Recognizing and Managing Lead and Mercury Poisonings

URGENT CARE Special Section

After iron, which was covered in EM’s May issue, lead and mercury are the two metals most likely to be implicated in heavy metal toxicity syndromes. The authors review the diagnostic considerations and update guidelines for detoxification.

hat constitutes a heavy metal? It de- W pends on who you ask. In industrial and environmental studies, heavy metals are generally defined as those elements that have high atomic weights—elements with a spe- cific gravity of 5 or higher. A strict chemistry definition classifies ev- Urgent Care Section Urgent Care erything between copper and bismuth on the periodic table as a heavy metal. Medical usage of the

term, however, is much more lib- Inc Researchers, Associates/Photo © 2009 Biphoto eral, encompassing lighter metals Chronic Effects of Lead Poisoning. Dark or bluish discoloration and metalloids that are excluded of the gum-tooth line, known as a “lead line,” may be noted on exam and is the result of a chemical reaction between lead and dental plaque. by other definitions. The list of medically recognized toxic metals and metalloids includes (but is not limited to) aluminum, arse- poisonings can often result in sig- nic, barium, bismuth, cadmium, nificant morbidity and mortality if cobalt, copper, chromium, gold, unrecognized and inappropriately lead, manganese, mercury, sele- treated. The physician also needs Christian Balmadrid, MD nium, silver, thallium, and zinc.1 to be prepared for the postdiag- Staff Physician Heavy metal or metalloid tox- nostic responsibility of identifying Durham Emergency Physicians Durham Regional Hospital icity is relatively uncommon in possible exposures to the same Durham, North Carolina urgent care centers, but for that toxin within the patient’s family, very reason it is important to workplace, or community that Michael J. Bono, MD Professor of Emergency Medicine maintain familiarity with its signs, may warrant testing, treatment, Eastern Virginia Medical School symptoms, and treatment. These or both. Norfolk, Virginia

www.emedmag.com SEPTEMBER 2009 | EMERGENCY MEDICINE 35 Urgent Care Section 36 >> HEAVY METAL POISONING households. children inayearUS of asmany4million screening assessments lead havebeenfoundin Toxic levelsofserum

FAST EMERGENCY MEDICINE metals otherthanironin2005. there werealmost13,000exposurestoheavy American AssociationofPoisonControlCenters, respiratory system atarateofabout40%, com- skin. Inadults,itisabsorbed primarilythroughthe through thelungs,gastrointestinal tract,orthe accounted fornearly35,000casesin2004 eral formandasaningredientinmultivitamins glass production. repair, bridgeandshipconstruction,welding, as leadsmelting,batterymanufacturing,radiator workers areatriskforleadexposureinsuchjobs in UShouseholds,andabout3millionindustrial ments ofasmany4millionchildreninayear serum leadhavebeenfoundinscreeningassess- loys intheirplumbingsystems.Toxic levelsof and anunknownnumberhaveleadpipesoral- 30 millionhomesstillcontainlead-basedpaints, 1970s. However, itisestimatedthatmorethan products intheUnitedStateswasbanned leaded gasoline.Fortunately, theuseofthose resulting fromexposuretolead-basedpaintsand ization, withthemajorityofpoisoningsworldwide Lead toxicityisconsideredadiseaseofindustrial- LEAD: ALINGERINGTHREAT sure include lead-contaminated soils (especially sure includelead-contaminatedsoils(especially picion ofmetaltoxicity. poison controlcenterwheneverthereisanysus- cian shouldconsultatoxicologistortheregional that eventhebest-informedurgentcarephysi- heavy metaltoxicity. We wouldcaution,though, and mercury—afteriron,themostlikelycausesof try, andclinicalaspectsoftoxicexposurestolead fresher courseontheepidemiology, biochemis- 2009, page36). and management,see our recentdiscussionofirontoxicitydiagnosis According tonationwidedatacollectedbythe The aimofthisarticleistoprovideabriefre-

