Springs). Before consuming any bottled water on a consistent basis, therefore, you should verify that the fluoride content is less than 0.2 ppm, and ideally less than 0.1 ppm. You can find out the level of fluoride level in some of the popular brands here. You can also find out the fluoride level by calling the number on the water label. (Most companies have this information readily available.) 275
3. Water Distillation: A third way to avoid fluoride from the tap is to purchase a distillation unit. Water distillation will remove most, if not all, of the fluoride. The price for a distillation units varies widely depending on the size. Small counter-top units cost as little as $200, while large units can exceed $1,000. If you don’t know if your area is fluoridated, you can find out by contacting your local water department. If you live in the U.S., you can also find out by going to FAN’s State Fluoride Database. 2) Don’t Let Your Child Swallow Fluoride Toothpaste Fluoride toothpaste is often the largest single source of fluoride intake for young children, and is a major risk factor for disfiguring dental fluorosis. This is because children swallow a large amount of the paste that they put in their mouth. In fact, research has shown that it is not uncommon for young children to swallow more fluoride from toothpaste alone than is recommended as an entire day’s ingestion from all sources. If you have a young child, therefore, we recommend that you use a non-fluoride toothpaste. If, however, you do use fluoride toothpaste, it’s very important that you supervise your children while they brush to make sure they use no more than a “pea-sized amount” of paste, and that they fully rinse and spit after they finish. And, lastly, do not purchase candy flavored toothpaste (e.g., bubble-gum and watermelon) as these toothpastes (which still contain adult-strength concentrations of fluoride) increase the risk that your children will swallow it (and actually want to swallow it).
3) Do NOT Get Fluoride Gel Treatments at the Dentist
Although dental researchers have stated on numerous occasions that fluoride gel treatment should ONLY be used for patients at highest risk of cavities, many dentists continue to apply fluoride gels irrespective of the patient’s cavity risk. The fluoride gel procedure requires the patient to clamp down on a tray for 4 minutes and uses an extremely concentrated, acidic fluoride gel (12,300 ppm). Because of the fluoride gel’s high acidity, the saliva glands produce a large amount of saliva during the treatment, which makes it extremely difficult (both for children and adults) to avoid swallowing the gel. 276
Even when dentists use precautionary measures such as suction devices, children and adults still ingest significant quantities of the paste, which can cause incredibly high spikes of fluoride in the blood (for up to 15 hours). These fluoride levels place patients, particularly children, at risk for stomach pain, nausea and vomiting, and places a person at risk for short-term kidney damage, harm to the reproductive system, and impairment to glucose metabolism. The next time your dentist asks you whether you want a fluoride gel treatment, say NO.
4) Eat Fresh Food, Not Processed Food and Preferably Organic
When water is fluoridated, it is not just the water that is fluoridated, but all beverages and foods that are made with the water. As a general rule, therefore, the more processed a food is, the more fluoride it has. The good news is that the naturally occurring levels of fluoride in most fresh water (e.g., spring water) and most fresh food (e.g., fruits, vegetables, grain, eggs, milk) is very low. Use this fact to your advantage by trying to shift as much as you can from processed foods to fresh. Also, since processed beverages (e.g., sodas, reconstituted juices, sports drinks) contribute far more to fluoride intake than processed foods, it is most important to focus on reducing your consumption of processed beverages. For more detailed information on how you can cut down on your fluoride intake from processed foods, see “FAN’s Grocery Store Guide: 7 Ways to Avoid Fluoride in Beverages and Food.” Note: Non-organic processed foods are stored in warehouses and are often fumigated with sulfuryl fluoride – see the allowable levels of fluoride and sulfuryl fluoride that EPA has approved.
5) Buy Organic Grape Juice and Wine
In the United States, many vineyards use a fluoride pesticide called cryolite. As a result, the levels of fluoride in U.S. grape juice and wine (particularly white grape juice and white wine) are consistently elevated. Indeed, in 2005, the USDA reported that the average level of fluoride exceeded 2 ppm for both white wine and white grape. The levels of fluoride in red wine are also elevated (1 ppm), and so are raisins (2.3 ppm). If you buy 277
grape juice and wine, or if you are a heavy consumer of raisins, buy organic. In the case of wine, if don’t want to spend the extra money on organic, consider purchasing a European brand, as Europe uses far less cryolite than the U.S.
6) Reduce Your Black & Green Tea Consumption (and/or Drink Tea with Younger Leaves)
Be careful of drinking too much tea, particularly bottled and instant varieties. The tea plant accumulates high levels of fluoride, and excess intake of tea is known to cause a painful bone disease called skeletal fluorosis. Some teas, however, contain high levels of health-boosting anti-oxidants, which are not only good for health in general, but help to protect against fluoride toxicity. In the ideal scenario, one could drink tea with high levels of anti-oxidants but low levels of fluoride. Recent research suggests that this might be a somewhat obtainable goal. It has recently been shown that the anti-oxidant levels in tea are far higher in young leaves than old leaves. This is important because young leaves also happen to have lower levels of fluoride. Indeed, it has been proposed that the fluoride content of tea is an indicator of its quality: the higher the fluoride, the lower the quality, and vice versa. If you love tea, therefore, try to purchase varieties that are made from young leaves (e.g., “White tea”). This will allow you to maximize tea’s known benefits, while reducing its known harm. Towards this end, avoid bottled and instant teas as they have been found to contain low-quality leaves that have very low levels of anti-oxidants. With bottled and instant tea, you get the risk (fluoride) without the benefit (anti-oxidants).
7) Avoid Cooking with Non-Stick (Teflon) Pans
Some research has found that cooking with Teflon-coated pans (i.e., stick-free pans) can significantly increase the fluoride content of food. If you have Teflon pans, therefore, consider switching to stainless steel. 278
8) Don’t Take Cipro and Be Mindful of Other Fluorinated Pharmaceuticals
Many pharmaceuticals are fluorinated, which means they contain something called a “carbon-fluorine bond.” Although the carbon-fluorine bond is strong enough to resist breaking down within the body, this is not always the case. Some fluorinated drugs have been found to metabolize into fluoride within the body and this greatly increases a person’s exposure to fluoride. The most notable example is Cipro. Other fluorinated chemicals that are currently known to break down into fluoride include fluorinated anesthetics (Isoflurane & Sevoflurane), Niflumic acid, Flecainide, and Voriconazole. If you are taking any of these drugs, find out if there are any safer alternatives available. 9) Minimize Consumption of Mechanically-Deboned Chicken: Most meats that are pulverized into a pulp form (e.g., chicken fingers, chicken nuggets) are made using a mechanical deboning processes. This mechanical deboning process increases the quantity of bone particles in the meat. Since bone is the main site of fluoride accumulation in the body, the higher levels of bone particle in mechanically deboned meat results in significantly elevated fluoride levels. Of all the meats that are mechanically deboned, chicken meat has consistently been found to have the highest levels. Thus, minimize consumption of mechanically-deboned chicken. 10) Avoid Fluoridated Salt If you live in a country which allows fluoridated salt to be sold, make sure that the salt you buy is unfluoridated. Consumption of fluoridated salt can greatly increase a person’s fluoride exposure. To see a list of countries that allow fluoridated salt, click here.
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30.) Dental water units are conductive to biofilm buildup because: A. Biofilm grows well on plastic tubing B. Tubing is small in diameter, therefore has an increase in surface area C. Microbes suspended in water have a shorter distance to fall before contacting the tubing surface D. Stagnation of water and low flow rates E. All of the above https://www.osap.org/general/custom.asp?page=Issues_DUWL_1 Although biofilm can form in all non-sterile fluid environments, dental waterlines provide particularly well-suited conditions. The tubing has a very narrow bore (1/8- to 1/16-inch), which provides a high internal surface-area-to-volume ratio. Low water pressure, low flow rates, and frequent periods of stagnation also encourage any bacteria introduced from the public water supply to accumulate within the tubing. The result is output water that is often many times more contaminated than tap water from the faucet in the same treatment room.
31.) Studies show most dental water systems deliver water to patients with microbial levels exceeding considered safe for drinking water. A. True B. False https://www.fda.gov/medicaldevices/productsandmedicalprocedures/dentalp roducts/ucm610545.htm
Dental Unit Waterlines
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Dental operative units are intended to supply power (electrical, air, water, etc.) and serve as a base for other dental devices, such as a dental handpiece and other dental accessories. The water supply of the dental operative unit is sourced from municipal water or a closed bottled water system. The waterlines of a dental unit, typically constructed from a polymer (e.g. polyurethane, polyvinyl chloride) or silicone rubber tubing, provide water from its source for irrigation, cooling, and flushing of the patient’s oral cavity during dental procedures. Dental operative units are Class I, FDA- regulated medical devices, and require premarket clearance (510(k)). Additional information on the regulatory requirements (general controls) for dental operative units can be found here. 280
Importance of Infection Control
Municipal water contains microorganisms that may be considered safe for drinking water, but could potentially cause patient infections when used during dental procedures. Dental unit waterlines, including those connected to municipal water sources or closed-bottle systems, typically cannot be sterilized; however, they should be routinely cleaned and disinfected. Without proper cleaning and disinfection, waterborne microorganisms can collect in the dental unit waterline and form a biofilm, a layer of microorganisms or bacteria adhered to the surface of the dental unit waterline, that can become dislodged and enter the water stream. Contaminated dental unit waterlines pose a risk of infection to the patient, particularly during surgical procedures by direct exposure of waterborne pathogens and to dental professionals due to inhalation of aerosols.
The Centers for Disease Control and Prevention (CDC) Guidance Document Guidelines for Infection Control in Dental Health-Care Settings — 2003 recommends treating the water used in dental units with commercial products such as chemical germicides to meet drinking water standards. Also, the American Dental Association (ADA) recommends routine monitoring of the water to demonstrate bacteria count of less than or equal to 500 Colony Forming Units (CFU) per milliliter of heterotrophic bacteria. Depending on the device design, sampling locations may include the connection to the water source, the dental handpiece connection, and a mid-point between these. Consult with the dental unit manufacturer’s instructions for the recommended maintenance schedule of the dental unit waterlines.
Recommendations
Dental practitioners should adopt appropriate infection control procedures for dental unit waterlines based on the manufacturer’s instructions for use. This should include infection control measures such as, but not limited to, monitoring water quality. The water management plan should include specific testing locations and frequencies, and actions to take (e.g., remediation, retesting at shorter intervals) based on test results.
Tips for Dental Practitioners
Dental professionals should establish written standard operating procedures to guide dental personnel in performing infection control procedures for dental unit waterlines. Implement the use of equipment and procedures such as separate reservoirs, chemical treatment protocols, use of filtration systems, and sterile water delivery systems. For units using separate water reservoirs, purge the dental unit waterlines each night and whenever units are out of service to prevent stagnant water from settling within the waterlines. Discharge water and air lines for a minimum of 20–30 seconds after each patient to physically flush out patient material that might have entered the dental water system during treatment. Monitor waterlines for damage or visible contamination and replace if needed or as directed by the manufacturer. Be alert to signs that may indicate biofilm formation including musty odor, cloudiness or particulates in the water, and clogging of lines.
DO:
For surgical procedures, use sterile irrigating solutions, such as sterile water or saline. Appropriate delivery devices (e.g., bulb syringe; sterile, single-use disposable products; or sterile water delivery systems that bypass the dental unit by using sterile single-use 281
disposable or sterilizable tubing) should be used to deliver sterile irrigating solutions during surgery. This may include a dedicated surgical irrigation system with components including handpieces that are single-use disposable or compatible with heat sterilization methods used in outpatient dental settings. Adhere to the recommended service life and maintenance of the dental operative unit and its components and accessories. Follow the manufacturer’s instructions to clean and disinfect the dental unit at recommended intervals. Contact the manufacturer of the dental unit to obtain the most up- to-date instructions or with any questions regarding the reprocessing of the dental unit. Monitor the water quality and microbial contamination of the dental unit waterlines using standard culturing methods at appropriate intervals to keep bacterial counts lower than 500 CFU/mL of water as recommended by ADA. Always properly dispose of single use disposable items after they have been used.
DO NOT:
Use the dental unit without following the cleaning and disinfection procedures in the manufacturer’s reprocessing instructions. Attach dental handpieces or dental instruments to dental unit waterlines that have not been cleaned or disinfected per the manufacturer’s instructions. Use cleaning and disinfection agents that are not recommended by the device manufacturer, as material incompatibility could result in structural damage that may increase the risk of biofilm formation or toxicity to patients.
Recommendations for Manufacturers
Ensure that your instructions for use comply with relevant FDA, Environmental Protection Agency, and state and local regulations applicable to the disinfection and maintenance of the dental unit waterlines. Follow recommended practices, including the FDA Guidance Document “Reprocessing Medical Devices in Health Care Settings: Validation Methods and Labeling” issued on March 17, 2015. Specifically, as outlined in this guidance, FDA expects that reprocessing methods for dental unit waterlines should be validated, and validations should be completed prior to submission of your 510(k). Your reprocessing instructions should reflect the validated methods. Consistent with our current practice for dental unit waterlines, submission of reprocessing validation data should be provided in your 510(k).
We recommend that the reprocessing instructions for your device be updated to contain comprehensive reprocessing instructions based on validation. Therefore, it is recommended that you:
Review your current reprocessing instructions to identify if your Instructions are comprehensive according to Section VI – “FDA’s Six Criteria for Reprocessing Instructions” of the FDA Guidance. Conduct an assessment to evaluate if additional validation testing is necessary to provide up- to-date comprehensive reprocessing instructions. Ensure your customers are notified promptly of any available updated Instructions for Use. Consult the FDA Guidance, “Deciding When to Submit a 510(k) for a Change to an Existing Device” to determine if a new 510(k) submission may be necessary for any labeling or design changes. Submit reprocessing validation test reports in future dental operative unit 510(k)s and describe how reprocessing was considered in the design of the device (e.g. water source, materials, connectors, etc.). 282
Contact the FDA if you have questions related to new validation and labeling instructions for dental unit waterlines. FDA recommends submission of reprocessing validation protocols via the Pre- Submission process prior to conducting testing. Please refer to the FDA Guidance document “Requests for Feedback and Meetings for Medical Device Submissions: The Q-Submission Program.”
Contact Information:
If you have questions, please contact CDRH’s Division of Industry and Consumer Education (DICE) [email protected], or via phone at 1-800-638-2041, or 301-796-7100.
References:
Ricci ML, Fontana S, Pinci F, Fiumana E, Pedna MF, Farolfi P, et al. Pneumonia associated with a dental unit waterline. Lancet 2012;379:684.
Hatzenbuehler LA et, al. Pediatric dental clinic-associated outbreak of Mycobacterium abscessus infection. J Pediatr Infec Dis 2017; 6(3):e116-e112.
Peralta G, et al. Notes from the field: Mycobacterium abscessus infections among patients of a pediatric dentistry practice—Georgia, 2015. MMWR 2016; 65(13)355-6.
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32.) Dr. Weston Price proved that
A. The bacteria in a root canal are most lethal B. The toxins from a root canal tooth are most lethal C. Neither the bacterial or toxins are lethal
https://www.westonprice.org/health-topics/dentistry/root-canal-dangers/
DNA Studies Confirm Dr. Weston Price’s Century-Old Findings
Toxic dental materials have created much havoc in the dental profession, as well as in patient health, for nearly two centuries. Dental mercury fillings, nickel crowns (especially in children, called “chrome crowns”), root canals and cavitations have been the target of concern for a long time.
Dental mercury was first exposed as a health-compromising product in 1840. The dental profession finally overcame the perception that putting toxic mercury in the mouth might be detrimental to human health; organized dentistry still considers the current fillings containing 50 percent mercury as “state of the art.”
The toxicity of root canals was disclosed by Mayo’s Clinic and Dr. Weston Price jointly back in about 1910. Close to a century ago. Price’s textbook on root canals, published in 1922, upset the dental associations at that time, and still does today. The American Dental Association (ADA), denies his findings and claims that they have proven root canals to be safe; however, no published data from the ADA is available to confirm this statement. Statements, but no actual research.
My attention was drawn to the increase in autoimmune disease after the high-copper amalgams of 1975 were initiated as “state of the ar1 t” fillings, which ADA claimed released no mercury. On the contrary, studies from Europe found that the high-copper amalgams released fifty times more mercury than previous amalgam!
In watching these changes regarding the onset of autoimmune disease, I noticed a blip in the statistics—an increase in amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease) in 1976 (See Figure 1).
Note in Figure 2 that the actual number of cases of multiple sclerosis increased tremendously, from an average of 8800 per year during the period 1970 to 1975, to an increase of up to 123,000 in one year. That year being 1976, the birth date of high-copper amalgams. 284
Figure 1 Figure 2
ROOT CANAL HAZARD
Is mercury the only dental hazard that can create conditions favorable to autoimmune diseases? No. There are bacteria in root canals that favor destruction of the nervous system and many other systems, resulting in the creation of autoimmune reactions.
What is the common denominator? The formation of a hapten (see page 46). A hapten is a small molecule that can elicit an immune response only when attached to a large carrier such as a protein; the carrier may be one that also does not elicit an immune response by itself. In general, only large molecules, infectious agents, or insoluble foreign matter can elicit an immune response in the body.
Healthy cells have a code imprinted on them. It is called the Major Histo-compatibility Complex (MHC). This is your personal code called “self.” Your body considers other code or alteration of this code to be “non-self.” The immune system is trained to kill and eliminate any “non-self” invaders.
If an atom of mercury attaches to a normal healthy cell, a hapten is formed and the immune system immediately identifies that cell as “nonself.” The immune system then proceeds to kill the contaminated cell. If mercury attaches to a nerve cell, the result is a neurological disease, such as multiple sclerosis, Lou Gehrig’s disease, seizures or lupus. If mercury 285
attaches to a binding site on a hormone, that endocrine function is altered. Mercury can attach to almost any cell in the body and create autoimmune diseases in those tissues.
Lately, it has become evident that toxins from anaerobic bacteria have the same ability to create non-self autoimmune diseases by interfering with the MHC. This is the project that Dr. Price began to study a century ago. Resistance from organized dentistry was the same then as it is today. Price wondered why dentistry was considered a “health” profession.
Price was concerned about the pathological bacteria found in nearly all root canal teeth of that time. He was able to transfer diseases harbored by humans from their extracted root canal teeth into rabbits by inserting a fragment of a root canal root under the skin in the belly area of a test rabbit. He found that root canal fragments from a person who had suffered a heart attack, when implanted into a rabbit, would cause a heart attack in the rabbit within a few weeks. Transference of heart disease could be accomplished 100 percent of the time. Some diseases transferred only 88 percent of the time, but the handwriting was on the wall.
Dr. Price discovered that root canals had within them bacteria capable of producing many diseases. They had no place in the body. Which is more important? The life of the tooth or the life of the patient? This is still the primary argument facing us today. ROOT CANALS AND NEUROLOGICAL DISEASE
Considering the difficulty of culturing anaerobic bacteria, it was hard to identify them with 1920s technology. Most of the bacteria reported by organized dentistry at that time were aerobes of unknown significance. Today, with DNA analysis available, anaerobic bacteria (the dangerous kind) can be identified whether dead or alive by the presence of their tell tale DNA signatures.
Let’s go back to the graphs of ALS up through the year 2000. Note an increase in 1976 and another increase in slope in 1991. In 1990, the dental association “suggested” that dentists perform thirty million root canals per year by the year 2000. Dentists accomplished that goal by 1999. As I understand it, the bar has now been raised to sixty million per year.
The unexplained increase in MS (8800 to 123,000) coincided with the advent of high copper amalgams. The increase in ALS in the same year is suggestive of the same cause. ALS also increased in 1991 as more root canals were performed. Statistical coincidence?
The goal of dentistry is to save teeth. Root canals allow dentists to maintain many teeth for years instead of extracting them. But is this goal appropriate considering the biological expense exposed with DNA research? What is more important? To save the life of the tooth or that of the patient? 286
HAVENS FOR BACTERIA
Dr. Price, while head of research for the now-defunct National Dental Association, took one thousand extracted teeth and reamed them out as dentists normally do, prior to filling the canals with wax. Price sterilized the canals with forty different chemicals far too toxic to be used in a live human situation; he wanted to see whether the canals could be permanently sterilized. After forty-eight hours, each tooth was broken apart, and cultured for the presence of bacteria. Nine hundred ninety out of one thousand cultured toxic bacteria just two days after treatment with chemicals designed to make the tooth sterile. Where did these bacteria come from?
An overview of the structure of a tooth (see Figure 4) shows the outer layer, known as enamel, the second layer, known as dentin, and the inner portion, known as the pulp chamber, where the nerve lives. On the outside of the tooth is what is called the periodontal ligament. Teeth are not attached directly to bone. Fibers come out of the tooth and intertwine with fibers coming out of the bone, and they unite to form what is called the periodontal ligament.
The second layer of the tooth, the dentin, is not really solid but composed of tiny dentinal tubules. In a front3 tooth, if all these tubules were attached end to end, they would reach over three miles. Note that the tubules have adequate space to house many thousands of bacteria (see Figure 5). This is where the bacteria were hiding in the thousand teeth Price tested. From the dentin tubules, bacteria can migrate either into the pulp chamber, where space is left as the gutta percha—a natural form of rubber used to fill the space inside the cleaned-out root—shrinks upon cooling, rebounding from the force applied to push the wax down the canal, and losing the liquid portion (see Figure 6), or into the periodontal ligament where a plentiful supply of food awaits them.
A tooth has one to four major canals. This fact is taught in dental school, but never mentioned are the additional “accessory canals.” Price identified as many as seventy-five separate accessory canals in a single central incisor (the front tooth). Figure 7 shows one of these canals filled with necrotic (dead) tissue.
There is no way that any dental procedure can reach into these accessory canals and clean out the dead tissue. This necrotic tissue creates a home for multiple bacterial infections outside the tooth in the periodontal ligament. With added food supply from this area, the anaerobic bacteria can multiply and their toxins can contribute to the onset of disease (see Figure 8).
Of course, the root apex (terminal end) is the primary area of concentration of infection. Even though this may be the last area to show infection, dentistry generally considers a tooth sterile unless areas of bone resorption show up on X-ray. Upon cooling and shrinking 287
of the gutta percha, space is left at the apex in which bacteria can thrive, where neither white blood cells of the immune system, nor antibiotics can reach them.
Figure 4 Figure 5
288
Figure 6 Figure 7
Figure 8 TOXIC MICROORGANISMS
Our first DNA studies examined bacteria retrieved from crushed root tips. We can identify eighty-three different anaerobic bacterial species with DNA testing. Root canals contain fifty-three different species out of these eighty-three samples. Some are more dangerous than others, and some occur frequently, some occasionally. Selecting those that occur more than 5 percent of the time, we found: Capnocytophaga ochracea Fusobacterium nucleatum Gemella morbillorum Leptotrichia buccalis Porphyromonas gingivalis
Of what significance are these? Four affect the heart, three the nerves, two the kidneys, two the brain and one the sinus cavities. Shouldn’t we question the wisdom of supplying a haven for these microbes so close to our brain and circulatory system? Does this information validate the claims of “sterile” root canals?
Dentists claim they can “sterilize” the tooth before forcing the gutta percha wax down into the canal. Perhaps they can sterilize a column of air in the center of the tooth, but is that really where the problem is? Bacteria wandering out of the dentinal tubules is what Price was finding, and what we were finding in the crushed tooth samples. But does the problem end there? Hardly. 289
Just out of curiosity, we tested blood samples adjacent to the removed teeth and analyzed them for the presence of anaerobic bacteria. Approximately 400 percent more bacteria were found in the blood surrounding the root canal tooth than were in the tooth itself. It seems that the tooth is the incubator. The periodontal ligament supplies more food, therefore higher concentration of bacteria.
But the winner in pathological growth was in the bone surrounding the dead tooth. Looking at bacterial needs, there is a smorgasbord of bacterial nutrients present in the bone. This explains the tremendous increase in bacterial concentration in the blood surrounding the root canal tooth. Try sterilizing that volume of bone.
Apparently, the immune system doesn’t care for dead substances, and just the presence of dead tissue will cause the system to launch an attack. Infection, plus the autoimmune rejection reaction, causes more bacteria to collect around the dead tissue. Every time a person with a root canal bites down, these bacteria are flushed into the blood stream, and they start looking for a new home. Chemotaxis, or the chemical attraction of a specific bacteria for a specific tissue, assists the anaerobes in finding new quarters in the heart, nervous system, kidney, brain, etc., where they will perform their primary damage.
Many of the bacteria in the surrounding bone are present in far more than 50 percent of the samples tested. Streptococcus mutans was found in 92 percent of the blood samples. It can cause pneumonia, sinusitis, otitis media, meningitis and tooth decay. Streptococcus mitis
was found 92 percent of the time. This microbe attacks the heart and red blood cells. It is a rather hearty bug, for it went to the moon (hiding in a camera) on an unmanned expedition, stayed there over two years in an environment without atmosphere, exposed to temperatures of 250 degrees Fahrenheit during the day, minus 250 in the shadow. Upon returning10 to Earth with the astronauts of Apollo 12, over two years later, this microbe was still alive. In humans, S. mitis binds to platelets and is involved in the pathogenesis of infective endocarditis. Want this guy living in your dead root canal tooth?
Of the top eight bacteria in the bloodrevotella adjacent intermedia to root canal teeth, five affect the heart, five the nervous system, two the kidney, two theStrep liver, intermedius and one attacks the brain sinus, where they kill red blood cells Of these, P (present in 76 percent of the samples) attacks heart, kidney and sinus; (present in 69 percent of the samples) attacks heart, nerves, lungs, liver and brain.
DNA examination of extracted root canals has shown bacterial contamination in 100 percent of the samples tested. This is quite the opposite of official claims that root canals are 97 percent successful. Do they need a new definition of success? 290
CAVITATIONS
Cavitations are the next big problem that result from dental procedures. Cavitations are areas of unhealed bone left over after a tooth extraction (see Figure 9).
Dentists are generally taught to remove a tooth and leave the periodontal ligament in the socket, a procedure which would be like delivering a baby and leaving the placenta in the uterus.
These socket areas with the ligament left in place rarely heal. After tooth removal, a cap of about 2 millimeters (one sixteenth of an inch) covers the extraction site, leaving a hole the size of the root of the tooth behind. In records of five thousand14 surgical debridements (cleaning) of cavitations, only two were found to be healed. When the periodontal ligament is left in the bone, the body senses that the tooth is still there, and the order for healing is canceled. These holes are lined with many of the same bacteria found in root canal sockets, but actually more different species. Whereas root canal teeth contain up to fifty-three different species of bacteria, cavitations yield up to eighty-two of the eighty- three we test for.
Of the five most frequently present bacteria found in cavitations, three affect the heart, two the nervous system and one the kidneys and lungs. They are as follows: Streptococcus mutans
(occurrence 63 percent of the samples), affects the nervous system, can cause pneumonia, sinusitis, otitis media and meningitis. It has also been blamed for causing dental decay in teeth, but this may be more the result of the2 fluid flow pulling bacteria into the tooth than actual active invasion by the bacteria. Porphyromonas gingivalis
(occurring in 51 percent of the samples), damages the kidney, alters integrity of endothelial lining of blood vessels, and induces foam cells from macrophages, contributing to atherogenesis. It contains proteasesP. thatgingivalis lyse red blood cells and extract nutrients (primarily iron) from the red blood cells. This action is called porin forming, which can destroy red blood cells rapidly. (By the way, can both up and down regulate about five hundred different proteins critical to maintaining our normal biochemical actions.) Candida albicans
(present in 44 percent of the samples), in its yeast form is beneficial in the process of demethylation of methyl-mercury as well as its ability to destroy pathogenic bacteria in the intestinal tract. When converted into the fungal form by a shift in pH in the digestive system, candida can penetrate the intestinal wall, leaving microscopic holes that allow toxins, undigested food particles, bacteria and other yeasts to enter the blood stream. This condition is sometimes referred to as Leaky Gut Syndrome, which can lead to environmental intolerances. 291
Prevotella intermedia P. intermedia (occurrence rate of 44 percent) has as its primary concern coronary heart disease (CHD). invades human coronary artery endothelial cells and smooth muscle cells. It is generally located in atheromatous11 plaques. Cellular invasion of cardiac muscle is central to the infective process. ANTIBIOTICS
So, if all these diseases of “unknown etiology,” that is, of unknown origin, are the result of bacterial invasion, why not just flood the body with antibiotics? They kill bacteria, don’t they? Ever hear of someone who was sick, was given antibiotics, and then got even worse? Most of us have heard the story. Perhaps the following information explains what happens in these cases, and why antibiotics cannot be used in infections of this nature.
Most antibiotics are “bactericidal”—think suicidal, or homicidal. Antibiotics kill. But this is not the same type of killing that John Wayne was noted for. When he fired at the bad guy, the bad guy fell over dead. Was then presumed to be buried. But when bactericidal antibiotics kill a bacterium, the bacterium explodes (see Figure 10).
The fragments12 are not eliminated immediately, for each piece is a lipopolysaccharide called endotoxin. By way of contrast, exotoxins are the toxic chemicals that are released by pathogenic bacteria, and endotoxins are toxic entities (fragments of the original bacteria) that are the result of the bacterial explosion caused by the antibiotic. Endotoxins present a huge challenge to the immune system, for now, instead of facing one bacterium, it has to process and eliminate perhaps one hundred endotoxins. With dozens of bacteria to confront from each single root canal or cavitation, no one antibiotic can kill all of them, and if there were one, the resulting dead bacterial corpses would overwhelm the body and produce either greater disease or death.
Broad spectrum antibiotics cannot be used for this reason. Sometimes even one capsule of antibiotic produces more problems than the immune system can tolerate. Plus, of course, it takes only two or three13 capsules to completely sterilize the gut of its four or more pounds of friendly bacteria. Antibiotics are far more powerful and potentially devastating than I ever thought they were. Antibiotics should be used with ultra caution, not routinely given for ten days or so after oral surgery, “just in case.”
There are other ways to get these microbes under control, and several are being tested at this time. It is advantageous to have intravenous vitamin C and occasionally a non-killing antibiotic is added to this solution. This combination does reduce the challenge to the immune system, but, overall, root canals represent the rock-and-hard-place situation.
Leave the root canal or cavitation in the body, and there is the potential of creating an unwanted autoimmune or degenerative disease that could be life threatening. Toxins and bacteria can both leak from these contamination sites wreaking havoc with a person’s 292
cardiovascular, endocrine, nervous and immune systems. The public needs to be informed, so they can make educated choices in the trade-off between toxic convenience and health.
Removing the offending tooth presents problems that must be confronted, or other problems can be induced—problems not as dangerous as the continuous bacterial spill, but ones that need to be avoided if possible. In order to allow the immune system to focus on healing, all other offending dental materials should be removed (mercury, copper, implants, tattoos and nickel crowns) so that the immune system can deal with the bacterial challenge instead of the bacteria plus toxic metals. Nutrition should be calculated from the aspect of the blood chemistries commensurate with one’s ancestral diet and in line with the dietary principles formulated by Dr. Price. Recovery from a root canal is complicated, but your patient’s life is worth salvaging.
These studies in DNA analysis of bacteria in root canals and cavitations confirm the fact that Dr. Weston Price, despite being one century ahead of his colleagues, was absolutely correct in determining that bacteria-laden root canals have no place in the body of people interested in their health. This toxic waste spill can be stopped, but not with the assistance of dental associations, which continue to insist that the procedure of root canals is perfectly safe. The recent increase in suggested quota up to sixty million root canals per year is not in the best interest of their patients, nor can that action do anything but increase health costs for the innocent patient.
Price was right. Root canals are not worth the price.
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Figure 9 Figure 10
SIDEBARS
HAPTENS
A hapten is a small molecule that can elicit an immune response only when attached to a large carrier such as a protein or toxic metal such as mercury; the carrier may be one that also does not elicit an immune response by itself. In general, only large molecules, infectious agents, or insoluble foreign matter can elicit an immune response in the body. Once the body has generated antibodies to a hapten-carrier adduct, the small-molecule hapten may also be able to bind to the antibody, but it will usually not initiate an immune response; usually only the hapten-carrier adduct can do this.
BACTERIA LURKING IN ROOT CANALS
Let’s look at five major bacterial species lurking in root canals more closely, keeping in mind that these are only five of the fifty-three that are routinely found in root canal teeth. 294
Capnocytophaga ochracea
: Found in brain abscesses associated with dental source of infection. Causes4 human disease in the central nervous system. Also related to septicemia and meningitis. Fusobacterium nucleatum
: Produces toxins that inhibit fibroblast cell divi5,6sion and wound healing processes. Causes infection in the heart, joints, liver and spleen. Gemella morbillorum 7 : Linked to acute invasive endocarditis, septic arthritis and meningitis. Leptotrichia buccalis
: Reduces the number of neutrophils8 (a critically important white blood cell), thus lowering immune competence. Porphyromonas gingivalis
: Destroys red blood cells by drilling holes (porinP. gingivaliss) in them, causing the cell to “bleed to death.” Low red cell counts that do not recover after dental revision are frequently responding to the porin activity of this microbe. also alters the integrity of the endothelial liningP. ofgingivalis blood vessels, which leads to inflammation and bleeding in the inner lining of blood vessels. This is the key step in formation of atherogenesis9 that leads to heart attacks. can change friendly bacteria into pathogens.
295
33.) When educating your patients, your office may supply educational information for patient’s use, but you may not advertise or claim that removing mercury fillings will cure a person’s disease.
A. True B. False https://web.stanford.edu/~bcalhoun/amalgam.htm
Dental AMALGAM and Mercury
by Birgit Calhoun
Quem Mercurius perdere vult, dementat prius (Alfred Stock, ca. 1926) [Originally: Quos deus perdere vult, dementat prius (Publius Syrius, ca. 43 B.C.)]
(Summer 2001 - Summer 2003)
For a translation of Alfred Stock's Die Gefährlichkeit des Quecksilberdampfes, (1926) see Birgit Calhoun's translation into English: The Dangerousness of Mercury Vapor, by Alfred Stock, as well as Medizin. Klinik Nr. 32/33; 22 (1926), 1209-1212 und 1250-1252, Nr.32/1209: Die Gefährlichkeit des Quecksilberdampfes und der Amalgame *), Von Prof. Dr. Alfred Stock, Berlin-Dahlem, and Stock, A: Die chronische Quecksilber- und Amalgamvergiftung; Zahnärztliche Rundschau 48 (1939), Spalten 371 - 377 und 403 - 407, (all Stock articles from http://people.blinx.de/sems/deutsch/stock1.htm#Stock 1); see also: Amalgam Removal: Alfred Stock, Louis Lewin, Erich Rudolf Jaensch,
For a review of the Kieler Amalgamgutachten view: http://www.stanford.edu/~bcalhoun/kieleram.htm
In case a link is no longer in service and you wish to see what it looked like at one time, please go to Internet Archive: The WaybackMachine
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According to Miriam Webster's OnLine Dictionary Amalgam: is an alloy of mercury with another metal that is solid or liquid at room temperature according to the proportion of mercury present and is used especially in making tooth cements. Mercury, according to Webster's, is "a heavy silver-white poisonous metallic element that is liquid at ordinary temperatures and is used especially in scientific instruments - - also called quicksilver". The word Amalgam comes from the Arabic al-malgam, meaning softening ointment (presumably because, when it is first mixed, it is soft and putty-like). Amalgam is the word for the liquid or solid alloys of mercury with other metallic elements or alloys.
In some countries dental amalgam is classified as a medicine. If that were the case in the United States it would be subject to many more regulations than it is now. As far as the U.S. Code of Federal Regulations is concerned amalgam is a prosthetic device and not a drug:
Amalgam Alloy, (a) Identification. An amalgam alloy is a device that consists of a metallic substance intended to be mixed with mercury to form filling material for treatment of dental caries. (b) Classification. Class II (21 CFR 872.3050 (2001)).
What is an alloy? According to Webster's an alloy is a "substance composed of two or more metals or of a metal and a nonmetal intimately united usually by being fused together and dissolving in each other when molten." Therefore, strictly speaking, given this definition, "amalgam is not a true alloy. It is made up of 50% mercury, which is not locked into a set filling but escapes continuously during the entire life of the filling in the form of vapor, ions and abraded particles" according to the Australasian Society Of Medicine And Toxicology (ASOMAT) fact sheet, which contains an extensive bibliography.
To this day there are still dentists who believe mercury amalgam is stable despite hundreds of observations and studies proving the opposite. As early as 1883 amalgam was proven to give off mercury vapor sufficient to shorten the life of the hardy cockroach (Talbot E. S., "Injurious Effects of Mercury as Used in Dentistry", MISSOURI DENT J, 15:124-30, March, 1883).
There is a lot of disagreement about the dangers of mercury in the medical and dental professions. This is because many of their members were taught by professors who are old enough to have been introduced to mercury before the advent of antibiotics, at a time when mercury and its compounds were thought to be useful medicines. Science has made giant strides toward recognizing what causes disease, what makes cells grow and how chemicals interact. There was no knowledge of DNA, and there were no electron microscopes. Testing medicines for approval by the FDA with its many 297
stages and double blind studies is a relatively recent safety net for the consumer and the pharmaceutical companies alike.
In the beginning of the 20th century much of how pharmaceuticals worked was left to educated guessing. For instance, the Encyclopedia Britannica of 1911 gives, at least the way we see it now, a somewhat illogical description of what mercury does to the human body. The following paragraphs are excerpts of the then accepted understanding of mercury:
...In discussing the pharmacology of mercury and its compounds it is of the first importance to observe that metallic mercury is inert, as such, and that the same may practically be said of mercurous salts generally. Both mercury itself and mercurous salts tend to be converted in the body into mercuric salts, to which the action is due. When metallic mercury is triturated or exposed to air, it is partly oxidized, the first stage of its transformation to an active condition being reached.... (Encyclopedia Britannica, Vol. 18, p.158)
Saying that an active condition is being reached, in this single paragraph, already contradicts the statement that mercury is inert. The next paragraph continues
...Metallic mercury can be absorbed through the skin, passing in minute globules through the ducts of the sweat glands. ...
[and]...One part of the perchloride in 500,000 will prevent the growth of anthrax bacilli and one part in 2,000--the strength commonly employed in surgery--kills all known bacteria....(Ibid. p.158)
...Single doses of mercury or its compounds have no action upon the mouth, the characteristic salivation being produced only after many doses. Their typical action on the bowel is purgative the effect varying with the state of the mercury. So relatively inert is metallic mercury that a pound of it has been given without ill effects in cases of intestinal obstruction which it was hoped to relieve by the mere weight of the metal. (Ibid, p.158)
The general tenet seems to be that mercury has no action. Yet why would mercury use result in salivation if there is no action. Why indeed would it be used for any medical purposes if there were no action?
...Mercury is largely used in affections of the alimentary canal, and has an obscure but unquestionable value in many cases of heart-disease and arterial degeneration. But its value in syphilis (see VENEREAL DISEASES) far outweighs all its other uses. ... (Ibid, p.159) 298
An example of how sexually transmitted diseases were treated with mercury before the discovery of antibiotics in the middle of the 20th century can be found in Sex Trans Inf (STI); 1998; 74;20-26: Sexually Transmitted Diseases and the Raj
Finally the entry of the Encyclopedia Britannica discusses the poisonous aspects of mercury in some detail. It is stated that mercury can kill and that it can produce some rather severe allergic reactions especially on the skin and mucous membranes of the mouth.
Those were the ideas then. There are very few doctors who would still go along with that type of thinking. And yet there are still many anachronisms to be removed to get to the truth of what mercury really does.
For current general information about mercury and a link to the Periodic Table of Chemical Elements consult the Mercury website and for an explanation of why mercury is poisonous see: Mercury, HG
Mercury is poisonous. But how poisonous is it really? In its metallic form it is relatively harmless. Many people talk about how they played with mercury as children after the fever thermometer broke. My neighbor told me that when she was a child her teacher let her play with the mercury. There used to be toys that included mercury. People all remember playing with the shiny, silvery substance because it is so fascinating to watch. However, they usually can't remember that it made them sick, and they don't often wonder, as my elderly neighbor did recently, whether the mercury might have caused her to be edentulous by the time she was 30 years old or whether it caused the scleroderma she has been suffering from for years.
The mercury vapors are poisonous. Most people have heard about that. But when they examined themselves after exposure they didn't notice any symptoms. So they figured that they probably didn't inhale enough to make themselves sick. They did not know about the possible connection of Lupus or Arthritis to the mercury they had played with in their youths. There are stories of children eating mercury bubbles. They did not die from it. A New England Journal of Medicine (June 15, 2000, Elemental Mercury Embolism To the Lung) article reported that a suicidal dental assistant injected mercury into herself. She apparently recovered although her chest x-ray shows what the mercury did to her lungs.
