DOCSLIB.ORG

Diagnosis of Acute Poisoning

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Diagnosis of Acute Poisoning MAIN TOPIC Diagnosis of acute poisoning As all chemicals can act as poisons in the right quantity, effective lines of communication between the attending clinician or health worker, the laboratory and the toxicologist are essential. Virtually all known chemicals can rating (LD50 < 400 mg/kg), 2 is edible’ substances ingested acci- cause injury or death, depending intermediate (LD50 of 400 - 4 000 dentally is usually small. The aver- on the dose of the substance. The mg/kg), and 1 is low (LD50 of age quantity of liquids swallowed lethal dose may vary widely. For 4 000 - 40 000 mg/kg). Safety, the accidentally by a child under the example, 4 000 mg/kg of table salt opposite of risk, is the probability age of 5 years is 5 ml, and that by will be lethal to 50% of a popula- that harm will not occur under an adult 15 ml. In contrast, the tion of experimental animals specified conditions.2,3 quantity swallowed intentionally (expressed as the LD50), while the (by adults) is usually considerably LD50 of arsenic trioxide is 1 - 2 larger, and should be taken into mg/kg, and that of botulinum toxin consideration when potential haz- 0.00001 mg/kg. A number of fac- Virtually all known ard or risk is assessed. tors may contribute to toxicity: chemicals can cause Table I lists the most frequently physico-chemical characteristics injury or death, ingested household agents consid- such as the pKa, lipid solubility, ered ‘usually non-toxic’. This table the route of entry (e.g. orally or depending on the is intended as a guide only, and percutaneously), the nature of the dose of the sub- should be used in conjunction with exposure (e.g. acute or chronic) the information given above.4,5 and the susceptibility of the victim. stance. This refers to factors such as the For clinical purposes, poisons state of fetal development, child- (including therapeutic drugs) may ‘Non-toxic ingestion’ refers to the hood, advancing age and underly- be divided into two broad cate- consumption of a non-edible agent ing pathology. In addition, the gories: or product usually not associated vehicle in which the agent is dis- with harmful effects. The practical solved or suspended, and other • Poisons (and their metabo- value of knowing that a product is formulation factors, may markedly lites) which directly cause ‘usually non-toxic’ prevents: influence toxicity. There is no irreversible or slowly reversible structural or entirely ‘safe’ chemical since all • an inappropriate response that functional tissue damage in have the potential to cause death causes panic and injury under specific circum- one or more organ systems. • over-treatment of the patient stances. It should also be empha- These are also considered com- • unnecessary visits to the doctor sised that some adverse reactions pounds with a high inherent or hospital emergency facility.4 to chemicals, such as allergic and toxicity (Table II). Arsenic and idiosyncratic reactions, are not For an agent to be considered the organophosphates are good dose-related.1,2 ‘usually non-toxic’, it should meet examples of poisons which may the following criteria: cause irreversible damage, long- In practice the critical factor is not lasting (slowly reversible) organ • positive identification of the whether or not a substance is poi- dysfunction, or lead to compli- product, its ingredients, and its sonous, but whether someone is at cations which may require concentration risk from exposure to it. Risk is extended periods of supportive the probability that a substance • positive assurance that it was therapy. Significant symptoms 1,4 will cause harm under specified the only product ingested. and signs of a substantial num- conditions. This is reflected in a Because of unpleasant or disagree- ber of poisons in this group may hazard rating on a scale of 1 - 3, able tastes, the quantity of ‘non- appear late (1 - 3 days post where 3 indicates a high hazard 438 CME August 2003 Vol.21 No.8 Table I. Most frequently ingested household agents considered ‘usually non-toxic’4 Abrasives Detergents (phosphate type, anionic) Lozenges (without local anaesthetic) Shampoos (non-pediculicides) Adhesives Deodorants Lubricant Shoe polish (most do not con- Antacids Deodorisers (spray and refrigerator) Lubricating oils (lipid pneumonia tain aniline dyes) Antibiotics (most) when aspirated) Sesame oil Eye make-up Silica Baby products, cosmetics Magic markers Silly putty (99% silicones) Ballpoint pen inks Fabric softeners Make-up (eye, liquid, facial) Soap and soap products Bathtub floating toys Fertiliser (if no insecticides or herbicides Matches Suntan preparations Bath oil (castor oil and perfume) added) Mineral oil (unless aspirated) Sweetening agents (saccharin, Bleach (< 3.5% hypochlorite) Fish bowl additives Motor oil cyclamate) Body conditioners Bubble-bath soaps Glues and pastes (for wood or paper) Newspaper Talc (not inhaled) Golf ball (core may cause mechanical Teething rings (containing Calamine lotion injury) Paint (indoor or latex) water, if sterile) Calcium sulphate Greases Pencil (lead, graphite, colouring) Thermometers (elemental mer- (plaster of Paris) Perfumes cury or alcohol) Candles (beeswax or Hair products (dyes, sprays, tonics) Peroxide 3% Toilet water paraffin) Hand lotions and creams Pet food Toothpaste (with or without Caps (toy pistol, potas- Homeopathic medication (excl. herbal Petroleum jelly (Vaseline) fluoride) sium chlorate) medicines) Phenolphthalein laxatives (Brooklax) Chalk (calcium carbonate) Hydrogen peroxide (medicinal 3%) Plasticine Vaseline Charcoal Play-Doh Vitamins (without iron) Cigarettes or cigars (nicotine) Ice bricks (water and edible thickener) Polaroid picture coating fluid Clay (modelling) Incense Porous-tip ink marking pens (koki) Water colours CME Colognes Inedible markers Prussian blue (ferricyanide) Contraceptives Ink (black and blue — non-permanent) Putty (less than 60 g) Zinc oxide Corticosteroids Iron filings (chemical sets) Zirconium oxide August 2003 Vol.21 No.8 August 2003 Vol.21 Cosmetics Rouge Crayons (marked ‘non-toxic’) Lanolin Rubber cement Laxatives MAIN TOPIC Dehumidifying packets Lipstick (silica or charcoal) Adapted from Ellenhorn and Barceloux,4 with permission 439 MAIN TOPIC exposure). At this stage symp- which are rapidly and com- maintenance of normal respira- toms may not be expected, or pletely reversible. Although tory, circulatory and renal func- the incident may have been par- many agents in this category tion with monitoring of blood tially forgotten. This can mean have the potential to cause gases, acid/base balance, serum that the patient and/or doctor serious organ dysfunction or electrolyte and glucose levels, may not immediately (if at all) even death, appropriate support- etc. Benzodiazepines and opi- associate the cause of the symp- ive care during the acute phase ates taken in overdose, and even toms with exposure, leading to will ensure complete recovery in strychnine, are examples of poi- delayed optimal therapeutic most instances. Fortunately, sons with a relatively low inher- intervention. Examples include most potential poisons dealt ent toxicity. paracetamol and Amanita phal- with in the clinical setting fall When dealing with a suspected loides poisoning. into this category. Consequently, case of poisoning, one of the main • Poisons which do not cause most poisoned patients require priorities should be to attempt to tissue damage directly or treatment of symptoms and identify poisons with a high inher- which cause toxic effects appropriate supportive care ent toxicity as soon as possible only. ‘Supportive care’ is the Table II. Examples of drugs and poisons with a high inherent toxicity* Drug or poison Specific treatment† Reason for early antidotal/ active removal therapy Carbon monoxide‡ Oxygen Tissue damage (nervous system) Cyanide‡, § Oxygen. In serious poisoning: Extremely toxic, often with a morbid course and sodium nitrite/sodium thiosulphate death or Kelocyanor (Restan) Digoxin Digoxin-specific antibodies With massive overdose poisoned membranes can no longer maintain electrolyte gradients; this leads to extremely high potassium levels Ethylene glycol‡, ¶ Ethanol, haemodialysis Tissue damage (nervous system, kidney) Isoniazid‡ Pyridoxine, haemodialysis Tissue damage (nervous system) Lithium carbonate** Haemodialysis Tissue damage (nervous system, kidney) Metals and metalloids Arsenic** Dimercaprol, penicillamine Tissue damage (nervous system, liver, kidney) Tissue damage (gastrointestinal, liver, CVS) Iron‡, ** Deferoxamine Tissue damage (nervous system) Lead** Dimercaprol, calcium disodium Tissue damage (nervous system, kidney) edetate Mercury** Dimercaprol, penicillamine Methanol‡, ¶ Ethanol, haemodialysis Tissue damage (nervous system, blindness) Methyl bromide Dimercaprol, N-acetylcysteine Tissue damage (nervous system, CVS, kidneys) Mushrooms — cyclopeptides as in Silibinin Tissue damage (liver, kidney, heart, pancreas) Amanita phalloides** Organophosphates** Obidoxime chloride, atropine To prevent extended periods of intensive care Paracetamol N-acetylcysteine Tissue damage (liver, kidney) Paraquat (diquat)**, †† Immediate, aggressive Multisystem failure (kidney, liver, nervous decontamination procedures plus system, heart, lungs) activated charcoal or a watery slurry of clay Salicylates‡ Haemodialysis Tissue damage (nervous system) Theophylline‡, ** Haemoperfusion Tissue damage (nervous system) *Examples are those in which antidotes or special toxin removal procedures may prevent permanent tissue damage or serious complications (paraquat
Load more