TRACK <<

| 3

Othervehiclesforleadexpo- SEPTEMBER 2009 role. It can be absorbed role. Itcanbeabsorbed and folkremedies. some ethnicmedications lead-glazed pottery, and moonshine whiskey, shot, fishingweights, leaded gasoline),buck- in countriesstillusing EMERGENCY Lead has no biological Lead hasnobiological 2

(Iron initsmin-

MEDICINE 4,5 , May 1 ; for 3 can alsobeabsorbedthroughtheskin. a rateof50%.Theorganicleadfoundingasoline absorption isthroughthegastrointestinaltract,at Conversely, inchildrenthepredominantrouteof diets lowincalcium,iron,phosphorus,orzinc). pregnancy andmalnourishedstates(particularly nal absorptionratesandefficiencycanincreasein ondary, atarateof10%to15%,butgastrointesti- ing processes.Gastrointestinalabsorptionissec- paints fromsurfacesorcertainsmeltingburn- monly duringactivitiessuchasremovingleaded times ofboneturnover, asinhyperthyroidism, individuals withnormalrenalfunction. by thekidneysandhasahalf-lifeof30daysin liver, andbonemarrow. Leadisprimarilyexcreted form, abletoaffecttissuessuchaskidney, brain, erythrocytes, whiletheremaining1%isinafree extend todecades, lead canbestoredinbone,whereitshalf-life Prolonged exposure may cause renal disease that Prolonged exposure maycauserenaldisease that short-term memory, anddifficultyconcentrating. tigue, irritability, insomnia,anorexia,impaired onset ofvaguesymptoms suchasmyalgias,fa- and maybeasymptomatic orhaveaninsidious menopause, pregnancy, sis oftheproximaltubules. nephropathy andrenalimpairmentduetofibro- disabilities, andothersigns. ity, overaggressiveorcriminalbehavior, learning manifested indecreasedIQscores,hyperactiv- to correlatewithneuropsychiatricdisordersas dren, chronicleadexposureshavebeenfound resulting inacuteleadencephalopathy. Inchil- brain capillarypermeabilityandcerebraledema, thies andwristfootdrop.Italsoincreases degeneration thatresultinperipheralneuropa- system, itinducesdemyelinationandaxonal biosynthesis, causinganemia.Intheneurologic In thehematopoieticsystem,leadinhibitsheme hematopoietic, neurologic,andrenalsystems. only amildlyelevatedBLL (lessthan10μg/dL) nation. Adultswithchronicexposuresmayhave toxic bloodleadlevel(BLL)onascreeningexami- sure, orareferralfromproviderwhofound cious symptomswithapossiblehistoryofexpo- sent witheitheraknownleadexposure,suspi- In thebloodstream,99%ofleadisboundto Clinical features. Pathophysiology. 7 andmaybereleasedduring Lead primarilyaffectsthe Patients willtypicallypre- 9 andbreastfeeding. 3 Leadalsocauses www.emedmag.com 7 However, 6 10 3 8 Urgent Care Section 38

>> HEAVY METAL POISONING environment. back toacontaminated not todischargethem exposure, itisimportant patients afteralead When discharging

EMERGENCY MEDICINE FAST continued frompage36 senting aswristorankledropmayalsooccur. As previouslynoted,peripheralneuropathiespre- in permanentneurologicandbehavioralchanges. and convulsions.Thiscanberapidlyfatalorresult changes tofull-blownencephalopathywithcoma tion rangingfrommildheadacheorpersonality also presentwithcentralnervoussystemdysfunc- tion, nausea,vomiting,andanorexia.Theymay as colickyabdominalpain(“leadcolic”),constipa- typically complainofgastrointestinaleffectssuch the severityofpresentingsymptoms.Patients higher BLLs,whichwillgenerallycorrelatewith nitrogen andcreatinine(toassessrenalfunction). basophilic stippling)andmeasuresofbloodurea smear (whichmayrevealtheclassicallydescribed ing includeacompletebloodcountwithperipheral may behelpfulintheevaluationofleadpoison- BLL canbegreaterthan100μg/dL.Otherteststhat lesions, lossofbrainvolume, pendent oflead’s effectsonthekidneys), can progresstorenalfailure,hypertension(inde- rocognitive dysfunction, usually passitharmlesslythroughthegastro- lead foreignbody, suchasafishingsinker, will tion delays. μg/dL tobetoxicinchildren. and PreventionhasdefinedaBLLgreaterthan10 to obtainisaBLL.TheCentersforDiseaseControl sure isessential.Themostimportantlaboratorytest history toassesstheriskandseverityofleadexpo- and motorneuropathies, rapidly fatal. Treatment inthesecases consists cause acuteleadencephalopathy, whichcanbe opposite extreme,significant leadpoisoningcan therapy neededformildlead poisoning.Atthe be consideredtopreventfurther leadtoxicity. Management. Assessment. Patients withacuteexposurewillpresent Often, removalfromexposure istheonly