So, is mercury really that poisonous? The question can only be answered when it is specified in what form the mercury presents itself. Also, the degree of toxicity is a matter which seems to not have been fully explored, especially when it comes as a function of time. What time frame is necessary for this substance to be causing or 299
exacerbating autism or amyotrophic lateral sclerosis--if indeed it is? Does it take a day, a week, months or years to cause symptoms? Both diseases have been mentioned in connection with mercury. There seems to be a paucity of data on the longterm effects of lowgrade exposure. What is known is that there are varying degrees of toxicity.
The relatively less poisonous metal and vapor forms of elemental mercury are not the only forms in which mercury occurs. There are many chemical combinations, inorganic and organic ones. All of them are poisonous. The most poisonous ones are organic. To illustrate how poisonous mercury can be, one only has to mention dimethyl mercury. Dimethyl mercury is an odorless, colorless liquid with the appearance of and weighing about three times as much as water. The extreme toxicity of dimethyl mercury is brought home in the WETTERHAHN LABORATORY POISONING CASE: FINAL MEDICAL REPORT, "Dimethyl Mercury Poisoning" (New England J. Med. 4 Jun 98 338:1672)(Science-Week 26 Jun 98), which describes the death of a scientist from mercury poisoning. Karen Wetterhahn spilled only a few drops of the liquid on her latex-gloved hands. Methylated mercury is relevant in the discussion of amalgam because under certain circumstances the mercury from amalgam may be methylated (Heintze, U., Edwardsson, S., Derand, T. and Birkhed, D.: "Methylation of Mercury From Dental Amalgam and Mercuric Chloride by Oral Streptococci in Vitro." Scand. J. Dental Research 91(2) 150-152, 1983; Yamada, Tonomura: "Formation of Methyl Mercury Compounds from Inorganic Mercury by Chlostridium cochlearium," J Ferment Technol 1972 50:159- 166, and Field study on the mercury content of saliva, by P.Krauß and M. Deyhle*, K.H. Maier, E. Roller, H.D. Weiß, Ph. Clédon). See also Journal of Nutritional & Environmental Medicine (1996)6,33-36; Methyl Mercury in Dental Amalgams in the Human Mouth, by WILLIAM A. SELLARS MD, RODNEY SELLARS JR DDS, LIAN LIANG PHD AND JACK D. HEFLEY PHD
The Canadian Edmonton Journal, March 27, 2001, states in its headline: "Mercury Fillings Toxic -- Report U of C Researchers Say 'Visual Evidence' Brain Cells Affected," by Robert Walker. The article further states:
New research vividly demonstrating the damage mercury has on brain cells -- in concentrations seen in people with amalgam fillings -- was published by University of Calgary medical school researchers Monday...Drs. Fritz Lorscheider and Naweed Syed's research, published in the British journal, NeuroReport, is supported by a time-lapse video showing how brain cells die within 10 minutes when they are exposed to mercury in minute concentrations... 300
Owen Hamill summarizes Lorscheider/Syed in an article "Mercury induced growth cone collapse: another reason for flossing" (NeuroReport 2001;12:A23) saying
...evidence indicates that mercury vapor is continuously released from tooth fillings where it is breathed in by the lungs and converted into mercuric ions. Although there is no debate on the toxic effects of high concentrations of mercury (i.e. associated with urinary concentrations > 50 µg/l), a challenge exists to demonstrate more subtle, preclinical effects associated with chronic low level mercury exposure in the general population with fillings. At least consistent with this notion is the study published in this issue [5] showing that exposure to mercury concentrations of < 0.1 M results in rapid (i.e. within 10 min) retraction of growth cones in snail neurons and is correlated with disruption of microtubules. Interestingly, the authors point out that similar disruption of microtubules is associated with Alzheimer's disease. These recent findings give added impetus for the development and implementation of alternative materials for fillings and may provide parents with added ammunition in teaching their children to floss. (Christopher C. W. Leong; Naweed I. Syed; Fritz L. Lorscheider CA "Retrograde degeneration of neurite membrane structural integrity of nerve growth cones following in vitro exposure to mercury, Neuroreport 2001;12:733-737).
Significantly
...the other metals [also present in amalgam] – aluminum, lead, cadmium and manganese – did not produce this type of degeneration.
A news item in the Calgary Gazette provides further information about the study in which the researchers added mercury ions to snail neuron cell cultures, which were subsequently observed to degenerate rapidly. Fritz Lorscheider (physiology and biophysics) elaborates: "Our study illustrates how mercury ions alter the cell membrane structure of developing neurons. This discovery provides visual evidence of our previous findings that mercury produces a molecular lesion in the brain." (University of Calgary Gazette on the Web, April 2, 2001, "Researchers present evidence of mercury’s effect on brain neurons," April 2, 2001, Lorscheider, Syed, Leong).
The first reported cases of methyl mercury poisoning occurred in 1863: 301
A 30 year-old male who had been exposed to dimethyl mercury for three months "complained of numbness of the hands, deafness, poor vision and sore gums...[He was] unable to stand without support," although no motor palsy was detected. His condition rapidly worsened; he became restless and comatose within a week and died 2 weeks after the onset of symptoms. Another victim was a 23-year-old laboratory technician who had been working in the laboratory for 12 months, although he had handled dimethyl mercury for only 2 weeks.
He complained of sore gums, salivation, numbness of the feet, hands and tongue, deafness and dimness of vision. He answered questions only very slowly and with indistinct speech... Three weeks later he had difficulty in swallowing and was unable to speak... [He] was often restless and violent. He remained in a confused state and died of pneumonia 12 month after the onset of symptoms (from Environmental Health Perspectives, Vol. 104, Supplement 2, April 1996).
These two men had obviously been affected very severely. Milder cases outside of a mercury-laden environment would not have gotten much attention at a time when death from an infectious disease was so common and would probably be the suspected reason for a person's demise. The toxicity of mercury could be seen much more easily in context with a known mercury environment. In addition metallic toxins were ubiquitous. People still ate from pewter plates. Houses were painted with lead paint. People boiled tea water in copper kettles. All those metals are now known to be poisonous. The comparative symptoms of poisoning from the various heavy metals are remarkably similar and mercury was just one of them. There were no blood or urine tests, yet, sensitive enough to positively mark one or the other metal as the greater culprit for the symptoms at hand.
It is not known at which point mercury is not toxic any more. Mercury works at the molecuar level. At which point can it be said that no damage occurs? 150 years ago it was common for people to complain about symptoms of all sorts and it was even more common to label someone a hypochondriac.
All that said, already over a hundred years ago there existed reports and studies concerning the dangers of mercury from amalgam. The ADA cannot claim that amalgam has always, and by everyone, been considered to be harmless. The dentist E. S. Talbot writes in 1883:
The subject of mercurial poisoning from the use of amalgam fillings in decayed teeth, has given rise to numberless articles, and has been a source of discussion in dental societies since its introduction into this country. Symptoms of mercurial poisoning 302
have manifested themselves in cases where these amalgams have been employed, causing the scientific members of the profession to investigate these fillings, to determine if these symptoms are due to the mercury contained in its composition. Nor is this investigation confined to men of science; the ordinary practitioner is constantly meeting these symptoms, and by careful observation will be able to diagnose these cases when met with. I will mention two cases which have come under my notice. ("Injurious Effects of Mercury as Used in Dentistry", MISSOURI DENT J, 15:124-30, March, 1883)
The article describes cases of amalgam poisoning. It also describes tests Dr. Talbot-- the same dentist who witnessed the demise of the cockroaches--performed to prove that mercury constantly leaks from amalgams.
H. Sheffield, also a dentist, wrote an article Amalgam and Other Kindred Poisons in "The Dental Headlight", 17:14-18, 1896, where he decries the use of mercury in dentistry. He points to the chronic nature of mercury poisoning from amalgam. Among other things he states: Let me enumerate some of the poisonous effects of mercury on the human family. A metallic taste in the mouth, headache, soreness and sponginess of the gums, pain in the sockets of the teeth when pressed together, fetid breath, ptyalism, ulceration of the mucous membranes of the mouth, fauces, larynx, and bronchia, loss of voice, hectic fever, profuse perspiration, emaciation, and death.... and in the same article he says: Those persons who have ... amalgam fillings in their teeth, frequently suffer from mercurial rheumatism and other symptoms of that poison; in fact, some are walking barometers, and by their pain can foretell the weather.
But even in those days recognizing amalgam toxicity would have had to depend on an observant dentist who was aware of the dangers of mercury or on the rare truly fulminant case that forced the dying patient to see a doctor. Doctors were even less aware that their patients' symptoms were the symptoms of mercury poisoning since the medicines doctors commonly prescribed for baby's teething pains, kidney problems, syphilis, constipation etc. contained mercury (Calomel, mercurous chloride, Hg2Cl2, teething powder, mercuro-chrome, Blue Mass). Moreover, what was prescribed as a cure always resulted in side effects, which, I venture to say, were not advertised by the doctor as being mercury poisoning. The side effects, which were sometimes worse than the cure and probably killed many a patient, usually happened 303
with a time delay so that the patient was unaware that his new ailment was really an after-effect of the mercury-containing "remedy." It should not surprise, then, that the symptoms of, e.g., syphilis became nearly identical to those of mercury poisoning.
One mercury poisoning symptom, depression, then called melancholia, and all the other numerous symptoms that were lumped together and called "hypochondriasis" were considered less problematic because the chance of dying from an untreated "real" illness was much greater in those days. President Lincoln, who was thought to be such a "complainer," regularly took "Blue Mass." This medicine contained mercury according to an article in Perspectives in Biology and Medicine 44.3 (2001) 315-33: "Abraham Lincoln's Blue Pills, Did our 16th President Suffer from Mercury Poisoning?" by Norbert Hirschhorn, Robert G. Feldman, and Ian A. Greaves, also summarized in National Geographic Magazine - National Geographic News: "Did Mercury in 'Little Blue Pills' Make Abraham Lincoln Erratic?" by Hillary Mayell for National Geographic News, July 17, 2001.
All in all it was very unlikely that those people who had had only a whiff of mercury would have known that those vapors had affected them enough to make them sick. By the time the mercury started to show symptoms, they would have forgotten about the exposure to it and assumed that they had fallen ill because of some infectious agent. Mercury is insidious because one of the symptoms of mercury poisoning is short term memory loss. If they couldn't remember what they had touched or inhaled or ingested, how were they going to tell the doctor--in the rare event that he might have asked-- about what they had taken when they couldn't recall the offending agent? Karen Wetterhahn, who had known what she was working with and did remember, did not feel that she was poisoned until months after her deadly exposure--her long term memory was apparently not affected. She knew that she was working with a very dangerous substance. The New England Journal of Medicine reported that it took at least 90 days before any symptoms arose. It took nearly five months (154 days) for the 48 year-old scientist to complain about neurological symptoms which brought her to the hospital.
The following events might be typical for mercury exposure. More than forty years ago, let's say starting in the late 40s, a child, I'll call her Lisa, broke a fever thermometer. She picked up a bubble of mercury from the floor and ate it. The girl's younger brother, Werner, watched the remaining mercury roll on the floor until it magically disappeared. The older brother, Juergen, also watched. Doing that they unknowingly inhaled some of the vapor. Here is another scenario: Supposing a dentist's two-year old grandson, I'll name him Karsten, sneaked into the office where amalgam had just been mixed and inserted into a patient's mouth. The child inhaled 304 the still lingering vapor, which by now, being heavier than air, had sunk to the level of the child's mouth. Here is another scenario: Supposing a young woman, Gigi, somewhat compromised in her calcium intake because she didn't drink milk and ate candy all through her childhood, had received a multitude of fillings in her teeth. Also, her two upper front teeth were not straight. She wanted them to look nice. To straighten out the crooked teeth she had gone to a dentist for porcelain crowns. In the process of grinding down the teeth the dentist had killed the nerves of those teeth. To aleviate the pain she went to yet another dentist who suggested removing the damaged nerves. The resulting root canals were filled with amalgam.
Here is what happened to the just mentioned people: The little girl, Lisa, who ate the mercury had no obvious ill effects from ingesting the beads of mercury. She was not as smart as one would have hoped. But she was going to be a wife and mother and nobody cared whether she was likely to go to the university or not. As for her brother, Werner, who had watched? He was sickly much of the time. I remember him bundled up in the backyard. He literally couldn't move because the blankets were tied around him with a rope to keep him on the stretcher that had been placed near where we played. He was not allowed to play. He watched us. He was thought to be too ill. It may seem far fetched to blame such a small amount of mercury vapor for the Attention Deficit and Hyperactivity Disorder--in those days that term was not used, yet--he experienced once he was better. Werner's mother was mainly resigned to the fact that her second child was not going to be as smart as his parents or his older brother, Juergen. Werner became a massage therapist, instead of the doctor she had wanted him to be.
Curiously the metallic mercury Lisa ingested affects the organism less severely than the vapor. It goes through the system and is absorbed only minimally. Whether the little girl had no ill effects at all is to be questioned. Was there really no ill effect or do we simply not know what ill effects she may have suffered? After all, our knowledge of what a small amount of tobacco smoke is capable of doing should alert us not to be casual about what a small amount of mercury vapor might do. A puff of smoke here and there (passive smoke) from another person's cigarette is also only a very small amount of smoke. And yet, the cumulative puffs have been known to cause lung cancer. Note! There is one important difference between tobacco smoke and mercury. Smoke is visible and easily detectable by its smell; mercury vapor is not.
Nothing happened to Werner's brother, Juergen, nothing to the dentist's grandson, Karsten, at the time when they inhaled the vapors. The nasty effects came years later when they were young adults, both Juergen and Karsten, came down with Multiple Sclerosis. 305
About Gigi, the young woman who had a root canal done, she did not know that she had been given mercury. The dentist who had performed the then (1965) new procedure did not know that a root canal should never be filled with mercury amalgam and thus set into action a process that would cause Gigi to suffer pain and several surgeries nearly thirty years later.
According to Dr. Meinig, who wrote a book about research done in the early 1900s, all root-filled teeth harbor harmful bacteria. Dr. Price, a dentist who later became head of the ADA, did the early research. He advanced a theory that bacteria coming from root filled teeth can cause infections. They quasi metastacize to remote locations such as heart, bones, brain etc. These infections can become life-threatening even without mercury. [Ref.: http://www.curezone.com/dental/root_canal.html: Dr. Joseph Mercola: ROOT CANALS POSE HEALTH THREAT - AN INTERVIEW WITH GEORGE MEINIG, D.D.S. Dr. George Meinig, one of the founders of the American Association of Endodontists (Root Canal Specialists), has written the book: "Root Canal Cover-Up Exposed - Many Illnesses Result."]
If bacteria and mercury are mixed methyl mercury results. Therefore root canals should not be filled with amalgam. It is likely that a root canal eventually turns into a bone cyst, also called cavitation. This is how a cavitation develops. Bacteria trapped at the tip of the root remain--despite all precautions-- in the recesses of the tooth after the root canal is filled. The anaerobic bacteria multiply. The only place they can go is into the jaw bone. There they may cause the bone to erode. What is worse, the mercury causes the surrounding tissue to become infarcted because the mercury causes the blood vessels to die. That means there is no blood supply to the bone. Thus the bone cannot heal. It becomes necrotic. The bacteria cannot be eradicated with antibiotics because the blood carrying the medicine does not reach the affected bone. Furthermore, the bacteria could convert the accessible mercury from amalgam into methylated mercury, which may--possibly through osmosis--continually reach the blood stream and be dispersed all over the body and into the brain. It seems methyl mercury seeps through tissues fairly easily. (It entered Karen Wetterhahn's system through Latex gloves and the skin). Furthermore mercury helps the bacteria to survive better because it compromises the immune system. Thus the mercury indirectly causes the cavitation to get bigger and bigger. What makes the situation worse is that cavitations are not visible in x-rays. They do not show any inflammation nor do they cause a fever, and they may remain painless for many years because the nerves do not reach into the bone and tell the person that something is wrong. (Scand. J. Dental Research 91(2) 150-152, 1983). The patient only notices the problem when the cyst finally gets large enough and breaks through to the outside or comes in contact with functioning blood vessels and/or nerves. That would be the point at which the bone is nearly completely destroyed. See also: Cavitations, by Karen Shrimplin 306
Another explanation for the erosion of bone is given in a web site about osteonecrosis/osteomyelitis, which, when it happens to the mandible and maxilla, is also called Phossy (or more recently Fossy) Jaw or Maxillofacial Osteonecrosis. This condition used to be very common in the 19th century. It is a condition where the bone dies due to "intramedullary ischemia and infarction." The ischemia is thought to have resulted from "environmental pollutants, such as lead and the phosphorus used in safety matches, as well as from popular medications containing mercury, arsenic or bismuth."
Maxillofacial Osteonecrosis of the maxillofacial region is not new to dentistry. During the pre-antibiotic era "phossy jaw" and other forms of "chemical osteomyelitis" resulted from environmental pollutants, such as lead and the phosphorus used in safety matches, as well as from popular medications containing mercury, arsenic or bismuth.[23-29] This disease was well established by 1867, did not often occur in individuals with good gingival health, and appeared to "attack" the mandible first.[25] It was associated with localized or generalized deep ache or pain, often of multiple jawbone sites. The teeth often appeared sound and suppuration was not present. Even so, the dentist often began extracting one tooth after another in the region of pain, often with temporary relief but usually to no real effect.[24] Occasionally, large fragments of necrotic bone would come out with the tooth, sometimes involving much of an entire quadrant, as depicted in the figure at the top of this page. Apparently, Lorinser of Vienna in 1845 was the first to call attention to the problem.[25]
( http://www.maxillofacialcenter.com/NICOhistory.html#History, and http://www.maxillofacialcenter.com/NICO1v55.html#Why)
According to the above web sites the chemical osteomyelitis described in Phossy Jaw can be seen in other parts of the body, i.e. for necrosis in the head of the femur it is called Legg-Calvé-Perthes disease. "G. V. Black,[29] the father of modern dentistry, described in 1915 an osteomyelitis look-alike disease which he called 'chronic osteitis.'" Other conditions are Osgood-Schlatter Disease, Panner's Disease and many others. (Appendix B)
In a new development, osteonecrosis is appearing in patients being treated with bisphosphonates such as Fosamax, Boniva, Actonel etc. (The New York Times, June 2, 2006, p.1; Drug for Bones is Newly Linked to Jaw Disease). According to http://orlando.craigslist.org/lgs/160483544.html "bisphosphonates are drugs that suppress or reduce bone resorption by osteoclasts. They do this both directly, by hindering the recruitment and function of osteoclasts (the bone-resorbing cells) and 307
perhaps indirectly, by stimulating osteoblasts (the bone-forming cells) to produce an inhibitor of osteoclast formation."
Getting back to the young mother, she became pregnant a few days after the root canal procedure. She and her fetus were exposed to a good dose of mercury already then because of the root canal. The mother also took fluoride pills and vitamins. Fluoride might matter if the mother brushed with a fluoride toothpaste or had a fluoride treatment while pregnant. Fluoride should not be used as long as there are amalgam fillings in the mouth. It is likely to free mercury from the amalgam. The loss of mercury causes the filling to deteriorate and add to the mercury body burden. talkinternational.com: Egypt Dent J 1994 Oct;40(4):909-18 (ISSN: 0070- 9484) Role of Fluoride on Corrodability of Dental Amalgams. See also Deutsche Amalgam Page: Fluoride, noch ein Betrug im Gesundheitssystem? July 19, 2002
The baby boy born nine months later would seem to be normal and happy. Of course, he received his DPT shots on time and was, to be more efficient, inoculated on the same day, against whatever else there might be to guard against illnesses. By age three this same child also had received thirty amalgam fillings. The baby's teeth looked perfect. Still, the pediatric dentist discovered many tiny pin-hole cavities, which needed to be taken care of. (This dentist is still working as a pediatric dentist and professor). He said not filling those teeth would cause them to fall out prematurely, and that would later affect the bite in the growing child. I wonder if he knew that he was putting poison into the boys mouth that was being mobilized later on, every time the school insisted on giving him fluoride treatments
This is what happened to the baby when he grew up. As already said, he seemed to be normal. Still, it was disconcerting that he did not learn to talk until age three and a half, much later than his peers. At least he did not wait to talk until age five as Einstein did. Talking late would be of no concern if the boy turned out to be another Einstein. But this boy also had a difficult time falling asleep and his mother would wear herself out trying to wake him up in the morning to get him ready for school. Was that like Einstein? Later when he was tested at school, the boy had an Intelligence Quotient of 137--quite a bit above average. So nobody worried. Maybe he would be like Einstein after all. But then, as a teenager, he withdrew from social interaction. He was very shy and after a while he suffered from depression. His mood swings caused disruptions for his family. Indeed his mother and father were afraid to criticize him for fear that he would react with outbursts of anger at any given moment. He is now thirty-five years old, and he is still depressed.
The next child born two years later was a healthy boy. He has had only one cavity. No problems with him. But then there was the third child. Four years after her first son was born, and after more dental work--done during pregnancy--the same mother gave 308
birth to a third son. This boy had a number of birth defects, which the doctors lumped together as midline defects. The boy's profound psycho/motor retardation became obvious after the craniosynostosis, the partially missing corpus callosum, hypospadias, the inguinal hernia and problems having to do with his teeth and ears were diagnosed. These defects may be explained by what Dr. Hal Huggins, DDS, refers to in his essay about mercury and Birth Defects:
How can dental mercury produce birth defects? What are the mechanisms? During normal cell division, our cells undergo a process called mitosis in which all the internal substance of a cell duplicates itself, then the contents divide evenly, and migrate to opposite ends of the cell until the cell looks something like an exercise dumbbell. Finally it squeezes itself in the middle until it separates into two identical cells. Mercury can stop this duplication process at any of its multiphasic steps resulting in an abnormal cell. If this new cell is capable of reproduction, then the abnormality may show up as a birth defect. If it is deep within a tissue, it may alter the function of a tissue or organ without being readily observed. To say with certainty that a birth defect happened one way or another is presumptuous. But recent research clearly shows the deleterious effect of mercury on cells in vitro. According to Y. ISSA1, A.J. DUXBURY, D.C. WATTS, and C.M. WATERS, of the Turner Dental School, University of Manchester, United Kingdom, School of Biological Science, United Kingdom HgCl2 was found to have a very potent toxic effect on MO3.13 (10-50 µM), as did Cd. Caspase activation was observed and morphological analysis showed that cells exposed to low concentrations of HgCl 2 exhibited features of apoptotic cell death including shrinkage and condensation of chromatin. High doses of HgCl2 (250 µM) revealed necrotic characteristics (cell swelling and lysis). Conclusion: mercury is extremely toxic to differentiated oligodendrocytes at relatively low concentrations and thus is potentially damaging in vivo. 3764 Mercury chloride: toxicity and apoptosis in a human oligodendroglial cell line MO3.13 (March 2002, San Diego)
All this said the retarded boy never talked. He is the size of a small nine-year old and looks like a child. He learned to walk at age 4. He was toilet trained already before that. At age 32 he is confined to a wheelchair due to the unfortunate after-effects of Legg-Calvé-Perthes disease. Doctors examined him long ago, thinking that he might be autistic. This child certainly would not have been able to diagnose himself. 309
As for the other above-mentioned three boys, they would never be able to connect the earlier events with their later illnesses, either, and, even though all the examples are not hypothetical, they are not meant to be proof that amalgam actually caused the neurological, psychological and behavioral difficulties just mentioned. There are too many confounding factors. They do, however, point out that the connections between cause and effect are not always visible within a short time span. Here it is worth mentioning that it takes years for the nicotine in tobacco to cause cancer, for the AIDS virus to do its damage, and the prion to cause Bovine Spongiform Encephalopathy (BSE). The children who were exposed to mercury would not remember that they had inhaled the vapors while watching brother or grandfather. The parents of the third boy could not relate the delay in speech acquisition, his shyness and, later, his depression to the fact he had been exposed to mercury via his dental fillings or his mother's amalgam-filled root canal while he was still in the womb. They did not know that "silver fillings", that's what amalgams are called, contained mercury.
On the subject of delay in toxicity of methyl mercury D. C. Rice writes in Neurotoxicology, 1996 Fall/Winter, 17 3-4, p.583-96:
Delayed toxicity as a result of developmental methyl mercury exposure was identified in mice two decades ago by Spyker, who observed kyphosis, neuromuscular deficits, and other severe abnormalities as the mice aged. Delayed neurotoxicity was also observed in monkeys... http://www.web-light.nl/AMALGAM/EN/SCIENCE/medl_neuro.html
There are so many reasons why things can go wrong in a person's life. A mother looks for all the known factors of what might have influenced her child. Was he traumatized somehow? Maybe his mother got impatient and yelled at him because he was so difficult to handle. What other psychological scars might there be? Depression and anger are supposed to originate from early childhood experiences. What about childhood illnesses that might have left neurological scars? The guessing game does not stop when a child has difficulties. Were those many vaccines to blame? They sometimes cause a fever and mimic the illness the vaccine is meant to inoculate against. The doctor tells the frightened mother that those symptoms are a natural reaction. You are supposed to have a reaction to the vaccine. The reaction means that the vaccine is making antibodies. The mother is somewhat reassured and stops worrying about the inevitable suffering. Meanwhile, one thing that is never mentioned--just as it is never mentioned that amalgam contains mercury--is that the vaccines contained a preservative called Thimerosal (it, too, contains mercury). Neither the parents nor, of course, the children had knowledge or control over receiving mercury (Children must be vaccinated. It's the law). 310
No doctor made the parents aware of the mercury. Even though Thimerosal, which contains ethyl mercury (chemical cousin to methyl mercury) and salicylic acid, has been used in vaccines since the 1930s, most doctors are unaware that those vaccines contain preservatives, let alone mercury. What might come as a surprise in this context--in addition to the fact that vaccines contain mercury--is that Eli-Lilly, the company that invented the preservative Thimerosal, first tested the vaccine on 22 patients dying of meningitis. I guess Eli-Lilly did not want to test mercury injections on healthy subjects. There is no indication that Thimerosal had no ill effect on those patients. ( WFAA.com, June 21, 2002, Dallas Fort Worth: Mercury in Childhood Vaccines: What did the Government Know? (Part II)). According to the original study at least 60% of the patients died while they were still in the hospital. The substance-- called merthiolate at the time--was not injected, but rather applied in some form to the nose. It was not injected as would be imperative if today's stringent rules were applied. The preservative Thimerosal, it could be said, was snuck into the list of FDA acceptable substances by fraudulent means.
Disclosing that mercury might be an ingredient in a vaccine is the law in California just as it is the law for a dentist to diclose that there is mercury in amalgam. That law (resulting from Prop. 65) is constantly being sidestepped today. Nobody suspects mercury in a vaccine. What's more vaccines don't need Thimerosal to work. As a matter of fact, there are several studies where it is shown that Thimerosal does not kill bacteria at all and causes a diminished immune response. Refuting pharmaceutical manufacturers' claims that Thimerosal kills bacteria, Leonard J. Goldwater states in his book "Mercury: A History of Quicksilver," (York Press, Baltimore, 1972) that merthiolate is thought to not be a particularly good preservative. Rather than being a real antiseptic it should be considered a bacteriostatin (it does not reliably kill bacteria). Thimerosal is not mentioned in the book. That leads me to conclude that the name Thimerosal for merthiolate is of a more recent date. One wonders if the name change was instituted in order to make it more difficult to find research done previously on the substance.
On immune response Dr. John Whitman writes in his website:
The presence of mercury in dental amalgam fillings has been shown conclusively to adversely affect the body's immune response. It has been shown that after amalgam removal the red and white blood cell levels tend to seek normal range with a corresponding increase in the body's immune response as evidenced by T- lymphocyte count increase (Bio-Probe References: Immunologic Adverse Effects) 311
That gets me to wondering whether an AIDS patient getting an amalgam filling or a flu-shot might inadvertently be risking his life by receiving Thimerosal with the vaccine.
Thimerosal is useful only to the manufacturer. Thimerosal allows the manufacturer to be a little sloppier in his laboratory. What Thimerosal does is mask the expression of contamination during the manufacturing process, and diverts attention from a potential defect in the vaccine. It serves the manufacturer well, but not the patient. The patient is not likely to connect the dots because they are hidden from view. Ask your doctor next time if the flu shot he is giving you contains mercury. His answer will most likely be: "Of course not." Then ask for the insert that comes with the shot. The insert will, most likely, tell you that it contains mercury. The next thing you'll hear is: "You got me there. But its only a trace amount." Most doctors don't know that those trace amounts can make your baby sick. For more information on the subject of organic mercury poisonings read Chiho Watanabe and Hiroshi Satoh who wrote about the "Evolution of Our Understanding of Methylmercury as a Health Threat."
Returning to amalgam I am assuming that mercury from tooth fillings does similar damage as mercury from Thimerosal depending on the oral environment. Thus it is entirely conceivable that mercury from amalgam that interacts with aspirin, taken for a headache, becomes something very similar to Thimerosal.
The main ingredient in dental amalgam is mercury. Amalgam has been used for centuries. The Chinese used it 1400 years ago to fill cavities. In the western world it became popular less than 200 years ago. It is a malleable material, similar to putty, and much easier to work with than gold when the dentist lays it into the cavity. That and the fact that it was much cheaper than gold, eventually made it the material of choice in all dentists' offices despite the fact that American dentists in the first half of the 19th century were amalgam-free.
Before the 1850s, there were strong efforts to ban the substance because it was thought to be poisonous. For economic reasons and convenience the proponents of amalgam prevailed. At that time the evidence that mercury compounds are poisonous was not found sufficiently compelling to discontinue it considering all its "beneficial" properties. By and large amalgam was thought to be stable. It was thought to be a special material that absolutely did not dissolve, at all. Since then chemists have learned that there is no substance, including amalgam, that does not dissolve in water over time.
Mercury's poisonous effects were well known in the days when mercury was used indiscriminately in certain industries. For instance, madness was an occupational hazard for workers in the felt industry. That was an accepted fact. That is why the 312
saying "Mad as a Hatter" was coined. The "Mad Hatter" syndrome was a symptom complex thought to be due to mercuric nitrate used in the processing of animal fur for felt hats. The mercury made you "mad" but it was thought that it didn't kill you (In Danbury, Connecticut, where the expression "Danbury Shakes"--shaking is a symptom of mercury poisoning--was coined, mercury was used by felt makers until 1941). For more on the interesting history of felt making please see: Was the Mad Hatter Really Mad? by Sharon West, March 20, 2001. Still, it was known that mercury could kill; that is why prisoners were, and maybe still are in some places, used for mercury mining. It was not widely known, though, that you could die from mercury poisoning the way Karen Wetterhahn did.
It should be added that the expression "mad scientist" was worn almost as a badge of honor. Chemical labs had always been thought to be places where an abundance of poisons made their way into the world. Among all those poisons amalgam was indeed a very safe substance. Yes, you could get poisoned. Laboratories were not the safest places to be. But the alchemist's goal was to make gold, and create wealth. The prospect of winning praise from the king for making porcelain and gun powder or ultimately gold was worth the risk. A good description of the Norwegian scientist Kristian Birkeland who, it appears, was affected by mercury and other noxious vapors in his laboratory can be found in Lucy Jago's "Bright Lights, Big Trouble - How The Aurora Drove A Genius Mad - The Bright Stuff" (The Independent On Sunday: The Sunday Review, 29 April, 2001, p.11). Arnold Orville Beckmann, founder of Beckmann Instruments, a medical insturmentation company, was so severely affected by mercury that he had to
...switch over from organic chemistry to physical chemistry, away from mercury and toward a whole new realm of fascinating chemical questions and puzzles. Carl Wilhelm Scheele, the famous chemist and pharmacist of the 18th century who dicovered oxygen, was thought to have died of mercury poisoning.
Besides being the discoverer of gravity and his writings about mathematics Isaac Newton dabbled in alchemy--in Newton's days that meant he worked with mercury. The signs of mercury poisoning were already noticeable long before his death. His shyness, on the one hand, his inability to make friends, his nasty disposition even towards those he adored and his unkempt appearance all fit into a picture of chronic mercury poisoning:
His character, at least as painted here, was almost pathologically solitary. At Cambridge, he rarely left his room. He had no friends, and was roused from his lonely musings and scribblings only to write vicious letters to those who seemed to 313
have stolen his ideas. To other scientists, even the adoring Halley, he was curt and ungenerous. He seems to have acquired social graces, such as combing his hair, only after becoming Warden of the Mint in 1696. (From a book review of "Isaac Newton", by James Gleick in The Economist, August 23, 2003)
Because it is commonly thought to be a stable substance, in other words non-toxic, amalgam has not been subjected to the strict regimen the Food and Drug Administration prescribes for all new medicines, applied internally as well as externally. Amalgam was approved (grandfathered in) without actually ever having been tested for toxicity. Environmentalists, on the other hand, have made sure that mercury amalgam outside the human body was included in the list of hazardous substances. It is poisonous before the dentist puts it into the mouth and after he takes it out. The only place dental amalgam is still considered to be safe is in the mouth. It is considered hazardous in any other place.
The recent lawsuits (See also below under Additional Websites: Stanford Law School - Dental Amalgam Litigation) filed in the United States dealing with the environmental hazard of dental amalgam (Tibau v. American Dental Association, BC252124, and Kids Against Pollution v. American Dental Association, BC 252125; San Francisco Daily Journal, Wed. June 13, 2001, p.2) have brought renewed interest in whether dental amalgam is really as safe as dentists have us believe. In spite of all the recent studies, ADA President Dr. Robert M. Anderton (ADA.org: Today's News - Association Responds to Amalgam Litigation, June 15, 2001) responds to these suits stating:
There is no sound scientific evidence supporting a link between amalgam fillings and systemic diseases or chronic illness. This is a position shared by the ADA and all major U.S. public health agencies and is a matter of public record.
Dr. Murray J. Vimy, DMD, Clinical Associate Professor, Faculty of Medicine, University of Calgary, Canada, counters Dr. Anderton's letter by pointing to 9 critical facts why amalgams are harmful. After referencing carefully those facts he concludes that
... statements by ADA spokespersons suggest that the ADA and its advisors may be knowingly disinforming the public through the media or they lack an understanding of the scientific research about mercury release from amalgam published in their own journals 314
Another lawsuit was filed in Maryland. The Wall Street Journal headline reads: "Dentists Battle 'Gag' on Warning About Mercury," by Kathryn Kranholt (Thursday, May 10, 2001, p.B1). The suit pits five dentists and seven patients against the American Dental Association. At issue is control (by dental regulators) of dental licenses to punish, or threaten punishment of dentists who criticize mercury amalgam. A Los Angeles Times (Wed., June 27, 2001) article, "Legislative Panel Moves to Disband Entire Dental Board" deals with the inertia of the California Dental Board on matters dealing with Prop. 65 compliance. It describes the ouster of the California Dental Board because they were slow to respond to ...legislative demands for creation and distribution of a warning sheet on the potential side effects of mercury cavity fillings. As an answer to this pressure the San Francisco Chronicle from August 4, 2001, p.A12, reports that "Dentists Yield On Mercury In Fillings - State Board Agrees To Cite Experts' Concerns." The Dental Board, the Chronicle says, finally agrees to put together a fact sheet that had been required by a 1992 law but had never been implemented. Ten days later the Daily Journal from August 13, 2001, contains the headline "Environmental Law: Despite Lack of Proof, Suit On Mercury Use Is Revived; Proposition 65 places the burden of proof on the dentists to show the fillings are safe, the appellate court says." It puts the importance of this judgment into perspective by including: ...Lawyers for Attorney General Bill Lockyer, who weighed in on the case on the side of the plaintiffs, called the decision an important reaffirmation of one of the basic foundations of the 1986 voter-approved law...
The Chicago Tribune entered the discussion with the headline: "Health Risks of Mercury Debated" (Chicago Tribune, August 22, Wednesday, 2001, p.N1). The article states among other things that:
The fillings slowly release tiny amounts of odorless, colorless mercury vapor. Their effect on health has been the subject of scores of conflicting studies, and no federal agency has moved to prohibit the fillings.
"You can't say mercury fillings are bad for you," said Dr. Myron Bromberg, a dentist in Reseda, Calif., and spokesman for the Academy of General Dentistry, an industry 315
group. "You can't say it because it's inaccurate. ...I have silver fillings in my mouth. I have silver fillings in my kid's mouth. If there were any problem with them, I wouldn't use them."
Mercury seems to be protected from scrutiny in other forms of internal use in humans as well. The article "Mercury-Autism Debate Left Open" in the Los Angeles Times (October 2, 2001, Tuesday, p.A10) about the mercury-containing preservative Thimerosal pronounces: "It should be reassuring to parents that we found no convincing evidence linking Thimerosal to any neurological disorder," said Dr. Marie McCormick of the Harvard School of Public Health...
This statement is being made even though ethyl mercury (mercurochrome, merthiolate), a chemical cousin to methyl mercury, has been banned for external use. Apparently, as long as mercury is applied internally it magically loses its toxicity. Furthermore, as long as there is any evidence at all, convincing or not, the medical community ought to be erring on the side of caution when it comes to toxic substances like mercury.
In spite of the above assurance, law suits keep coming. law.com published an article "Drug Companies Sued Over Vaccines Containing Traces of Mercury" by William McCall (October 3, 2001) where it states:
A coalition of law firms went to court across the nation Tuesday, trying to force the pharmaceutical industry to study whether vaccines containing a trace of mercury cause autism and other brain damage in young children.
Getting back to mercury in teeth, the California Lawyer joins into the debate by featuring Shawn Khorrami in an article about his multiple amalgam lawsuits filed in Los Angeles as well as San Francisco (Getting Drilled - The Controversy Over Mercury Fillings Turns Litigious, October 2001, p.18):
Shawn Khorrami calls it "the m-word," and the Van Nuys attorney wants dentists to open wide and say it. The m-word is mercury, a component in countless dental fillings that speckle the mouths of millions of Americans.
Further down on the same page it becomes evident that law makers keep busy, too. The same article comments about the California Dental Board saying 316
Senator Liz Figueroa (D-Fremont) has a bill pending (SB 26) that would shut the current board down altogether, with the intention of forming a new board. "I've never seen any government agency that is more alligned with a trade association than this board," says Julianne D'Angelo Fellmeth of the Center for Public Interest Law at the University of San Diego.
On October 11, 2001 the Feat Daily Newsletter (www.feat.org) reported that Governor Gray Davis had "signed SB 134 (Figueroa), the Dental Board sunset reform bill. One of the reforms in the bill requires a dentist to provide a fact sheet on possible health risks related to mercury to a patient prior to performing a dental restoration that could involve the use of dental amalgam. The bill also requires new patients to receive and acknowledge receipt of the mercury risk fact sheet."
In February 2002 under the Section: FDA Forum, Pharmaceutical & Medical Devices the Web Postings report among other news that the FDA's Center for Devices and Radiological Health has created a web page, http://www.fda.gov/cdrh/consumer/amalgams.html (updated Feb. 11) with the latest safety information on the amalgam materials used in dental fillings. The FDA and other organizations of the U.S. Public Health Service continue to investigate the safety of amalgams used in dental restorations (fillings). However, no valid scientific evidence has ever shown that amalgams cause harm to patients with dental restorations. The FDA is aware that some manufacturers have advised in their labeling against using amalgam in very young children and pregnant and nursing women. The FDA Plans to uniformly regulate dental mercury, amalgam alloy, and pre- encapsulated dental amalgam. To reduce allergic reactions from restorative materials, FDA will propose in labeling guidance that the products's labeling list the ingredients in descending order of weight by percentage and include lot numbers, appropriate warnings and precautions, handling instructions and expiration dating.
The Daily Journal (March, 21, 2002, Mercury In Dental Fillings Caused Autism, Family Claims, by Erin Carroll) covers what it claims is the "first case to link [autism] to mercury in dental fillings:"
LOS ANGELES - A Burbank family has sued the American Dental Association and 29 other dental corporations, claiming that they concealed the dangers of mercury in dental fillings, a toxin the family believes contributed to their child's autism. 317
In the suit, lawyers for Kathy Galeano allege that her nine amalgam fillings released enough mercury into her system during her pregnancy to help cause her son Daniel, now 5, to develop severe autism. While lawsuits have been filed alleging a link between mercury in pediatric vaccines and autism, plaintiffs' lawyer Shawn Khorrami of Van Nuys believes this is the first case to link the disease to mercury in dental fillings. Galeano v. American Dental Association, BC270306 (L.A. Super. Ct., filed March 20, 2002).
The FDA defends itself in the Daily article by making the same statement it had already made in its Web Postings (Vide supra): "...no valid scientific evidence has ever shown that amalgams cause harm to patients with dental restorations. The FDA is aware that some manufacturers have advised in their labeling against using amalgam in very young children and pregnant and nursing women."
Shawn Khorrami, however, states that the "metal's link to autism has been documented and that, despite mercury's known dangers, the dental profession continues to use it in fillings."
The Seattle Post-Intelligencer (Wednesday, March 20, 2002, Suit: Fillings Caused Child's Autism by Erica Werner, also Charleston Gazette, March 21, 2002, also San Jose Mercury News, Mar. 21, 2002, p.11A, DENTAL GROUPS SUED OVER CHILD'S AUTISM) reports about the same suit, and quotes ADA chief counsel Peter Sfikas as saying that
mercury in fillings is chemically bound with metals including silver, copper and tin into a "hard, stable and safe substance"
whereas Boyd Haley, chairman of the chemistry department at the University of Kentucky, states in the Seattle Post-Intelligencer: "I don't know that it's [the connection between amalgams and autism] proven, but it's very credible. Mercury is one of the most neurotoxic compounds known to man."
Haley said some studies show people with amalgam fillings have four to five times as much mercury in their blood and urine as people without such fillings.
Not surprisingly the ADA counters with a newsletter (ADA.org, Todays News, April 5, 2002) saying that
Eleven lawsuits claiming that mercury in dental amalgam caused autism in the plaintiffs' children were filed this week in Fulton County (Georgia) State Court. 318
Named as defendants were the American Dental Association and Georgia Dental Association; pharmaceutical firms American Home Products (now Wyeth), Glaxo Smith Kline, Armour Pharmaceutical and Johnson & Johnson; and Utility Georgia Power Co.
...these complaints are an "egregious abuse of the legal system," the ADA immediately responded. "Actions like these mislead vulnerable people, using information with no scientific basis to give false hope to those with chronic, often incurable illnesses."
As quasi proof for the harmlessness of amalgam the article quotes:
Dr. Dean Edell, whose syndicated "Health Talk" radio program is broadcast nationwide, characterized the autism suits as prime examples of "junk science" in the courtroom.
"Autism is not caused by vaccines or [amalgam fillings] in your mouth," Dr. Edell told his audience April 4. "A jury doesn't understand the science in this.... We all pay for this."
Natural Health (March 1, 2002, p.26) asks its readership to comment on the controversy by asking: "Should Amalgam Fillings Be Banned? Evidence On The Risks Of Mercury Fillings Is Mixed. Should They Be Outlawed Anyway? Backtalk." The article refers to a bill recently introduced to Congress by Diane Watson, D-Calif., that would prevent dentists from using amalgam fillings nationwide by 2006. It also mentions that results from two trials currently underway at the National Institute of Health are expected in 2005.
The ADA, instead of expressing interest in the bill and merely being cautiously skeptical rather than concerned about all dental patient's wellbeing, finds Diane Watson's proposed bill threatening enough to respond with an ADA.org Newsletter (April 16, 2002):
"In plain terms, Rep. Watson is attempting to legislate based on junk science," ADA Executive Director James B. Bramson said in an April 12 statement posted online. "We have requested meetings with her numerous times and thus far have been shut out. But we will continue to attempt a dialogue with her."
Further down in the same newsletter it states:
"Concern about amalgam, because of its mercury content, is intuitive but unfounded," the ADA executive director said. "The process by which amalgam is made renders the 319
bound mercury component stable and therefore safe for use in accepted dental applications."
Rep. Watson's proposed Mercury in Dental Filling Disclosure and Prohibition Act would prohibit after 2006 introduction into interstate commerce of mercury intended for use in a dental filling. The bill would require new labeling, with consumer warnings about mercury content, for dental amalgam materials regulated by the U.S. Food and Drug Administration.
The CDA states: Studies show that no filling material has been proven superior to amalgam in safety, durability, and cost effectiveness. Amalgam has been researched worldwide and no study has ever caused a professional dental organization or agency to recommend a ban of amalgam (Fact Sheets: Dental Health by the California Dental Association)
If it were so easily proven that amalgams are not dangerous why does it take no time at all to find the following study that confirms the dangers of mercury. B. Fredin comes to the following conclusion in Studies on the Mercury Release from Dental Amalgam Fillings:
...It is concluded that dental amalgam should be considered an unstable alloy constituting a long term Hg exposure and toxicologically unsuitable as a dental filling material. (Swed J Biol Med no 3, 1988 pp 8-15)
This study may be from a foreign country and it may be small. But it gives a clue about the validity of the tenet that amalgam causes symptoms. Amalgam has been researched worldwide; but the ADA has never acknowledged the importance of studies in other countries. Dental associations have not recommended a ban on amalgam because this very recommendation would mean--in the absence of long- overdue ADA initiated studies--admitting that amalgam has always been a toxic substance.
Apparently there is no need to acknowledge the facts of basic science that there is no such thing as absolut stability in science, and that chemists have known for a long time that mercury is not stable even in amalgam form (See Alfred Stock).
It is much easier to stick with conventional wisdom. That attitude does not convert conventional wisdom into modern science. It merely leaves us in the dark. The media have forgotten how to expose powerful forces such as the ADA and various amalgam manufacturers. Thus, unfortunately, even the usually outspoken Washington Post is 320
not convinced of the dangers of amalgam. Jennifer Huget discusses amalgam in two articles (March 26, 2002, Tuesday, p.F01 and p.F04). The headline for the first one reads: "Filling In For Mercury; There's No Proof Dental Amalgam Is Unsafe" (p.F01). The second one gives a synopsis of the two opposing views titled "Mercury Fillings: The Cases For And Against; Mercury Amalgam's 150-Year History As A Dental Restorative Has Been Marked By Occasional Eruptions Of Controversy Over Its Safety. Following Is A Synopsis Of The Opposing Arguments" (p.F04). While her discussion gives voice to both sides of the argument, the main points of the anti- amalgam argument--that it is poisonous to many systems in the human organism--are only discussed in the most general terms.
The mercury amalgam issue may be somewhat trickier than the mercury vaccine issue. But behind both amalgam and thimerosal hides mercury. They have a lot more in common than might be suspected at first glance. Dentist and doctors both have something at stake keeping the truth from coming out.
The ones who are not fooled so easily are the lawyers. A law.com headline on April 29, 2002, reads "National Lawyer Network Gears up for Mercury Litigation; Two Miami Lawyers Launch Attacks on Vaccine Makers, Saying Mercury Component Leads to Autism," by Julie Kay. She points out, among other things that
Robles is one of hundreds of plaintiffs' lawyers around the country who are filing or about to file negligence lawsuits against companies that manufactured or distributed vaccines containing thimerosal, a mercury-containing preservative that until the past few years was used in many pediatric vaccines. It is still used in some adult vaccines and While Robles has advertised on daytime television, in the National Enquirer and on his Internet site for clients in other types of cases, he says he isn't scouting for mercury clients. "I don't have to," says the attorney, who heads the Robles Law Center. "There are thousands of them. This is definitely the next big thing."
Relevant Laws for California:
Health & Safety Code: Section 25249.6 et seq., Business & Prof. Code 17200 et seq. Labor Code 6382(b)(1) and 6382(d) discussing the list of chemicals known to cause cancer and reproductive toxicity 321
Chapter 3.2. California Occupational Safety and Health Regulations (CAL/OSHA) Subchapter 1. Regulations of the Director of Industrial Relations, §339. The Hazardous Substances List
The U.S. requirement for preservatives in multi-dose vaccines was incorporated into the CFR in January 1968, although many biological products had contained preservatives, including thimerosal, prior to this date. Specifically, the CFR states:
Products in multi-dose containers shall contain a preservative, except that a preservative need not be added to Yellow Fever Vaccine; Polio-virus Vaccine, Live Oral; viral vaccine labeled for use with the jet injector; dried vaccines when the accompanying diluent contains a preservative; or to an Allergenic Product in 50 percent or more volume (v/v) glycerin. [21 CFR 610.15(a)]
The CFR also requires that the preservative used
…[s]hall be sufficiently non-toxic so that the amount present in the recommended dose of the product will not be toxic to the recipient, and in combination used it shall not denature the specific substance in the product to result in a decrease below the minimal acceptable potency within the dating period when stored at the recommended temperature. [21 CFR 610.15(a)] (from an FDA website dealing with Thimerosal toxicity: Thimerosal in Vaccines)
Even thought the law clearly states that there is a need for preservatives in vaccines, it does not specify that this preservative has to contain mercury. The reason why Thimerosal is preferred by all the pharmaceutical companies is that it doesn't have to hold up to any standards. Thimerosal has never been adequately tested. Any new preservative would have to hold up under the current standards, and that costs lots of money and time. Since testing is not required for this "time-tested" material, no one sees it necessary to bother with a new risky product that has no chance of making extra money for the company even if the mercury contained in Thimerosal is poisonous. Let whomever it may concern prove that Thimerosal is not safe.
While dentists are shying away from the "m-word," dental amalgam manufacturers are worried about future litigation. According to ASOMAT, a letter was sent out March 13, 1998 by the Australian Dental Association to 10,500 dentists stating, among other things, that
Contrary to the claims made by the Australian Dental Association that amalgam is safe, the manufacturers are now acknowledging the intrinsic dangers of this 322
material. The legal implications of this latest development are far reaching. If you continue to use dental amalgam you may be playing legal roulette with your assets. Caulk, Australian amalgam manufacturer of Dispersalloy, warns that their product is not safe contradicting the Australian Dental Association's own statement that it is. This information comes from http://www.zip.com.au/~rgammal/letdent.html. Another manufacturer of dental amalgam, Dentsply, issued the following warning: "Contraindications: The use of amalgam is contraindicated:
In Proximal Or Occlusal Contact To Dissimilar Metal Restorations. In Patients With Severe Renal Deficiency. In Patients With Known Allergies to Mercury. For Retrograde or Endodontic Filling. As A Filling Material For Cast Crown. In Children 6 and Under. In Expectant Mothers.
Most mercury is mined in Spain and in the Near East in countries such as Uzbekistan and Tajikistan. Amalgam manufacturers are found all over the globe. Amalgam has been used in more or less identical formulation for more than 160 years. Nowadays it is supplied in two parts. Part 1. is mercury and Part 2. is a mixture of ground mercury and other metals. After the two parts are mixed, the resulting amalgam often contains more than 50% mercury. The other ingredients, by the way, are also poisonous. The percentages of the other ingredients vary from manufacturer to manufacturer depending on how strict the manufacturer country's environmental regulations are. This matters because the global marketplace does not respond to the rules of the country to which the amalgam is shipped unless the country's regulators are watchful. Individual countries' governments have to see that their own environmental laws are obeyed.
The mercury contents, depending on who supplies the amalgam, vary from as low as 50% to as high as 70% depending on the source.
According to http://www.ericdavisdental.com/facts_and_figures_mercury.htm the amount of mercury in amalgam is sometimes as high as 65%. This means that the amounts of copper, zinc, and other heavy metals vary, as well.
Usual percentages mentioned are approximately: 323
Mercury: 50% Silver: 34-38% Tin: 12-14% Copper: 1-2% Zinc: 1-2%
These figures do not tell the whole story, however. There are two versions of amalgam. One, the gamma-2 amalgam, is more corrosion-prone because of the greater possibility of the following equation: AgSn + 2Hg = AgHg + HgSn. Here the HgSn part is the most poisonous. When this phase occurs, there is supposedly a greater chance for mercury vapors to develop, which are harmful to dental personnel and patients. The second, the gamma-2-free amalgam is supposedly more stable. Also, instead of the black color of corrosion, it retains the color of silver. When the two amalgams are compared, the change in the percentages of copper and silver are the following:
The gamma-2-phase amalgams contain equal parts, 50% of liquid mercury, and 50% of an alloy powder containing:
> 65% silver (Ag) (poisonous) < 29% tin (Sn) (Highly poisonous) < 6% copper (Cu) (poisonous) < 2% zinc (Zn) < 3% mercury (Hg) (poisonous)
The gamma-2-free amalgams contain equal parts, 50% of liquid mercury, and 50% of an alloy powder containing:
> 40% silver (Ag) (poisonous) < 32% tin (Sn) (Highly poisonous) < 30% copper (Cu) (poisonous) < 2% zinc (Zn) < 3% mercury (Hg) (poisonous) 324
Note: It is rather disturbing that, according to Ulf Bengtsson and others, studies have found that the desired stability of gamma-2 free amalgam was not achieved. Not only are the modern non-gamma-2 amalgams shown to release even more mercury vapors than the gamma-2 containing ones, but they have a strange propensity to form mercury droplets on the amalgam surfaces after polishing (On the Instability of Amalgams, by Ulf Bengtsson, January 1, 1997).
Another problem is posed by the interaction of dissimilar metals, which are, if not part of the amalgam, often found in gold crowns or other protheses next to the fillings. According to the Kieler Amalgam Gutachten-- reviewed by Birgit Calhoun (excerpts in English: http://www.zan.cc/AG5.htm)-- Loebich, the leader of the metallographic laboratory of Degussa AG, a former German amalgam manufacturer, published a report already in the 1950s warning that "...amalgam has 'caused complaints and Illnesses.'" Also according to Loebich (1955), it is not necessary that the metals in question need touch each other. Merely the presence in the mouth is enough to cause generalized malaise. Loebich says: "This can happen via two fundamentally differing pathways:
Either the ions (metal salts) work as poisons, which may form from the metal (chemical Influences). Or the potential difference (voltage) effects some sort of functional disturbance in the organism (physical influence)." (Translated from the German by B. Calhoun). The author of the just mentioned web site has the following comments about the subject of differing metals:
It is part of the basics of the knowledge of physics that a voltage difference, the so- called "potential difference," exists between two different metals or metal alloys. Now, if these two metals make contact, or if there is a conductor or a conducting medium, then this voltage difference is being evened out by an electrical current. In an oral cavity, which has been treated with differing alloys, appears - explained in this way - the phenomenon of the co-called "mouth battery." In order to get an idea about the "quantities" and "strengths" of this equalization of potential only this needs to be mentioned: In order to effect a stimulus transfer on a healthy neuron, the cells have to produce 95 millivolts (the so-called "action potential"). The measurements between two alloys in the oral cavity amount to up to 300 millivolts. A detailed description of how the mouth may act as a battery may also be found in an article by Jeff Clark (1997) "Chronic Fatigue Syndrome? Or Mercury Poisoning?" under the title: Candida's Fire 325
The daily intake of mercury per person (measured in Micrograms) in the population (World Health Organization Bulletin, 1991) is:
Amalgam Filling: 3.0 - 17.0 Seafood: 2.34 Other Foods: 0.0035 Air: 0.001
It is to be noted that the sum of the total daily average intake (<2.6 Micrograms) of mercury from the environment, by and large, is still less than the lowest measured mercury from dental amalgam. There are certain lakes and streams where the methyl mercury content in fish is high. But to downplay the mercury content in amalgams just because there are poisonous fish in the lake is not the answer to the problem of environmental mercury.
The information on gamma-2 amalgam and the daily amounts each person is exposed to, reported by WHO, was translated by B. Calhoun after obtaining it from a German Amalgam website.
In view of the great differences in amounts of mercury between one type of amalgam and another there is really no way of telling what the dentist puts into our mouths. Any person allergic to mercury or pregnant or just interested in the poisons in our environment has a right to know. Proposition 65 (The Safe Drinking Water and Toxic Enforcement Act of 1986) became effective January 1, 1987. Since then people in California presume that they can rest assured they know what toxins they are exposed to. It is important to make an informed choice about the material the dentist uses, whether it is amalgam, porcelain, gold or plastic. Environmental poisons abound. Women are told they cannot eat certain types of fish when they are pregnant because the waters are polluted with mercury. They are warned not to take any medicines, or most recently common medicinal plants such as Echinacea or Valerian unless they consult with their doctors. The most recently broadcast environmental scare comes to us in the form of chocolate, which apparently contains lead and cadmium (American Health Line, 10, 2002, Fri., California, "Group Files Suit Over Toxic metals In Chocolate"). But so far there is no public warning about mercury coming from amalgam or the vaccine preservative Thimerosal. Babies are exposed to mercury by way of vaccines sometimes as early as the day they are born, if not before because the mother needed dental work or took Rhogam because her blood was Rh-negative.
Because mercurial medicines such as mercurochrome and merthiolate as well as the former diuretic and antisyphilis drug mercuric chloride are inherently dangerous, they are no longer on the market. You can no longer buy fever thermometers containing 326
mercury. House paint containing mercury was banned in the early nineties. Thimerosal, now under investigation with respect to DPT (Diptheria, Pertussis, Tetanus), was often given to infants together with flu, Hepatitis B, and other shots containing Thimerosal. In the past, they were given without any hesitation. Now they are quietly being eliminated. But there is no law, yet, forbidding mercury preservatives, just as there are no laws forbidding the use of amalgam in the dentist's office or tobacco in cigarettes etc. (See also: Hearings Before The Committee On Government Reform, House Of Representatives, One Hundred Sixth Congress: "Vaccines--Finding The Balance Between Public Safety And Personal Choice," Aug. 3, 1999, and "Mercury in Medicines--Are We Taking Unnecessary Risks?" July 18, 2000, http://www.access.gpo.gov/congress/cong017.html). In order to calm its readership about the fear of exposing themselves and their children to vaccines the Wall Street Journal (Review & Outlook, Editorial: Immune To Reason, Tuesday, October 23, 2001) downplays Thimerosal's risk and calls "modern" America "risk- phobic." The writer prefaces that statement by saying:
The hysteria this time is over Thimerosal, an organic mercury compound that since the 1930s has been used in very small quantities as a preservative in vaccines. The Food and Drug Administration requires such preservatives to keep vaccines from being contaminated by bacteria and fungus. But back in 1999, the FDA released a report fretting that some children receiving the entire schedule of vaccines might ingest slightly more mercury than considered safe by (controversial) Environmental Protection Agency standards.
That report rallied a number of advocacy groups that claim Thimerosal is behind childhood neurodevelopmental disorders such as autism and attention- deficit disorder. Parents groups like Safe Minds have for years demanded that thimerosal be outlawed, even though there is no credible evidence whatsoever -- none -- linking the low levels of mercury in vaccines to any disorders.
But if there were no dangers at all why does the letter to the editor by Jane Maroney El-Dahr, MD, in The Wall Street Journal (Nov.7, p.A23) say "Thimerosal in Vaccines Best Avoided For Now." Her letter states
As a presenter during the Institute of Medicine's workshop on Thimerosal-Containing Vaccines and Neurodevelopmental Disorders, I must respond to your Oct. 30 [SIC] editorial "Immune to Reason." The IOM report did not find "no evidence that mercury-containing vaccines cause harm," but rather that there was not yet enough direct evidence to either accept or reject the hypothesis. This is quite different from 327
concluding that there was no credible evidence and rejecting the hypothesis, as your editorial suggests.
More importantly, it was the IOM, whose responsibility it is to make such difficult recommendations, that concluded it is in the best interest of the public health to use thimerosal-free vaccines exclusively for children at this time and to move toward removing mercury form all vaccines.
The goals of protecting the public from vaccine-preventable diseases while providing the safest possible vaccines are equally important to the health of America's children and are not mutually exclusive. Jane Maroney El-Dahr, MD, Tulane University Medical Center, New Orleans - The author is associate professor, clinical pediatrics and Head, Section of Pediatric Allergy/Immunology/Rheumatology
To confound the situation, MMR (Measle, Mumps, Rubella) vaccine seems to many parents to be the cause for their children's autism. As it turns out this vaccine contains no preservatives and thus no Thimerosal (Physician Desk Reference). So, not surprisingly a study in Denmark (The Wall Street Journal, Danish Study Finds No Links Between Vaccine And Autism, by Rachel Zimmerman, Thur., November 7, 2002, p.D4, reporting on an article in The New England Journal of Medicine, Nov. 7, 2002, p.1477, A Population-Based Study of Measles, Mumps and Rubella Vaccination and Autism) discounts the theory that the MMR vaccine might be the cause for autism.
... More than 400,000 of the Danish children received the MMR vaccine for measles mumps and rubella--the same shot given to children in the U.S. About 100,000 of the children weren't vaccinated with MMR...
The study found that in both the vaccinated and the unvaccinated groups...about three in every 1,000 children were diagnosed with autism or related disorders... That means no autism from MMR inoculations. Were all those parents wrong about vaccines? They may be wrong about MMR, but what about the other shots their babies received, possibly on or around the same day? There is no reason to believe that the children did not get exposed to mercury just because they received none in MMR vaccine. As already mentioned they could have gotten it any number of ways. Is the discussion about MMR and autism being taken up, merely to divert from the mercury in other vaccines? Curiously, as the fears over MMR are being allayed, Arthur Allen of The New York Times Magazine (November 10, 2002, p. 66, The Not- So-Crackpot Autism Theory) steps forward and states: "Reports of autism seem to be 328
on the rise. Anxious parents have targeted vaccines as the culprit. One formerly skeptical researcher [Dr. Neal Halsey ( Institute for Vaccine Safety: Perspectives on the Use of Thimerosal-Containing Vaccines, by Dr. Neal Halsey, Maryland, August 11- 12)] now thinks it's an issue worth investigating." The vaccine in question here is the Hepatitis-B vaccine. Since the start of the universal vaccination of infants in the early '90s there has been a tremendous increase in autism.
Going by the Danish study the MMR vaccine thus could easily be a "red herring," possibly designed to "exhonorate" all vaccines. The late conscience of Dr. Neal Halsey does not alter the fact that there is only luke-warm questioning of Thimerosal's safety. In the '90s, Dr. Halsey used to advocate the vaccination of all infants, and the sooner the better.
Of course children need to be vaccinated. That does not mean all children need mercury. I wonder if Dr. Halsey even knew, then, that Thimerosal was an ingredient. Not many physicians knew. But in the face of all the evidence, showing toxicity coming from Thimerosal, it is amazing that the only response the doctor can muster is ambivalence.
On June 18, 2003 an articles in The New Scientist reviews a report to be published in the September Issue of the International Journal of Toxicology, Toxic Metal Clue To Autism, that there is indeed a connection between mercury in autism:
A study of mercury levels in the baby hair of children who were later diagnosed with autism has produced startling results. The babies had far lower levels of mercury in their hair than other infants, leading to speculation that autistic children either do not absorb mercury or, more likely, cannot excrete it.
The possibility that the Danish study was a "Red Herring" is even more plausible knowing that only two months later another Danish study was published in Pediatrics Magazine (Thimerosal and the Occurrence of Autism: Negative Ecological Evidence From Danish Population-Based Data, by Kreesten M. Madsen, MD*, Marlene B. Lauritsen, MD, Carsten B. Pedersen, Msc, Poul Thorsen, MD, PhD*, Anne-Marie Plesner, MD, PhD, Peter H. Andersen, MD and Preben B. Mortensen, MD, DMSc; Vol. 112, September 3, 2003, pp.604-606) that is trying, once and for all, to eliminate the idea that Thimerosal is the culprit causing autism. All major newspapers and magazines carried the story claiming that Thimerosal was not to blame any longer for the rising incidence of autism. Yet reading the article it becomes soon obvious that the data must have been massaged and manipulated to make them fit the wanted conclusion. Two of the scientists had a conflict of interest working for the Danish 329
manufacturer of Thimerosal. The scientists, if indeed any were involved, employed the scientific method only minimally. In addition the pool from which the subjects were drawn was enlarged some time after Thimerosal was removed from Danish vaccines so that the numbers became meaningless. ( PR Newswire, Tuesday September 2, 8:06 am ET; Vaccine Health Officials Manipulate Autism Records To Quell Rising Fears over Mercury in Vaccines; Safe Minds Cites Unscientific Trending Techniques and Conflicts of Interest, Call Study's Conclusions Doubtful)
Mercury from Thimerosal is not the same as mercury from amalgam. Still the following question presents itself: Can we really presume all is being done to keep us secure in our belief that public entities such as the ADA, the CDA, CDC, and our dentists tell us the truth about what they are putting into our bodies? The psychological harm by not telling us what we are exposed to might be even greater than the actual harm that amalgam causes. Rumors run rampant on the internet about Chronic Fatigue Syndrome, Alzheimer's, and MS being caused by amalgam.
The institutionalized complacency of the above-mentioned organizations reminds of the complacency with which NASA ignored warnings in both the Challenger and the Comlubia space shuttle disasters as well as some aspects of 9-11. In the first two disasters administrative personell only saw what they wanted to see and not what sciencists had warned of all along.
But ignoring the influence of mercury on our bodies, even if it is only a small amount, allows us to ignore not only the fact that it could poison individual cells, but also that it could wreak havoc with our enzyme, vitamin, mineral and protein metabolism. It could interfere with our state of nutrition and whether we are making good use of the things we eat on a day to day basis.
For example, it is not often mentioned that mercury displaces zinc when it courses through the body. The zinc deficiency thus caused could leave a child stunted and immature. It is also not mentioned that the presence of mercury deprives the body of an optimal level of thiamin (Vitamin B1). Thiamin deficiency causes beriberi (in Sighalese this word means "I can't, I can't"). The presence of mercury in our bodies also could cause the signs of methionine deficiency, a form of protein malnutrition. Methionine is an essential amino acid, i. e. it cannot be synthesized by the human body. In African countries this type of malnutrition is called kwashiorkor. The reason why both thiamin and methionine deficiency can arise in the presence of mercury is because thiamin and methionine have a sulfur component and are very unstable. Mercury thus has no trouble destroying the two essential nutrients. We humans compensate for the lack of that deficiency by eating more. It is no wonder that there is so much discussion about obesity, particularly in teenagers. 330
The symptoms of both thiamin and methionine deficiency show some similarities to mercury poisoning, such as depression, fatigue, mental deterioration, numbness in the distal extremities etc. To find out how severe this problem is deserves further investigation.
Since there are no results of official studies in the USA, as yet, of how great the danger from amalgam actually is, it could be implied that there are also no studies on the effects of mercury from amalgam on human physiology, not to speak of human psyche and behavior. Anyone will tell you that the difficulty lies in the fact that double blind studies cannot be considered relevant unless they are done on human subjects. Testing animals would not allow for the testing of characteristics specifically human in nature. To add to the problem, the following two qualifications have to be met. First the test subjects have to be willing to submit to tests involving one of the most toxic metals known to man, and second the subjects would have to be free of mercury. Even if there were willing subjects, it would be unethical and highly irresponsible to use human subjects to test the effects of a substance that is known to cause illness.
The Nuremberg Code became the standard for testing after World War II and the Nuremberg Trials: "Permissible Medical Experiments." Trials of War Criminals before the Nuremberg Military Tribunals Under Control Council Law No. 10. Nuremberg October 1946 - April 1949, Washington. U.S. Government Printing Office (n.d.), vol. 2., pp. 181-182. "Recommendations guiding physicians in biomedical research" involving human subjects followed in 1964 in the Declaration of Helsinki; adopted by the 18th World Medical Assembly, Helsinki, Finland, June 1964, amended by the 29th World Medical Assembly, Tokyo, Japan, October 1975, and the 35th World Medical Assembly, Venice, Italy, October 1983
The first qualification, studying mercury double blind on humans, would be akin to studying the toxicity of poisonous mushrooms on people. The second, finding subjects unexposed to mercury, is almost impossible to meet. Mercury is ubiquitous. Almost everyone is exposed these days. The consumption of fish containing ever-increasing amounts of methyl mercury, due to environmental overload from coal-fired power plants etc., is rising exponentially. Adding to that, most people have mercury fillings by the time they are ten years old, and the first exposure of mercury arrived in our bodies when we were still infants in the form of thimerosal (a mercury antifungal preservative) in vaccines or even in the womb if our mothers had amalgam fillings or ate a lot of fish.
Most of us have been exposed to mercury from car exhaust and air pollution. Fish contains mercury because that is where all mercury winds up eventually. It winds up in the water either naturally through soil erosion or after it has been used in various 331
manufacturing processes. It is being released into lakes, rivers and eventually the oceans. There the algae metabolize the metallic mercury. These algae are eaten by smaller sea creatures, which in turn are eaten by the bigger fish etc. The oldest, largest fish eventually wind up with the highest mercury content. Whales, dolphins, sharks, tuna, swordfish, king makarel are the most likely to contain a lot of mercury. Tin cans, in which tuna is stored, have also been known to contain mercury. Paint and toilet paper from recycled paper products contain residues of mercurial antifungicides. The New England Journal of Medicine (Mercury Poisoning in Paper Pica, April 29, 1982, p. 1056) reported that an Inuit woman showed the typical signs of mercury poisoning (headaches, dizzy spells, tunnel vision) after having habitually eaten paper over a stretch of ten years. She had eaten a box of Kleenex (83ppb) and cigarette packages (108ppb) daily and sometimes consumed whole paperback books (341ppb). She did not eat fish. Her hair was tested and found to contain hair mercury levels that corresponded to 251 ppb in blood. Given all these sources of mercury, it is easy to see that there are no straight-forward solutions to the study of mercury in the human body. The only way to find out about most chronic, non-lethal, mercury poisonings is, therefore, through epidemiologic processes.
A table of the many forms in which mercury is used can be found in a web site called the Mercury Use Tree. It was acurate as of April 20 1998.
Most of the symptoms of mercury poisoning have been gathered empirically in the same way people found out about poisons since prehistoric times. Eat a toadstool or deadly nightshade berry and you die. Touch poison oak and you get a rash. Cyanide or strychnine are bad for you because you die from those poisons. The toxicity of chemicals ranges from mildly allergenic to mind-altering to medicinal to lethal. The outward signs of toxicity can vary from very mild to severe.
Once more the "Mad Hatter" comes to mind. Workers in the felt industry seemed to all have the same psychological symptoms. People around them thought of them as being "mad." They also got a pink rash if they were "allergic." The symptoms of "madness" expressed themselves in a "mercurial" personality also called erethism (See again Miriam Webster's OnLine Dictionary: abnormal irritability or responsiveness to stimulation). Erethism was attributed to mercuric nitrate, which was used to roughen the animal hair so that it would mat more easily. The mercury was taken out of the felt making process and the symptoms disappeared. In epidemiological terms that constituted proof that mercury caused the illness. 332
Meanwhile it is often forgotten that acrodynia still exists. It just does not show up as a result of calomel. Nowadays acrodynia results from other sources of mercury. The source of mercury could be a pesticide, fungicide, paint, floor cleaner/preservative etc.
Another example for empirically determining mercury poisoning is the story of a "cure" for syphilis by using mercuric chloride. This mercury salt had been the drug of choice and the only "cure" for that venereal disease for centuries. The "madness" syphilitics experienced was thought to be a symptom of syphilis. Mercury made it worse. But that was but a small price to pay for regaining your "health." If there were side-effects, they would not have been immediately recognized as being connected to the mercury. At any rate, with the arrival of antibiotics, the, by now, apparent harm mercury caused was eliminated. Epidemiologically speaking, this proved that mercury had caused the "madness."
Calomel had been used as a teething powder on babies for over a hundred years. That is how long they had been suffering from "Pink Disease." Not until the middle of the 20th century did it dawn on a few Australian doctors that mercurous chloride, Hg2Cl2, was causing it. The proof that Calomel was the culprit, though, was not brought until ten years later when it became evident that babies did not suffer from acrodynia any longer. See Mats Hansen: ACRODYNIA OR HOW TO FAIL TO RECOGNIZE MERCURY POISONING FOR MORE THAN 100 YEARS. The reason why mercury was implicated so late was partly due to the fact that it was known to cause "allergies" and partly due to the typical delay of neurological symptoms in chronic mercury poisoning.
Epidemiological studies are not ideal because of the many confounding factors. Marcia Angell, MD, writes in "Science On Trial", pp. 166-167:
Probably the chief difficulty in epidemiologic studies is chosing groups of people who are alike in every way except for the exposure in question (in cohort studies) or the disease in question (case control studies). Yet this is essential. Otherwise, some other differences between the groups might account for the results and badly mislead everyone. Other differences between groups that may confuse the results are "confounding variables." For example, cigarette smokers are more likely to drink alcohol than nonsmokers. So when an epidemiologic study shows a link between cigarette smoking and a disease, it is necessary to determine whether the real association is with smoking or whether it might possibly with drinking (the condounding variable in this case). It could be the combination--or even some other factor that might be different between smokers and nonsmokers.
Although there are statistical methods for neutralizing confounding variables, they are not perfect, and they are of no use whatsoever unless the confounding variables are 333
known and measured. For example, epidemiologic studies have shown an association between premature births and lack of prenatal care, but maybe there are confounding variables that explain the association. Maybe it has nothing to do with the prenatal care itself. For example, it could be that women who can afford prenatal care are more likely to carry babies to term because such women are better nourished.
But back to the subject of amalgams. While all this was going on, mercury was considered "safe" in the form of amalgam. There were "no" acute symptoms (or were there?) right after the filling was put in, and there were no "apparent" symptoms later on that could be clearly labeled as having resulted from amalgam. The symptoms "mild" mercury poisoning is known for are usually not recognized as medical problems, but fall into into the realm of psychiatry. If there were symptoms after a visit to the dentist they might have been a migrain headache or some ringing in the ears or diarrhea. The symptoms were only very mild, and they could have come from exposure to almost any substance produced in our industrialized world.
Dentists have claimed that amalgam is the filling material of choice. It it relatively harmless, they say. It is, in any case, better than not filling cavities at all. The question poses itself: Is there even a way to connect amalgam to the many symptoms that have been attributed to the exposure of mercury from amalgam, and could one deduce from empirical studies whether amalgam causes poisonings that are not easily correlated to the amounts of mercury in blood or urine samples at a given time? In order to answer that question, the symptoms have to be definable. There has to be a clear-cut set of signs that separates mercury poisoning from other heavy metal poisonings.
In addition it would be desirable to clarify what the word allergy means, and if it should not be eliminated from the vocabulary when it comes to mercury. The pink skin in mercury poisoning is no more an allergic reaction than the pink skin in scarlet fever or the rash in measles. Just because sensitivity to mercury looks like an allergy does not mean that it is one. The pink skin is the result of toxicity. It was first described as acrodynia or "pink disease". Even though acrodynia is almost always mentioned in the context of teething powders, it can also be the result of inhaling paint vapors containing too much mercury anti-fungicide:
In August 1989, a previously healthy 4-year-old boy in Michigan was diagnosed with acrodynia, a rare manifestation of childhood mercury poisoning. Symptoms and signs included leg cramps; rash; itching; excessive perspiration; rapid heartbeat; intermittent low-grade fevers; irritability, marked personality change; insomnia; headaches; hypertension; swelling; redness and peeling of the hands, feet, and nose; weakness of the pectoral and pelvic girdles; and nerve dysfunction in the lower extremities. A urine mercury level of 65 ug/L was measured on a 24-hour urine 334
collection. Treatment with intensive chelation therapy increased his urine mercury excretion 20-fold. Examination of his mother and two siblings found urine mercury levels greater than or approximately equal to his; his father had elevated, although lower, levels. Parents and siblings were asymptomatic, although electromyographic abnormalities were detected in one sibling.... identified inhalation of mercury- containing vapors from phenylmercuric acetate contained in latex paint as the probable route of mercury exposure for the family; 17 gallons of paint had been applied to the inside of the family's home during the first week of July. Samples of the paint contained 930-955 ppm mercury, the Environmental Protection Agency (EPA) limit for mercury as a preservative in interior paint is 300 ppm. During July, the house was air conditioned, and the windows were not opened... The preceding quote is an excerpt from an article by Aronow R, Cubbage C, Weiner R, Johnson B, Hesse J & Bedford J, Mercury Exposure from Interior Latex Paint - Michigan, Morbidity and Mortality Weekly Report (MMWR) 39(8):125-126 (1990)
Because of this case a study was done to see if mercury from latex paint can produce toxic levels. The result was described in the New England Journal of Medicine; Oct. 18, 1990; Volume 323:1096-1101, Nr.16 "Mercury Exposure From Interior Latex Paint", by MM Agocs, RA Etzel, RG Parrish, DC Paschal, PR Campagna, DS Cohen, EM Kilbourne, and JL Hesse:
We found that potentially hazardous exposure to mercury had occurred among persons whose homes were painted with a brand of paint containing mercury at concentrations approximately 2 1/2 times the Environmental Protection Agency's recommended limit.
The problem with the diagnosis of mercury poisoning is that there are so many purported symptoms and that it takes so long for them to develop. And, just because of these two circumstances it is often said about people who blame mercury for everything that they are not realistic and that they must just have latched onto a fad. This criticism can be countered by pointing out that there has never been a limit to how many symptoms a disease may have. It is entirely possible for a disease to have 1,500 symptoms as Professor Hahnemann pointed out. The reason for this is that mercury works on the cellular level of the human organism and that the science of determining symptoms is confined to what a doctor can remember. It is neat and tidy when a disease can be easily recognized and has only very few pathognomonic signs. Therefore it is also not surprising that certain diseases are much more often described 335
and diagnosed. But just because they have not been described and named, doesn't mean that they don't exist
The symptoms of mercury poisoning, depending on the amount and type of mercury consumed, range from imperceptible to dire. The Merck Manual's Centennial Edition (17th Ed., p.2636) lists the following symptoms in the chronic category: Gingivitis, Mental Disturbances, Neurological Deficits. Mercury vapor is listed as causing severe pneumonitis. The symptoms that go along with any kind of toxicity, such as liver and kidney disease are not mentioned here even though they present themselves often, especially in chronic mercury poisoning. The accumulation of mercury in the liver causes a constant strain on the organism. It causes fatigue and weakness to the body and compromises the immune system. The first signs of kidney disease might be albuminuria, frequent urination, and urgency to urinate. [See: Alfred Stock, Die Gefaehrlichkeit des Quecksilberdampfes, (1926); also Fatal Mercury Intoxication in a Dental Surgery Assistant, BRITISH DENTAL JOURNAL, 127:553-5 (12/16/69): A 42-year-old dental surgery assistant with at least a 20-year history of exposure to mercury developed a rapidly fatal nephrotic syndrome...]
There are no thorough U.S. studies as yet to quantify the level of distress the human body feels as a function of the amount of mercury absorbed from inhaling it as a vapor, swallowing it, or absorbing it through the skin. As mentioned already, the results of a U.S. study in this direction are not expected until 2005. A very exhaustive study on 20,000 people at the University of Tuebingen in Germany ( "Field Study on the Mercury Content of Saliva", by Peter Krauss, Universität Tübingen - Institut für Organische Chemie - AK Prof. Dr. Peter Krauß) deals with the saliva content of mercury from amalgam. It has so far not evaluated the effects of mercury on the people studied. In the meantime the overt symptoms, gathered empirically over centuries, have been well documented. The only U.S. study that deals with the question whether amalgam actually releases mercury into the human body by testing blood and urine samples (Mercury Concentrations in Urine and Whole Blood Associated with Amalgam Exposure In a U.S. Military Population, by Kingman, A., Albertini, T., Brown, L.J., J Dent Res, 1998;77(3): 461- 471) http://nnd40.med.navy.mil/Gen_Dent/Gen_Dent/Pearlsb5.htm states the following:
...Correlations between amalgam exposure and Hg concentrations in urine were statistically significant. Hg concentrations are modeled as a function of amalgam exposure, adjusted for age, alcohol consumption, and the presence of restorations containing other metals for each measurement scale separately. The whole blood organic mercury concentration and the current number of alcoholic drinks per day 336
were also consistently statistically significant. As alcohol consumption increases, lower urinary total mercury levels are to be expected...
Could this mean that the liver of a person drinking alcohol is not able to detoxify mercury as efficiently as necessary? That conclusion is likely, yet equally as unproven as the hypothesis that people who drink alcohol have found a way to eliminate their mercury overdose more effectively via the digestive tract, thus bypassing the already damaged kidneys. In any case there is a known correlation between alcohol consumption and mercury levels in urine and blood. This thought leads to the next question: Could it be that alcoholics, by getting drunk, are really choosing the lesser of two evils? Unfortunately, rather than becoming only mercury impaired they also become alcohol impaired. Either way the liver suffers.