TRACK 16 An occupational and environmental An occupationalandenvironmental

SEPTEMBER 2009 Patients whoingestasingle treatment required. intestinal tract,withno surgical removalshould not passedin2weeks, the leadforeignbodyhas passage hasoccurred.If however, toensurethat graph maybewarranted, follow-up KUBradio- 12,13 15 andcardiacconduc- white matter brain whitematterbrain 3 In acute exposures, In acuteexposures, 14 distal sensory distalsensory 11 neu- 17 A 15 3 therapy is kg every12hoursforanother14days.Second-line mg/kg every8hoursfor5days,followedby10mg/ acid), and netetraacetic acid),DMSA(2,3-dimercaptosuccinic or BAL),calciumdisodiumEDTA (ethylenediami- include dimercaprol(alsocalledBritishantilewisite and renalexcretion.Thechelatingagentsavailable form nontoxiccomplexesthatcanundergobiliary ory behindtheiruseisthattheywillbindtolead been performedtoassesstheirefficacy. Thethe- been used,butcontrolledclinicaltrialshavenot absorption oflead. in continuedexposuremay actuallyincreasethe are undergoingchelationtherapy, becauseitsuse a contaminatedenvironment,particularlyifthey sure, itisimportantnottodischargethemback sorbed throughthegastrointestinaltract. irrigation candecreasetheamountofleadab- lular pathology. Inacuteingestions,wholebowel enhance elimination,andpreventorreversecel- prevent furtherexposure,minimizeabsorption, ate toseveretoxicity, thegoalsoftherapyareto tive measures. site evaluationsandidentifying possiblepreven- medicine maybehelpfulin makingenvironmental ment oraphysicianspecializing inoccupational apy withDMSAisrecommended. system symptoms,outpatientoralchelationther- patient hasnogastrointestinalorcentralnervous ing therapy. ogy constitutethemostusefulguidetodetermin- Blood leadlevelsandthepatient’s symptomatol- lowing havebeenrecommendedinsometexts. for thetreatmentofleadpoisoning,butfol- and canbeusedforoutpatienttherapy. sion, whilethelattertwoagentsareoralchelators are usedforseveretoxicitiesthatrequireadmis- come inintramuscularorintravenousformand verity ofsymptoms.Thefirsttwoagentslisted to useisdictatedbythepatient’s BLLandthese- sive intracranialpressuremonitoring. including intubation(tohyperventilate)andinva- of standardmeasurestocontrolcerebraledema, and hasanincreasedsideeffectprofile. To enhanceelimination,chelatingagentshave When dischargingpatientsafteraleadexpo- If the BLL is between 45 and 69 μg/dL and the If theBLLisbetween45and69μg/dL Consensus guidelineshavenotbeenproposed D D -penicillamine -penicillamine. Which chelating agent -penicillamine. Whichchelatingagent 3 Eitherthelocalhealthdepart- , but it is not as effective butitisnotaseffective continued onpage 40 www.emedmag.com 19,20 Dosing is 10 Dosingis10 3 Inmoder- 3 18 Urgent Care Section

40 >> HEAVY METAL POISONING polluted areas. ingestion ofseafoodfrom form ofmercuryisthrough exposure totheorganic The mostcommon