None of those above mentioned studies evaluate the symptoms that might accompany higher blood or urine mercury levels in persons with amalgams compared to those without. And do the blood and urine levels really tell the whole story? The inference that the alcohol-impaired liver changes the urine levels of tested subjects demands this question. What other substances are there to change the values? The horrible physical effects on the body don't show up until the mercury has damaged the interior of the affected cells. By the time mercury has done its damage you might not find it in bodily fluids but only inside the cells. It takes quite a different test to assess the amount of mercury a cell might contain.
The Merck Manual describes the symptoms of mercury poisoning rather superficially. A physician is presumed to know what it means to have mental and neurological deficits. Mental and neurological deficits are rather subjective terms, however. What exactly do they mean when it comes to mercury? For a general description of what the terms entail please read this University of Iowa Web site on Neurotoxicity
The "Mad Hatter" whom Lewis Carroll's described in "Alice In Wonderland" had only a few symptoms and they appeared to be more behavioral than neurological. This particular hat maker did not even show erethism the way it is described in the dictionary. He had few signs of mood swings or at best only very mild ones, unless we are already too jaded by all the craziness around us in today's polluted world to think of him as mad. He seems merely a little confused, or perhaps excentric, in his choice of words. He is forgetful. But who doesn't forget things once in a while? And he shakes at one point when he is put under stress on the stand when he is being asked about what he knows about a theft. After all, he is being threatened with execution if he can't answer. Wouldn't we all shake? Could his behavior be considered a neurological symptom of mercury poisoning? Lewis Carroll apparently thought so. He was a mathematician who was familiar with the afflictions of hat makers. Carroll 337
describes the "Mad Hatter's" sense of time. The hatter's interpretation of it could be one of the most telling signs of early onset mercury poisoning. The subtleties in his logic and his insistence on it are the beginnings of a certain willfullness that at this point escape Alice; she sees him as rude. But the reader sees the "Hatter's" logic as not entirely farfetched and even somewhat philosophical. The problem is not in his logic (he seems rather intelligent), but in his unwillingness to communicate patiently with Alice who cannot understand what he means when he comes up with a new way of looking at time. After all she is only a child. Off-hand what we can tell from the hatters behavior is that he is childish, slightly moody, unable to communicate with people, and, in the end, not unintelligent. It is known that hatters had all those symptoms and more.
At the other extreme, the inventor of homeopathy Dr. Samuel Hahnemann, a physician, who had seen quacks use mercury and became increasingly concerned about its indiscriminate use, listed over 1200 distinct symptoms of mercury poisoning. Because of the huge differences in opinion about what constitute symptoms of mercury poisoning it seems wise to look for other sources. The question is: Which symptoms could realistically be attributed to the effects of mercury?
There are two prominent examples of mercury poisonings in recent times. The first one, which occurred in the mid-fifties and early sixties at and around the Japanese fishing village of Minamata, affected thousands of people, and killed hundreds. The agent here is presumed to have been methyl mercury. It had made its way into Minamata Bay as an end-product in the process of making acetaldehyde. The people ate the mercury-laced fish caught in the bay and became sick. Many of them died. In a website from American University (TED Case Studies, Case Number 246) http://www.american.edu/TED/MINAMATA.HTM a paragraph gives the following account:
Not until the mid-1950's did people begin to notice a 'strange disease'. Victims were diagnosed as having a degeneration of their nervous systems. Numbness occurred in their limbs and lips. Their speech became slurred, and their vision constricted. Some people had serious brain damage, while others lapsed into unconsciousness or suffered from involuntary movements. Furthermore, some victims were thought to be crazy when they began to uncontrollably shout. People thought the cats were going insane when they witnessed 'suicides' by the cats. Finally, birds were strangely dropping from the sky. Series of these unexplainable occurrences were bringing panic to Minamata. 338
See also: LewRockwell.com: Minamata: Real Life Horror Show, by Mike (In Tokyo) Rogers,
The second incident refers to the poisonings and deaths of peasants in Iraq. Approximately 100,000 tons of grain had been shipped to a starving population. Because it was already fall in Iraq, not spring when it might have done them some good for planting, they baked pink bread made from the grains coated with a pink- colored mercury-containing preservative. This Purdue University website http://abe.www.ecn.purdue.edu/~mercury/src/iraq.htm describes the following scenario:
In 1956 over 100 people were poisoned in Northern Iraq by eating flour mixed with wheat seed. The wheat seed had been treated with a fungicide containing 7.7% ethylmercury-p-toluene sulfonamide. Fourteen deaths were reported, and probably even more occurred. As a trial, the seeds had been fed first to chickens for several days and no ill effects were observed. Besides central nervous system manifestations, a number of other clinical symptoms were observed: polydypsia, polyuria, weight loss, severe proteinuria, deep musculoskeletal pain refractive to analgesics, and pruritus of the palms, soles, and genitals. Researchers credit the other symptoms to the prevalence of a parasitic disease called ancylostomiasis, and to dietary deficiencies of protein and vitamins. The event repeated itself 4 years later when an additional 100 people were poisoned by a flour and wheat seed treated this time with a fungicide containing 1% ethylmercury chloride and phenylmercury acetate. Four of 34 patients died, and it is probable that others died as well after refusing hospitalization and medical advice.
According to Medicine-Worldwide 100,000 Iraqis came in contact with the mercury and about 2,000 people died of mercury poisoning.
These two cases illuminate the major impact mercury had on the affected populations in Japan and Iraq. Both countries had deaths. In both countries the poisoning resulted in a permanently maimed part of the population. What is significant in Iraq is that the people there knew that the seed grain was poisonous. They just didn't know in which way. They didn't know that it may take a long time to poison with mercury. Because, even though acute poisoning can kill within a few days, the insidiousness of chronic mercury poisoning lies in the delayed effect of methyl and ethyl mercury. It takes months even for a potentially lethal dose to take effect. The people fed the grain to the chickens to see if those chickens might show signs of poisoning. When nothing happenend, after what seemed a reasonable time, the grain was used to bake bread. 339
The poisoned chickens did not die as had been expected. So they were slaughtered and eaten, too. That, too, caused poisoning.
What could have prevented the poisoning? Maybe nothing. However, the failure to detect the poisoning of the chickens showed the basic lack of understanding of how slowly organic mercury may poison the body. They gave the ckickens too little time to be poisoned. If they had waited half a year, the chickens would have died from mercury poisoning and the grain would not have poisoned anyone. But Iraq had a famine at the time, and it is not certain how long the population could have waited. Still, if the people had been better informed, they might have lived.
Why do I mention these two examples of mercury poisoning when amalgam seemingly does not cause any overt symptoms? My point is that it took time to discover that mercury had caused the deaths in those countries. Mercury from amalgam has the same potential for harm as any other mercury. Its toxicity depends mainly on how the mercury binds to organic or inorganic matter in the body. Neither in Minamata nor in Iraq was mercury suspected right away. In Minamata the prime suspect for the characteristic animal and people behavior was at first thought to have been the acetaldehyde, a building block for plastic, that had been manufactured at the Chisso plant in Minamata since the 1930s. But to discover the connection to mercury still took close to thirty years. Mercury was a necessary ingredient for the manufacture of acetaldehyde.
The symptoms were so subtle that at first the population was in denial. They were perceived as behavioral deviations. Furthermore, in Japan any disease process was considered a reflection of the individual's own failure. Therefore quaint names were given to the behavior so nobody would hold it against you if you acted strange. The behavior in cats was called "dancing cat" disease. The corresponding human behavior was called the "elegant" disease. Only after years of investigations and worsening symptoms was it discovered that mercury used in the process of making plastics was the cause of birth defects and deaths (Bitter Sea, Akio Mishima, The Human Cost of Minamata Disease, 1992).
The difficulty diagnosing vague symptoms coming from continued slow leakage of mercury vapors or compounds from dental amalgam thus becomes much more plausible when it is put in perspective.
Chronic mercury poisoning has many faces. Some are psychological, some behavioral and some are physical. The following quote was part of an article published by the Zeitschrift für angewandte Chemie under the title "Die Gefährlichkeit des Quecksilberdampfes," Von ALFRED STOCK, Berlin-Dahlem, Kaiser-Wilhelm-Institut für Chemie, (Eingeg. 9. Febr. 1926): 340
Seit beinahe 25 Jahren litt ich an Beschwerden, die, anfangs schwach und nur gelegentlich auftretend,allmählich mehr und mehr, schließlich fast bis zur Unerträglichkeit zunahmen, so daß ich schon daran verzweifelte, weiter wissenschaftlich arbeiten zu können. Die Ursache wurde von mir und vielenausgezeichneten Ärzten, die ich um Rat anging, nicht erkannt. Man hielt für möglich, daß sie in besonders engem Bau der Nasenwege und in einer ungewöhnlichen Reizbarkeit der Nasenschleimhaut zu suchen sei. Ich unterzog mich infolgedessen jahrzehntelanger Behandlung der Nase mit Ätzen, Brennen, Massieren, Elektrisieren, blutigen Operationen. Ohne Erfolg! Vor etwa zwei Jahren endlich kam durch einen Zufall - einige meiner Mitarbeiter erkrankten unter ähnlichen Erscheinungen - heraus, daß es sich um eine schleichende Vergiftung mit Quecksilberdampf handelte. (web link vide infra, Alfred Stock, Die Gefaehrlichkeit des Quecksilberdampfes, 1926; translated by Birgit Calhoun: The Dangerousness of Mercury Vapor)
In the above-mentioned quote Dr. Afred Stock, head of a Berlin University laboratory, talks about his 25-year long illness [headaches, sinus infections sore throats etc.]. He reports that he consulted numerous outstanding physicians without finding relief. It was thought possible that the reason for his problems could be found in the narrow built of his nasal passages and the unusual irritability of his nasal mucosa. Because of this he underwent decade-long treatments of the nose with cauterizations, burnings, massages, electrical stimulations and bloody operations. Without success! By accident he found out about the illnesses in some of his co-workers with symptoms similar to his. They were diagnosed as having a slow form of mercury poisoning. With the help of Dr. Lewin, an expert in toxicology, he heard about the fact that amalgams leak mercury. He tested various amalgam specimens himself to prove that this indeed was true. The article among other things, states that, even though these symptoms were real and not brushed off as "being all in his head," it took again a long time before an answer was found. Stock suffered from his illness until he had all the mercury, including his amalgams, removed from his environment. His condition improved, and, for the rest of his life, he went on a campaign against the indiscriminate use of mercury, particularly in amalgam fillings.
Sub-clinical symptoms are hard to assess. Very mild symptoms of exposure to a very small dose of poison would not be connected to the cause. Indeed they might be dismissed as psycholgical or some form of hysteria. In the vernacular, intoxication is connected to immediate results. When you drink wine you become inebriated almost right away. When you take a sleeping pill you become drowsy. Drinking and drugs are meant to produce quick results. If the symptoms were not immediate, nobody 341
would be tempted to abuse alcohol and drugs. But, the toxicity of alcohol and drugs, as well as that of mercury and other heavy metals, and their possible long-range neurological damage are rarely discussed unless the symptoms become clinical.
Toxicity over time by small amounts of mercury is not obvious. And yet, when large numbers of people show the same signs of being different in a variety of characteristics--I refer again to the "Mad Hatter" syndrome, or what was called the "Danbury Shakes" in the United States--then the connection eventually becomes a confirmation.
When tobacco was suspected of causing lung cancer there was at first no more than a hunch. It took years before a clear picture emerged. Asbestos causes mesothelioma. It took a while to make that connection. The same can be said for lead in paint (by the way until 1990 mercury was used in paint, as well, see EPA Environmental News: Use of Mercury Compounds in Indoor Latex Paint to be Eliminated, by Al Heier, June 29, 1990, Friday). Lead causes mental retardation. Now a connection is being made between mercury from amalgam and symptoms that seem to be not only physical but also mental and behavioral. The voices on the internet speak loudly and clearly. They are not just the voices of individuals giving really credible anecdotal evidence that used to be the basis for "Old Wives' Tales." These voices come from the scientific community from all over the world. Here are some quotes: http://www.amalgam.ukgo.com/amquotes.htm.
The following mercury poisoning website from Purdue University gives a good synopsis what chronic mercury poisoning might entail:
Chronic Mercury Poisoning
If you are exposed to any form of mercury repeatedly or for an extended period, chronic mercury poisoning can result. Health effects include nervous system effects, kidney damage, and birth defects. There are several symptoms:
1. Gingivitis: The gums become soft and spongy, the teeth get loose, sores may develop, and there may be increased salivation.
2. Mood and mental changes: People with chronic mercury poisoning often also have wide mood swings, becoming irritable, frightened, depressed, or excited very quickly for no apparent reason. Such people may become extremely upset at any criticism, lose all self-confidence, and become apathetic. Hallucinations, memory loss, and inability to concentrate can occur. 342
3. Nerve damage: It may start with a fine tremor (shaking) of the hand, loss of sensitivity in hands and feet, difficulty in walking, or slurred speech. Tremors may also occur in the tongue and eyelids. Eventually this can progress to trouble balancing and walking. It has even caused paralysis and death in rare cases. (Chronic Mercury Poisoning: http://danpatch.ecn.purdue.edu/~epados/mercbuild/src/chronic.htm)
The DAMS (Dental Amalgam Mercury Syndrome) Support Group uses the ICNR web site's set of symptoms
One of the many web sites quoting symptoms due to chronic mercury exposure from amalgam is Leif Hedegard's. His background includes medical school--he also has experience taking care of disabled children. He states in his Swedish Amalgam page http://www.algonet.se/~leif/AmFAQk02.html that the most commonly named symptoms in inorganic Hg-intoxication are: Tremor, Erethism and Gingivitis. Tremor and gingivitis are not always present. The first sign is usually erethism (increased excitability). Erethism goes along with some or all of the following psychological and behavioral symptoms:
irritability outbursts of temper stress intolerance decreased simultaneous capacity increased sensitivity to sounds and light resentment of criticism loss of self-confidence timidity excessive shyness embarrassment with insufficient reason self-consciousness anxiety indecision insomnia vivid dreams lack of concentration memory loss depression fatigue... 343
The above mentioned symptoms are repeated more or less in the the same form in many websites. Of course anyone could have any one of those symptoms without being exposed to mercury. A bad hair day doesn't mean that mercury caused it. A nightmare or a bout of insomnia doesn't automatically mean that your amalgams acted up. What is significant in this context, however, is that the probability of having only one of those symptoms by itself resulting from mercury exposure is slim. Typically a person suffering from low-level mercury exposure experiences most, if not all, of the symptoms listed above.
Lou's Page (see link below) lists the almost identical symptoms as above to be the first ones to appear in a victim of mercury poisoning: The Erethismus (from Greek; excite) is a pathologically increased excitability. Erethism is usually the first symptom to develop. It goes along with some or many of the following symptoms; irritability, outbursts of temper, stress intolerance,... (see symptoms above) all these together can cause a complete change of personality. The memory loss could be disabling:"...memory loss such that young mothers would forget to retrieve children from baby-sitters on the way home from work... Non- verbal memory tested by facial recognition was no better than chance..." (Vroom 1972).
A group of psychologists reported on a single case of low grade mercury exposure (Chronic Neuropsychological Effects of Long-Term Mercury Exposure: A Longitudinal Study; James B. Pinkston, Wm. Drew Gouvier, Jeffrey N. Browndyke, & Paula J. Varnado-Sullivan, Dept. of Psych., Louisiana State Univerity, Baton Rouge, LA). They introduce their abstract by saying Although the short-term deleterious effects of mercury exposure have been explored, the residual, chronic effects of mercury poisoning have received far less attention. Mercury poisoning has been attributed to deficits in cognition problems with intellectual functioning, attention, and memory. It has also been seen as the impetus for changes in personality including depression, anxiety, and paranoia.
After three years of psychological testing they conclude that 344
... Neuropsychological testing...revealed a profile of continued psychological disturbance including pronounced personality changes as well as persistent mild cognitive deficits on sensory/perceptual testing as well as dexterity and frontal lobe tasks along with preserved intellectual functioning This confirms what victims of low level poisoning experience in the following accounts of mercury poisoning - Victims of Mercury Poisoning & Their Stories: http://www.talkinternational.com/adaletters.htm. The Hearing by the Committee on Government Reform also contains numerous personal accounts of symptoms relating to amalgam illness "Mercury in Medicines--Are We Taking Unnecessary Risks?" (July 18, 2000), http://www.access.gpo.gov/congress/cong017.html).
Reading patients' accounts makes it obvious that most of them had symptoms for years, and it took years of suffering before a diagnosis was made. It is not easy to diagnose such an illusive illness. So, when it comes to proving that the symptom complex actually is the result of mercury exposure, it is important to be aware of how complex the situation is. The following Position Paper, "Now to the Question of Toxicity," by Tom Clarkson, Universities of Rochester Medical School, and David Bellinger, Harvard University Medical School, March 3, 1998, http://www.iadr- dentalfaculty.org/plenary/Plenary2/0000002f.htm gives only a glimpse of the difficulties in testing whether the above-mentioned symptoms are indeed related to mercury poisoning. Yet, for those involved, the importance of finding the reason for their disability can make the difference between a life worth living and the constant struggle of fighting depression and other forms of disfunction.
The connection between low-level mercury poisoning and amalgam is being contested by dental associations and dentists. It is after all possible that the above symptoms could have originated from other toxins. There are so many environmental toxins that it is impossible to completely separate one from the other. On the other hand a major study "Link Between Dental Fillings And Disease" http://www.vimy-dentistry.com/nhanesstudy.htm makes one ponder if there is not indeed something to the notion that mercury from amalgam is an active chemical, and that this most poisonous of all metals could result in the symptoms described above. ...looked at the Survivor Rates using the International Classification of Disease Codes (ICD-9-CM) from the U.S. National Health and Nutritional Exam Survey 3 (NHANES 345
III), and found dramatic differences in dental filling rates for people suffering from a variety of diseases, as compared to the dental fillings rate in the general population. The NHANES III sample represents 180,072,328 Adult Americans, who are the General Adult Population 17 Years of age and older between 1988 and 1994. For more information about the background of the study please see the following Canadian News Release from April 18, 2001, by Wayne Obie of Talk International.com representing CFMR & Americans against Mercury: All That Glitters Is Not Silver, Multi Million Dollar U.S. Government Study Connects Dental Fillings To MS and other Diseases
For centuries scientists, historians and well-educated people in general have postulated and found, not too surprisingly, that the Romans lost their super power status in the Western World because they used lead pipes in their water delivery systems. It was also insinuated that the Spanish Kings were thought as lacking in mental accuity because they had the money to paint their palaces with white lead paint as soon as there was the slightest blemish. It has been known since ancient times that the vapors from heavy metals such as lead and tin cause neurologic symptoms. So it makes one wonder why mercury is not getting more attention, especially since mercury has been used in the United States as an antifungicide into the early 'nineties.
What's more, the toxic metals just mentioned are known to interact with mercury. The various metals contained in amalgam become more toxic when they are released simultaneously. ASOMAT's address is: The Australasian Society for Oral Medicine and Toxicology (ASOMAT), Robert Gammal, PO Box A860, Sydney South, NSW 2000, AUSTRALIA), states:
The synergistic effects of mercury combined with various other substances is also an area of significant concern which has been under-researched to date. The toxic effects of mercury are further enhanced when mercury is in combination with other metals such as zinc and lead.
In a study (24) which looked at a common amalgam (Dispersalloy), the researchers reported [that]... "Dispersalloy was severely cytotoxic initially when Zn release was greatest, but was less toxic between 48 and 72 hours as Zn release decreased." Zn, at the amount released from an amalgam, should not reach cytotoxic levels. It does however, potentiate the toxicity of the mercury released by tying up protective mercury chelators due to the fact that Zn and Hg both have a high affinity for sulfhydryls. In experiments investigating this effect, it was found that addition of non- toxic amounts of Zn2+ (5-10 micromolar) enhanced the toxicity of mercury about 5- 346
fold. (Personal communication: Prof. Boyd Haley. Prof. and Chair, Dept of Chemistry, Univ of Kentucky).
The effects of mercury and lead combined have also been reported. One study showed that when a lethal dose (LD1) of mercury was combined with 1/20 LD1 of lead, the combination of the two resulted in a LD100 in the test animals (44). This has not been investigated in human subjects but it is clearly reasonable to assume the possibility of similar effects in amalgam-bearing humans.
More of Prof. Dr. Boyd Haley's communication to Representative Dan Burton (D) can be found in "Dr. Haley Rebuts the American Dental Association Position on Mercury Amalgam Safety," 23-May-01, http://www.bioprobe.com/ReadNews.asp?article=36
Neurologic symptoms caused lead-based paint to be banned and pewter plates and spoons to become merely decorative antiques. Especially in view of the fact that various studies have connected lead and manganese in drinking water with crime, it should not be too far-fetched to mandate scientific studies to lay to rest any lingering doubts about the nature of mercury, and whether dental mercury shouldn't be treated with more caution. It takes time to investigate potential connections. The sooner those connections have been either confirmed or eliminated the sooner we can put aside our fears. Or can we, considering the history of the ADA over the last 150 years? It is time for the ADA and amalgam manufacturers to prove that amalgam is safe, or else warn people of its harmful effects. It is the dentist's professional responsibility to make his patient aware of any potential harm.
Even if the connection between mercury and illness is too difficult to establish, the overwhelming evidence points to the fact that mercury is being released from amalgam, and that mercury in even minute quantities causes harm. Even if mercury is not the main reason for Alzheimer's (CFS Radio Interview, August 15th, 1999: Roger G. Mazlen, M.D. Host with Prof. Boyd E. Haley (Commenting on his research relating to Alzheimer's and mercury) or Multiple Sclerosis or autism or..., there is no doubt that mercury can not help but worsen the outcome in affected people. To be on the safe side it is best to eliminate mercury from the environment in general and the oral cavity in particular.
Even if the ADA does not recognize studies that have been done, an attempt should be made to dispel the fears of patients. I see it as an ethical duty to refute research done by Robert L. Siblerud, John Motl and Eldon Kienholz who investigate mercury as a root of depression, anger, anxiety and violence (Psychological Reports, 1994, 74; pp.67-80; Psychometric Evidence That Mercury From Silver Dental Fillings May Be An Etiological Factor In Depression, Excessive Anger, And Anxiety) in a scientific manner, if indeed it can be refuted, before criticizing its validity. 347
Another thought comes to mind. When Alzheimer's and autism are compared, the two diseases seem very similar. The only difference seems to be the neurofibrillary tangles and other signs of neuro-cellular damage. Is it possible that autism and Alzheimer's are the same? It seems entirely plausible that the only reason why Alzheimer's patients show cell damage is because they lose the ability to regenerate new cells. A young child's organism tends to prune and restructure its cell systems, particularly nerve cells, all the time. Any cells that become redundant are being "pruned," and then flushed out and filled in with new ones. An old person cannot regenerate cells as fast as they are being destroyed (possibly by mercury). The space is therefore not being filled in with new cells and old worn out cells are not carried away. Therefore the damage can actually be seen. See also Autism - Alzheimer's -- Mercury Poisoning Comparison Chart, January 19, 2002
Concerning the law and how amalgam obtained this lofty protected status, I suggest calling amalgam what it is: bad medicine. It is not merely a medical device. It contains mercury. If it were a medical device, such as a metal screw or a rod inserted into a broken bone, any medical doctor would not hesitate removing it (expenses paid by the Health Maintainance Organization) if it causes pain or irritation. The ADA claims that dentists are on the same level as medical doctors. How is it possible that the poisonous amalgam is not treated the same as a metal rod in a person's bone. Pulling a metal rod out of a person's bone is much more expensive than amalgam from a tooth. Why the unequal treatment? When I had to have a bone transplant because of cavitation caused by a root canal, the dental insurance did not pay for the damage amalgam had done. The HMO did not pay either. It thinks cavitation is a dental problem. Where does the mouth end and the person begin? Why the unequal treatment?
One more comment, when it comes to the safety of products such as dental amalgam and Thimerosal in vaccines, eventually the courts are going to have to be involved. I am quoting from another website (http://www.algonet.se/~leif/bdafactf.pdf):
In the end, no product can be proved safe, and new hazards can always be discovered. The courts ultimately decide the issue, rather than scientists. For example, breast implants were the subject of successful litigation, even though they had achieved wide acceptance following extensive use prior to the introduction of regulatory controls.
Proving what particular mercury poison [vapor from a fever thermometer or amalgams or paint from an old house (Arch Env Cont Tox 21:62-64 (1991): Beusterien KM, Etzel RA, Agocs MM, Egeland GM, Socie EM, Rouse MA & Mortensen BK.: Indoor air mercury concentrations following application of interior 348
latex paint; MMWR 39(8):125-126 (1990): Aronow R, Cubbage C, Weiner R, Johnson B, Hesse J & Bedford J: Mercury Exposure from Interior Latex Paint - Michigan), inorganic salts from the soil or water around mercury mines, skin whitening ointments, organic ethyl mercury from Thimerosal or methyl mercury from fish or amalgams] is the culprit for specific symptoms is even more difficult than tying just one of those forms of mercury to a symptom complex.
But to leave the subject mercury unexplored as a cause of illness (mental or physical), just because the law has difficulty finding specific connections that hold up in a court of law, must not be the reason for inaction. With mercury there is always the likelihood of reasonable doubt about who gave it to the baby or the child or the mother. Was it the doctor, the dentist, the fisherman, the painter or mother earth?
The bottom line is: Mercury is poisonous. Mercury is known to cause toxicity. Therefore companies and agencies that knowingly put or leave mercury in their products should be required to remove it or else be held accountable for exposing people to it whether there is proof of damage or not. Any product should be clearly labeled for mercury. Any doctor should state that he is injecting mercury with the vaccines, even if there are only traces. Water companies should not be allowed to state that mercury is non-detectable when, in fact, it is. The law has no trouble labeling heroin or marijuana prohibited substances. The only difference is that those substances are taken voluntarily, and for pleasure, to boot. Mercury is known to be a far greater poison than those controlled substances. Why is mercury protected? Mercury is a money-maker and it keeps physicians, pharmaceutical companies, psychiatrists and dentist in business.
It seems so convenient to excuse mercury from scrutiny because it has been applied to the human body for such a long time. It seems so sonvenient that good studies cannot be done to establish a clear-cut cause and effect scenario because mercury has already been dispensed for millennia. But since mercury is poisonous in very small quantities and attacks cells, the only necessity for proof of effect is its presence in human tissues or fluids. It doesn't take much to kill cells. If it can be detected, it is likely to be harmful.
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34.) Pathogenic gut bacteria:
A. Facilitate Hg excretion B. Facilitate Hg absorption C. Protect the host in a commensal symbiotic manner D. Convert inorganic Hg forms to more potent organic forms
https://iabdm.org/wp-content/uploads/2012/04/mildent_hg.pdf
MERCURY FILLINGS Special Report: 10 Reasons to Avoid Mercury Fillings 3 They expand over time and result in tooth breakage This results in the need for further treatment such as a crown or extraction. The expansion of the filling is readily acknowledged by all dentists. Of this, there is no disagreement. The pressures that are exerted in an outward direction are great against the tooth which is, for the most part, an unyielding structure. The expansion is ongoing and relentless. The first thing that usually occurs then is a small fracture that helps to relieve the pressures and stresses of the expanding mass. This compromises the structural integrity of the tooth itself, rendering it more susceptible to overt fracture. Add to this situation normal wear and tear and you have a condition where the tooth can more readily fracture in an overt manner. The feeling you have when this happens is that there can be pressure upon biting that is relieved upon the release of the bite. They release mercury vapor continuously The vapor is absorbed by the oral tissues as well as your nose. For years, the formal body known as the American Dental Association (ADA) asserted that the mercury in the fillings were bound tightly together and that there was no “leakage”. This myth was promulgated for several decades because technology did not exist to prove otherwise. Eventually, the vapor was able to be readily visualized emanating from a filling with the use of a black light. In fact, there is a video from the International Academy of Oral Medicine and Toxicology that demonstrates this phenomenon quite clearly, to even a casual observer. Mercury can also be demonstrated coming off a filling while in the mouth through the use of a Mercury Vapor Analyzer. This device is used today, in industry, to detect unsafe levels of mercury in the ambient air in a particular space. To detect it in the mouth, the probe is placed into the mouth and a reading is obtained. You are then given some paraffin wax to chew for about 60-90 seconds. Then, another reading is obtained. This illustrates then that they are indeed exposing themselves to mercury vapor every time you chew. Acidic foods (i.e. vinegars, pickles, etc.) accelerate the amount of mercury vapor being liberated from the surface of the fillings. Special Report: 10 Reasons to Avoid Mercury Fillings 4 Mercury creates a battery effect in your mouth It is known as oral galvanism. The high school science definition of a battery is having 2 dissimilar metals in the presence of an electrolyte. For you non-science people, just know that a mercury filling has at least 5 metals in it and you have in your saliva: calcium, sodium, chloride, potassium, and a whole bunch of other elements in the solution. So as you can see, you create a battery. You may have experienced this by touching a metal filling with a fork. You will get a decided metallic taste in your mouth. This is a great example of oral galvanism. This is present all the time if you have any metals present in your mouth. For those that have metal fillings, some type of malady (disease) may occur related to this phenomenon. Constituents migrate out of the filling They can “plate out” resulting in what is called an amalgam tattoo (see photos to left). These spots can be either quite small or almost invisible due to size or location. They may be barely visible to the eye or they can be HUGE and visible to even a casual observer. However, they can also migrate elsewhere with grave consequences. Mercury causes brain changes “Neurofibrilar tangles” (essentially, warped fibers) are considered the hallmark finding of an Alzheimer’s victim’s brain, as seen on an autopsy. According to Dr. Boyd Haley, Chemistry Professor Emeritus and Mercury researcher of the University of Tennessee, neurofibrilar tangles are present in 100% of cases. The only substance known to cause this is mercury. There is a molecule in our body known as Apo lipoprotein. There are different variations of this molecule but 3 major versions that we must pay attention to. Two of these versions are coded with the genes for binding mercury in the body. The third one does not bind mercury at all. Studies have shown that an Alzheimer’s victim will have only the version that does not bind mercury. This means that you have an extremely high chance of having Alzheimer ’s disease if you have what is known as the ApoE-4 Allele. You must take extra steps to bind this heavy metal in your body for your brain health. BEFORE AFTER 350
Mercury helps in the creation of antibiotic resistant superbugs in the gut Because the mercury has been present for so long, bugs in the gut have become adapted to the forms of mercury that would have killed them in the past. Now with Superbugs in the news on a regular basis, one has to ask why we keep poisoning ourselves and setting ourselves up for failure. These fillings contain approximately 50% mercury, the most powerful neurotoxin As of 2015, mercury is roughly 50% (by volume) the filling material. Mercury has the unique property, as it is a liquid, which other metals will dissolve into. The proportions worked out decades ago puts the mercury content at about 50%, while the others metals: Silver (35%), Tin (9%) Copper (6%) Zinc (trace). All values are approximate. Mercury fillings are the only filling authorized by some government agencies In spite of the availability of alternative materials that do not contain mercury, it has been memorialized in and around the world. Some countries in Europe have banned it but most take the lead from the US. Due to the mythology of the materials and the lobbying power of the insurance companies and the American Dental Association, mercury fillings live on and on.
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35.) What biological pathways, structures and/or chemicals are blocked by Hg?
A. Neurotransmitters B. Enzymes C. Mitochondria D. All of the above
https://iabdm.org/education/articles/
Biological Dental Medicine: Changing Lives A selection of patient comments on working with a biological dentist to improve their oral and overall health and well-being… Could a Root Canal Be the Cause of Your Chronic Health Problem? Root canal treated teeth may harbor harmful microbes, the toxic metabolic waste products of which can have systemic health impacts and contribute to a variety of chronic diseases. The Netflix documentary “Root Cause” investigates these issues, interviewing doctors and dentists around the world, including yours truly (although briefly), who believe many health problems can be traced back to these infected teeth... Why Is It Called "Biological" Dentistry Anyway? You often hear “holistic dentistry,” “integrative dentistry” and “biological dentistry” used interchangeably. They’re not actually the same thing. Biological dentistry is holistic and integrative, but in and of themselves, neither holistic nor integrated is biological. For the why, you have to go back to when the term was originally coined – back in the mid- 1980s... I Was Poisoned by My Teeth, excerpt This excerpt from Dr. Gloria Gilbere's I Was Poisoned by My Teeth focuses on infant oral health, with special emphasis on fluoride and fluoridation. Shared with permission. Fluoride Ingestion: Connecting the Dots A must-read position paper on fluoridation by toxicologist Steve Gilbert, PhD, of the Institute of Neurotoxicology & Neurological Disorders. Shared with permission. Fluoridation's Neurotoxicity An essential position statement from the Fluoride Action Network on the neurotoxic risks of ingesting fluoridated water. 352
10 Reasons to Avoid Mercury Fillings In this report you will find multiple reasons why you will not want to have mercury fillings in your teeth or those of your loved ones. Mercury fillings are an archaic practice from the past and do not belong in dental practice today, especially considering there are more aesthetic and non-toxic options readily available. Mercury & Human Health: A Comprehensive Bibliography, 2003 - 2009 40 Years of Electro Acupuncture According to Voll (EAV) A summary of studies and scientific publications by Bernhard A. Weber (Marburg). Important Vitamins Help Reducing Gum Disease Risk Information concerning a new study from Journal of Dental Research on periodontal disease by using Vitamin E and C. Are Dental X-rays Harmful? A collection of articles to assist in education about the concern of the safety of dental xrays and radiation exposure. Chelation Therapy: Stepping Into the Next 60 Years (A Historical Commentary) By John Trowbridge, MD, FACAM (from the Townsend Letter, April 2013) “Mind-body medicine,” a term well known in medicine, has major roots in observations made in the 1960s by one of my lab directors at Stanford, George Solomon, M.D. Intensive study of the “relaxation response,” “healing touch,” “acupuncture,” and similar “soft science” technologies has led to widespread acceptance in the medical and lay communities. At about the same time, startling observations were being made of reversals of increasingly prevalent coronary and peripheral vascular maladies by chelation therapy with intravenous EDTA. Despite “hard science” showing that these beneficial discoveries have been replicated time and again, chelation remains largely unknown or, at worst, vigorous defiled. Has the Dental Work in Your Mouth Turned You into a Walking Antenna? By Lina Garcia, DDS, DMD We should not overlook the impact of metal dental work, electromagnetic and microwave-attracting stress on the increasing prevalence of chronic illness in our 353
society. "I strongly suspect," writes Dr. Garcia, "that this is an unrecognized source of insidious stress on our physical, mental, and emotional health." Root Canals Are Dead Bodies By Dr. Ronald Carlson Root canals are dead bodies - and as such, should be buried six feet below Earth’s surface! The Microbiology of the Acute Dental Abscess By D. Robertson & A.J. Smith (from the Journal of Medical Microbiology) The microbiology and treatment of the acute localized abscess and severe spreading odontogenic infections are reviewed. Circulation of Lymph in the Dentinal Tubules with some Observations on the Metabolism of the Dentine By E. W. Fish, MD, ChB, LDS (From the Department of Bio-Chemistry and Physiology, University College, London. 1926) Endodontic-Endotoxemia: Our Current Dilemma By Dr. Ronald Carlson The author’s research on the oral systemic linkage to good and enduring health reveals the potential deleterious effects of “modern root canal therapy” and “implant dentistry.” Be Part of Dentistry’s Green Future By Ina Pockrass, Co-Founder, Eco-Dentistry Association How to be part of dentistry’s clean, green and highly profitable future by embracing abundant high technology and good old common sense.
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36.) Hg can cause a hyper sensitization of the hosts immune system. What test can detect this body response?
A. MELISA B. Serum Compatibility Test C. EAV https://www.ncbi.nlm.nih.gov/pubmed/3457765 http://www.melisa.org/testing/
Hypersensitivity to mercury, nickel and chromium in relation to dental materials. Burrows D. Abstract Three metals which are used in dental materials are recognized as causing sensitization sufficiently frequently to consider whether problems might arise from their use in dentistry. These metals are, mercury, nickel and chromium. Nickel is by far the commonest sensitizer, 10 per cent of women are allergic to nickel; sensitization usually occurs through jewellery or fasteners on articles of clothing. Chromium (as chromate) is a much less common sensitizer for several reasons. Sensitization only occurs through hexavalent salts of chromate and the degree of exposure of humans to these salts is much less than to either nickel or mercury. The true incidence of mercury sensitization is difficult to ascertain because many of the materials which were used for patch testing previously and on which statistics were based, contained unnecessarily high concentrations of mercury, and the pattern of mercury allergy is changing because many substances which contain mercury and were used frequently are not now employed. Although metallic mercury can sensitize the evidence would suggest that if dental amalgams ever cause people to become allergic to mercury, it is an extremely rare occurrence. Problems with mercury-containing amalgams in those sensitized are also rare, only 28 cases have been recorded in the literature. Thus, it is likely that at the present time sensitization to mercury is uncommon and decreasing. There is even less evidence that nickel or chromate in dental materials actively sensitize and it is exceptionally rare to have problems with these metals in a prosthesis in someone who is already sensitized.(ABSTRACT TRUNCATED AT 250 WORDS).
Metal allergy – a possible cause of health problems 355
People with metal hypersensitivity may have numerous symptoms associated with an overactive immune system, including chronic fatigue, joint and muscle pain, cognitive impairment, depression, headaches, fibromyalgia and skin rashes. MELISA is a scientifically proven and clinically validated blood test that detects type-IV allergy to multiple metals, such as mercury, gold, palladium and titanium.(1) Why use MELISA? Exposure to metals in dental fillings and crowns, surgical implants, joint prostheses and environmental pollutants can lead to health problems in sensitive individuals (if they cause an allergic reaction). MELISA can identify the individuals who may suffer side effects from metal exposure. The test indicates which metals the immune system will tolerate and which will cause an immune reaction. This information may be useful prior to surgery or to dental work to establish the optimal type of materials the body will tolerate. High success rates Seventy-six percent of chronic fatigue patients in a clinical trial experienced health improvement after removing dental restorations containing allergenic metals, as identified by the MELISA test (2). An additional study of patients with autoimmune diseases showed that 71% of those with positive responses in MELISA improved after having their fillings removed (3). In a further study, patients with fibromyalgia were tested for allergy to metals with MELISA. By reducing their exposure to metals identified as problematic, significant health benefits were seen. 50% of patients no longer fulfilled the criteria for fibromyalgia diagnosis; the remaining 50% all reported an improvement in their symptoms (4). Allergy vs. toxicity MELISA measures whether the immune system reacts to specific metals: it does not measure the levels of metals in the body. Other tests, such as hair analysis, quantify excreted or current levels of mercury or other metals, but these are usually found to be below the official “safe limit”. For hypersensitive individuals, there may be no “safe” level; even trace amounts may trigger symptoms if the immune system reacts (5). This reaction will be on-going unless the source of exposure is removed. Metal allergy and orthopaedics Metal allergy is a well-documented factor in the failure of implants. The need for allergy testing in sensitive patients is recognized by both implant manufacturers and by surgeons alike. The prevalence of metal hypersensitivity in patients with implants is significantly higher than in the general population, with an even higher prevalence rate among patients with failing implanted devices (6). Studies show that lymphocyte transformation tests are better suited for diagnosing possible metal sensitivity in patients with implants than traditional patch testing (7). Implant-related hypersensitivity reactions are mediated by sensitized T cells and the relationship between skin hypersensitivity and systemic hypersensitivity is ill defined. Lack of standardization, subjective evaluation and irritative reactions also contribute to reduced reliability. MELISA is particularly useful in diagnosing titanium allergy The Mayo clinic found no positive reactions to titanium in over a decade of patch testing despite many published cases of titanium allergy (8). In a 2006 study, 56 symptomatic patients exposed to titanium through dental implants were tested with MELISA. Of the 56 patients tested, 21 (37.5%) were positive to titanium. Conversely all patients were patch test negative to titanium. Following the removal of titanium implants in hypersensitive patients showed remarkable clinical improvement (9). It is important to remember that traces of other metals such as nickel and aluminium are found even in commercially pure titanium due to the production process (5, 10). 356
Recent studies have shown that allergy to the constituents in bone cements (11, 12) may be a causal factor in joint failure. MELISA is able to test for certain constituents of bone cements to determine whether an individual is hypersensitive. Additional uses Lyme Disease: MELISA testing is has been clinically validated for the diagnosis of Lyme disease (13). MELISA testing is a particularly useful tool in diagnosing Lyme in serologically and clinically unclear cases (14). Gluten: An additional application for MELISA is in furthering the diagnosis of non-coeliac gluten sensitivity. How the MELISA test works MELISA tests the patient’s white blood cells against a panel of suspected allergens based on the patient’s medical and dental history. The reaction is measured by two separate methods: uptake of radioisotope by dividing lymphocytes and evaluation by microscope. The test report shows the strength of the reaction as a Stimulation Index and lists the most common sources of exposure. How to get tested Before testing it is helpful to establish which metals the patient is currently exposed to. A pre-test questionnaire can be used to establish this. A blood sample may be sent to any licensed MELISA laboratory as long as it arrives within 48 hours (ideally 24). The blood should be kept at room temperature and sent in special tubes, which will be provided by the lab. The amount of blood required depends on how many antigens are to be tested. For a screening of 10 metals, 36 ml blood, or 4 large tubes of blood, is needed. Steroids or other immuno-suppressant drugs may affect the test result, as well as any ongoing systemic infections (Staphylococcus etc).