FAST EMERGENCY MEDICINE continued frompage38 particularly marine fish(shark,swordfish, tuna) form ofmercuryisthrough ingestionofseafood, therapy. tient shouldbeadmittedandundergoIVchelation signs ofcentralnervoussystemtoxicity, thepa- are protractedgastrointestinalsymptomsorany age isbasedoneither50mg/kgor1000mg/m dose ofdimercaprolafterthefirstone.Dailydos- tion ofcalciumdisodiumEDTA isgiven witheach to 12hoursforthelast7days.Aseparateinjec- 4 to6hoursforanother2days,andthenevery days. After2days,dosingisspacedouttoevery to 4mg/kgdeepIMinjectioneveryhoursfor2 tion). birth defectsmanifestedinthefollowinggenera- more morbidityinthepopulation(inaddition, caused atleast1000deathsandsignificantly tion offishfrommercury-contaminatedwaters Bay tragedy, whenfrom1932 to1968,inges- toxicity occurredinJapanduringtheMinamata ous toxin.Themostinfamouscasesofmercury However, it isalsowellrecognizedasadanger- a diuretic,antiseptic,andantisyphiliticagent. 2000 years,continuingintothe19thcenturyas Mercury hasbeeninmedicinaluseformorethan MERCURY: KNOWTHEGUISES to fourdivideddosesforup5days. of bodysurfacearea,giveneitherIVorIMintwo ther subcutaneouslyorintravenously. injecting themselveswith elemental mercuryei- inorganic. Themostcommonrouteofexposure cause toxicity:elemental(metallic),organic,and that gaverisetotheterm“madhatters.” and symptomsofcentralnervoussystemtoxicity workers exposedtoitsvaporsdevelopedsigns manufacture offelthatsinthe19thcentury, when The mostcommonexposure totheorganic If theBLLisgreaterthan70μg/dLorthere There arethreeprimaryformsofmercurythat

22,23 TRACK 3 Mercurywasalsocommonlyusedinthe Dimercaprolisinitiallyadministeredat3 <<

SEPTEMBER 2009 of patientsintentionally have alsobeenaccounts and thermometers.There sphygmomanometers cury includespillsfrom sources ofelementalmer- tilized vapor. Common via inhalationofitsvola- to theelementalformis 3 3

21 2 fillings. through mercury-containingamalgamdental duce anytoxicity sinceitisnotabsorbed bythe gested, elementalmercury willusuallynotpro- in thelungs,leadingtoacute toxicity. Whenin- absorbed, andIVinjections canbesequestered not beenrecommended. nervous system,andremovalofthesefillingshas to mercury’s knowntoxiceffectsonthecentral have notrevealedevidencelinkingdentalfillings levels arelessthanabout5μg/L). in bloodmercurylevelsofupto20μg/L(normal these fishcanreach1mg/kgorhigher, resulting age exposureof10μg/day. accurately assess.Onestudyestimatesanaver- and totalamalgamsurfaceareaisdifficultto dental fillingsdependsonthenumberof polluted areas. and freshwaterfish(pike,walleye,bass)from the “madhatters.” inability toconcentrate;itwasthesyndromeof nervousness, insomnia,memoryproblems,and is characterizedbyshyness,emotionallability, toms, andaconditioncallederethism.Erethism neuropathies, dysarthrias,parkinsoniansymp- posures canresultinfinetremors,peripheral the brain. ebellum, postcentralgyri,andcalcarineareasof Chronic exposurecancauseatrophyofthecer- by stimulatinganimmunereactioninthekidneys. nephrotoxicity bothbydirectcausticeffectsand zyme function.Additionally, mercuryleadsto parts itstoxiceffectsbydisruptingcellularen- syndrome, andacuterenalfailure. may occur, presenting asproteinuria,nephrotic ficient systemicabsorption,acutenephrotoxicity provoke seizuresandencephalopathy. With suf- brain barrier, andlargeconcentrationscanrapidly tal mercuryalsoreadilypenetratestheblood- respiratory distresssyndrome. rect lunginjury, chemicalpneumonitis,andadult inhalation ofitsaerosolizedform,resultingindi- cury, asnotedbefore,ismost oftenabsorbedvia route, andacuityoftheexposure.Elementalmer- of mercurytoxicityaredeterminedbytheform, Pathophysiology. Patients mayalsobeexposedtomercury Subcutaneous injectionscan besystemically Clinical features. 24 Theamountofmercuryreleasedfrom 3 24 Concentrationsofmercuryin 21 Like allmetals,mercuryim- The presentingsymptoms 26 24 Subsequentstudies 3 Inhaledelemen- www.emedmag.com 25 21 Chronicex- Urgent Care Section 41