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37.) Mercury has a strong bacteriostatic effect:
A. True B. False
https://jamanetwork.com/journals/jama/article-abstract/298167 https://courses.lumenlearning.com/microbiology/chapter/using-chemicals-to-control-microorganisms/
Using Chemicals to Control Microorganisms LEARNING OBJECTIVES
• Understand and compare various chemicals used to control microbial growth, including their uses, advantages and disadvantages, chemical structure, and mode of action In addition to physical methods of microbial control, chemicals are also used to control microbial growth. A wide variety of chemicals can be used as disinfectants or antiseptics. When choosing which to use, it is important to consider the type of microbe targeted; how clean the item needs to be; the disinfectant’s effect on the item’s integrity; its safety to animals, humans, and the environment; its expense; and its ease of use. This section describes the variety of chemicals used as disinfectants and antiseptics, including their mechanisms of action and common uses.
Phenolics In the 1800s, scientists began experimenting with a variety of chemicals for disinfection. In the 1860s, British surgeon Joseph Lister (1827–1912) began using carbolic acid, known as phenol, as a disinfectant for the treatment of surgical wounds (see Foundations of Modern Cell Theory). In 1879, Lister’s work inspired the American chemist Joseph Lawrence (1836– 1909) to develop Listerine, an alcohol-based mixture of several related compounds that is still used today as an oral antiseptic. Today, carbolic acid is no longer used as a surgical disinfectant because it is a skin irritant, but the chemical compounds found in antiseptic mouthwashes and throat lozenges are called phenolics. Chemically, phenol consists of a benzene ring with an –OH group, and phenolics are compounds that have this group as part of their chemical structure. Phenolics such as thymol and eucalyptol occur naturally in plants. Other phenolics can be derived from creosote, a component of coal tar. Phenolics tend to be stable, persistent on surfaces, and less toxic than phenol. They inhibit microbial growth by denaturing proteins and disrupting membranes.
Figure 1. Phenol and phenolic compounds have been used to control microbial growth. (a) Chemical structure of phenol, also known as carbolic acid. (b) o-Phenylphenol, a type of phenolic, has been used as a disinfectant as well as to control bacterial and fungal growth on harvested citrus fruits. (c) Hexachlorophene, another phenol, known as a bisphenol (two rings), is the active ingredient in pHisoHex.
Since Lister’s time, several phenolic compounds have been used to control microbial growth. Phenolics like cresols (methylated phenols) and o-phenylphenol were active ingredients in various formulations of Lysol since its invention in 1889. o-Phenylphenol was also commonly 358
used in agriculture to control bacterial and fungal growth on harvested crops, especially citrus fruits, but its use in the United States is now far more limited. The bisphenol hexachlorophene, a disinfectant, is the active ingredient in pHisoHex, a topical cleansing detergent widely used for handwashing in hospital settings. pHisoHex is particularly effective against gram-positive bacteria, including those causing staphylococcal and streptococcal skin infections. pHisoHex was formerly used for bathing infants, but this practice has been discontinued because it has been shown that exposure to hexachlorophene can lead to neurological problems. Triclosan is another bisphenol compound that has seen widespread application in antibacterial products over the last several decades. Initially used in toothpastes, triclosan is now commonly used in hand soaps and is frequently impregnated into a wide variety of other products, including cutting boards, knives, shower curtains, clothing, and concrete, to make them antimicrobial. It is particularly effective against gram-positive bacteria on the skin, as well as certain gram-negative bacteria and yeasts.[1]
TRICLOSAN: ANTIBACTERIAL OVERKILL? Hand soaps and other cleaning products are often marketed as “antibacterial,” suggesting that they provide a level of cleanliness superior to that of conventional soaps and cleansers. But are the antibacterial ingredients in these products really safe and effective? About 75% of antibacterial liquid hand soaps and 30% of bar soaps contain the chemical triclosan, a phenolic.[2] Triclosan blocks an enzyme in the bacterial fatty acid-biosynthesis pathway that is not found in the comparable human pathway. Although the use of triclosan in the home increased dramatically during the 1990s, more than 40 years of research by the FDA have turned up no conclusive evidence that washing with triclosan-containing products provides increased health benefits compared with washing with traditional soap. Although some studies indicate that fewer bacteria may remain on a person’s hands after washing with triclosan-based soap, compared with traditional soap, no evidence points to any reduction in the transmission of bacteria that cause respiratory and gastrointestinal illness. In short, soaps with triclosan may remove or kill a few more germs but not enough to reduce the spread of disease. Perhaps more disturbing, some clear risks associated with triclosan-based soaps have come to light. The widespread use of triclosan has led to an increase in triclosan-resistant bacterial strains, including those of clinical importance, such as Salmonella enterica; this resistance may render triclosan useless as an antibacterial in the long run.[3][4] Bacteria can easily gain resistance to triclosan through a change to a single gene encoding the targeted enzyme in the bacterial fatty acid-synthesis pathway. Other disinfectants with a less specific mode of action are much less prone to engendering resistance because it would take much more than a single genetic change. Use of triclosan over the last several decades has also led to a buildup of the chemical in the environment. Triclosan in hand soap is directly introduced into wastewater and sewage systems as a result of the handwashing process. There, its antibacterial properties can inhibit or kill bacteria responsible for the decomposition of sewage, causing septic systems to clog and back up. Eventually, triclosan in wastewater finds its way into surface waters, streams, lakes, sediments, and soils, disrupting natural populations of bacteria that carry out important environmental functions, such as inhibiting algae. Triclosan also finds its way into the bodies of amphibians and fish, where it can act as an endocrine disruptor. Detectable levels of triclosan have also been found in various human bodily fluids, including breast milk, plasma, and 359
urine.[5] In fact, a study conducted by the CDC found detectable levels of triclosan in the urine of 75% of 2,517 people tested in 2003–2004.[6] This finding is even more troubling given the evidence that triclosan may affect immune function in humans.[7] In December 2013, the FDA gave soap manufacturers until 2016 to prove that antibacterial soaps provide a significant benefit over traditional soaps; if unable to do so, manufacturers will be forced to remove these products from the market.
Figure 2. Triclosan is a common ingredient in antibacterial soaps despite evidence that it poses environmental and health risks and offers no significant health benefit compared to conventional soaps. (credit b, c: modification of work by FDA)
THINK ABOUT IT
• Why is triclosan more like an antibiotic than a traditional disinfectant? Heavy Metals Some of the first chemical disinfectants and antiseptics to be used were heavy metals. Heavy metals kill microbes by binding to proteins, thus inhibiting enzymatic activity. Heavy metals are oligodynamic, meaning that very small concentrations show significant antimicrobial activity. Ions of heavy metals bind to sulfur-containing amino acids strongly and bioaccumulate within cells, allowing these metals to reach high localized concentrations. This causes proteins to denature. Heavy metals are not selectively toxic to microbial cells. They may bioaccumulate in human or animal cells, as well, and excessive concentrations can have toxic effects on humans. If too much silver accumulates in the body, for example, it can result in a condition called argyria, in which the skin turns irreversibly blue-gray. One way to reduce the potential toxicity of heavy metals is by carefully controlling the duration of exposure and concentration of the heavy metal.
Figure 3. Heavy metals denature proteins, impairing cell function and, thus, giving them strong antimicrobial properties. (a) Copper in fixtures like this door handle kills microbes that otherwise might accumulate on frequently touched surfaces. (b) Eating utensils contain small amounts of silver to inhibit microbial growth. (c) Copper commonly lines incubators to minimize contamination of cell cultures stored inside. (d) Antiseptic mouthwashes commonly contain zinc chloride. (e) This patient is suffering from argyria, an irreversible condition caused by bioaccumulation of silver in the body. (credit b: modification of work by “Shoshanah”/Flickr; credit e: modification of work by Herbert L. Fred and Hendrik A. van Dijk)
Mercury Mercury is an example of a heavy metal that has been used for many years to control microbial growth. It was used for many centuries to treat syphilis. Mercury compounds like mercuric 360
chloride are mainly bacteriostatic and have a very broad spectrum of activity. Various forms of mercury bind to sulfur-containing amino acids within proteins, inhibiting their functions. In recent decades, the use of such compounds has diminished because of mercury’s toxicity. It is toxic to the central nervous, digestive, and renal systems at high concentrations, and has negative environmental effects, including bioaccumulation in fish. Topical antiseptics such as mercurochrome, which contains mercury in low concentrations, and merthiolate, a tincture (a solution of mercury dissolved in alcohol) were once commonly used. However, because of concerns about using mercury compounds, these antiseptics are no longer sold in the United States.
Silver Silver has long been used as an antiseptic. In ancient times, drinking water was stored in silver jugs.[8] Silvadene cream is commonly used to treat topical wounds and is particularly helpful in preventing infection in burn wounds. Silver nitrate drops were once routinely applied to the eyes of newborns to protect against ophthalmia neonatorum, eye infections that can occur due to exposure to pathogens in the birth canal, but antibiotic creams are more now commonly used. Silver is often combined with antibiotics, making the antibiotics thousands of times more effective.[9] Silver is also commonly incorporated into catheters and bandages, rendering them antimicrobial; however, there is evidence that heavy metals may also enhance selection for antibiotic resistance.[10]
Copper, Nickel, and Zinc Several other heavy metals also exhibit antimicrobial activity. Copper sulfate is a common algicide used to control algal growth in swimming pools and fish tanks. The use of metallic copper to minimize microbial growth is also becoming more widespread. Copper linings in incubators help reduce contamination of cell cultures. The use of copper pots for water storage in underdeveloped countries is being investigated as a way to combat diarrheal diseases. Copper coatings are also becoming popular for frequently handled objects such as doorknobs, cabinet hardware, and other fixtures in health-care facilities in an attempt to reduce the spread of microbes. Nickel and zinc coatings are now being used in a similar way. Other forms of zinc, including zinc chloride and zinc oxide, are also used commercially. Zinc chloride is quite safe for humans and is commonly found in mouthwashes, substantially increasing their length of effectiveness. Zinc oxide is found in a variety of products, including topical antiseptic creams such as calamine lotion, diaper ointments, baby powder, and dandruff shampoos.
THINK ABOUT IT
• Why are many heavy metals both antimicrobial and toxic to humans? Halogens Other chemicals commonly used for disinfection are the halogens iodine, chlorine, and fluorine. Iodine works by oxidizing cellular components, including sulfur-containing amino acids, nucleotides, and fatty acids, and destabilizing the macromolecules that contain these molecules. It is often used as a topical tincture, but it may cause staining or skin irritation. An iodophor is a compound of iodine complexed with an organic molecule, thereby increasing iodine’s stability and, in turn, its efficacy. One common iodophor is povidone-iodine, which includes a wetting 361
agent that releases iodine relatively slowly. Betadine is a brand of povidone-iodine commonly used as a hand scrub by medical personnel before surgery and for topical antisepsis of a patient’s skin before incision.
Figure 4. (a) Betadine is a solution of the iodophor povidone-iodine. (b) It is commonly used as a topical antiseptic on a patient’s skin before incision during surgery. (credit b: modification of work by Andrew Ratto) Chlorine is another halogen commonly used for disinfection. When chlorine gas is mixed with water, it produces a strong oxidant called hypochlorous acid, which is uncharged and enters cells easily. Chlorine gas is commonly used in municipal drinking water and wastewater treatment plants, with the resulting hypochlorous acid producing the actual antimicrobial effect. Those working at water treatment facilities need to take great care to minimize personal exposure to chlorine gas. Sodium hypochlorite is the chemical component of common household bleach, and it is also used for a wide variety of disinfecting purposes. Hypochlorite salts, including sodium and calcium hypochlorites, are used to disinfect swimming pools. Chlorine gas, sodium hypochlorite, and calcium hypochlorite are also commonly used disinfectants in the food processing and restaurant industries to reduce the spread of foodborne diseases. Workers in these industries also need to take care to use these products correctly to ensure their own safety as well as the safety of consumers. A recent joint statement published by the Food and Agriculture Organization (FAO) of the United Nations and WHO indicated that none of the many beneficial uses of chlorine products in food processing to reduce the spread of foodborne illness posed risks to consumers.[11]
Another class of chlorinated compounds called chloramines are widely used as disinfectants. Chloramines are relatively stable, releasing chlorine over long periods time. Chloramines are derivatives of ammonia by substitution of one, two, or all three hydrogen atoms with chlorine atoms.
Figure 5. Monochloroamine, one of the chloramines, is derived from ammonia by the replacement of one hydrogen atom with a chlorine atom. Chloramines and other cholorine compounds may be used for disinfection of drinking water, and chloramine tablets are frequently used by the military for this purpose. After a natural disaster or other event that compromises the public water supply, the CDC recommends disinfecting tap water by adding small amounts of regular household bleach. Recent research suggests that sodium dichloroisocyanurate (NaDCC) may also be a good alternative for drinking water disinfection. Currently, NaDCC tablets are available for general use and for use by the military, campers, or those with emergency needs; for these uses, NaDCC is preferable to chloramine tablets. Chlorine dioxide, a gaseous agent used for fumigation and sterilization of enclosed areas, is also commonly used for the disinfection of water. 362
Although chlorinated compounds are relatively effective disinfectants, they have their disadvantages. Some may irritate the skin, nose, or eyes of some individuals, and they may not completely eliminate certain hardy organisms from contaminated drinking water. The fungus Cryptosporidium, for example, has a protective outer shell that makes it resistant to chlorinated disinfectants. Thus, boiling of drinking water in emergency situations is recommended when possible. The halogen fluorine is also known to have antimicrobial properties that contribute to the prevention of dental caries (cavities).[12] Fluoride is the main active ingredient of toothpaste and is also commonly added to tap water to help communities maintain oral health. Chemically, fluoride can become incorporated into the hydroxyapatite of tooth enamel, making it more resistant to corrosive acids produced by the fermentation of oral microbes. Fluoride also enhances the uptake of calcium and phosphate ions in tooth enamel, promoting remineralization. In addition to strengthening enamel, fluoride also seems to be bacteriostatic. It accumulates in plaque-forming bacteria, interfering with their metabolism and reducing their production of the acids that contribute to tooth decay.
THINK ABOUT IT
• What is a benefit of a chloramine over hypochlorite for disinfecting? Alcohols Alcohols make up another group of chemicals commonly used as disinfectants and antiseptics. They work by rapidly denaturing proteins, which inhibits cell metabolism, and by disrupting membranes, which leads to cell lysis. Once denatured, the proteins may potentially refold if enough water is present in the solution. Alcohols are typically used at concentrations of about 70% aqueous solution and, in fact, work better in aqueous solutions than 100% alcohol solutions. This is because alcohols coagulate proteins. In higher alcohol concentrations, rapid coagulation of surface proteins prevents effective penetration of cells. The most commonly used alcohols for disinfection are ethyl alcohol (ethanol) and isopropyl alcohol (isopropanol, rubbing alcohol). Alcohols tend to be bactericidal and fungicidal, but may also be viricidal for enveloped viruses only. Although alcohols are not sporicidal, they do inhibit the processes of sporulation and germination. Alcohols are volatile and dry quickly, but they may also cause skin irritation because they dehydrate the skin at the site of application. One common clinical use of alcohols is swabbing the skin for degerming before needle injection. Alcohols also are the active ingredients in instant hand sanitizers, which have gained popularity in recent years. The alcohol in these hand sanitizers works both by denaturing proteins and by disrupting the microbial cell membrane, but will not work effectively in the presence of visible dirt.
Last, alcohols are used to make tinctures with other antiseptics, such as the iodine tinctures discussed previously in this chapter. All in all, alcohols are inexpensive and quite effective for the disinfection of a broad range of vegetative microbes. However, one disadvantage of alcohols is their high volatility, limiting their effectiveness to immediately after application.
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Figure 6. (a) Ethyl alcohol, the intoxicating ingredient found in alcoholic drinks, is also used commonly as a disinfectant. (b) Isopropyl alcohol, also called rubbing alcohol, has a related molecular structure and is another commonly used disinfectant. (credit a photo: modification of work by D Coetzee; credit b photo: modification of work by Craig Spurrier)
THINK ABOUT IT
• Name at least three advantages of alcohols as disinfectants. • Describe several specific applications of alcohols used in disinfectant products. Surfactants Surface-active agents, or surfactants, are a group of chemical compounds that lower the surface tension of water. Surfactants are the major ingredients in soaps and detergents. Soaps are salts of long-chain fatty acids and have both polar and nonpolar regions, allowing them to interact with polar and nonpolar regions in other molecules. They can interact with nonpolar oils and grease to create emulsions in water, loosening and lifting away dirt and microbes from surfaces and skin. Soaps do not kill or inhibit microbial growth and so are not considered antiseptics or disinfectants. However, proper use of soaps mechanically carries away microorganisms, effectively degerming a surface. Some soaps contain added bacteriostatic agents such as triclocarban or cloflucarban, compounds structurally related to triclosan, that introduce antiseptic or disinfectant properties to the soaps.
Figure 7. Soaps are the salts (sodium salt in the illustration) of fatty acids and have the ability to emulsify lipids, fats, and oils by interacting with water through their hydrophilic heads and with the lipid at their hydrophobic tails. Soaps, however, often form films that are difficult to rinse away, especially in hard water, which contains high concentrations of calcium and magnesium mineral salts. Detergents contain synthetic surfactant molecules with both polar and nonpolar regions that have strong cleansing activity but are more soluble, even in hard water, and, therefore, leave behind no soapy deposits. Anionic detergents, such as those used for laundry, have a negatively charged anion at one end attached to a long hydrophobic chain, whereas cationic detergents have a positively charged cation instead. Cationic detergents include an important class of disinfectants and antiseptics called the quaternary ammonium salts (quats), named for the characteristic quaternary nitrogen atom that confers the positive charge. Overall, quats have properties similar to phospholipids, having hydrophilic and hydrophobic ends. As such, quats have the ability to insert into the bacterial phospholipid bilayer and disrupt membrane integrity. The cationic charge of quats appears to confer their antimicrobial properties, which are diminished when neutralized. Quats have several useful properties. They are stable, nontoxic, inexpensive, colorless, odorless, and tasteless. They tend to be bactericidal by disrupting membranes. They are also active against fungi, protozoans, and enveloped viruses, but endospores are unaffected. In clinical settings, they may be used as antiseptics or to disinfect surfaces. Mixtures of quats are also commonly found in household cleaners and disinfectants, including many current formulations of Lysol brand products, which contain benzalkonium chlorides as the active ingredients. Benzalkonium chlorides, along with the quat cetylpyrimidine chloride, are also found in products such as skin antiseptics, oral rinses, and mouthwashes. 364
Figure 8. (a) Two common quats are benzylalkonium chloride and cetylpyrimidine chloride. Note the hydrophobic nonpolar carbon chain at one end and the nitrogen-containing cationic component at the other end. (b) Quats are able to infiltrate the phospholipid plasma membranes of bacterial cells and disrupt their integrity, leading to death of the cell.
THINK ABOUT IT
• Why are soaps not considered disinfectants? HANDWASHING THE RIGHT WAY Handwashing is critical for public health and should be emphasized in a clinical setting. For the general public, the CDC recommends handwashing before, during, and after food handling; before eating; before and after interacting with someone who is ill; before and after treating a wound; after using the toilet or changing diapers; after coughing, sneezing, or blowing the nose; after handling garbage; and after interacting with an animal, its feed, or its waste. Figure 9 illustrates the five steps of proper handwashing recommended by the CDC. Handwashing is even more important for health-care workers, who should wash their hands thoroughly between every patient contact, after the removal of gloves, after contact with bodily fluids and potentially infectious fomites, and before and after assisting a surgeon with invasive procedures. Even with the use of proper surgical attire, including gloves, scrubbing for surgery is more involved than routine handwashing. The goal of surgical scrubbing is to reduce the normal microbiota on the skin’s surface to prevent the introduction of these microbes into a patient’s surgical wounds. There is no single widely accepted protocol for surgical scrubbing. Protocols for length of time spent scrubbing may depend on the antimicrobial used; health-care workers should always check the manufacturer’s recommendations. According to the Association of Surgical Technologists (AST), surgical scrubs may be performed with or without the use of brushes.
Figure 9. (a) The CDC recommends five steps as part of typical handwashing for the general public. (b) Surgical scrubbing is more extensive, requiring scrubbing starting from the fingertips, extending to the hands and forearms, and then up beyond the elbows, as shown here. (credit a: modification of work by World Health Organization)
To learn more about proper handwashing, visit the CDC’s website. Bisbiguanides Bisbiguanides were first synthesized in the 20th century and are cationic (positively charged) molecules known for their antiseptic properties. One important bisbiguanide antiseptic is chlorhexidine. It has broad-spectrum activity against yeasts, gram-positive bacteria, and gram- negative bacteria, with the exception of Pseudomonas aeruginosa, which may develop resistance on repeated exposure.[13] Chlorhexidine disrupts cell membranes and is 365
bacteriostatic at lower concentrations or bactericidal at higher concentrations, in which it actually causes the cells’ cytoplasmic contents to congeal. It also has activity against enveloped viruses. However, chlorhexidine is poorly effective against Mycobacterium tuberculosis and nonenveloped viruses, and it is not sporicidal. Chlorhexidine is typically used in the clinical setting as a surgical scrub and for other handwashing needs for medical personnel, as well as for topical antisepsis for patients before surgery or needle injection. It is more persistent than iodophors, providing long-lasting antimicrobial activity. Chlorhexidine solutions may also be used as oral rinses after oral procedures or to treat gingivitis. Another bisbiguanide, alexidine, is gaining popularity as a surgical scrub and an oral rinse because it acts faster than chlorhexidine.
Figure 10. The bisbiguanides chlorhexadine and alexidine are cationic antiseptic compounds commonly used as surgical scrubs.
THINK ABOUT IT
• What two effects does chlorhexidine have on bacterial cells? Alkylating Agents The alkylating agents are a group of strong disinfecting chemicals that act by replacing a hydrogen atom within a molecule with an alkyl group (CnH2n+1), thereby inactivating enzymes and nucleic acids. The alkylating agent formaldehyde (CH2OH) is commonly used in solution at a concentration of 37% (known as formalin) or as a gaseous disinfectant and biocide. It is a strong, broad-spectrum disinfectant and biocide that has the ability to kill bacteria, viruses, fungi, and endospores, leading to sterilization at low temperatures, which is sometimes a convenient alternative to the more labor-intensive heat sterilization methods. It also cross-links proteins and has been widely used as a chemical fixative. Because of this, it is used for the storage of tissue specimens and as an embalming fluid. It also has been used to inactivate infectious agents in vaccine preparation. Formaldehyde is very irritating to living tissues and is also carcinogenic; therefore, it is not used as an antiseptic. Glutaraldehyde is structurally similar to formaldehyde but has two reactive aldehyde groups, allowing it to act more quickly than formaldehyde. It is commonly used as a 2% solution for sterilization and is marketed under the brand name Cidex. It is used to disinfect a variety of surfaces and surgical and medical equipment. However, similar to formaldehyde, glutaraldehyde irritates the skin and is not used as an antiseptic.
A new type of disinfectant gaining popularity for the disinfection of medical equipment is o- phthalaldehyde (OPA), which is found in some newer formulations of Cidex and similar products, replacing glutaraldehyde. o-Phthalaldehyde also has two reactive aldehyde groups, but they are linked by an aromatic bridge. o-Phthalaldehyde is thought to work similarly to glutaraldehyde and formaldehyde, but is much less irritating to skin and nasal passages, produces a minimal odor, does not require processing before use, and is more effective against mycobacteria.
Ethylene oxide is a type of alkylating agent that is used for gaseous sterilization. It is highly penetrating and can sterilize items within plastic bags such as catheters, disposable items in 366
laboratories and clinical settings (like packaged Petri dishes), and other pieces of equipment. Ethylene oxide exposure is a form of cold sterilization, making it useful for the sterilization of heat-sensitive items. Great care needs to be taken with the use of ethylene oxide, however; it is carcinogenic, like the other alkylating agents, and is also highly explosive. With careful use and proper aeration of the products after treatment, ethylene oxide is highly effective, and ethylene oxide sterilizers are commonly found in medical settings for sterilizing packaged materials. β-Propionolactone is an alkylating agent with a different chemical structure than the others already discussed. Like other alkylating agents, β-propionolactone binds to DNA, thereby inactivating it. It is a clear liquid with a strong odor and has the ability to kill endospores. As such, it has been used in either liquid form or as a vapor for the sterilization of medical instruments and tissue grafts, and it is a common component of vaccines, used to maintain their sterility. It has also been used for the sterilization of nutrient broth, as well as blood plasma, milk, and water. It is quickly metabolized by animals and humans to lactic acid. It is also an irritant, however, and may lead to permanent damage of the eyes, kidneys, or liver. Additionally, it has been shown to be carcinogenic in animals; thus, precautions are necessary to minimize human exposure to β-propionolactone.[14]
Figure 11. (a) Alkylating agents replace hydrogen atoms with alkyl groups. Here, guanine is alkylated, resulting in its hydrogen bonding with thymine, instead of cytosine. (b) The chemical structures of several alkylating agents.
THINK ABOUT IT
• What chemical reaction do alkylating agents participate in? • Why are alkylating agents not used as antiseptics? DIEHARD PRIONS Prions, the acellular, misfolded proteins responsible for incurable and fatal diseases such as kuru and Creutzfeldt-Jakob disease (see Viroids, Virusoids, and Prions), are notoriously difficult to destroy. Prions are extremely resistant to heat, chemicals, and radiation. They are also extremely infectious and deadly; thus, handling and disposing of prion-infected items requires extensive training and extreme caution. Typical methods of disinfection can reduce but not eliminate the infectivity of prions. Autoclaving is not completely effective, nor are chemicals such as phenol, alcohols, formalin, and β- propiolactone. Even when fixed in formalin, affected brain and spinal cord tissues remain infectious. Personnel who handle contaminated specimens or equipment or work with infected patients must wear a protective coat, face protection, and cut-resistant gloves. Any contact with skin must be immediately washed with detergent and warm water without scrubbing. The skin should then be washed with 1 N NaOH or a 1:10 dilution of bleach for 1 minute. Contaminated waste must be incinerated or autoclaved in a strong basic solution, and instruments must be cleaned and soaked in a strong basic solution. 367
For more information on the handling of animals and prion-contaminated materials, visit the guidelines published on the CDC and WHO websites. Peroxygens Peroxygens are strong oxidizing agents that can be used as disinfectants or antiseptics. The most widely used peroxygen is hydrogen peroxide (H2O2), which is often used in solution to disinfect surfaces and may also be used as a gaseous agent. Hydrogen peroxide solutions are inexpensive skin antiseptics that break down into water and oxygen gas, both of which are environmentally safe. This decomposition is accelerated in the presence of light, so hydrogen peroxide solutions typically are sold in brown or opaque bottles. One disadvantage of using hydrogen peroxide as an antiseptic is that it also causes damage to skin that may delay healing or lead to scarring. Contact lens cleaners often include hydrogen peroxide as a disinfectant. Hydrogen peroxide works by producing free radicals that damage cellular macromolecules. Hydrogen peroxide has broad-spectrum activity, working against gram-positive and gram- negative bacteria (with slightly greater efficacy against gram-positive bacteria), fungi, viruses, and endospores. However, bacteria that produce the oxygen-detoxifying enzymes catalase or peroxidase may have inherent tolerance to low hydrogen peroxide concentrations. To kill endospores, the length of exposure or concentration of solutions of hydrogen peroxide must be increased. Gaseous hydrogen peroxide has greater efficacy and can be used as a sterilant for rooms or equipment.
Figure 12. Catalase enzymatically converts highly reactive hydrogen peroxide (H2O2) into water and oxygen. Hydrogen peroxide can be used to clean wounds. Hydrogen peroxide is used to sterilize items such as contact lenses. (credit photos: modification of work by Kerry Ceszyk) Plasma, a hot, ionized gas, described as the fourth state of matter, is useful for sterilizing equipment because it penetrates surfaces and kills vegetative cells and endospores. Hydrogen peroxide and peracetic acid, another commonly used peroxygen, each may be introduced as a plasma. Peracetic acid can be used as a liquid or plasma sterilant insofar as it readily kills endospores, is more effective than hydrogen peroxide even at rather low concentrations, and is immune to inactivation by catalases and peroxidases. It also breaks down to environmentally innocuous compounds; in this case, acetic acid and oxygen.
Other examples of peroxygens include benzoyl peroxide and carbamide peroxide. Benzoyl peroxide is a peroxygen that used in acne medication solutions. It kills the bacterium Propionibacterium acnes, which is associated with acne. Carbamide peroxide, an ingredient used in toothpaste, is a peroxygen that combats oral biofilms that cause tooth discoloration and halitosis (bad breath).[15] Last, ozone gas is a peroxygen with disinfectant qualities and is used to clean air or water supplies. Overall, peroxygens are highly effective and commonly used, with no associated environmental hazard.
THINK ABOUT IT
• How do peroxides kill cells? Supercritical Fluids 368
Within the last 15 years, the use of supercritical fluids, especially supercritical carbon dioxide (scCO2), has gained popularity for certain sterilizing applications. When carbon dioxide is brought to approximately 10 times atmospheric pressure, it reaches a supercritical state that has physical properties between those of liquids and gases. Materials put into a chamber in which carbon dioxide is pressurized in this way can be sterilized because of the ability of scCO2 to penetrate surfaces.
Supercritical carbon dioxide works by penetrating cells and forming carbonic acid, thereby lowering the cell pH considerably. This technique is effective against vegetative cells and is also used in combination with peracetic acid to kill endospores. Its efficacy can also be augmented with increased temperature or by rapid cycles of pressurization and depressurization, which more likely produce cell lysis.
Benefits of scCO2 include the nonreactive, nontoxic, and nonflammable properties of carbon dioxide, and this protocol is effective at low temperatures. Unlike other methods, such as heat and irradiation, that can degrade the object being sterilized, the use of scCO2 preserves the object’s integrity and is commonly used for treating foods (including spices and juices) and medical devices such as endoscopes. It is also gaining popularity for disinfecting tissues such as skin, bones, tendons, and ligaments prior to transplantation. scCO2 can also be used for pest control because it can kill insect eggs and larvae within products.
THINK ABOUT IT
• Why is the use of supercritical carbon dioxide gaining popularity for commercial and medical uses? Chemical Food Preservatives Chemical preservatives are used to inhibit microbial growth and minimize spoilage in some foods. Commonly used chemical preservatives include sorbic acid, benzoic acid, and propionic acid, and their more soluble salts potassium sorbate, sodium benzoate, and calcium propionate, all of which are used to control the growth of molds in acidic foods. Each of these preservatives is nontoxic and readily metabolized by humans. They are also flavorless, so they do not compromise the flavor of the foods they preserve. Sorbic and benzoic acids exhibit increased efficacy as the pH decreases. Sorbic acid is thought to work by inhibiting various cellular enzymes, including those in the citric acid cycle, as well as catalases and peroxidases. It is added as a preservative in a wide variety of foods, including dairy, bread, fruit, and vegetable products. Benzoic acid is found naturally in many types of fruits and berries, spices, and fermented products. It is thought to work by decreasing intracellular pH, interfering with mechanisms such as oxidative phosphorylation and the uptake of molecules such as amino acids into cells. Foods preserved with benzoic acid or sodium benzoate include fruit juices, jams, ice creams, pastries, soft drinks, chewing gum, and pickles. Propionic acid is thought to both inhibit enzymes and decrease intracellular pH, working similarly to benzoic acid. However, propionic acid is a more effective preservative at a higher pH than either sorbic acid or benzoic acid. Propionic acid is naturally produced by some cheeses during their ripening and is added to other types of cheese and baked goods to prevent mold contamination. It is also added to raw dough to prevent contamination by the bacterium Bacillus mesentericus, which causes bread to become ropy. 369
Other commonly used chemical preservatives include sulfur dioxide and nitrites. Sulfur dioxide prevents browning of foods and is used for the preservation of dried fruits; it has been used in winemaking since ancient times. Sulfur dioxide gas dissolves in water readily, forming sulfites. Although sulfites can be metabolized by the body, some people have sulfite allergies, including asthmatic reactions. Additionally, sulfites degrade thiamine, an important nutrient in some foods. The mode of action of sulfites is not entirely clear, but they may interfere with the disulfide bond formation in proteins, inhibiting enzymatic activity. Alternatively, they may reduce the intracellular pH of the cell, interfering with proton motive force-driven mechanisms. Nitrites are added to processed meats to maintain color and stop the germination of Clostridium botulinum endospores. Nitrites are reduced to nitric oxide, which reacts with heme groups and iron-sulfur groups. When nitric oxide reacts with the heme group within the myoglobin of meats, a red product forms, giving meat its red color. Alternatively, it is thought that when nitric acid reacts with the iron-sulfur enzyme ferredoxin within bacteria, this electron transport-chain carrier is destroyed, preventing ATP synthesis. Nitrosamines, however, are carcinogenic and can be produced through exposure of nitrite-preserved meats (e.g., hot dogs, lunch meat, breakfast sausage, bacon, meat in canned soups) to heat during cooking.
Natural Chemical Food Preservatives The discovery of natural antimicrobial substances produced by other microbes has added to the arsenal of preservatives used in food. Nisin is an antimicrobial peptide produced by the bacterium Lactococcus lactis and is particularly effective against gram-positive organisms. Nisin works by disrupting cell wall production, leaving cells more prone to lysis. It is used to preserve cheeses, meats, and beverages.
Natamycin is an antifungal macrolide antibiotic produced by the bacterium Streptomyces natalensis. It was approved by the FDA in 1982 and is used to prevent fungal growth in various types of dairy products, including cottage cheese, sliced cheese, and shredded cheese. Natamycin is also used for meat preservation in countries outside the United States.
THINK ABOUT IT
• What are the advantages and drawbacks of using sulfites and nitrites as food preservatives? KEY CONCEPTS AND SUMMARY • Heavy metals, including mercury, silver, copper, and zinc, have long been used for disinfection and preservation, although some have toxicity and environmental risks associated with them. • Halogens, including chlorine, fluorine, and iodine, are also commonly used for disinfection. Chlorine compounds, including sodium hypochlorite, chloramines, and chlorine dioxide, are commonly used for water disinfection. Iodine, in both tincture and iodophor forms, is an effective antiseptic. • Alcohols, including ethyl alcohol and isopropyl alcohol, are commonly used antiseptics that act by denaturing proteins and disrupting membranes. • Phenolics are stable, long-acting disinfectants that denature proteins and disrupt membranes. They are commonly found in household cleaners, mouthwashes, and hospital disinfectants, and are also used to preserve harvested crops. • The phenolic compound triclosan, found in antibacterial soaps, plastics, and textiles is technically an antibiotic because of its specific mode of action of inhibiting bacterial fatty- acid synthesis.. 370
• Surfactants, including soaps and detergents, lower the surface tension of water to create emulsions that mechanically carry away microbes. Soaps are long-chain fatty acids, whereas detergents are synthetic surfactants. • Quaternary ammonium compounds (quats) are cationic detergents that disrupt membranes. They are used in household cleaners, skin disinfectants, oral rinses, and mouthwashes. • Bisbiguanides disrupt cell membranes, causing cell contents to gel. Chlorhexidine and alexidine are commonly used for surgical scrubs, for handwashing in clinical settings, and in prescription oral rinses. • Alkylating agents effectively sterilize materials at low temperatures but are carcinogenic and may also irritate tissue. Glutaraldehyde and o-phthalaldehyde are used as hospital disinfectants but not as antiseptics. Formaldehyde is used for the storage of tissue specimens, as an embalming fluid, and in vaccine preparation to inactivate infectious agents. Ethylene oxide is a gas sterilant that can permeate heat-sensitive packaged materials, but it is also explosive and carcinogenic. • Peroxygens, including hydrogen peroxide, peracetic acid, benzoyl peroxide, and ozone gas, are strong oxidizing agents that produce free radicals in cells, damaging their macromolecules. They are environmentally safe and are highly effective disinfectants and antiseptics. • Pressurized carbon dioxide in the form of a supercritical fluid easily permeates packaged materials and cells, forming carbonic acid and lowering intracellular pH. Supercritical carbon dioxide is nonreactive, nontoxic, nonflammable, and effective at low temperatures for sterilization of medical devices, implants, and transplanted tissues. • Chemical preservatives are added to a variety of foods. Sorbic acid, benzoic acid, propionic acid, and their more soluble salts inhibit enzymes or reduce intracellular pH. • Sulfites are used in winemaking and food processing to prevent browning of foods. • Nitrites are used to preserve meats and maintain color, but cooking nitrite-preserved meats may produce carcinogenic nitrosamines. • Nisin and natamycin are naturally produced preservatives used in cheeses and meats. Nisin is effective against gram-positive bacteria and natamycin against fungi.
371
38.) Toxic dental materials include:
A. BPA B. Porcelain crowns containing aluminum C. Crowns containing nickel or cadmium E. Amalgams F. All of the above
http://www.naturalawakeningssa.com/toxic-metals-in-your-mouth-be-aware-of-the-potentially- harmful-metal-components-in-your-dental-work/
Toxic Metals in Your Mouth: Be Aware of the Potentially Harmful Metal Components in Your Dental
Work
Date: January 9, 2014 Author: publisher
by Dr. Paul Wilke, DDS
There are lots of factors to consider when it comes to restorative dental materials. Physical properties include tensile and compressive strength, resistance to corrosion and tarnish, ability to cast well and bond with ceramic opaque and porcelain, the coefficient of expansion and contraction, and yield strength, to name a few.
These physical properties are important to dentists because the human mouth is a hostile environment with moisture, chemical attack with acid and alkaline foods, high loads and temperature changes all take their toll on dental restorative materials.
Another factor that is very important to me is biocompatibility. Why? Because of the potentially harmful components in dental materials, which are implanted into human tissue.
Toxic Metals
Dental amalgams are about 50 percent mercury, which is the second most toxic naturally occurring element on the planet, next to radioactive plutonium. Amalgam does not render the mercury harmless, like I was taught in dental school. It actually vaporizes continuously. Mercury is a potent neurotoxin and immune suppressant, and it negatively impacts the cardiovascular and connective tissue systems. Another component is nickel, which is used in most silver-colored cast metals for crowns, usually partially covered by porcelain. These alloys typically contain 75 percent nickel and 2 percent beryllium. Nickel is the most carcinogenic metal known, and many women are allergic to it. Many orthodontic brackets are about 10 percent nickel. 372
Other metal components include nickel, chromium and cobalt in partial dental frameworks. Titanium dental implants can be made with 100 percent titanium or a common alloy that includes 6 percent aluminum and 4 percent vanadium. All of these materials have great physical properties, but biologically they are a disaster. For example, aluminum has been implicated in many health problems, including breast cancer, according to research published in the Journal of Applied Toxicology.¹
Safe Options
Fortunately, modern biologic dentistry is now able to get away from almost all metal. Fillings can be tooth- colored composite or milled ceramic. Crowns and bridges can be made with many different types of ceramics, from feldspathic, to lithium disilicate, to zirconia. Partial dentures can now be made from a thermoplastic called acetyl that is very strong and inert. It doesn’t absorb or give off any chemicals or bacteria and comes in many tooth shades. It’s strong enough to use in occlusal rest preps and for clasps.
Biocompatible, metal-free implants from zirconia, such as those from Z-systems in Switzerland, are widely used in Europe and now available in the U.S. Being non-metallic, they do not conduct electricity and therefore have no effect on electrical meridian pathways, and being pure white, they are much better looking in upper anterior tooth replacement cases.
Many orthodontic cases, can be treated with hard plastic retainers that progressively straighten teeth. These plastics don’t give off any bisphenol A (BPA). Familiar brand names are Clear Correct and Invisalign. There are some difficult cases, however, that still require bonded brackets and wires.