<< 21 TRACK

EMERGENCY MEDICINE FAST

HEAVY METAL POISONING METAL HEAVY | 3,21

HEAVY METAL POISONING METAL HEAVY Methylmercury readily crosses the placenta and will accumulate in higher concentrations in cord blood than in the maternal circulation. >> 27-29 3,21 Initial management of acute SEPTEMBER 2009 Additionally, there is little correlation be- there is little Additionally, 3,21 The ideal laboratory value to obtain in a sus- The ideal laboratory Management. As noted earlier, organic mercury cannot be As noted earlier, Other tests that may be helpful in the initial to arrive at the diagnosis of mercury poisoning. of mercury poisoning. at the diagnosis to arrive available to confirm few practical tests There are poisoning. mercury is a 24-hour urine mer- pected mercury exposure after a 5-day seafood-free cury level measured detect both inorganic and el- diet. This test can compounds but cannot detect emental mercury are excreted predominantly organic forms, which urine mercury level is less through bile. A normal a level greater than 100 to than 20 μg/L, while significant mercury exposure, 150 μg/L suggests ther- in which chelation apy is recommended. mercury toxicity should include aggressive pulmonary support in cases of aspiration and aggressive cardiovascular support in cases of in- However, there are no However, recommendations for urine mercury levels between 20 and 100 μg/L, partially due to the fact that urine assays detect both recent exposures of tissue bur- and continued renal elimination den. tween mercury levels and actual toxicity. A spot tween mercury levels and actual toxicity. there are few urine mercury test is available, but to that studies to confirm its validity compared some studies of a 24-hour sample. Furthermore, in uri- suggest the existence of diurnal variation urine test nary mercury excretion, making a spot likely even less useful. detected in urine assays. It does, however, con- detected in urine assays. It does, however, centrate in erythrocytes, so serum mercury levels can be obtained to confirm organic mercury exposure. A normal serum mercury level is less than 10 μg/L. Chelation therapy is recommended for values greater than 35 μg/L. evaluation include a urinalysis (looking for proteinuria) and a basic metabolic panel (looking for elevated creatinine). A complete blood count and a type-and-screen should be obtained because of the potential for gastrointestinal hemorrhage and per- plain film radiographs may foration. Occasionally, identify ingested, aspirated, or injected mercury.

21 3,21 21 Once ingested 24,26 The best-known form of 3,21 21 As with the other heavy metal Assessment. Perhaps the largest health concern regarding Organic mercury is also readily absorbed Organic mercury is also readily Ingestion of inorganic mercury salts, on theIngestion of inorganic

poisonings, signs and symptoms are relatively nonspecific, so a thorough history and physical and high index of suspicion are often needed and absorbed systemically, methylmercury can and absorbed systemically, penetrate the central nervous system, to which its toxic effects are generally limited. organic mercury is methylmercury, which is the organic mercury is methylmercury, often publi- compound found in seafood and is cized for its teratogenic effects. gastrointestinal tract. It can be subsequently as- be subsequently tract. It can gastrointestinal toxicity as causing pulmonary pirated, however, inhalation. it does via mercury poisoning to emerge in recent medical literature is with the effects of methylmercury exposure in utero. Methylmercury readily crosses the placenta and will accumulate in higher concentrations in cord blood than in the maternal circulation. It can inhibit brain cell division and migration, resulting in micrognathia, microceph- developmental disorders, mental retardation, aly, blindness, and symmetric motor deficits. through the gastrointestinal tract. Exposure to through the gastrointestinal tract. generally does not however, organic mercury, delayed neurologic Rather, lead to acute toxicity. paresthe- symptoms (ataxia, tremors, dysarthria, visual field sias of the hands, feet, and mouth), and hyper- constriction, hearing loss, spasticity, and months reflexia typically develop over weeks with chronic exposure. other hand, does lead to a significant and poten- other hand, does gastrointestinal toxicity. tially life-threatening a corrosive gastroen- Acute ingestions precipitate as abdominal pain and he- teritis that presents vomiting, third spacing, andmatemesis. Severe can cause massivegastrointestinal hemorrhage leads to acute renal failurefluid loss that rapidly Shock with cardiovascularand tubular necrosis. are the end result if fluid losscollapse and death of inor- progresses. Other signs and symptoms discolor- ganic mercury ingestion include a grayish patients mayation of the mucous membranes, and exposuresalso complain of metallic taste. Chronic mercury tox- present similarly to chronic elemental ranging from proteinuria Renal dysfunction, icity. to nephrotic syndrome, may also occur. www.emedmag.com Urgent Care Section 42

>> HEAVY METAL POISONING has begun. decontamination process be initiatedsoonafterthe chelation therapyshould is suspected,empiric If mercurypoisoning

EMERGENCY MEDICINE FAST poisoning, dimercaprol shouldbeused. Itshould treatment forelemental or inorganicmercury 2-week “drugholiday.” els, treatmentcoursesshould beseparatedbya cury levelshavedroppedbelowaspecificvalue. ratory measurementshaveconfirmedthatmer- days. Treatment shouldbecontinueduntillabo- day forthefirst5days,thentwicedaily14 administered at10mg/kgorallythreetimesper chelating agentforallformsofmercuryisDMSA, In patientswithnormalrenalfunction,thefirst-line able containsulfhydrylgroupsthatbindmercury. process hasbegun.Allthechelatingagentsavail- should beinitiatedsoonafterthedecontamination poisoning issuspected,empiricchelationtherapy able inacutecaresettings.Therefore,ifmercury mercury toxicityaregenerallynotreadilyavail- debridement topreventsystemicabsorption. antibiotics. Injectedmercurywillrequiresurgical drainage. Thereisnoroleforsteroidsorempiric suctioned andplacedinapositionfavoringpostural halational exposures,however, patientsshouldbe ingested, requiringnogastriclavage.Incasesofin- abdominal radiographs. sponse totreatmentcanbefollowedwithserial be consideredinlargeingestions,andthere- bowel irrigationwithpolyethyleneglycolshould and thusisnotgenerallyrecommended.Whole milk. Activatedcharcoalbindsverylittlemercury binding sulfhydrylgroupssuchaseggwhitesor performed withsolutionscontainingmercury- should beplaced,andgastriclavage cury ingestion,anasogastricororogastrictube decontaminated. Inorganicandinorganicmer- prominent. Thepatientshouldalsobequickly gestion wheregastrointestinalsymptomsare In patientswithrenaldysfunction needing As notedearlier, laboratoryteststhatconfirm Elemental mercuryisgenerallyharmlesswhen