Some metal brackets are low nickel, 0.5 percent versus 10 percent, for standard brackets. Ceramic brackets are also an option, but they do slow down treatment and cost more. Also, some orthodontic wires are nickel free. Today’s modern dentist has many restorative options that were not available even 10 or 20 years ago. Fortunately, modern dentistry can be entirely biocompatible and beautiful at the same time.
¹ J Appl Toxicol, 2011 Apr; 31 (3):262-9.
Dr. Paul G Wilke, DDS, owns Total Mouth Fitness, a practice that has served the San Antonio community for more than a quarter century. Dr. Wilke is certified in biological dentistry through The International Academy of Biological Dentistry and Medicine. For more information about Dr. Wilke and his practice, visit www.TotalMouthFitness.com or call 210-495-5588. Total Mouth Fitness is located at 14310 Northbrook Dr., Independence Plaza III, Suite 150, in San Antonio.
373
39.) Galvanism can occur:
A. Within a single tooth containing dissimilar metals. B. Between gold crowns and aluminum containing porcelain crown. C. Between gold crowns and an amalgam filling D. A & C E. All of the above
https://iabdm.org/wp-content/uploads/2012/04/mildent_hg.pdf
Mercury creates a battery effect in your mouth
It is known as oral galvanism. The high school science definition of a
battery is having 2 dissimilar metals in the presence of an electrolyte.
For you non-science people, just know that a mercury filling has at
least 5 metals in it and you have in your saliva: calcium, sodium, chloride, potassium, and a whole bunch of other elements in the
solution. So as you can see, you create a battery.
You may have
experienced this by touching a metal filling with a fork. You will get
a decided metallic taste in your mouth. This is a great example of oral
galvanism. This is present all the time if you have any metals present
in your mouth. For those that have metal fillings, some type of
malady (disease) may occur related to this phenomenon
374
40.) Galvanism can decrease the release of Hg vapor from a filling:
A. True B. False
https://www.ncbi.nlm.nih.gov/pubmed/26544100 http://orthomolecular.org/library/jom/1983/pdf/1983-v12n03-p184.pdf https://www.fremontnaturaldentistry.com/blog/mixed-metals-in-the-mouth-can-be-trouble-oral- galvanism/
Mixed Metals in the Mouth Can Be Trouble: Oral Galvanism
For all the amazing things modern dentistry has to offer, it still holds forth some pretty bad ideas. Filling teeth with neurotoxic mercury amalgam is one. Another? Placing a variety of metals in a person’s mouth.
Now, there are a number of ways you could wind up with more than one metal in your mouth. For instance,
• You could have a “silver” amalgam filling in one tooth and a gold inlay or crown on another. • You may have titanium implants holding false teeth in your jaws. • You may wear a partial or removable bridge that has metal clasps. • If you’ve had dental work done by more than one dentist or multiple restorations over many years, those restorations likely differ in the metal alloys used to make them. These types of situations create conditions similar to what you find in a classic galvanic or voltaic cell battery. Electrical currents can generate in the mouth, in a phenomenon known as oral galvanism. You may also hear it described as “electric teeth,” “tooth currents,” or “a battery in the mouth.”
A battery has two electrodes – the cathode and the anode – made of different metals or other material. When placed in an electrolyte solution, chemical reactions occur at each electrode: One produces electrons while the other consumes them.
This movement of electrons generates an electrical current.
The same thing can happen in your mouth, but in this case, the electrodes are your fillings or other metal restorations or prosthetics. Your saliva provides the electrolyte solution in which chemical reactions occur.
Under the right conditions, a reaction at one restoration produces electrons which are consumed at another, creating an electrical current between the two sites. But instead of that energy being directed to an electrical device, as with a conventional battery, the electrical current flows through your mouth and into surrounding tissues. 375
The amount of current produced is relatively small. You can’t be electrocuted by it. There’s no immediate harm. What you might notice at first is a slight metallic taste or burning sensation.
Sometimes the two sites are positioned so that they can periodically come into contact with each other. For instance, you could have a mercury filling on an upper tooth and a gold crown on the lower tooth right below it. When the teeth come into contact, the circuit is “shorted,” resulting in a burst of pain.
Oral galvanism even happens temporarily if you put a metal object in your mouth or accidentally chew on piece of foil.
Even if you can’t feel it, oral galvanism can affect your health. After all, your nervous system runs on electrochemical energy. Having extra currents running in your mouth can interfere with these. They can also disrupt energy flow along the meridians associated with the metal-restored teeth and may interfere with the healthy function of other organs on the same meridian.
Commonly reported symptoms of chronic oral galvanism include headaches, fatigue, memory problems, sleep deprivation, irritability and other mood issues, and trouble concentrating.
Oral galvanism may also result in increased mercury release from mercury amalgam fillings, resulting in increased mercury exposure with all of its toxic ill effects.
The solution, of course, is to replace the metal in your mouth with biocompatible alternatives – composite or ceramic restorations and implants, say, or lightweight, metal-free partials. Depending on how long you’ve been living with the effects of galvanism, additional work with an integrative physician or other health professional may be needed to help bring the body back into balance.
And if you don’t have metals in your mouth now, keep it that way. Stick with a dentist who will fix or replace teeth as needed only with metal-free materials. As ever, prevention remains the best insurance there is.
Posted by fndyoshida on Jul 30th, 2018 7:58 am Filed under Oral-Systemic Health . You can follow any responses to this entry through the RSS 2.0 feed. Both comments and pings are currently closed.
Tags: mercury fillings, metal-free dentistry, oral galvanism, silver fillings, titanium implants
376
41.) Name the entity not known to cause facial pain.
A. Trigeminal Neuralgia B. NICO C. Pulpitis D. Amalgam Tattoo
https://www.sciencedirect.com/topics/medicine-and-dentistry/amalgam- tattoo
https://www.healthline.com/health/amalgam-tattoo
Amalgam tattoos don’t cause any symptoms and they’re not raised or painful. They also don’t bleed or grow over time.
42.) Which are possible benefits of functional appliances?
A. Enhancing hormone function through the pituitary gland B. Increase the IQ C. Restore normal sleep D. Reduce muscle tension E. All of the above
http://www.columbia.edu/itc/hs/dental/D5300/Functional%20Appliances%20Sli de%20Show%20with%20sounds_Mod6_04.ppt%206-1_BW.pdf
https://www.dentalexcellenceva.com/airway-improvement/
Airway Development Research
Treating Airway and Breathing Disorders
DeWitt C. Wilkerson, DMD
Inside Dentistry
Abstract
Patients can develop airway and breathing disorders at any stage of life. Issues such as allergic reactions, chronic congestion, malocclusions, mouth breathing, improper tongue position or tongue-tie, and other age-related and associated risk factors must be treated to correct the source of obstruction and reestablish proper naso-diaphragmatic breathing. Other conditions with similar symptoms, such as TMD, must be considered during treatment planning in order to avoid complications during therapy. Among older patients, treatment for airway and breathing disorders not only restores proper breathing function, but can also reverse some of the damage seen in brain scans. Because an open airway and proper breathing are foundational to oral and systemic health, every patient treated, regardless of age, should be screened for disordered breathing. 377
Dentistry continues to grow as a true medical specialty. In the 1970s, the primary focus was on dental occlusion and restorative dentistry. In the 1980s, the focus shifted to dental implants and the treatment of temporomandibular joint disorders (TMDs). In the 1990s, the new focus was on esthetics, cosmetics, and ceramic materials. Since 2000, dentistry’s focus has concentrated on digital technology and is now moving toward integrative dental medicine. Integrative dental medicine looks at the dental patient as a whole person and is concerned with issues such as diabetes, systemic inflammation, cardiovascular health, gastric reflux, toxins, stress factors, drug interactions, and other issues related to the convergence of oral and overall health. In addition to these concerns, addressing airway and breathing disorders, both during childhood and throughout life, will be a key focus of integrative dental medicine moving forward.
An understanding of the critical role of airway obstructions and disordered breathing significantly influences proper treatment planning in dentistry. Manifestations may include signs and symptoms such as dental malocclusions, bruxism, tongue-tie, attention deficit, poor sleep, sleep apnea, daytime fatigue, TMD, and morning headaches. Every patient treated, regardless of age, should be assessed for the presence of potential airway problems. (Note: Dentists are not trained or qualified to diagnose obstructive sleep apnea; this diagnosis must be made by a medical doctor. Dentists should work under the guidance of a qualified physician when treatment planning such cases.)Risk Factors and Treatment for Children These concerns may start at a very young age—even at birth. Adenoid hypertrophy is the most common cause of nasopharyngeal obstruction in children, the most common cause of pediatric sleep-disordered breathing, and a potential etiologic cause of altered craniofacial growth, characterized by a long face, retrusive chin, and narrow maxilla.1
Roger Price, PharmD, describes a common childhood scenario in which an allergic reaction to dairy products induces mouth breathing. “This mouth breathing results in a lack of filtration and cleansing of the air, allowing airborne bacteria to settle and flourish; an increase in the volume of dirty air over the lymphoid tissue; an increase in inflammation and congestion as a result of over breathing; a lack of release of NO from the sinuses, preventing bacterial control and vasodilation; and diminution of diaphragmatic breathing, which can lead to a reduced lymph flow to the tonsils and adenoids to remove the toxins,” Price explains. “After eliminating the allergic triggers, restoring nasal breathing is a must.”
Mouth breathing has also been associated with dental malocclusions in children.2 Zicari and colleagues’ analysis of 71, 6- to 12-year-old mouth breathing children revealed a 72.5% incidence of reduced transverse diameter of the maxilla and increased vertical dimension, a 32.5% incidence of cross bite, a 43.7% incidence of skeletal class II malocclusions, and a 90% incidence of atypical swallowing patterns. The results showed a strong correlation between oral breathing and malocclusions, which manifests as both dentoskeletal and functional alterations, leading to a dysfunctional malocclusive pattern (Figure 1 through Figure 3). The study concludes that “this dysfunctional malocclusive pattern makes it clear that the association between oral breathing and dental malocclusions represents a self-perpetuating vicious circle in which it is difficult to establish if the primary alteration is respiratory or maxillofacial. Regardless, the problem needs to be 378
addressed and solved through the close interaction of the pediatrician, otorhinolaryngologist, allergologist, and orthodontist.”
Children can suffer from both obstructive and central sleep apnea. Approximately 10% of children snore and 2% to 4% of them have obstructive sleep apnea (OSA) (including babies, but especially those between 2- and 8-years-old). Up to 40% may experience subtle breathing disturbances, including those related to upper airway resistance syndrome (UARS) with sympathetic nervous system “flight or fight” response and blood cortisol stress hormone surges. Signs and symptoms of sleep apnea among children can include insulin resistance, cardiac modulation, mood swings, cognitive dysfunction/attention deficit, and behavioral changes such as hyperactivity and poor impulse control. In addition, these children are at an increased risk of future cardiovascular disease, especially those with childhood obesity. Most children with sleep apnea are mouth breathers, and many of them snore.
Bruxism commonly accompanies airway obstructions in children. DiFrancesco and colleagues evaluated 69 consecutive children who presented to the Otolaryngology Department of the University of São Paulo Medical School for tonsil and adenoid removal.3 Before surgery, the children’s parents reported that 100% experienced sleep apnea, 45.6% engaged in bruxism, and 60.7% possessed dental malocclusions. Three months after surgery, none of the children presented with breathing problems, and 11.8% presented with bruxism. Because there was a significant improvement in bruxism after surgery, the study data suggests that there is a positive correlation between sleep-disordered breathing and bruxism. The researchers conclude that otolaryngologists must be aware that bruxism is associated with airway obstruction and consider it when evaluating tonsil and adenoid hyperplasia (Figure 4 and Figure 5).
When screening children for breathing and airway disturbances, integrative orthodontist, Barry Raphael, DMD, recommends that clinicians ask the following questions:
● Does the child have any sleep issues such as restlessness, bedwetting, frequent awakening, or snoring? ● Is the nose chronically obstructed or congested in any way? ● Are the lips apart at rest? ● Does the tongue rest on the palate and stay there during swallowing? ● Are the chest and shoulders moving during breathing instead of the diaphragm? ● Is the child’s respiratory rate greater than 16 breaths per minute? ● Is the child holding his or her head in front of the shoulders to keep the airway open?
Treatment for children’s sleep-disordered breathing involves correcting the sources
of obstruction and reestablishing naso- 379
diaphragmatic breathing. There are several areas of focus, including the following:
Treatment of any food and environmental allergies that may be causing upper airway inflammation and obstruction.
Ear, nose, and throat treatment of airway obstructions, including nasal stenosis, deviated septum, and enlarged adenoids and tonsils. It is always best to treat the potential causes of lymphoid infection and inflammation, such as allergies or mouth breathing, before considering removal of the tissues, which provide a valuable first line of defense against invading pathogens.
● Surgical removal of restrictive tongue frenum. ● Orthodontic expansion of the maxillary and mandibular dental arches (Figure 6 and Figure 7). ● Orofacial myofunctional therapy to train proper tongue position and swallowing. ● Training in proper naso-diaphragmatic breathing, including breathing exercises such as the Buteyko method.
Pediatric dentist and anthropologist Kevin Boyd, DDS, MSc, has uncovered published papers from the University of Michigan’s archived dental library collection that clearly show that physicians, orthodontists, and general dentists from the mid-19th through the early 20th century were keenly aware of a possible connection between pediatric naso-respiratory dysfunction, somatic and neurological/neurobehavioral growth deficits, and dental malocclusion in the primary/early mixed dentition. Moreover, these medical and dental professionals of yesteryear were collaboratively exploring how preventing or reversing early malocclusion might also prevent or reverse associated systemic and neurological problems.
An open airway and proper breathing are foundational to oral and systemic health. Screening all children for disordered breathing should be a top priority in every dental practice.
Airway/Breathing Disorders and TMD
Young adults often present to the dental office with signs and symptoms that are categorized under the “basket syndrome” TMD. Common manifestations of TMD include sore muscles of mastication, clenching/bruxism, morning headaches, joint soreness, joint clicking/locking, restricted range of mandibular movement, dental malocclusions, cervical neck problems, poor sleep quality, and chronic fatigue.
One of the pioneers in sleep medicine, Christian Guilleminault, MD, studied young, thin men and women who were exhausted despite regularly sleeping 8 hours and having sleep study results in the “normal” range.4 In his classic experiment, he placed thin pressure sensors inside each patient’s 380
esophagus and measured pressures during sleep. All of the subjects had multiple episodes of only partial obstruction; however, they exhibited severe respiratory efforts that led to significantly negative pressures in the esophagus. After multiple episodes of labored breathing, patients would awaken from deep to light sleep, which is called an “arousal” in sleep medicine. Although the apneas and hypopneas among these patients were minimal, they experienced severely fragmented sleep. Guilleminault coined the term “UARS” to describe this common phenomenon.
In another Guilleminault study involving 30 subjects age 21 to 24 who were diagnosed with UARS, all reported chronic fatigue, 28 reported non-refreshing sleep, 26 reported disrupted nocturnal sleep, 29 reported daytime performance impairment, and 17 reported morning headaches.5
These are common complaints expressed when interviewing patients diagnosed with TMD as well. UARS and TMD can have many similar symptoms. In practice, it is not unusual to find patients who are suffering from both disorders simultaneously (Figure 8). When determining the appropriate treatment plan, it is important to clarify the cause and effect relationships that are resulting in the patient’s symptoms.
Some patients with both TMD and airway/breathing disorders may actually suffer negative effects from traditional TMD therapy. Yves Gagnon, DMD, and Giles Lavigne, DMD, MSc, PhD, conducted a pilot study involving 10 subjects who were previously diagnosed with snoring and sleep apnea through polysomnography.6 Each subject was fitted with a maxillary occlusal splint (ie, nightguard). After one week of wearing the splint to sleep each night, the participants underwent a new overnight polysomnography, during which the splint was worn. The results indicated that, with the splint in the mouth, the apnea-hypopnea index increased by approximately 50% in half of the subjects and the total time snoring while asleep was increased by 40% overall. When airway/breathing disorders are present, including UARS and OSA, it is important to avoid prescribing overnight intraoral splint therapy that may crowd the tongue or allow the mandible to drop back during sleep.
Screening all TMD patients for disordered breathing should be a top priority in every dental practice.
Considerations for Middle-Aged Patients
Another segment that frequently suffers from airway and breathing disorders is the population of middle-aged men and women. For these patients, poor sleep, frequent sleep arousals, daytime fatigue, foggy thinking, early memory loss, tired eyes, bruxism, and gastric reflux can indicate the presence of an airway or breathing disorder (Figure 9).
Research conducted at UCLA by Paul Macey, PhD, concluded that sleep apnea can take a toll on brain function7. Due to neurotransmitter imbalances, sleep apnea can result in poor concentration, difficulty with memory and decision-making, depression, and stress. There are two key neurotransmitters involved: gamma-aminobutyric acid (GABA) and glutamate. The 381
neurotransmitter GABA acts as a brake pedal in the brain, producing a calming mood and helping to make endorphins, whereas the neurotransmitter glutamate acts as an accelerator in the brain, increasing when the brain is in a state of stress. Chronic high levels of glutamate can be toxic to nerves and neurons.
Sleep apnea may result in low levels of GABA and high levels of glutamate that can essentially produce brain damage. This is indicated by signs of memory loss and foggy thinking and may appear to mimic the early signs of Alzheimer’s disease. The good news is that effective therapy can often reverse the damage. After less than one year of continuous positive airway pressure (CPAP) therapy, reversals attributed to increased oxygenation have been seen in brain scans.
Millions of middle-aged men and women across the United States suffer from this reversible form of memory loss and brain damage, and dental professionals are perfectly positioned to screen and intervene. As such, screening all mature adults who snore or are overly tired for disordered breathing should be a top priority in every dental practice.
Conclusion
In October 2017, the American Dental Asso-ciation (ADA) released a policy statement addressing dentistry’s role in sleep-related breathing disorders. The policy encourages dental professionals to screen their patients for OSA, UARS, and other breathing disorders; advocates working with medical colleagues; and emphasizes the effectiveness of intraoral appliance therapy for treating patients with mild to moderate OSA and CPAP-intolerant patients with severe OSA. With the endorsement of the ADA, screening for and treating sleep-related breathing disorders has indeed become the newest focus of integrated dental medicine.
References
1. Major MP, El-Hakim H, Witmans M, et al. Adenoid hypertrophy in pediatric sleep disordered breathing and craniofacial growth: the emerging role of dentistry. J Dent Sleep Med. 2017; 5(4):83-87. 2. Zicari AM, Albani F, Ntrekou P, et al. Oral breathing and dental malocclusions. Eur J Paediatr Dent.2009; 10(2):59-64. 3. DiFrancesco RC, Junqueira PA, Trezza PM. Improvement of bruxism after T & A surgery. Int J Pediatr Otorhinolaryngol. 2004;68(4):441-445. 382
4. Guilleminault C, Stoohs R, Clerk A, et al.. A cause of excessive daytime sleepiness. The upper airway resistance syndrome. Chest. 1993;104(3): 781–787. 5. Guilleminault C, Lopes MC, Hagen CC, et al. The cyclic alternating pattern demonstrates increased sleep instability and correlates with fatigue and sleepiness in adults with upper airway resistance syndrome. Sleep. 2007;30(5): 641-647. 6. Gagnon Y, Mayer P, Morisson F, et al. Aggravation of respiration disturbances by the use of an occlusal splint in apneic patients: a pilot study. Int J Prosthodont. 2004;17(4):447-453. 7. Perry, L. Sleep apnea takes a toll on brain function Page. https://newsroom.ucla.edu/releases/sleep-apnea-takes-a-toll-on-brain-function. Updated February, 11, 2016. Accessed November 22, 2017.
Airway Improvement – Epigenetic Orthodontics
Before ending up with sleep apnea there are sign and symptoms of Airway obstruction that leads to sleep apnea 10 or 20 years down the road, take these signs seriously and get the correction today. This can keep you ache and pain free, organ failures due to even mild apnea at night and high cost of health care due to illnesses that you cannot recover from due to lack of quality deep sleep.
When the body adapts to poor conditions, the whole body pays the price.
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43.) Titanium implants have been shown to have no correlation to autoimmune disease.
A. True B. False
https://iabdm.org/root-canals-dental-implants-endotoxemia/
Root Canals, Dental Implants, Endotoxemia by IABDM | May 30, 2014 | Biological Dentistry, Root Canals | 9 comments From “Controversy? Not for Me!” by Ronald S. Carlson, DDS In dental surgery, we (I do not!) advocate, unlike our medical colleagues, the retention of gangrenous tissues within the oral cavity. You may know them as “root canals.” Controversy abounded 100 years ago about these “root cadaver canals,” but that was swept under the rug of dental history, about 1945. Well evidenced now is the oral- systemic relationship to arthritic conditions and pain, “oral sepsis.” One hundred years ago, however, we did not have so-called modern dental implants and their open wounds inviting infection. I liken them to stakes being driven into the jaws, being hit with poisoned arrows. A known fact is that 80% of these dental implants are immediately attended with “peri-implant mucositis,” pain, swelling, similar to “gingivitis” or “periodontitis.” Periodontal medicine now encompasses both periodontal disease and per-implant disease – infected open wounds. Orthopedic surgeons with whom I associate often remark to me about the blackness and cheese-like quality of the bone of the spinal column when they enter a year later to retrieve rusted titanium screws, exactly the same as [used in] dental implants. My experience is the same! Unlike the orthopedic surgeons, I send tissue samples routinely to Queen’s Medical Center for histo-pathological review and get reports back such as, “present are marked acute/chronic inflammation, fibrosis, granulation tissue, reactive bone, necrotic (dead) bone, cysts, odontogenic tumors, non-supportive condensing osteitis, abscesses with actinomyces” (a gram negative fungal bacteria which produces pus in the body – like candida). My over 30 years of clinical scientific research has 240 samples that verify the above conditions around root canal teeth and dental implants. Google Endodontic- Endotoxemia: Our Current Dilemma or look for the work of Weston Price, DDS, or George Meinig’s book Root Canal Cover-Up Exposed.
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44.) Teeth can be effectively and permanently sterilized by:
A. Antibiotics B. Homeopathic remedies C. Sodium Hypochlorite D. Lasers
E. Teeth cannot be permanently and effectively sterilized
https://iabdm.org/wp-content/uploads/2013/10/iabdm_rct_position_paper.pdf
IABDM Position Paper on Root Canal-Treated Teeth By Michael D. Margolis, DDS Controversy surrounds the removal of teeth with root canal-treatment, teeth that are diseased with an abscess or exposed nerve. There are four options: 1. Do nothing. 2. Root canal-treatment. 3. Re-treatment of the existing root canal-treated tooth. 4. Extraction of the tooth with the proper cleaning of the tooth socket and appropriate grafting of the site. According to the American Association of Endodontists, “There is no valid, scientific evidence linking root canal-treated teeth and disease elsewhere in the body. A root canal is a safe and effective procedure.”1 At first glance, this statement seems to settle the issue once and for all. But where are the facts to back it up? There is a significant and growing body of compelling evidence linking root canal-treated teeth to systemic disease. Much of it has been published in peer-reviewed endodontic, periodontal, dental, and medical journals, and has even reported in daily newspapers. Early Research on Root Canal Toxicity Early in the 1900s, a group of medical and dental researchers independently saw an unmistakable connection between systemic disease and various bacteria. These pathogens seemed to originate from oral sources in and around periodontally involved teeth, infected teeth, root canal-treated teeth, and extraction sites. Early, important researchers in this area include • Dr. Charles Mayo, founder of the Mayo Clinic. • Dr. Frank Billings, past President of the American Medical Association and creator of the Council on Medical Education, “which brought about the standardization of medical education in the United States” in the early 1900s..4 • Dr. Weston Price, founder of the research institute of the National Dental Association (which became the American Dental Association) and chair of the NDA from 1914 to 1928. 5,6,7 • Dr. Edward C. Rosenow, a prolific researcher who consistently produced welldocumented works, nearly 300 articles between 1902 and 1958. Rosenow in particular “built upon two venerable medical concepts: (a) the concept of oral focal infection, whereby distant and/or generalized diseases have been attributed to the dissemination of microorganisms or their toxins through the bloodstream from an oral "focus" or reservoir; and (b) the ability or perhaps even tendency of microorganisms to exist in different phases as a result of dissociation or mutation, depending on environmental conditions.8 All four of these clinicians, three physicians and a dentist, independently conducted thousands of experiments implanting extracted root canal teeth from patients who suffered from a multitude of diseases. In every case, the experimental animal (rats or mice) became ill with the same disease the patient had suffered. Perhaps the most famous research was done by Dr. Weston Price. ( After a 16-year old boy had died of endocarditis two weeks after Price had performed root canal therapy, Price successively implanted that same tooth into two hundred rabbits. All died with endocarditis. The 16-year old boy was his son. Dr. Price worked furiously to find a way to make root canals safe. This research was summarized in his two volume work, Dental Infections, Oral and Systemic and Dental Infections and the Degenerative Diseases. After 25 years of research, he concluded: There was no viable way to sterilize a root canaled tooth. All this research was performed before the advent of antibiotics, which prevented infections from spreading and killing the advancing organisms causing the disease. Unfortunately, we do see these organisms express themselves over time but not always in the patient’s mouths. These men had no hidden agendas. They only wanted to expose the truth. In the 1930s, approximately three years after Price’s death, Dr. W. L. Holman wrote an article to dismiss all the research of Price, Billings, Mayo, and Rosenow, doing so without performing any bacteriological research or experiments himself. Holman’s dishonest treatment of Rosenow’s work in particular was clearly self-motivated and wrong.9 The wholesale dismissal of Dr. Rosenow’s in no small part seems attributable to a clearly fraudulent misrepresentation of his research results.10, 11 The discrediting of the oral-systemic connection has had an impact on modern dentistry for over eighty 385
years. Over the next couple of decades, Holman's portrayal came to serve as the indispensable foundational citation for a body of incestuously cross-referenced literature,12 which confronted Dr. Rosenow's otherwise unassailable work. This body of contrary literature continues to undermine and influence modern medical and dental attitudes, theory and practice, establishing Holman's deception as probably the grandest fraud in the history of medicine, if not science.13 Crossing the Research Gap One article in the Journal of Endodontics’ January 1982 special issue try to make a case that a pulpless tooth is not a dead tooth. It still has a definite and vital relationship with the surrounding tissue; the author insists; the life of the tooth depends on the attachment apparatus, i.e., the periodontium and adnexa. In the words of Dr. Grossman and Dr. Marshall, The life of the tooth is dependent upon the integrity of the periodontal membrane and not upon the integrity of the pulp…. If a pulpless tooth were a dead tooth, it should be exfoliated since the body does not tolerate dead tissue. That a pulpless tooth is not dead may be quickly demonstrated by an attempt to remove such a tooth without an anesthetic.13, 14, 15, 16 Of course, these doctors had everything to gain and everything to lose if the root canaltreated teeth were declared dead and unhealthy. What is the current scientific literature, peer-reviewed articles connecting periodontal disease, 17, 18 root canal-treated teeth, and ischemic osteonecrotic or chronic avascular necrotic bone lesions connecting these conditions with systemic disease? Today, research on both periodontal disease bacterial microbiology 19,20 and toxicity of root canal-treated teeth 21 have been published, using advanced biopsy techniques ranging from polymerase chain reaction technique (DNA) to the Limulus amoebocyte lysate (LAL) assay, quantitative kinetic chromogenic LAL assay (KQCL) and kinetic turbidimetric LAL assay (Turbidimetric), with the exception of the histological techniques. 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33 There is a lack of peer reviewed articles connecting histological analysis and DNA testing of microorganisms present. In fact, there is very little incentive for researchers to investigate an established dental procedure that generates over $22,900,000,000.00 annually34 in the United States of America* for fear of retribution by established dental institutions, whose membership consists of governor-appointed positions recommended by their state dental associations and state dental boards, the American Dental Association, as well as organizations such as: the American Association Of Endodontists, the American College of Oral and Maxillofacial Surgeons, the American Academy of Periodontology, and the American Dental Association. It is safe to conclude that few if any members of state dental boards have any idea or concept of biological, holistic, or integrative dentistry. Practical Matters for the Biological, Holistic, or Integrative Dentist Exemplary record keeping is certainly a cornerstone of your defense if a state board, attorney or insurance company asks why you extracted a “perfectly healthy” root canal-treated tooth. Do not trust a board member to interpret your findings and understand what you are doing. You have to write out all the information. In your records you must list 1. The patient’s chief complaint. 2. Why the patient wants their root canal-treated teeth removed. 3. Any experience of pain, infection, or a systemic-related condition the patient has had. 4. Radiographic (both CBCT and 16 to 18 full mouth series), EAV, and/or quantitative ultrasound (QUS or CAVITAT™) documentation of dental conditions. 5. A signed and dated informed consent form from the patient and a written statement why they want their root canal-treated teeth (past extraction sites and Titanium implants) removed. 6. The patient’s expression of pain level or statements like “After I had my root canal done,I got sick, and I believe these two situations are related.” Chart the facts: existing conditions, missing teeth, restorations, periodontal health, bone health oral cancer screening, TMJ condition, and sinus health. Include the condition of each tooth number or area: failed root canal-treated tooth with granulation tissue, cracked tooth, etc. Note why you recommend extraction. If the patient had persistent pain and discomfort despite root canal treatment and an absence of positive periapical findings on radiograph, write it in the record. Why is it a failure? Pain? Suppuration? Mobility? Fracture? Un-restorability? Record your diagnosis. This is where the board will say they “gotcha” because until the biopsy is returned, you may only give possibilities (i.e., differential diagnosis) and not a formal diagnosis. If you use a DNA biopsy report, many dentists do not get the connection between a histological report or a DNA report. Therefore, state possible differential diagnoses of 1. AVN. 2. Asymptomatic chronic fibrosis. 3. Failed root canal due to radiolucency at the apex of the tooth, no pain. 4. Abscess present with draining fistula. 5. Non-supportive osteomyelitis. In his book Six-foot Tiger, Three-foot Cage, Dr. Felix Liao states the case for connecting the oral cavity to the rest of the body, with and without endodontic care. The book supports the perioendo-systemic connections: • A 2016 study in PLoS Medicine showed the link between periodontitis (gum disease) and memory decline. “The presence of 386 periodontitis at baseline,” it said, “was not related to baseline cognitive state but was associated with a six fold increase in the rate of cognitive decline….” (35) • Bacteria from the mouth have been shown to spread to the rest of the body. For instance, people with periodontal disease have double or triple the risk of having a heart attack or stroke.(36) • Oral bacteria have been found in heart attack clots. “Dental infection and oral bacteria, especially viridans streptococci, may be associated with the development of acute coronary thrombosis,” wrote researchers in the journal Circulation. (37) • One study found that DNA from endodontic (root canal) bacteria was found in 56% of 36 samples of heart attack clots. Periodontal bacteria was found in 47% of those samples. The authors concluded that “dental infection could be part of pathophysiology in intracranial aneurysm disease [stroke].” (38) • Bacterial DNA was detected in 21/36 (58%) of specimens. A third of the positive samples contained DNA from both endodontic and periodontal bacteria. DNA from endodontic bacteria were detected in 20/36 (56%) and from periodontal bacteria in 17/36 (47%) of samples. Bacterial DNA of the Streptococcus mitis group was found to be most common. (39) Upon the arrival of biopsy reports, a diagnosis may be stated or the personal opinion given on the patient’s situation. This maybe entered at the time you review patient results or in a letter to the patient, with a copy placed in the patient's chart. State dental boards have no idea how to interpret a DNA report because it does not list a diagnosis like a histology report does. Therefore, they will argue the validity of the biopsy. There are new insurance dental codes that distinguish between Histological Reports (D7285) and DNA (0422) Reports.35 Always have a biopsy of either type for all surgical procedures that include surgery of avascular necrosis sites, removal of root canal-treated teeth, bone lesions, or soft tissue excisions. Protocol for the Removal of Root Canal- Treated Teeth In Root Canal Cover-up, Dr. George E. Meinig explains the method he has suggested since 1993. There have been many good suggestions added to his basic protocol, but his lays the foundation for the basics.36 The basic protocol is also recommended for the extraction of nonroot canal-treated teeth, but it is not the only way to prepare an extraction site. Once the tooth has been extracted and tooth, tissues and blood samples have been collected for biopsy, a #8 or #10 round burr is used to remove one to two millimeters of the entire bony socket, including the apex area. Of course, there are exceptions to every rule. In mandibular third and second molar areas, one should know exactly where the neurovascular bundle is and the mental foreman/nerve. On occasion, I avoid cleaning the lower one- third of the socket to avoid neurological damage. In the upper arch, the round burr is started in the apex area and brought to the surface, avoiding the possibility of going directly into the sinus. It is very common to extract a failed root canaltreated tooth or abscessed tooth and discover an oral-antral fistula exists into the sinuses. If this happens, a protein rich fibrogen (PRF) or collagen membrane can be inserted into the apex of the socket or in the sinus via the opening and a bone augmentation material, such as artificial bone, cadaver bone, autologous bone, or a beta-tri-calcium phosphate paste may be placed in the sinus area and socket. A similar membrane may be secured in the socket, sutured into place by suturing the tissues in such a manner to secure the healing site. Make sure there is a good blood flow into the area by not injecting an anesthetic with epinephrine, unless there is a contraindication. Whenever a lower third molar appears to be entangled around the neurovascular bundle, always refer that patient to an oral surgeon for removal. If the surgeon encounters a problem, their license makes it less likely they will be involved in a board complaint or legal action. Never attempt to be a dental hero. The purpose of removing the first 1 to 2 mm of bone is to perform a partial ostectomy squestrectomy for removal of the periodontal ligament (PDL), non-vital, loose, or sloughed- off dead bone caused by infection or reduced blood supply. aiding healing of the site. As we learned in school; the PLD has four purposes: • To secure the tooth to jawbone. • To facilitate fluid flow through the dentinal tubule structures. When the tooth is “depressed” into the socket, it acts as a cushion. When the pressure is released, the tooth moves back to its original position and acts as plunger to the fluids in the dentinal tubules, creating pressure to pull the liquids out from the tooth’s inner structures into the PDL and the interstitial spaces. • To give feeling without pain. • To prevent bone growth. (Teeth are considered bone by the body.) Ligaments allow freedom of movement between bones. So if a tooth is removed but the PDL remains in the socket, the body reacts as if the tooth is still present. It prevents the creation of capillary beds which bring in the blood vessels establishing circulation. Without proper circulation, osteoblasts and osteoclasts cannot be generated and no new bone will grow. A lesion is created, and an anaerobic environment is established for bacteria, viruses, and toxins to live in and thrive. With root canal teeth, endotoxins have been found 100% of the time,37, 38 This means the PDL 387
and adjacent bone were exposed to toxins and should be completely cleaned. The basic principles of cleaning the jawbone socket are recognized in the American Dental Association’s Dental Procedures Codes 2017. The principle of cleaning the surgical sites is the same for a root canal-treated tooth, a non- root canal tooth, and areas of avascular necrotic lesions. D7140: extraction, erupted tooth or exposed root (elevation and/or forceps removal). [Includes removal of tooth structure, minor smoothing of socket bone, and closure, as necessary.] D7210: extraction, erupted tooth requiring removal of bone and/ or sectioning of tooth, and including elevation of mucoperiosteal flap if indicated. [Includes removal of tooth structure, minor smoothing of socket bone, and closure, as necessary.] D7550: Partial ostectomy/squestrectomy [for removal of non-vital, loose, or sloughedoff dead bone caused by infection or reduced blood supply].40 While the procedure is being performed, the area should be irrigated with copious amounts of sterile saline water via your surgical hand piece or a separate water syringe. While cutting the bone, the PDL and toxins are removed and the bone is “perturbed” or stimulated. As the blood vessels are established in the socket or other bony lesions, this perturbation of the bone stimulates a change from osteocytes to osteoblasts. The latter are the cells that generate new bone formation. After the socket has been cleaned, it is recommended to prepare it. There is no one set method to perform any or all of the suggestions below. Whatever works in the specific, individual case is appropriate. 1. Fill the socket with a non-vasoconstrictor (no epinephrine) local anesthetic. Allow the liquid local anesthetic to set for about thirty (30) seconds, then gently remove most of the anesthetic, leaving a small amount to continue stimulating osteoblastic activity. 2. Irrigate the surgical site with sterile saline water, hydrogen peroxide (and set for 30 seconds), ozonated water (and left to set for 1 minute), or other preferred cleaning solutions. 3. Rinse the site with another antiseptic solution. Once the surgical site has been cleaned, place your bone augmentation material(s) or PRF/PRP tissues along with primary closure via suturing the site. Each practitioner needs to decide whether to place anything into the surgical site. Materials used by many of our members include: nothing, sterilized cadaver or xenograft materials, synthetic bone; and protein rich fibrogen or plasma rich protein, with or without the addition of homeopathic remedies. Some biological and integrative dentists will simply clean the site, placing nothing because their patients often suffer from autoimmune conditions. Their experience with this type of patient is less is more. All surgical sites should be closed as much as possible by suturing the surgical site with an absorbable or Teflon suture for better healing and less build-up of plaques. Addition of homeopathic remedies, PRF, PRPP liquids, ozone, or another product may be added to the sites to aid in healing. For postoperative care, gentle mouth swishing with salt water or a nontoxic mouth wash is recommended
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45.) Oral bacteria, such as: S. Mitior, S. Mutans, S. Sanguis and a fungi, Candida Albicans all have been found to convert inorganic mercury to methyl mercury.
A. True B. False https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1392265/
Methylmercury, Amalgams, and Children’s Health
Gianpaolo Guzzi
Claudio Minoia
Paolo D. Pigatto
Gianluca Severi
Author information Copyright and License information Disclaimer
See the article "Transport of Methylmercury and Inorganic Mercury to the Fetus and Breast-Fed Infant" in volume 113 on page 1381.
See the reply "Methylmercury, Amalgams, and Children’s Health: Björnberg et al. Respond" on page A149b.
This article has been cited by other articles in PMC. In their excellent article, Björnberg et al. (2005) stated that exposure to methyl-mercury in humans occurs primarily through fish consumption. We would like to make one observation about the sources of potential exposure to methylmercury in the general population. We were surprised that Björnberg et al. (2005) failed to mention saliva as a plausible biologic source of methylmercury in individuals who have mercury dental fillings. Leistevuo et al. (2001) found a correlation between the total amalgam surfaces and organic mercury—presumably as methylmercury + (CH3Hg )—in saliva. Previous studies have reported that mouth air levels of elemental mercury (Hg0) significantly correlate with the number of occlusal surfaces (Lorscheider et al. 1995; Clarkson 2002). Hence, when mercury vapor (Hg0) 389 is released from amalgams and dissolved into the saliva, it exists mainly as Hg0 and partly as inorganic divalent mercury (Hg2+). Consistent with this background, saliva has high levels of inorganic mercury associated with the total number of amalgam surfaces, which markedly increased during mastication and bruxism. In approximately 270 individuals with amalgams, we used inductively coupled plasma-mass spectrometry to measure a wide range of possible values of total mercury in saliva. Mercury levels ranged from the limit of detection [LOD; 0.1 μg/L] to 780 μg/L in both salivary baseline flow rate in unstimulated condition and in a post–chewing- gum test (Guzzi et al. 2005). Trace amounts of elemental and inorganic mercury from saliva are taken up by oral bacteria, which in turn release methyl-mercury as their by- product. Heintze et al. (1983) and Lyttle et al. (1993) reported direct evidence that organic mercury in saliva is due to the transformation of bacteria. As shown in our article (Pigatto et al. 2005), the proximate cause of mercury alkylation in oral microbial communities—which occurs in dental plaque— appears to be associated with the presence of some bacteria. Furthermore, our ongoing investigation seems to support the work of Leistevuo et al. (2001), suggesting evidence that subjects with dental amalgams have shown higher levels of methylmercury compared with controls (Guzzi et al. 2005). Once ingested in the gastrointestinal tract, the methylmercury in saliva is therefore nearly all absorbed (> 95%), as is methylmercury in fish. Leistevuo et al. (2001) reported that the levels of methyl-mercury in saliva ranged from 0 to 174 nmol/L (0–37.523–μg/L), with a mean methylmercury level estimate of 14.0 nmol/L (3.019–μg/L). (Leistevuo et al. 2001). Assuming that daily adult salivary secretion is at least 800 mL, speciation analyses indicate that exposure to methyl-mercury through ingestion—apparently derived from oral bacteria biomethylation of inorganic mercury—is about 2–3 μg/day (Leistevuo et al. 2001). Perhaps Björnberg et al. (2005) did not deem this exposure significant? Considering that the relevant feature of methylmercury in humans is accumulation in both adult and fetal brain, it is quite clear that, over time, the extensive exposure to methylmercury associated with dental amalgams 390 should be taken into account. We believe that organic mercury found in saliva may indeed represent a potential nondietary source of methylmercury.