TRACK

SEPTEMBER 2009 quired toobtaintheselev- of DMSAtherapyarere- 20 μg/L.Ifrepeatcourses levels shouldbelessthan sonings, bloodmercury L. Inorganicmercurypoi- should belessthan20μg/ hour urinemercurylevels mercury poisonings,24- In elementalandinorganic 3,21 21 3,21 cury inthecentralnervoussystem. the toxinandactuallyincreaselevelofmer- as thereissomeconcernthatitwillredistribute be avoided,however, inorganicmercury toxicity, for debridementoftheaffectedsofttissue. hospitalized andwillrequiresurgicalconsultation have self-injectedmercurywillalsoneedtobe DMSA) willneedtobeadmitted.Patientswho intramuscular dimercaproltherapy(versusoral renal failure,oracutepneumonitis,requiring toxicity, suchasencephalopathy, shock,acute hibiting anysignsofpotentiallylife-threatening confirm theclearanceofmercury. Patientsex- patients withfollow-upurineorbloodtestingto is exclusivelyexcretedbythekidneys. cillamine iscontraindicatedinrenalfailure,asit mg/kg/day infourdivideddosesisgiven. day orallyfor1to2weeks;children,2030 rol. Typical adultdosingis250mg fourtimesa group, comparedtotwoinDMSAanddimercap- fective becauseitcontainsonlyonesulfhydryl or twicedailyfor10days. is 5mg/kginitiallyfollowedby2.5once . Velez LI,DelaneyKA.Heavymetals.In:MarxJA,ed. 3. 2.Bronstein AC,SpykerDA,CantilenaLR,etal.2007Annual 1.Watson WA, LitovitzTL,RodgersGCJr. 2004Annualreport REFERENCES . 7.Rabinowitz MB.Toxicokinetics ofbonelead. Fischbein A,HuH.Occupationalandenvironmentalexposure 6. World HealthOrganization.Lead.In:AirQualityGuidelinesfor 5. 4. Agency forToxic SubstancesandDiseaseRegistry. 10. Gulson BL, MahaffeyKR, Riess ML,HalmJK.Leadpoisoninginanadult:leadmobiliza- 9. Goldman RH,WhiteR,KalesSN,HuH.Leadpoisoningfrom 8. Asymptomatic patientscanbetreatedasout- D Toxicol (Phila). National PoisonDataSystem(NPDS):25thAnnualReport. Report oftheAmericanAssociationPoisonControlCenters’ 2005;23(5):589-666. Toxic Exposure SurveillanceSystem. of theAmericanAssociationPoisonControlCenters Wilkins; 2007:954-990. Occupational Medicine. to lead.In:RomWN,MarkowitzSB,eds. pdf. Published2001.AccessedSeptember11,2009. Europe. 2nded.http://www.euro.who.int/document/aiq/6_7lead. 2009. tp13.html#bookmark05. Updated2007.AccessedSeptember11, Toxicological profileforlead.www.atsdr.cdc.gov/toxprofiles/ Philadelphia, PA: MosbyElsevier;2006:2418-2427. Emergency Medicine:ConceptsandClinicalPractice. lead fromtheskeleton duringthepostnatalperiodislarger than tion bypregnancy? Med. mobilization ofbonestoresduring thyrotoxicosis. Perspect. -penicillamine isathird-lineagent,lessef- 1994;25(3):417-424.

1991;91:33-37. 2008;46(10):927-1057. J GenInternMed. Philadelphia,PA: LippincottWilliams& Jameson CW, etal.Mobilizationof

2007;22(8):1212-1215. www.emedmag.com Am JEmergMed Environmental and 3,21 Environ Health Thedose 21 Am JInd D -peni- 6thed. Rosen’s 3,21 Clin Q .

Urgent Care Section 43

J N Engl J Med. EMERGENCY MEDICINE

J Occup Environ Med. HEAVY METAL POISONING METAL HEAVY | Philadelphia, PA: WB WB PA: Philadelphia,

1996;277(1):239-244. Variability in urinary mercury excretion. in urinary mercury excretion. Variability