46.) Which statement is true?
A. No difference in tooth decay exists between fluoridated and non- fluoridated countries B. Cavities do not increase when fluoridation stops C. Fluoridation does not prevent oral health crisis in low income areas D. All of the above https://iaomt.org/wp-content/uploads/IAOMT-Fluoride-Position-Paper.pdf https://iaomt.org/wp-content/uploads/IAOMT-Fluoride-Position-Paper.pdf
Moreover, there is even doubt about fluoride’s efficacy in preventing tooth decay. For example, research has indicated that fluoride does not aid in preventing pit and fissure decay (which is the most prevalent form of tooth decay in the U.S.) or in preventing baby bottle tooth decay (which is prevalent in poor communities). Also, research has suggested that in malnourished children and individuals of lower socio-economic status, fluoride can actually increase the risk of dental caries due to calcium depletion and other circumstances.
47.) Teeth and gums of a root canal treated tooth are a perfect hiding place for bacteria because
A. The cementum is porous. B. The dentinal tubules of a single tooth have approximating three miles of length. C. Fluid flow in the tubules is stagnant E. The presence of lateral accessory canals. F. All of the Above
https://www.westonaprice.org/health-topics/dentistry/root-canal-dangers/
See Question 32 – Pages 283-294
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48.) Spirochetes are considered a healthy microflora.
A) True B) False
https://www.sciencedirect.com/topics/immunology-and- microbiology/spirochete
Host Defenses to Spirochetes Nicolás Navasa, ... Juan Anguita, in Clinical Immunology (Fifth Edition), 2019 Conclusions Spirochetes are a phylogenetically ancient and distinct group of microorganisms. Because of their propensity to cause diseases in humans, B. burgdorferi and T. pallidum are the two most- well-studied spirochetes. However, the inability to culture T. pallidum in vitro has made researching this spirochete very difficult, and as a consequence, the immune response that follows infection with this spirochete remains poorly understood. The etiological agents of Lyme disease and syphilis are similar in that they have relatively small genomes, surviving only in association with a host and eliciting inflammatory disease, but genomic comparison clearly shows that T. pallidum and B. burgdorferi are not closely related. It seems likely that despite some similarities, these spirochetes evolved independently from a more complex ancestor, resulting in differences in their life-cycles, environmental adaptations, and the pathology associated with their infection. Therefore it is not surprising to learn of the differences in the host immune responses to B. burgdorferi and T. pallidum. Both the host response to these spirochetes and their infectivity determine the extent of pathology following infection. Please check your eBook at https://expertconsult.inkling.com/ for self-assessment questions. See inside cover for registration details.
HViewost dchapterefensePurchases to spir bookochetes Chris M. OlsonJr., ... Juan Anguita, in Clinical Immunology (Fourth Edition), 2013 Conclusion Spirochetes are a phylogenetically ancient and distinct group of microorganisms. Because of their propensity to cause diseases in humans, B. burgdorferi and T. pallidum are the two most well-studied spirochetes. However, the inability to culture T. pallidum in vitro has made researching this spirochete very difficult, and as a consequence our understanding of the immune response following infection with this spirochete is more limited. The etiologic agents of Lyme disease and syphilis are similar in having relatively small genomes, surviving only in association with a host and eliciting inflammatory disease, but genomic 392
comparison clearly shows that T. pallidum and B. burgdorferi are not closely related. It seems likely that, despite some similarities, these spirochetes evolved independently from a more complex ancestor, resulting in differences in their life cycles, environmental adaptations and the pathology associated with their infection. Therefore, it is not surprising to learn of differences in the host immune response to B. burgdorferi and T. pallidum. Both the host response to these spirochetes and the infectivity of the bacterium determine the extent of pathology following infection.
CViewlass ichapterficationPurchase and pat bookhogenicity of microbes D.C. Shanson MB, FRCPath, in Microbiology in Clinical Practice (Second Edition), 1989 Spirochaetes Spirochaetes are thin-walled spiralled flexible organisms which are motile by means of an axial filament. They are not seen in a Gram-stain (except B. vincenti), but may be seen either by dark- ground illumination microscopy, or in a silver stain under the light microscope. Borrelia spirochaetes in the blood may also be seen in a Giemsa stain. The three groups of spirochaetes include: 1 Treponema Spirochaetes with regular spirals, approximately 1 μm apart from each other, 5–15 μm long and about 0·2 μm wide, e.g. Treponema pallidum (cause of syphilis) 2 Leptospira Spirochaetes which have tightly coiled spirals, 5–15 μm long and about 01 μm wide. Characteristically, there is often a ‘hooked’ end, e.g. Leptospira icterohaemorrhagiae (cause of Weil's disease). 3 Borrelia Large spirochaetes, 10–30 μm long and about 0·3 μm wide, with irregular spirals 2–4 μm apart from each other, e.g. Borrelia recurrentis (a cause of relapsing fever).
EViewxtra cchapterellularPurchase Organis mbooks Amy C. Valenciano DVM, MS, DACVP, ... Ronald D. Tyler DVM, PhD, DACVP (Clinical and Anatomic Pathology), DABT, in Atlas of Canine and Feline Peripheral Blood Smears, 2014 Distinctive Features: Spirochetes are rarely seen in peripheral blood and are bacteria of the order Spirochaetales. Spirochetes appear as small, thin, corkscrew-shaped, extracellular organisms. Diagnostic Significance: 393
The presence of spirochetes in peripheral blood suggests borreliosis or lyme disease, which is a tickborne disease caused by the bacterium Borrelia burgdorferi. Finding spirochetes on peripheral blood films warrants further testing, empirical antibiotic therapy, or both.
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Plate 6-3. Spirochetes
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Make sure not to confuse activated platelets with spirochetes and platelet fragments. A, Activated Platelet B, Platelet Fragment C, Spriochetes Next Topic Plate 6-3a Plate 6-3b Plate 6-3c Plate 6-3d Plate 6-3e Plate 6-3f Plate 6-3g Plate 6-3h Plate 6-3i Plate 6-3j
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IViewnfec tchapterious DiPurchaseseases book Thea Brabb, ... Martha Hanes, in The Laboratory Rabbit, Guinea Pig, Hamster, and Other Rodents, 2012 Background and Etiology Spirochetes of the genus Brachyspira (formerly Serpulina) have been associated with diarrhea and colitis in a variety of animals including birds and mammals. Brachyspira contains seven distinct species. Of these, two species have been implicated in guinea pigs, either in natural infections or as an animal model; B. hyodysenteriae, the primary cause of swine dysentery, and B. pilosicoli, a zoonotic agent associated with disease in chickens, pigs, and 403
humans. Spirochetes have been associated with disease in guinea pigs in several publications, although purposeful infection to demonstrate causality has not been done and in many cases, identification of the species involved has also not been accomplished (Duhamel, 2001). Guinea pigs have been used as an animal model for B. hyodysenteriae infection.
CReadlinic fullal B chapteracterioViewlogy PDFDownload book Jeffrey K. Actor PhD, in Elsevier's Integrated Review Immunology and Microbiology (Second Edition), 2012 Spirochetes Spirochetes are long, slender bacteria, usually only a fraction of a micron in diameter but anywhere from 5 to 250 μm long. The best known spirochetes of clinical importance are those that cause disease. Among spirochetal diseases are syphilis and Lyme disease. Treponema Treponema pallidum is the causative organism of syphilis. It is a motile spirochete that is generally acquired by close sexual contact and which enters host tissue by breaches in squamous or columnar epithelium. Disease is marked by a primary chancre (an area of ulceration and inflammation) seen in genital areas, which manifests soon after the primary infection. Progression to secondary and tertiary syphilis is marked by maculopapular rashes and eventual granulomatous response with CNS involvement. Nonvenereal treponemal diseases include pinta, caused by Treponema carateum, and disfiguring yaws, caused by Treponema pallidum ssp. pertenue. Borrelia Borrelia burgdorferi is the spirochete that causes Lyme disease. In contrast to T. pallidum, Borrelia has a unique nucleus containing a linear chromosome and linear plasmids. Borrelia is transmitted by tick bites (Ixodes) during blood feeding. An early indication of Lyme disease is a distinctive skin lesion called erythema migrans. If it is left untreated, an erosive arthritis similar to rheumatoid arthritis can occur and, eventually, chronic progressive encephalitis and encephalomyelitis. A number of other Borrelia spp. can cause endemic relapsing fever, with causative agents including B. duttonii, B. hermsii, and B. dugesi. Leptospira Leptospira spp. (leptospires) are long, thin motile spirochetes. They are the causative agent of leptospirosis, a febrile illness that may lead to aseptic meningitis if left untreated. Symptoms of infection include fever, chills, and headache, with occasional presentation of jaundice. Organisms can be spread in water contaminated by infected animal urine. Pathology 404
Erythema Migrans of Lyme Disease Erythema migrans (also called erythema chronicum migrans) is the skin lesion that develops at the site of a bite from a deer tick infected with borreliosis. The early lesion is characterized by an expanding area of red rash, often with a pale center (“bulls-eye”) at the site of the tick bite, indicative of early signs of Lyme disease.
LViewarge chapter IntestiPurchasene book In Canine and Feline Gastroenterology, 2013 Pathophysiology Pathogenic spirochetes intimately attach to the apical membrane of cecal and colonic epithelial cells. The mechanism(s) by which their cellular interaction results in diarrhea remains unclear. Spirochetes can be found in large numbers in the colonic crypts of normal dogs. In dogs with diarrhea, spirochetes can appear in the feces in large numbers. Whether the spirochetes are causal to the diarrhea or alternatively, mechanically dislodged from the crypts by diarrhea induced by other etiologic factors, remains an area of active debate. In a small number of cases, it has been observed that B. pilosicoli can be isolated from dogs with diarrhea and intestinal spirochetosis, whereas B. canis were commonly isolated from healthy dogs.53,54 Furthermore, B. pilosicoli will attach to cecal epithelial cells from chicks, whereas B. canis will not.55 Accordingly, the current presumption is that B. pilosicoli may be pathogenic and B. canis commensal. A characteristic, but not invariable feature of B. pilosicoli infection is the attachment of one pole of the spirochete to the intestinal epithelium, resulting in a dense “false brush-border.”53,56 Other pathologic changes include colonic inflammation, thickening of the colonic mucosa, and enlarged Peyer patches and lymphoid follicles.
RReadelap fullsin gchapter FeverViews PDFDownload book David A. Warrell, in Infectious Diseases (Fourth Edition), 2017 Borrelia–Tick Complexes Spirochetes have been identified in a larval Amblyomma tick in fossilized amber from the Dominican Republic, dated at 15–20 million years old. Different species of Borrelia spirochetes are transmitted by particular species of soft ticks of the genus Ornithodoros (Argasidae) in different parts of the world (Table 131-1). These ticks are found in dry savanna areas and scrub, particularly near rodent burrows, caves, piles of timber and dead trees, or in cracks and crevices in walls, roof spaces and beneath the floors of log cabins, anywhere inhabited by small rodents. Unlike louse-borne relapsing fever, tick-borne relapsing fevers are zoonoses with the exception of B. duttonii infection. Vertebrate reservoir species are 405
rodents such as rats, gerbils, mice, squirrels and chipmunks, and also dogs and birds. Ticks ingest spirochetes while sucking blood from infected animals or humans. They attack at night, remaining attached for less than 30 minutes before returning to their hiding places. Infection is either by a bite, through infected saliva, or by contaminating mucosal membranes with infected coxal fluid. Borreliae are not excreted in tick feces. Ticks remain infected for life, even while starved of blood for as long as 7 years. Spirochetes can be transmitted transstadially, through successive stages of development of the tick; venereally from male to female ticks; and transovarially, by females to their progeny (except, perhaps, ticks of the O. moubata complex).
TABLE 131-1. Geographic Distribution of some Important Borrelia and Ornithodoros spp. Borrelia spp. Ornithodoros spp. Geographic Distribution
NEW WORLD TICK-BORNE RELAPSING FEVER BORRELIAE
B. hermsii O. hermsi Canada, Central and Western United States, Mexico
B. turicatae O. turicata Southwestern United States, Mexico
B. parkeri O. parkeri Western United States, Baja California
B. mazzotti O. talaje Mexico, Central America
B. O. (venezuelensis) Colombia, Venezuela, Argentina, Bolivia, Paraguay venezuelensis rudis
OLD WORLD TICK-BORNE RELAPSING FEVER BORRELIAE
B. duttonii O. moubata Sub-Saharan Africa
B. crocidurae O. (erraticus) sonrai West, North, East Africa, Middle East
Middle East, Central Asia from Uzbekistan to western B. persica O. tholozani China
B. hispanica O. erraticus Iberian peninsula, Greece, Cyprus, North Africa
B. latyschewi O. tartakowskyi Eastern Europe, Iran, Iraq, Afghanistan
B. caucasia O. asperus Iraq, Eastern Europe
Copyright D.A. Warrell. 406
Borrelia miyamotoi was first described in Japan in 1995. Recently it was recognized as a human pathogen in the relapsing fever group of Borrelia. It is prevalent in hard ticks (Ixodidae), such as Ixodes persulcatus in Russia, I. ricinus in Western Europe and I. scapularis and I. pacificus in the USA. These ticks are also vectors of Lyme disease group Borrelia.3
IViewnfec tchapterious DiPurchaseseases book Mark F. Ditmar MD, in Pediatric Secrets (Fifth Edition), 2011 33 What causes leptospirosis? Spirochetes of the genus Leptospira. These are typically acquired from animal contact, or water or soil contaminated by the urine of dogs, rats, or livestock in the course of recreation or work. Animals may remain asymptomatic shedders for years, and the organisms can remain viable after shedding for weeks to months. Acquisition of illness is more common after heavy rainfalls or flooding. The incubation period can be up to 1 month. In 90% of cases, the disease is self- limited. American Academy of Pediatrics: Leptospirosis. In Pickering LK, editor: 2009 Red Book: Report of the Committee on Infectious Diseases, ed 28, Elk Grove Park, IL, 2009, American Academy of Pediatrics, pp 427–428.
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49.) If your office writes a prescription for an antibiotic, should you inform her that it may disable her birth control pill?
A. No B. Yes
https://www.medicinenet.com/effects_of_antibiotics_on_birth_control_pills/ask.h tm
https://www.medicinenet.com/coronavirus/focus.htm
Do Antibiotics Interfere With Birth Control Pills? Ask the experts What are the effects of antibiotics on birth control pills? Doctor's response There are two ways that antibiotics potentially can reduce the action of birth control pills. Birth control pills contain estrogens. Some antibiotics, e.g., rifampin, griseofulvin, cause the enzymes in the liver to increase the break-down of estrogens and thereby can decrease the levels of estrogens in the body and the effectiveness of the pills. This can result in unwanted pregnancy. Therefore, individuals taking birth control pills should use a second method of birth control when taking these antibiotics or other drugs that can increase the break-down of estrogens. The other way that antibiotics could interfere with the effectiveness of birth control pills is by reducing the re-circulation of estrogens within the body. Estrogens, e.g., ethinyl estradiol, in birth control pills are broken-down by conversion in the liver to other chemicals which are then secreted into the intestines in the bile that is produced by the liver. Bacteria in the intestine are able to convert these chemicals back into the active estrogen which is then reabsorbed into the body. This re-circulation is called entero-hepatic cycling. Theoretically, antibiotics can kill the bacteria that convert the inactive chemicals to the active estrogen, and, therefore, may interfere with the effectiveness of birth control pills. Unwanted pregnancies could occur. Although it has not been proven that unwanted pregnancies can occur by this means, drug manufacturers caution that antibiotics could decrease the effectiveness of birth control pills. Since it is better to be safe than sorry, individuals taking birth control pills are advised to use a second reliable method of birth control when taking antibiotics.
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50.) If you have a patient on Nitrous Oxide do you have to write the percentage of Nitrous to Oxygen?
A. Yes B. No http://icourses.uthscsa.edu/courses/nitrous2/technique.html
V. Technique for Administering Nitrous Oxide Conscious Sedation
The following is a suggested "step by step" technique for administering nitrous oxide - oxygen conscious sedation. Techniques may vary slightly from patient to patient, as each patient is an individual with different responses to different types and levels of stress. The same patient may respond differently from day to day depending on emotional conditions. Changes in medical or physical conditions, or drugs and medications the patient may be taking, can also make a substantial difference in patient reaction to nitrous oxide. Therefore, it is important to always reassess the patients physical and emotional state, as well as review all drugs the patient may be taking prior to each nitrous oxide administration.
A. Pre-induction Considerations
Before administering N2O-O2 Conscious Sedation:
1. Eating prior to receiving N2O is acceptable, but only a light meal. If the patient becomes nauseated easily (for example tends to get "car sick" or "air sick"), consider having the patient refrain from eating.
2. Many dentists permit patients who have had N2O sedation to leave the office unaccompanied, and to drive an automobile or operate potentially dangerous 1 machinery. Jastak and Orendurff in their study to test driving safety following N2O - O2 sedation found most subjects show adequate recovery to drive in 5 minutes, but one subject (of 19 studied) required additional recovery time. The maximum duration of time in the study was 30 minutes, and all subjects were young healthy volunteers that did not undergo dental treatment. The authors noted that patients who have undergone stressful treatment or receive N2O for longer than 30 minutes may require more time for recovery. In a more recent study, Conry, et. al2 subjected volunteers to 90 minutes of N2O levels sufficient to produce subjective symptoms. They concluded that following 90 minutes exposure, psychomotor function impairment continued to be detectable 10 minutes after termination of treatment, and probably continued longer. At the same time, they detected no impairment of vigilance, immediate memory or mental tracking ability. 409
Occasionally, for no apparent reason, patients seem to recover much more slowly from N2O. Therefore, the wisest precaution would be to require the patient be accompanied by a responsible adult who can take responsibility for seeing the patient home safely. When this is not practical, the patient should be asked, and be prepared to remain under observation in the office for at least an additional 20 minutes, or more, and be released only when all effects of the N2O appear to be gone. The bottom line issue is, if the patient has an accident, there is no way to prove beyond all doubt that the N2O was not a contributing factor.
An additional precaution, and one that may be an aid legally, is the Trieger
Test. Trieger Test This test would be administered both preoperatively and postoperatively. Once the postoperative drawing matches the preoperative drawing, the patient should be considered recovered well enough to leave your office.
3. If it is the first N2O experience for the patient, describe the benefits and obtain "informed"consent.
4. Check the equipment daily before the first patient receives nitrous oxide. Be sure the tanks are turned on and contain sufficient gas for the procedure. Check the machine for proper function and gas flow. Check the calibration of any machine that provides a dial for regulating the percentage of gases being delivered. Most machines guarantee an accuracy of plus or minus five percent. Insure that the fail-safe is working and the machine will cut off the N2O in the event that the O2 supply is lost. Check to see that the O2 flush valve, the air inlet valve and the non-rebreathing valve are all functioning properly.
B. Pre-induction - Patient Considerations
1. It is important to establish a good rapport, especially with the apprehensive patient. The patient must have confidence in the dentist and the technique of N2O. 3 Malamed suggests introducing the patient to N2O at an appointment prior to the one in which the stressful procedure is to be done. This permits the apprehensive patient to become familiar with the nasal hood, the smells and effects of N2O in a relaxed, non- threatening atmosphere.
2. When discussing N2O with patients, describe the technique in terms the patient can understand. Stress the positive features of N2O but don't oversell or promise a successful outcome. (Some patients don't respond well, and may reject it.) Certainly, 410
never coerce or force a patient (including pediatric patients) to receive N2O. An unpleasant result is almost assured for an unwilling recipient. If the patient enters treatment with the expectation of success, he likely will achieve it, and vice-versa.
3. Patients must understand the objective of N2O is relaxation and sedation and not anesthesia or sleep! It may be compared to a couple of beers or cocktails but with no hangover and a quick recovery. However, if referral to alcoholic beverages offends the patient because of religious or personal beliefs, it may make them reluctant to try it, and some other comparison should be used. It has been suggested that recovering alcoholics should not be given N2O because the euphoria that can accompany N2O may lead to a desire to return to alcohol.
4. Loosen tight clothing such as ties and collars. The patient should remove contact lenses.
5. Provide quiet relaxing surroundings for the patient. Avoid discussing difficulties with the assistant when the patient can hear you.
6. Recheck the medical history for any change; specifically determine if there has been any change in drugs the patient may be taking. Also take a moment to "read" the patient's physical and emotional state that particular day prior to starting N2O.
7. Suggest the patient visit the restroom prior to starting N2O. This should prevent the possible interruption of treatment, oxygenating the patient and then re-inducing the patient to resume treatment, all of which can take 10 or more minutes.
SUGGESTED PRE-INDUCTION ROUTINES
check equipment each morning & log inspection light meal - NPO if frequent car sickness, etc rest room immediately pre-op signed informed consent updated medical history set up relaxing surroundings / comfortable clothing encouraging suggestions
C. Initial Inducement
1. Place patient in a SEMISUPINE position.
2. Obtain preoperative baseline blood pressure and pulse. 411
3. Turn on 100% O2....6-8 liter flow; the normal range for most adults. (Always begin and end with 100% oxygen) Pre oxygenation is to establish flow rates and some "comfortability" and to diminish anxiety. It will increase saturation some but is unnecessary for this reason.
4. Place the hood over patient's nose and have the patient adjust for a snug but comfortable fit...check for leaks.
5. Establish a proper flow rate for the patient by observing the expansion of the bag.
6. Maintain personal contact with patient (verbal and/or tactile) throughout the procedure.
7. Introduce N2O gradually, start with 20-25% N2O, 75-80% O2.
8. Make suggestions to patient that are pleasant and relaxing. This effort can make the experience successful; your assistant may be better at this than you.
9. After 2-3 minutes, increase N2O concentrations in stages to the desired effect -but not exceeding a maximum, in most cases, of 50% (30% - 40% N2O is usually sufficient). The patient should breathe a given level for 3-5 minutes before increasing the concentration to the next higher level.
10. Continue to monitor the patient, but do not allow the patient to talk excessively...(also monitor the machine).
11. Reduce N2O mixture to the lowest percentage with which the patient is comfortable. Near end of procedure cut off N2O and give 100% O2.
12. In Texas, the dentist can not leave the operatory while the patient is receiving N2O unless the hygienist or assistant present in the operatory has passed the Texas State Board N2O certification test. The dentist may leave the room if O2 only is being administered. This, of course, may vary in different states; so each state's requirements must be reviewed.
13. Post oxygenate for 3-5 minutes, or longer if the patient exhibits continued signs of N2O effects.
14. Upright the chair slowly, and keep in the patient in the sitting position for a few minutes before allowing to get up out of the chair. 412
15. Obtain post operative blood pressure and pulse.
16. Always compliment the patient on how well he or she performed.
17. If unaccompanied, the patient should remain in the office for an additional 20 minutes after completion of oxygenation, or longer if the patient can still feel the effects of N2O.
D. Comments
1. 50-50 is average maximum...for most patients 30-40% N2O is sufficient, and many patients do well with only 25-35% N2O.
2. A few patients may tolerate higher percentages, but generally most complications develop above 50% N2O. If you feel greater than 50% N2O is necessary to obtain the desired affect, consider using another form of patient sedation such as oral sedation.
3. At higher altitudes, somewhat higher percentages may be required.
RECORDS
Keeping accurate records of each N2O administration can be extremely helpful. For example, if after administration, it is noted that a certain patient does well on 35% N2O, time and N2O can be saved by going to that percentage and not giving more than is necessary. This does not mean that titration is not necessary for each patient each administration time, as the patient's needs and emotional state may vary from day to day; but, in general, one can expect to titrate near the same percentage each administration. In addition, records are invaluable in defense of a possible malpractice threat.
Records of the N2O administration are kept as a part of the regular patient's record. The following information should be retained:
1. Date of administration 2. Time of administration 3. Pre and postoperative vital signs 4. Settings (percentages of gases) plus total flow in liters 5. Premedication used (if any). What used, how much, how given, and any other medications being taken by patient. 6. Time started (actual) O2 + N2O. 413
7. Time ended (actual) N2O and O2 (indicates postoxygenation). 8. Any pertinent occurrences during administration. 9. Time patient left office. 10. Condition of patient when leaving office. (And who was with patient) 11. Names of persons in attendance during operation. (assistant if more than one working in office)
DISINFECTION OF EQUIPMENT
Nitrous oxide, like most inhalation anesthetic agents, are capable of depressing protective mechanisms, and thus increasing the incidence of respiratory disease. The rubber or plastic goods, such as the nasal hood, which have come in contact with the patient or the patient's exhaled breath become contaminated and must be disinfected before using again for another patient. Rubber goods are now on the market that are autoclavable; expensive but reuseability and a much improved method for preventing cross contamination makes the expense tolerable. Gas sterilization is also an alternative, but expensive. Chemical disinfection is still a choice, however, concern is surfacing that respiratory irritation following chemical disinfection may be present. It is very important, therefore, that all the equipment is rinsed thoroughly and allowed to dry before reuse.
Simply follow the autoclaving instructions that will be included with the equipment when autoclaving the rubber and scavenging system. According to Yegiela et al4, to chemically disinfect, perform the following: After each use, wash the nasal hood with soap and water to remove gross debris, and soak for 10 minutes in 2% glutaraldehyde. Rinse thoroughly with tap water and allow to dry. Yegiela also suggests weekly sterilizing all tubing, reservoir bags, and nasal hoods by storing them in glutaraldehyde for 10 hours, followed by rinsing in warm tap water for 1 hour.
Disposable nasal masks are available, often given to the patient or saved in the office for their next appointment. This eliminates cross contamination problems, but additional expense must obviously be absorbed somewhere. Nasal mask inserts are also an option from some manufactures. These inserts can be removed from the nasal masks after each patient and autoclaved or disinfected as suggested above.
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51.) Who invented the Ozone Generator?
A. Thomas Edison B. Christian Friedrich Schonbein C. Nikola Tesla D. Marie Curie https://www.lenntech.com/library/ozone/history/ozone-history.htm
History of ozone Past developments in ozone application
A Dutch chemist called Van Marum was probably the first person to detect ozone gas sensorially. In the description of his experiments, he mentioned the notion of a characteristic smell around his electrifier [1,3]. However, the discovery of ozone was only just mentioned by name decennia later, in a writing of Schönbein that dates back to 1840. This discovery was presented to the University of München. Schönbein had noticed the same characteristc smell during his experiments, that Van Marum had tried to identify earlier. He called this gas 'ozone', which is distracted from ozein; the Greek word for scent. Generally, the discovery of ozone is ascribed to Schönbein. Moreover, Schönbein is mentioned as the first person to research the reaction mechanisms of ozone and organic matter.
After 1840, many studies on the disinfection mechanism of ozone followed. The first ozone generator was manufactured in Berlin by Von Siemens [1,3,6]. This manufacturer also wrote a book about ozone application in water. This caused a number of pilot projects to take place, during which the
disinfection mechanism of ozone was researched. Figure 1: Marius Paul Otto The French chemist Marius Paul Otto (figure 1) received a doctorate at the French University, for his essay on ozone. He 415
was the first person to start a specialized company for the manufacture of ozone installations: 'Compagnie des Eaux et de l’Ozone' [5].
The first technical-scale application of ozone took place in Oudshoorn, Netherlands, in 1893 [3,5]. This ozone installation was thouroughly studied by French sientists, and another unit was installed in Nice after that (in 1906). Since than, ozone was applied in Nice continuously, causing Nice to be called the 'place of birth of ozone for drinking water treatment'. In the years prior to World War I, there was an increase in the use of ozone installations in various countries. Around 1916, 49 ozone installations were in use throughout Europe (26 of which were located in France) [3]. However, this increase faltered soon afterwards. This was consequential to research of toxic gases, which evidently lead to the development of chlorine. This disinfectant appeared to be a suitable alternative to ozone, as it did not have the shortcomings in management, such as low applicative guarantee and low yield of ozone generation. Ozone production did not reach its prior level until after World War II. In 1940, the number of ozone installations that were in use worldwide had only grown to 119. In 1977 this number, had increased to 1043 ozone installations. More than half of the installations were located in France [1,3]. Around 1985, the number of applied ozone installations was estimated >2000 [2].
Today, chlorine is still preferred over ozone for water disinfection. However, the last decennia the application of ozone applications did start to increase again. This was caused by the discovery of trihalomethanes (THM) as a harmful disinfection byproduct of chlorine disinfection, in 1973. Consequentially, scientists started looking for alternative disinfectants [5]. Another problem was an increase in disturbing, difficultly removable organic micropollutants in surface waters. These compounds appeared to be oxidized by ozone faster than by chlorine and chlorine compounds. Furthermore, ozone turned out to deactivate even those microorganisms that develop resistance to disinfectants, such as Cryptosporidium. Finally, there has been a progress in the abolishment of shortcomings in ozone management.
Read more: https://www.lenntech.com/library/ozone/history/ozone-history.htm#ixzz6JLtSknMa
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52.) Ozone is measured in:
A. Milligrams B. Liters C. Ounces D. Gamma https://simplyo3.zendesk.com/hc/en-us/articles/360001680987-How-is-ozone- measured-What-is-gamma-and-ug-mL-
How is ozone measured? What is gamma and ug/mL?
Let’s take a second to learn about ozone concentrations.
Ozone is measured in a number of different ways. Ozone Generators measures ozone concentration in micrograms per milliliter (ug/mL), which is just a fancy way of saying how strong it is. The higher the concentration of ozone, the stronger it will be. We also use the term “gamma” instead of micrograms per milliliter (ug/mL) because it is easier to say, but they are the same thing.
Gamma = ug/ml = how strong the ozone is.
Your chart will look something like this. 417
As you will see in the instructions with an ozone generator, when you rotate the knob on the regulator you change the strength of the ozone.
The regulator is able to control how fast the oxygen is dispensed. Rotating the knob changes how fast the oxygen is dispensed. The speed of the oxygen is called “flow rate”.
How fast the oxygen is dispensed (flow rate) affects how strong the ozone is (ozone concentration).
The slower the flow rate, the higher the concentration of ozone. The faster the flow rate, the lower the concentration of ozone.
Seems kind of backward, huh?
Well, inside the ozone generator is a piece called the "reactor". This is where the ozone is made. So the more time the gas spends in the reactor, the more opportunity it has to make 418 ozone. It's kind of the difference between painting a deck for 4 hours vs. 8 hours. You are going to get more done in 8 hours.
So this is why we like pediatric oxygen regulator, they can go to slow flow rates like 1/8, 1/16, and 1/32 Liter Per Minute (LPM). Normal regulators only go to 1/2 or maybe 1/4LPM.
However, our Ozone+ oxygen tank regulator was specially designed for ozone generators. It can get twice the concentrations and flow rates of any other regulator in the world.
53.) Tubing for using ozone must be latex free
A) True B) False
https://www.ozonesolutions.com/knowledge-center/ozone-compatible- materials.html
Many of these materials were tested in-house at Ozone Solutions. Some are commonly known and rated as shown by others. All tests were performed at very high levels of ozone concentration.
For any materials not shown, please call. We may have data on file or we can use our labs to test the material for you!
Our Rating System
Rating Description
A Excellent Ozone has **no effect** on these materials. They will last indefinitely.
B Good Ozone has minor effect on these materials. Prolonged use with high concentrations of ozone will break down or corrode these materials beyond usefulness.
C Fair Ozone will break down these materials within weeks of use. Prolonged use with any ozone concentration will break down or corrode these materials beyond usefulness.
D Poor Ozone will break down these materials within days or even hours of use. These materials are not recommended for any use with ozone. 419
Ozone cracking in natural rubber tubing
Material Rating Material Rating
ABS Plastic B LDPE B
Acetal (Delrin®) C Magnesium D
Acrylic (Perspex®) B Monel C
Aluminum C (wet ozone) / B (dry Natural Rubber D ozone)
Brass B Neoprene C
Bronze B Nylon D
Buna-N (Nitrile) D PEEK A
Butyl A Polyacrylate B
Cast Iron C Polyamide (PA) C
Chemraz A Polycarbonate A
Copper B Polyethelyne B
CPVC A (does get brittle) Polypropylene C
Cross-Linked Polyethylene A Polypropylene (glass-filled) C (PEX) (GFPP)
Durachlor-51 A Polysulfide B
EPDM C (wet ozone) / B (dry Polyurethane, Millable A ozone)
EPR A PVC A (wet ozone) / B (dry ozone) brittle 420
Material Rating Material Rating
Ethylene-Propylene A PVDF (Kynar) A
Fiber Reinforced Plastics (FRD) D Santoprene A
Flexelene B Silicone A
Fluorosilicone A Stainless Steel - 304/316 A
Galvanized Steel C Stainless Steel - Other Grades B
Glass A Steel (Mild) D
Hastelloy-C® A PTFE A
HDPE A Titanium A
Hypalon® C Tygon B
Hytrel® C Vamac A
Inconel A Viton A
Kalrez A Zinc D
Kel-F (PCTFE) A
421
54.) When using ozone that has been bubbled through oil it becomes an Ozonide which is safer to breath.
A. True B. False https://globalhealing.com/natural-health/health-benefits-ozonides/
Health Benefits of Ozonides
Written by Dr. Edward GroupFounder
Georg Cronheim published two articles in 1947 that give a thorough and intriguing description of the pharmaceutical uses of ozonides. Since 1947 remarkably few scientific discussions have been made with regard to the chemotherapeutic effects of ozonides, however, those that have been published seem very worthy of review. Changes in chemical nomenclature over the past 66 years require that I take a few 422 sentences to clarify contemporary terms. Historically the term ozonide was used to describe any product or products that result from the ozonation of unsaturated compounds like waxes, rubbers, or oils. These "ozonides" were describing a mixture of ozonides, and or, hydroperoxides, and or, the many possible polymeric arrangements of each. As dozens of brilliant chemists, most notable, Christian Friedrich Schonbein, Carl Dietrich Harries, Rudolf Criegee, and Philip Bailey, have struggled to elucidate the true nature of ozonolysis, we now use the term ozonide to indicate a 1,2,4-trioxolane compound, as depicted in Figure 1.
The production of the 1,2,4-trioxolane functionality is highly dependent on both the structure of the alkene being ozonated, and on the conditions of the reaction. Many alkenes will not produce 1,2,4-trioxolanes, as the major product, regardless of reaction conditions. This information is Impeccably described by Philip Bailey in his comprehensive review of ozone chemistry, which still stands as the preeminent reference for the reactions with ozone. For this discussion the term ozonide will refer to a compound with the 1,2,4- trioxolane functionality, sometimes described as the secondary ozonide in chemical literature, where the primary ozonide is the first adduct of ozone and the alkene. Thus an ozonide is distinguished from the complicated mixture of compounds produced by the reaction of ozone with unsaturated mixtures like oils, waxes, and rubbers.
Review For those of you who don't remember the details of those 1947 journal articles I will reiterate a few of the more important references. The uses of ozonides described by Cronheim were mostly of topical preparations with germicidal properties, except the oral application for dogs and swine as described by Butz and La Lande. Inventors have been claiming dramatic medicinal uses for ozonides since 1902 when William Neel first described the medicinal use of ozonides for diseases of the blood and respiratory organs, where ozonated oils were inhaled. Then in 1917 William J. Knox ozonated ricinoleic acid or caster oil to produce a germicidal laxative. In 1921 James Todd published "Experiments with Oxygen on Disease" (Pittsburgh, PA) where he detailed the manufacture of ozonated olive, and cod-liver oils, that give "miraculous cures" with oral dosages. In 1937 Butz and La Lande successfully treated dogs infested with ascarides with oral dosages of an ozonide and diheptanol peroxide. They also found it of significance to note that no toxicity values could be determined for the ozonides or the diheptanol peroxide, as no toxicity was ever observed regardless of dosage. In 1942 Charles C. Johnson described the ozonation of the purified triglyceride 9 of oleic acid, and its fungicidal, germicidal, and deodorizing applications. Mr. Johnson also mentions 423
“exceptionally meritorious results in treatment of secondary or tertiary burns”. Then after nearly half a century of dormancy, ozonides have reemerged by many orthogonal routes as this discussion will try to make clear. In 1986 De Villez used ozonated oils to treat acne. From 1988 to 1994 Stephen Herman generated a long list of patent publications, and a far longer list of claims for the uses of ozonides. The list of claims covers thousands of compounds, and hundreds of uses. I will list several of the uses described: treatment for insect stings, athletes foot, nail fungus, warts, viral infection, HIV, insecticide, fungicide, sunburn, serious burn repair, scar inhibitor, cancer, spermicide, arthritis, protozoal infection, leishmaniasis, to name most of the applications. In 1992 Luiz-Claudio de Almeida Barbosa et al. Describe accidentally isolating a stable ozonide with anti-malarial activity. Starting in the early 1990s a multinational team of chemists have synthesized, purified, and analyzed many dozens of ozonides with anti-malarial activity. Both in vitro and in vivo work is reported for both oral and subcutaneous dosages giving much insight as to the structure activity relationship (SAR). In his 2002 patent publication Vennerstrom et. al. described the synthesis, purification and physical properties of 90 spiro and dispiro 1,2,4 trioxolane compounds their thermal stability and the degree of anti-malarial activity of each. Vennerstrom also mentions in this document that these compounds have anti-cancer properties. The work from this group is extensive and beyond the scope of this review, but I would like to digress a moment to discuss the very high yields reported by Vennerstrom using fully substituted alkenes. In my opinion, both Creegee and Baily would be surprised at these results as their work points to very low yields for tetra substituted alkenes and much higher yields 1,2-substituted alkenes. In 1994 Davy K. Koech reports "Trioxolanes: a new generation of compounds with Wide Ranging Activities". And in 2008 Koech et al. published "Clinical 16 Applications of Trioxolane Derivatives" where he specifically indicates, an ozonide compound prepared and used effectively for the treatment of both AIDS and arthritis. In 1999 Dr. Gerhard Steidl published "The Fight Against Bacteria, Funguses, and Parasites by Supporting the Oxidative System in the Human Organism". This is the first of three papers published by Dr. Steidl concerning the use of ozonides. The second and third papers are titled, "Medicinal Microbiology Elimination of Pathogenic Bacteria, Fungi, Parasites, Viruses by Oxygen and Bitter Drugs" (Sept. 2000), and the more extensive follow on paper, "Use of Ozonides in the Treatment of Malignant Disease - basic principles and clinical results" (Jan. 2002). These documents seem to be web based publications found by a web search of the titles. Dr. Gerhard Steidls’ papers again describe hundreds of medical applications where virtually all known parasitic, viral, fungal, and tumor cells, can be treated, at least partially, as bitter drugs are used concomitantly with an ozonized oil. I would like to add that Dr. Steidl also suggests that some forms of depression, anxiety, hyperactivity, and hypo-activity may also be treated with these oxidative therapies. Sasaki et al claim anti tumor activity with an ozonide. In Sept. 2004 Hofmann et al describe the treatment of coronary arteriosclerosis by an oxidative therapeutic formulation, followed in April 2005 by a second patent describing the successful treatment of horses infected with sarcocystis protozoal infections. And a third patent issued in 2009 describes the bone regeneration 20 properties of these oxidative therapies. The most recent excitement surrounding the use of ozonides is related to the 424 treatment of malaria. Most notable are the patents by Vennerstrom et al. describing antimalarial activity with dispiro-1,2,4-Trioxolanes.
Discussion One must wonder why with the seemingly endless list of medical uses claimed by ozonides, with no significant side effects noted, why the market is relatively void of oxidative therapies. I shall propose several reasons why this might be the case however the true answer will likely be the complicated equilibrium between these and other unknown factors. First, the chemical literature is strewn with references to the explosive danger of trying to isolate trioxolane molecules. I must confess to my excessive care (fear) when first working with these compounds as I understood from much of the chemical literature that ozonides were very unstable, and subject to explosive decomposition. Ozonides are traditionally thought of as only intermediates in ozonolysis, where an alkenes is converted to; alcohols, aldehydes, ketones, carboxylic acids, or peroxides, and the isolation of the ozonide has been strictly avoided by much of chemical literature. I would like to support this statement with a few quotes, wherein ozonides are specifically discouraged from being isolated: From the 1966 US patent 3,284,492, where Fremery and Fields state: "Ideally the highly reactive and unstable ozonide should be converted quickly and simply to the desired product.” From the current Organic-Chemistry.org description of ozonolysis, "while secondary ozonides are more stable than primary ozonides they should not be isolated from an unmodified ozonolysis as other explosive compounds may have been formed". And this online article written by Derek Lowe, indicated the current thinking of most pharmaceutical chemists, where Dr. Lowe questions the sanity of trying to develop an ozonide for use as a drug, as he states, “there are some structures that I just wouldn’t make on purpose, and which I wouldn’t submit for testing even if I made them by accident.” As far as the explosive reputation of ozonides, I think a few comments from Philip Bailey could go a long way to clear up the misconception about their stability, “...most of the explosive “ozonides” of early literature were not ozonides at all, but polymeric peroxides, or ozonides contaminated with such.” Bailey goes on to 25 describe how many ozonides have been safely isolated, and that discrete melting points of over 100 Centigrade is not uncommon. Clearly, the extensive work performed by Vennerstrom, and what must be a small army of other excellent chemists, clearly demonstrate the stability of these compounds as most decompose between 150-170C. Second, It may be that the continued bombardment by product advertisers about the benefits of "antioxidants" has, indirectly, given a bad reputation to oxidizing compounds. In fact, the opposite seems true, as I can think of many examples where peroxides and ozonides demonstrate healing properties, and can think of no therapeutic reducing agents. It has also been suggested that the technology of oxidative therapeutic treatments were abandoned as a result of the discovery of “modern” antibiotics, as might be corroborated by the disappearance of ozonide research after 1947.
Summary It seems clear that aerobic biology of eukaryotic organisms is very compatible with oxygen and reactive oxygen species (ROS) like singlet oxygen, superoxide, and other oxygen radicals. Whereas anaerobic organisms (prokaryote) like bacterium, and fungus, 425
do not generally tolerate these type of oxygen species. It also seems obvious that there are many pharmaceutical opportunities for the use of ozonides as antimicrobial agents. Lastly, it has been suggested that the technology of oxidative therapeutic treatments were abandoned as a result of the discovery of “modern” antibiotics. It's also has been suggested that our understanding of modern antibiotics is not perfect, and that they are a very poor treatment for parasitic and fungal infestation, is a good reason for reevaluation of the “early” chemical research. Let me end with a quote from my esteemed predecessor, "The pharmaceutical use of oxygen releasing compounds dates back to 1818 when Thenard discovered hydrogen peroxide. The compounds that have been employed since then are mostly inorganic and organic peroxides. Very little attention has paid to ozonides which can also decompose to release nascent oxygen and can be used in the same manner as peroxides." Georg Cronheim, 1947
55.) Ozone can be used to desensitize a tooth.
A. True B. False
https://dallasdentist.net/dentalozone/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5345329/
http://ispub.com/IJDS/7/2/6215
Ozone: A new face of dentistry R Garg, S Tandon
Keywords bleaching, caries, ozone, ozone oils
Citation R Garg, S Tandon. Ozone: A new face of dentistry. The Internet Journal of Dental Science. 2008 Volume 7 Number 2.
Abstract Most of people possess a fear towards dentistry. On account of this fear, they avoid the dental treatment. Infact, people fear injections and drills that are used in dental clinics. But, in recent 426
time, dentistry has been experiencing a period of dynamic changes and growth, perhaps like no other time before. The use of ozone in dental treatment is the result of this dynamics and growth. Incorporation of ozone in dental clinic set-ups would eradicate the feeling of pain during dental treatment and also cut off the treatment time, significantly. Ozone has been shown to stimulate remineralization of recent caries-affected teeth after a period of about six to eight weeks. Scientific support, as suggested by demonstrated studies, for ozone therapy presents a potential for an atraumatic, biologically-based treatment for conditions encountered in dental practice.
Introduction Until now, dentists have been convinced that caries can only be eliminated by the removal of the carious part of the tooth followed by replacement of that deceased substance with a suitable restorative material. Also, surgical treatment for caries involved usually the removal of healthy tooth substance, with occasionally ensuing pulpitic disorders. And, very oftenly, sooner or later, secondary caries appeared and filling needed replacing. But, all that has changed now. The treatment and prevention of tooth decay, it only takes seconds, has minimal physical intervention and is completely pain-free. This has become possible only because now, dentists have in their armamentarium, ozone. Ozone is a gas composed of three atoms of oxygen and is the most powerful oxidant. It is one of the most important gases in the stratosphere due its ability to filter UV rays which is critical for the maintenance of biological balance in the biosphere. It has been used in human medicine since the beginning of twentieth century. Today, ozone is used not only to disinfect wounds and improve blood circulation, but also as a treatment for carcinomas, leukemia, rheumatism and multiple sclerosis. In dentistry, now a days, ozone has got its own role. It is used in a safe and controlled manner to remove caries painlessly followed by remineralization of that demineralized tooth structure.1 This is very much true for the cases of incipient caries. But, still for the cases of open cavitations, scientists will have to go a long way. But definitely one day, ozone would be the single only answer to all types of caries.
What is ozone? Ozone is a gas composed of three atoms of Oxygen and present naturally in the upper layer of atmosphere in abundance. It has got the capacity to absorb the harmful ultra-violet rays present in the light spectrum from the Sun. Thus, ozone filters the light spectrum high up in the atmosphere and protects the living creatures from the ultra-violet rays. Ozone is an unstable gas and it quickly gives up nascent Oxygen molecule to form Oxygen gas. Due to the property of releasing nascent Oxygen, it has been used in human medicine since long back to kill bacteria, fungi, to inactivate viruses and to control hemorrhages. Medical grade ozone is made from pure medical oxygen because oxygen concentration in the atmospheric air is variable. Atmospheric air is made up of nitrogen (71%), oxygen (28%), and other gasses (1%) including ozone which is altered by processes related to altitude, temperature, and air pollution. 427
There are three different systems for generating ozone gas2: • Ultraviolet System: produces low concentrations of ozone, used in esthetics, saunas, and for air purification. • Cold Plasma System: used in air and water purification. • Corona Discharge System: produces high concentrations of ozone. It is the most common system used in the medical/ dental field. It is easy to handle and it has a controlled ozone production rate.
Brief History Christian Friedrich Schönbein, a German chemist is considered to be the father of ozone therapy (1840). When he passed an electrical discharge through water, a strange smell was produced, which he called ozon, from the Greek word ozein (odor). Edward Fisch was the first dentist to use ozone in 1950. He used ozone to treat Austrian surgeon Ernst Payr who then became an ozone enthusiast and began a line of research dedicated to its use in healthcare. At the time, ozone therapy was difficult and limited due to the lack of ozone-resistant materials, such as Nylon, Dacron, and Teflon, until 1950 when ozone-resistant materials were manufactured. At that time Joachim Hänsler, a German physicist and physician, joined another German physician, Hans Wolff, to develop the first ozone generator for medical use. Their design continues to be the basis for modern equipment. Medical grade ozone is a mixture of pure oxygen and pure ozone in the ratio of 0.05% to 5% of O3 and 95% to 99.95% of O2. Due to the instability of the O3 molecule, medical grade ozone must be prepared immediately before use. Within less than an hour after preparation only half of the mixture is still ozone while the other half is transformed into oxygen. As a result, it is impossible to store ozone over long periods of time. In order to control the decomposition of O3 into oxygen it can be associated with a vehicle with aqueous properties to promote the conversion more quickly or with a vehicle with more viscous properties to retard the conversion.
Dental ozone generators Recent studies have proven the effectiveness of applying ozone in both the medical and dental fields and its indications for use in a wide range of specialties.3 Application of ozone gas has been advocated in dentistry for sterilization of cavities,456 root canals,78 periodontal pockets,9 and herpetic lesions.10 CurOzone USA Inc. (Ontario, Canada) developed the HealOzone, which is now distributed by KaVo Dental (KaVo, Biberach, Germany), for use in dentistry. Millar and Hodson11 compared the safety of two ozone generating systems. These are the Ozicure device (which is no longer available and is not licensed for use in Europe) and HealOzone developed by CurOzone USA Inc., now distributed by KaVo Dental, Biberach, Germany, for use in dentistry. The two were compared based on the amount of ozone that escaped during gas application. The investigators found the Ozi-cure device, when used without adequate suction, allowed ozone to reach concentrations above the permitted levels and, therefore, should not be used. The HealOzone generator was found to be safe to use following the manufacturer’s recommendations. After the treatment, a special filter in the generator turns the residual ozone back into oxygen.12
Indications of Ozone in dental problems 428
Very recently, in dentistry, ozone has got its role in various dental treatment modalities. Interest in ozone use in dentistry is due to the infectious diseases associated with the oral cavity. Ozone therapy presents great advantages when used as a support for conventional treatments, for example, to dental caries, periodontal procedures, and endodontic treatment.13
● Prophylaxis and prevention of caries ● Remineralization of pit and fissure caries ● Remineralization of root and smooth surface caries ● Restoration of open cavitations along with conventional conservative measures ● Bleaching of discoloured root canal treated teeth ● Endodontic treatment ● Desensitization of extremely sensitive tooth necks ● Soft tissue pathoses Caries prevention and remineralization Ozone can be used to kill bacteria present in carious lesion, painlessly and even without anaesthetic. Ozone is applied to the carious lesion in a controlled manner, safely killing bacteria that have caused caries, thus requiring minimal of physical intervention and just a few seconds. In cases of incipient caries, ozone can kill bacteria in the demineralized part and this demineralized tooth structure then, can be remineralized using a special remineralization kit, containing Calcium, Fluorine, Phosphorus and Sodium, all in their ionic forms.114
Bleaching In root canal treated teeth, crown discolouration is a major aesthetic problem, especially in anterior teeth. Conventional walking bleaching requires much more time and results are not oftenly satisfactory. Also, capping the tooth with ceramic crown is not always a good idea. But, now, ozone has the answer to all these questions. After removing the root canal filler material from the pulp chamber, the canal is sealed tight at the level of cementoenamel junction. Then, the chamber is cleansed with sodium peroxide solution to remove any debris, cement particles and the smear layer, leaving the dentinal tubules opened-up. Now, a bleaching paste or a cotton pellet moistened in bleaching solution is packed in the chamber and the orifice is sealed with the Glass-inomer cement. After placing the bleaching agent in to the inner of the tooth, the crown is irradiated with ozone for minimum of 3- 4 minutes. This ozone treatment bleaches the tooth within minutes and gives the patient a happy and healthier-looking smile.
Endodontic treatment Ozone oils can be used to sterile the root canal systems and to clear the canals of necrotic debris by virtue of ozone’s bactericidal and effervescent properties. Ozone oils are ozonated sunflower oil or olive oil or groundnut oil. This ozone oil irrigation is more quick and efficient in canal sterilization than that conventional irrigation by the sodium hypochlorite and sodium peroxide combination.
Desensitization of sensitive root necks Quick and prompt relief from root sensitivity has been documented after ozone spray for 60 seconds followed by mineral wash onto the exposed dentine in a repetitive manner. This 429
desensitization of dentine lasts for longer period of time. Smear layer present over the expose root surface prevents the penetration of ionic Calcium and Fluorine deep into the dentinal tubules. Ozone removes this smear layer, opens up the dentinal tubules, broadens their diameter and then Calcium and Fluoride ions flow into the tubules easily, deeply and effectively to plug the dentinal tubules, preventing the fluid exchange through these tubules. Thus, ozone can effectively terminate the root sensitivity problem within seconds and also results last longer than those by conventional methods.
Soft tissue pathoses Ozone has been reported to accelerate the healing of soft tissue conditions, i.e. aphthous ulcers, herpes labialis, ANUG and other gum infections. It also reduces the post-extraction healing time by forming a pseudo-membrane over the socket, so protecting it from any physical and mechanical insults.
Ozone therapy contraindications The following are contraindications for use of ozone therapy:13
● Pregnancy ● Glucose-6-phosphate-dehydrogenase deficiency (favism) ● Hyperthyroidism ● Severe anaemia ● Severe myasthenia ● Active hemorrhage Conclusion Most people suffer anxieties about being treated for tooth decay or more precisely; they fear the injections and drills. But, now, with ozone treatment, this is all the thing of past. Studies have shown that 99 percent of all the bacteria causing tooth decay have been eliminated after 10 seconds of ozone exposure and even 99.9 percent bacteria after 20 seconds exposure. Thus, treating patients with ozone cuts off the treatment time with a great deal of difference, it eliminates the bacterial count more precisely and moreover, it is completely painless, so increasing the patients’ acceptability and compliance.111516 Ozone can now be incorporated in various other treatment modalities also, like bleaching of discoloured teeth, root canal treatment, desensitization and treatment of some soft tissue infections. Ozone, definitely, seems to be a promising treatment modality for various dental problems, in future.
References 1. Hickel R, Huth C. Initial therapeutic impressions of the use of Ozone for the treatment of caries. Deutscher Zahnarzte Kalender 2004; 1-10. 2. Nogales CG, Ferrari PA, Kantorovich EO, Lage-Marques JL. Ozone Therapy in Medicine and Dentistry. J Contemp Dent Pract 2008 May; (9)4:075-084. 3. Viebahn-Haensler R. The use of ozone in medicine. 4th ed, 2002. 4. Celiberti P, Pazera P, Lussi A. The impact of ozone treatment on enamel physical properties. Am J Dent. 2006; 19(1):67-72. 430
5. Baysan A, Whiley R, Lynch E. Anti microbial effects of a novel ozone generating device on microorganisms associated with primary root carious lesion in vitro. Caries Res. 2000; 34:498- 501. 6. Baysan A, Beighton D. Assessment of the ozone-mediated killing of bacteria in infected dentine associated with non-cavitated occlusal carious lesions. Caries Res. 2007; 41:337-341. 7. Nagayoshi M, Kitamura C, Fukuzumi T, Nishihara T, Terashita M. Antimicrobial effect of ozonated water on bacteria invading dentinal tubules. J Endod. 2004; 30(11):778-81. 8. Estrela C, Estrela CRA, Decurcio DA, Hollanda ACB, Silva JA. Antimicrobial efficacy of ozonated water, gaseous ozone, sodium hypochlorite and chlorhexidine in infected human root canals. Int Endod J. 2007; 40:85-93. 9. Nagayoshi M, Kitamura C, Fukuzumi T, Nishihara T, Terashita M. Efficacy of ozone on survival and permeability of oral microorganisms. Oral Microbiology and Immunology 2004; 19:240-6. 10. Macedo SB, Cardoso CC. [The use of ozone in Dentistry]. 16º Campinas International Conclave 2005; 115. 11. Megighian GD, Dal Vera MV. Patients’ attitude towards and satisfaction with managing caries with Ozone as a routine treatment in dental practice. J Dent Res 2003; 82B: 2069. 12. www.kavo.com/healozone. 13. Nogales CG. [Ozonetherapy: Medical and Dentistry application] [Dissertation]. São Paulo (Brazil): University of São Paulo; 2006. 14. Abu-Nab’a L, Shorman AL, Lynch E. Ozone treatment of primary occlusal pit and fissure caries. Caries Res 2003; 37: 272. 15. Dahnhard JE, Jaeggi T et al. Treating caries in anxious children with Ozone: Parents’ attitude after the first session. J Dent Res 2003; 82B: 2034. 16. Domingo H, Smith C et al. Patients’ attitude to managing caries with Ozone. J Dent Res 2002; 81A: 1337.
Author Information Rajeev Kumar Garg Dental surgeon, Dental surgery clinic
Sandeep Tandon Professor & Head, Dept. of Paedodontics, Govt. Dental College & Hospital
431
56.) If a patient begins to cough when using ozone on them. Having them chew Vit C can counteract the impulse to cough.
A. True B. False
https://isom.ca/article/increasing-the-effectiveness-of-intravenous-vitamin-c-as- an-anticancer-agent/
https://www.austinozone.com/therapies/ozonization-its-purpose-and-its-use-in-therapy/
Published Article by a UK Clinical Nutritionist Ozone is a natural gas that we breathe daily. It is created when oxygen (O2) molecules are split into two separate atoms by ultra violet radiation from the sun, lightning, and electric arc. The freed atoms recombine in 3-atom groups to form cousins of oxygen: ozone (O3). The word ozone comes from the Greek word ozein meaning smell, because of its distinctive sun-ray lamp smell. Ozone is nature’s way of cleaning pollution from our atmosphere.
HOW DOES OZONE WORK? Ozone tends to react with other substances by attaching the third oxygen atom to the other substance, thereby oxidizing it. Many of us have heard weather reports where the ozone levels were referred to in conjunction with pollution levels. Ozone is present in smog because certain processes that create pollution also produce ozone. Ozone recombines with those same pollutants and neutralizes them by breaking them down into water, carbon dioxide, sulphur, nitrogen and oxygen. Generated low levels of ozone used for water purification prove very successful, as it is possibly the most powerful antibiotic, sanitizer and deodorant known to man. It doesn’t merely mask harmful substances or smells – it seeks them out and eliminates them. The highest natural levels of ozone are found at the seashore and in forest/mountain locations, places where you automatically feel refreshed. The invigorating air after a thunderstorm is as a result of ozone, so is the smell of naturally dried laundry on a clothesline. USES OF OZONE Perhaps you are a smoker or live with someone who smokes or maybe work with people who do. That is a worrying scenario as cigarette smoke has over 3,600 chemicals. Ozone will break those chemicals down into their basic molecular components, neutralizing them. It is capable of destroying tar, soot and oil in the lungs, benzene, vinyl chloride and other hydrocarbons. Having performed this task the ozone itself reverts to just plain oxygen! 432
Dr. Clark regularly warns about the dangers of airborne gasses such as formaldehyde, carbon monoxide, and chemical pollutants given off by carpets, wallpaper, and furniture. Take for example formaldehyde. When formaldehyde is infiltrated by ozone it breaks down into carbon dioxide, water and oxygen. Well worth bearing in mind if you have pollutants in your house or workplace like these that you are not in a position to remove. Carbon monoxide is a lethal gas and cannot be detected easily. It bonds with human blood 600 times faster than oxygen. Ozone changes carbon monoxide to carbon dioxide, a harmless gas. Solvents from fresh paint are instantly neutralized by ozone as are cooking smells, animal odors, cigarette smoke, garbage smells and mildew, etc. Perfume can be intolerable for people suffering chemical insensitivities. An ozonator may be the answer. In some countries people wear tiny ozone generators around their neck just for this reason – to neutralize pollutants, perhaps on a journey through heavily polluted areas. Bacteria, molds, fungi and even mildew are destroyed when they react with ozone as the outer membranes or ‘shells’ of these micro-organisms contain receptors that absorb ozone to their own demise. They are anaerobic, meaning that they can thrive only where oxygen levels are depleted. Ozone increases oxygen levels. Viruses can also be destroyed by ozone on contact. In the case of polio only 0.012ppm removes all viral cells in seconds. As you know there isn’t an effective antibiotic that will touch a virus. Ozone is a particularly safe therapy to use provided that certain restrictions are respected. The Food and Drug Administration declares 0.05ppm as the safe level for 24 hour a day inhalation in the USA. However, natural outdoor levels vary between 0.03 and 0.05ppm and go several times higher than this at times and in certain ideal locations can reach 0.65ppm, so nature then breaks the FDA’s rulings! Even at these higher rates no harm has been caused, in fact the opposite is the case. In cleaning water, ozone is more efficient even than chlorine, in fact an ozone level of 0.04ppm in just 4 minutes has been shown to kill bacteria, mold and fungus. Giardia and Cryptosporidium cysts are susceptible to ozone but are unaffected by normal levels of chlorine in water. Ozone is 25 times more effective than hypochlorous acid, 2,500 times more effective than hypochlorite, and 5,000 times more than chloramine. (Results measured by the time needed to kill 99.99% of all micro-organisms). Chlorine reacts with organic materials to form chloroform, carbon tetrachloride etc generally known as trihalomethanes. These have been implicated as carcinogens in the development of kidney, bladder and colon cancer. However, ozone when used repeatedly and in conjunction with charcoal, reacts with organic materials to break them down into simpler compounds that are not dangerous. Ozone swimming pool cleaners are very popular and one of the reasons is that when water is ozonated, algae is oxidized and floats to the top, metabolic by products of algae are oxidized also, removing odor and taste. So cleaning the pool is not such a frequent or time-consuming job, chemicals are not required and the water is smelling good and clean (…just makes you want to jump in). In cleaning the air, ozone reacts with odors oxidizing them into harmless compounds or carbon dioxide. We would have sufficient ozone but all the chemical gasses released into the atmosphere by cars and factories are using it up. Surely oxygen generators would be sufficient? Well, ozone is approximately 3,500 times more potent an oxidant than oxygen. High mountain 433
areas produce high levels of ozone. This is why people with respiratory problems, TB etc. were sent to such areas. As with anything i.e. oxygen, water etc. too much can be harmful, (although ozone is an incredibly safe gas and consistently spoken of as the safest therapy, non toxic and with no evidence of free radical damage) yet no one has ever died from using ozone and it has been in use for many years. Only chronic high overdose may give problems and then there would be warning symptoms such as coughing for more than 30 minutes continuously. At such times Vitamin C (5,000mg) – an antagonist of ozone – can reverse the effect. THE HISTORY OF OZONE THERAPY Over 1000 scientific papers have been written about ozone and its benefits. The first ozone generators were developed by Werner von Siemens in Germany in 1857. In 1870 ozone was used therapeutically to purify blood by C. Lender in Germany. Today there are over 3,000 places around the world using ozone to clean their water and sewage. In 1885 The Florida Medical Association published ‘Ozone’ by Dr. Charles J. Kenworth, MD, detailing the use of ozone for therapeutic purposes. In 1896 Nikola Tesla patented his first ozone generator and went on to form a company selling ozone machines to doctors. Tesla also made ozonated olive oil and sold it to naturopaths, just as we do today. Some of Tesla’s generators are still working today. In 1902 J. H. Clark published a Dictionary of Practical Materia Medica (London) and described the successful use of ozonating water to treat anemia, diabetes, influenza, morphine poisoning, canker sores, strychnine poisoning, and whooping cough. Just a few years later ozone was used to treat Tuberculosis, anemia, chlorosis, tinnitus, asthma, bronchitis, hay fever, pneumonia, gout and syphilis. In World War I ozone was used to treat gangrene, the effects of poison gas and wounds. In 1915 Dr. A. Wolff used it to treat colon cancer and cervical cancer. But one man we may have all heard of is Dr. Otto Warberg of the Kaiser Institute in Berlin. In 1926 he announced that the cause of cancer is a lack of oxygen at the cellular level. He went on to become the only man to receive two Nobel Prizes for Medicine and be nominated for a third. Dr. Wendell Hendricks wrote, “cancer is a condition within the body where the oxidation has become so depleted that body cells have degenerated beyond control, the body is so overloaded with poisons that it sets up a tumor mass to harbor these poisons and remove them from general activity within the body”. Very similar to Dr. Hulda Clark’s views. In fact, recently Dr. Clark has said that to remove PCBs from the body – the fourth immune reducing factor in cancer patients – we need to take 2 tablespoons of ozonated olive oil three times a day for 2-3 weeks. So ozone has quite a history and is well established as a successful therapy with over 7,000 German doctors using it daily and Russian doctors even bubbling it into brine for use on burn victims. USES OF OZONE AT HOME To get back to uses within the home setting, ozone used for cleaning fruit and vegetables has an interesting side effect because ethylene given off by fruit accelerates the ripening process, 434
however, ozone reacts with ethylene reducing rapid ripening and thereby extending shelf life (Grocers note!). Regular use of ozone in the home can ensure high levels of immunity from most common diseases. Some state that ozonating water removes fluorine too. It is comforting to know that breathing the ozone bubbled through olive oil or water when using Dr. Clark’s recipes is not only safe but beneficial. Some recommend this for respiratory diseases such as bronchitis, asthma etc. If olive oil is ozonated for several weeks the oil will start to change, it foams and becomes a gel. If kept in a refrigerator this oil holds onto its ozone for up to 10 years and can be used as required on cuts, all skin complaints, burns, bites, herpes and as a lubricant when required in this setting. This gel is 95% as active as ozone gas. As this gas cleans up your body, the immune system responds, arteries and veins are cleaned, circulation improves with blood vessels unclogged, blood and lymph normalizes, inflammation reduces, bleeding stops, cardiac problems reduce as plaque is oxidized in arteries (such patients are often dependent upon oxygen tanks throughout the day), the brain and memory respond to the increases in oxygen produced, heavy metals are chelated, tumor metabolism is inhibited and the outer lipid layer of malignant cells is broken down and destroyed. Successful use of this therapy has been found with gangrene of the fingers and toes and with destroying the viruses that causes hepatitis. Many doctors are using it internally via rectum, vagina, mouth and ear. Some specialists inject it straight into the tumor, into the portal vein for the liver, or into the arm. There are ozone body suits that you can step into following a hot bath, so as to get it into the skin – referred to by nutritionists as the third kidney. Dr. Michael Carpendale wrote an article in Science magazine (Vol. 209 22 August 1980) and stated that the growth of human cancer cells from lung, breast and uterine cancers were selectively inhibited in a dose dependent manner by ozone at 0.3ppm to 0.8ppm in ambient air during 8 days of culture. Exposure to ozone at 0.8ppm inhibited cancer cell growth more than 90%. Evidently the mechanisms for defense against ozone are impaired in human cancer cells. Today both the FDA and EPA certify ozone as able to destroy 99.9992% of all pathogenic germs in the purification of water while destroying 99.9992% of all pollutants in the water simultaneously. Many doctors/therapists are testifying to the effectiveness of ozone with the HIV virus. I do not believe that there is a disease or health condition that ozone hasn’t been used with, there is no way I could list all the conditions it is successful with, all the cancers, all the bacterial, parasitic diseases etc. Unsolicited testimonials are sited on the Internet and covering such a wide variety of conditions including one of silicon poisoning following leakage from a breast implant! In recent years we have seen headlines such as ‘Burnt diesel fumes the worst carcinogen’. There are ozonators that you can have in your car plugged into the cigarette lighter (how ironic), household ozonators for water, oil and air, and larger industrial units. 435
Dr. Hulda Clark uses ozone therapy for different purposes in her therapy:
▪ To eliminate freon from the body, use 1 glass of ozonated water daily. Ozonate water for 3-4 minutes. Drink within 20 seconds of ozonating. ▪ To eliminate PCBs from the body, use ozonate olive oil. Ozonate oil for 30 minutes. Take 2 tbs. of ozonated olive oil 3 times daily for 2-3 weeks. PCBs are the fourth factor Dr. Clark has found that inhibits immunity in cancer patients (and other diseases, especially AIDS). It also makes zapping less effective. ▪ Much like frankincense oil, ozonated olive oil inhibits virus replication and is especially recommended for HIV victims or other viral conditions. ▪ To kill Ascaris and certain tapeworms. Ascaris and dog tapeworms are especially hardy, and when they are killed with the regular herbal program, they decay and release more eggs and stages than the body can handle. Ozonated oil can penetrate their membranes and kill the eggs and stages on the inside before they open up. Take 3 tbs. of ozonated oil per day, for 3 weeks, together with 2 Cysteine capsules. Caution: Do not allow this article to provoke you to experiment with ozone. Please contact a doctor or therapist with experience in this field or maybe read more about the uses of ozone in the many books printed on the subject, before beginning your own ozone progr
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57.) What is “PRF” abbreviation for?
A. Protein rich fibrin B. Platelet rich plasma C. Platelet rich fibrin D. None of these above
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4509294/
The development of bioactive surgical additives to regulate the inflammation and increase the speed of healing process is one of the great challenges in clinical research. In this sense, platelet rich fibrin (PRF) appears as a natural and satisfactory alternative with favorable results and low risks. The following review attempts to summarize the relevant literature regarding the technique of using PRF, focusing on its preparation, advantages, and disadvantages of using it in clinical applications. PRF alone or in combination with other biomaterials seems to have several advantages and indications both for medicine and dentistry, due it is a minimally invasive technique with low risks and satisfactory clinical results. Keywords: Blood platelet, fibrin, platelet-rich fibrin, bone regeneration, oral surgery
58.) Does Platelet rich fibrin secrete growth factors?
A. True B. False https://www.ncbi.nlm.nih.gov/pubmed/14691563
Platelets are known for their role in haemostasis where they help prevent blood loss at sites of vascular injury. To do this, they adhere, aggregate and form a procoagulant surface leading to thrombin generation and fibrin formation. Platelets also release substances that promote tissue repair and influence the reactivity of vascular and other blood cells in angiogenesis and inflammation. They contain storage pools of growth factors including PDGF, TGF-beta?and VEGF as well as cytokines including proteins such as PF4 and CD40L. Chemokines and newly synthesised active metabolites are also released. The fact that platelets secrete growth factors and active metabolites means that their applied use can have a positive influence in clinical situations requiring rapid healing and tissue regeneration. Their administration in fibrin clot or fibrin glue provides an adhesive support that can confine secretion to a chosen site. Additionally,the presentation of growth factors attached to platelets and/or fibrin may result in enhanced activity over 437 recombinant proteins. Dental implant surgery with guided bone regeneration is one situation where an autologous platelet-rich clot clearly accelerates ossification after tooth extraction and/or around titanium implants. The end result is both marked reductions in the time required for implant stabilisation and an improved success rate. Orthopaedic surgery, muscle and/or tendon repair, reversal of skin ulcers, hole repair in eye surgery and cosmetic surgery are other situations where autologous plate-lets accelerate healing. Our aim is to review these advances and discuss the ways in which platelets may provide such unexpected beneficial therapeutic effects.
59.) Studied indigenous groups and the “Isaac Newton of Nutrition”?
A. Isaac Newton B. Galileo Galilei C. Weston A. Price D. Albert Einstein
https://www.westonaprice.org/health-topics/nutrition-greats/weston-a-price- dds/
Dr.Weston A. Price (1870-1948), a Cleveland dentist, has been called the “Isaac Newton of Nutrition.” In his search for the causes of dental decay and physical degeneration that he observed in his dental practice, he turned from test tubes and microscopes to unstudied evidence among human beings. Dr. Price sought the factors responsible for fine teeth among the people who had them- the isolated “primitives.”
The world became his laboratory. As he traveled, his findings led him to the belief that dental caries and deformed dental arches resulting in crowded, crooked teeth and unattractive appearance were merely a sign of physical degeneration, resulting from what he had suspected- nutritional deficiencies.
Price traveled the world over in order to study isolated human groups, including sequestered villages in Switzerland, Gaelic communities in the Outer Hebrides, Eskimos and Indians of North America, Melanesian and Polynesian South Sea Islanders, African tribes, Australian Aborigines, New Zealand Maori and the Indians of South America. Wherever he went, Dr. Price found that beautiful straight teeth, freedom from decay, stalwart bodies, resistance to disease and 438 fine characters were typical of native peoples on their traditional diets, rich in essential food factors.
Photos Copyright © Price-Pottenger Nutrition Foundation®, All Rights Reserved, www.ppnf.org When Dr. Price analyzed the foods used by isolated indigenous peoples he found that they provided at least four times the calcium and other minerals, and at least TEN times the fat-soluble vitamins from animal foods such as butter, fish eggs, shellfish and organ meats.
The “primitive” Seminole girl (left) has a wide, handsome face with plenty of room for the dental arches. The “modernized” Seminole girl (right) born to parents who had abandoned their traditional diets, has a narrowed face, crowded teeth, and a reduced immunity to disease.
The importance of good nutrition for mothers during pregnancy has long been recognized, but Dr. Price’s investigation showed that 439 indigenous people understood and practiced preconception nutritional programs for both parents. Many tribes required a period of premarital nutrition, and children were spaced to permit the mother to maintain her full health and strength, thus assuring subsequent offspring of physical excellence. Special foods were often given to pregnant and lactating women, as well as to the maturing boys and girls in preparation for future parenthood. Dr. Price found these foods to be very rich in fat soluble vitamins A and D nutrients found only in animal fats.
These indigenous people with their fine bodies, homogeneous reproduction, emotional stability and freedom from degenerative ills stand forth in sharp contrast to those subsisting on the impoverished foods of civilization-sugar, white flour, pasteurized milk and convenience foods filled with extenders and additives.
The photographs of Dr. Weston Price illustrate the difference in facial structure between those on native diets and those whose parents had adopted the “civilized” diets of devitalized processed foods.
The discoveries and conclusion of Dr. Price are presented in his classic volume Nutrition and Physical Degeneration. The book contains striking photographs of handsome, healthy natives and illustrates in an unforgettable way the physical degeneration that occurs when human groups abandon nourishing traditional diets in favor of modern convenience foods.
In addition to his work on nutrition, Dr. Price conducted extensive research into the destructive effects of root canals, detailed in his two- volume work Dental Infections Oral & Systemic and Dental Infections & the Degenerative Diseases. His conclusions, ignored by the orthodox dental establishment for over 50 years, are gaining renewed acceptance as holistic practitioners are discovering that the first step to recovery from degenerative disease often involves removal of all root canals in the patient’s mouth. 440
The principles of holistic dentistry, based on the research of Weston Price and Francis Pottenger, are as follows:
Eat nutrient-dense whole foods, properly grown and prepared. Avoid root canals. If you have root canals that you suspect are causing disease, have them removed by a knowledgable dentist. Avoid mercury (amalgam) fillings. If you have amalgam fillings, have them removed by a holistic dentist who specializes in mercury filling replacement. Orthodontics should include measures to widen the palate. Extract teeth only when necessary, and then in such a way as to avoid leaving the jaw bone with cavitations, which can be focal points of infection.
Photos Copyright © Price-Pottenger Nutrition Foundation®, All Rights Reserved, www.ppnf.org Good dental health begins with the diet of the parents. The Samoan boy on the left was born to parents who ate nutrient-rich native foods. 441
The Samoan boy on the right was born to parents who had abandoned their traditional diet. He has crowded dental arches, and will be more susceptible to dental decay.
A Comparison of the Diets (Compiled from Nutrition and Physical Degeneration by Weston A. Price, DDS)
A comparison of indigenous groups which have shown a high immunity to dental caries and freedom from degenerative processes with the diets of modernized groups who have forsaken their native diets for the foods of commerce consisting largely of white flour products, sugar, polished rice, jams, canned goods and vegetable fats resulting in loss of this immunity to dental caries and in loss of freedom from degenerative processes. (Figures give the number of times the amount of minerals and vitamins which are found in indigenous diets compared with modernized diets.)
Group Minerals1 Vitamins2
Fat Water Ca P Fe Mg Cu I Soluble Soluble
large Native Eskimos 5.4 5.0 1.5 7.9 1.8 49.0 10 plus increase 442
Indians-far North of large 5.8 5.8 2.7 4.3 1.5 8.8 10 plus Canada increase
large Swiss 3.7 2.2 3.1 2.5 * * 10 plus increase
large Gaelic- Outer Hebrides 2.1 2.3 1.0 1.3 * * 10 plus increase
large Aborigines of Australia 4.6 6.2 50.6 17.0 * * 10 plus increase
large New Zealand Maori 6.2 6.9 58.3 23.4 * * 10 plus increase 443
large Melanesians 5.7 6.4 22.4 26.4 * * 10 plus increase
large Polynesians 5.6 7.2 18.6 28.5 * * 10 plus increase
Coastal Indians of large 6.6 5.5 5.1 13.6 * * 10 plus Peru increase
Andean Mountain large 5.0 5.5 29.3 13.3 * * 10 plus Indians of Peru increase
Cattle Tribes of Interior large 7.5 8.2 16.6 19.1 * * 10 plus Africa increase 444
Agricultural Tribes of large 3.5 4.1 16.6 5.4 * * 10 plus Central Africa increase
*Not given
1. Minerals: Ca=Calcium, P=Phosphorus , Fe=Iron, Mg=Magnesium, Cu=Copper, I=Iodine
2. Fat soluble vitamins include A,D,E,K. Water soluble vitamins include the B vitamins (folate, pantothenic acid, thiamin, riboflavin, niacin, B6, B12) and vitamin C
PERCENTAGES OF TEETH ATTACKED BY DENTAL CARIES IN INDIGENOUS AND MODERNIZED GROUPS
Group Indigenous Modern
Swiss 4.60 29.8
Gaelics 1.20 30.0
Eskimos 0.09 13.0
Northern Indians 0.16 21.5 445
Seminole Indians 4.00 40.0
Melanesians 0.38 29.0
Polynesians 0.32 21.9
Nutrition and Physical Degeneration is available from Amazon.com, Price-Pottenger Nutrition Foundation, and Radiant Life.
“We can now visualize our universe, its light, gravity and heat, its seasons, tides, and harvest, which prepare a habitation for the universe of vital forms, microscopic and majestic, which fill the oceans and the forests. We have a common denominator for universes within and around each other, our world, our food and our life have potentials so vast that we can only observe directions, not goals. We sense human achievements or ignominious race self-destruction. Every creed today vaguely seeks a utopia; all have visualized a common controlling force or deity as the most potent force in all human affairs. Yes, man’s place is most exalted when he obeys Mother Nature’s laws.” –Weston A. Price, DDS
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60.) pH levels present in our blood, saliva and urine, the three primary body fluids which should depict more alkalinity for proper cell functioning. Normal pH measurement should be?
A. 5.5 B. 6.0 C. 7.0 D. 8.0
https://scientificfilters.com/product-applications/tisch-laboratory-filter-paper/ph- papers/ pH Papers
Everything That You Should Know About pH Papers pH papers are test papers which are soaked and inseminated with one or more indicator mixtures and then dried and cut in the form of strips to be sold as pH indicator packages. pH strips are used to detect the acidity or alkalinity of substances or chemicals which depict varying colors on being exposed and reacting to pH ratings. They have widespread applications in the Healthcare, Educational Institutes as well as Chemical Laboratories and places where determination of pH levels of substances is necessary.
ph papers
What is pH Papers Made Of? pH indicator of which pH papers are made is a halochromic compound which detects hydronium ions or hydrogen ions via a color change. The pH value of a neutral solution that is one which is neither acidic nor alkaline is 7 at 25 Degree Celsius. The values below 7 are considered acidic, while those above 7 are alkaline in nature. Importance of pH in Human Life 447
If you thought pH testing is only done in chemical labs, well, it is time that you know the role of pH in our daily lives. You must have often heard your family physician or doctors attending your relatives refer to pH levels of the body increasing or decreasing. pH indicator strips are used to detect the level and action of Hydrogen in your body which, although present in less amounts is a Critical Element.
Hydrogen measures the balance of acid and alkaline in the bodies of all living organisms and plays some very critical roles. It triggers cell movement which is required for establishing communications through electrons. It also boosts cell growth and development, while being responsible for binding DNA through Hydrogen bonds.
Hence, pH papers measure the pH levels present in our blood, saliva and urine, the three primary body fluids which should depict more alkalinity for proper cell functioning. A pH value measurement below 7 indicates degeneration with augmented acidic levels. Alkaline imbalance makes your body vulnerable to diseases and formation and growth of bacteria, yeast and even cancer. Therefore, in order to live a long, healthy life an acid-alkaline balance is required to be maintained. Considering the importance of determining and knowing pH levels in the body, the significance of pH papers remains indubitable. Types of pH Papers At Tisch you can choose from a wide array of Whatman pH indicator papers according to your needs. Here are some types of pH indicator and test papers available on our online store. Ph Strips Type CF – These types of plastic supported strips possess dye-impregnated indicator papers of four varying segments and give out reliable and accurate results. Type CS Strips: Each of the strips present in the pack contain the indicator dye in the central segment along with 8 or more segments of varying colors printed on the side for matching. Dispensers Type SR: These dispensers are generally available in full ranges while, in some they come in narrow ranges. Dispensers Type TC: It embraces presence of 3 different color indicator bands. It comes with a comparison chart for accuracy in detection and reading. Indicator Books: They are usually used in schools or educational institutions as they pose a cost-effective means of pH testing for large number of pupils. Litmus Paper: These come in two varieties and are responsible for detection of acidity and alkalinity of solutions. Red Litmus is used for alkalinity or basicity and is identified by the red color turning blue. Blue Litmus paper, on the other hand when exposed to solution that is acidic turns red. If there is no color change with one type of Litmus paper it is essential to experiment with the other color Litmus. Other types of pH papers comprise Congo Red and Phenolphthalein Acid Alkali Test Papers and Potassium Iodide, Lead acetate and Universal Indicator Test Papers. All our pH papers and strips come with color comparison chart with detailed usage instructions for easy application, while depicting impeccable precision and dependability in results.
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