Clinical Toxicology. SEPTEMBER 2009 McCann T, Naleway C, et al. The validity of spot McCann T, 1982;24(8):590-595. J Pharmacol Exp Ther. tional Institute for Minamata Disease. Ministry of the Disease. Ministry of the tional Institute for Minamata iang WK. Mercury. In: Ford MD, Delaney KA, Ling LJ, Ling LJ, Ford MD, Delaney KA, In: iang WK. Mercury. orld Health Organization. Biological Monitoring of Metals. Biological Monitoring of Metals. orld Health Organization. http://whqlibdoc.who.int/hq/1994/WHO_EHG_94.2.pdf. Accessed http://whqlibdoc.who.int/hq/1994/WHO_EHG_94.2.pdf. September 14, 2009. current exposures and clinical manifestations. Erickson T, eds. Erickson T, Saunders; 2001:737-743. measures. http://www.env.go.jp/en/ disease the history and Accessed September 14, chemi/hs/minamata2002/index.html. 2009. of Japan. Mercury and Health. http:// Environment. Government Accessed September 14, www.nimd.go.jp/english/index.html. 2009. http://whqlibdoc.who.int/ipcs/IPCS_EHC_ Inorganic mercury. 14, 2009. 118.pdf. Accessed September 2003;349(18):1731-1737. excretion ples as a surrogate measure of 24-hour porphyrin mercu- rates. Evaluation of diurnal variations in porphyrin, subjects with very and creatinine concentrations among ry, low occupational mercury exposure. 1998;40(12):1090-1101. exposure urine samples for low-level occupational mercury excre- assessment and relationship to porphyrin and creatinine tion rates. Occup Med. 26. Clarkson TW, Magos L, Myers GJ. The toxicology of mercury— Magos L, Myers Clarkson TW, 26. 21. Ch21. of Japan. Minamata of the Environment. Government Ministry 22. Na23. Organization. Environmental Health Criteria 118: Health World 24. W 25. of spot urine sam- JS, Martin MD, Leroux BG. Validity Woods 27. 28. Martin 28. MD, G, Barber T. Wallis 29.

Pediatrics. Am J Cardiol. Am J Epidemiol. 2006;33(6):732-741. 1989;27(3):173-182. 1992;10(6):577-583. 1998;131(4):324-329. 2007;115(3):472-482. Muscle Nerve. J Lab Clin Med. 2006;67(9):1556-1562. Am J Emerg Med. 2006;66(10):1476-1484. J Toxicol Clin Toxicol. J Toxicol Neurology. Neurology. erican Academy of Pediatrics Committee on Drugs. on Drugs. erican Academy of Pediatrics Committee eisskopf MG, Wright RO, Schwartz J, et al. Cumulative J, et al. Cumulative RO, Schwartz eisskopf MG, Wright 2004;160(12):1184-1193. function in community-dwelling older exposure and cognitive adults. measured by brain exposure is linked to neurodegeneration MRI. sive exposure to lead. in association with low-level conduction disturbances lead exposure (the Normative Aging Study). 1998;82(5):594-599. body ingestion. lead intoxication. blood lead levels among young children: recommendations Poisoning from the Advisory Committee on Childhood Lead Prevention. http://www.cdc.gov/nceh/lead/casemanagement/ 2009. caseManage_main.htm. Accessed September 14, lead exposure in children. guidelines for Treatment 1995;96(1 pt 1):155-160. lead exposure and prospective change in cognition among change in cognition among lead exposure and prospective Normative Aging Study. elderly men: the VA exposure and cardiovascular disease—a systematic review. systematic review. cardiovascular disease—a exposure and Perspect. Environ Health during pregnancy. during pregnancy. Navas-Acien A, Guallar E, Silbergeld EK, Rothenberg SJ. Lead EK, Rothenberg SJ. A, Guallar E, Silbergeld Navas-Acien

13. Shih RA, Glass TA, Bandeen-Roche K, et al. Environmental lead Bandeen-Roche K, et al. Environmental Shih RA, Glass TA, 13. BS, Davatzikos C, et al. Past adult lead Schwartz Stewart WF, 14. with exces- Thomson RM, Parry GJ. Neuropathies associated 15. PS, et al. Electrocardiographic Schwartz J, Vokonas Cheng Y, 16. Seidler DE. Management of lead foreign GP, Wedin Durback LF, 17. 18. Roberge RJ, Martin TG. Whole bowel irrigation in an acute oral Roberge RJ, Martin TG. Whole bowel irrigation 18. elevated Centers for Disease Control and Prevention. Managing 19. Am20. 12. W 12. 11. www.emedmag.com