Recommended publications
  • 615.9Barref.Pdf
    INDEX Abortifacient, abortifacients bees, wasps, and ants ginkgo, 492 aconite, 737 epinephrine, 963 ginseng, 500 barbados nut, 829 blister beetles goldenseal blister beetles, 972 cantharidin, 974 berberine, 506 blue cohosh, 395 buckeye hawthorn, 512 camphor, 407, 408 ~-escin, 884 hypericum extract, 602-603 cantharides, 974 calamus inky cap and coprine toxicity cantharidin, 974 ~-asarone, 405 coprine, 295 colocynth, 443 camphor, 409-411 ethanol, 296 common oleander, 847, 850 cascara, 416-417 isoxazole-containing mushrooms dogbane, 849-850 catechols, 682 and pantherina syndrome, mistletoe, 794 castor bean 298-302 nutmeg, 67 ricin, 719, 721 jequirity bean and abrin, oduvan, 755 colchicine, 694-896, 698 730-731 pennyroyal, 563-565 clostridium perfringens, 115 jellyfish, 1088 pine thistle, 515 comfrey and other pyrrolizidine­ Jimsonweed and other belladonna rue, 579 containing plants alkaloids, 779, 781 slangkop, Burke's, red, Transvaal, pyrrolizidine alkaloids, 453 jin bu huan and 857 cyanogenic foods tetrahydropalmatine, 519 tansy, 614 amygdalin, 48 kaffir lily turpentine, 667 cyanogenic glycosides, 45 lycorine,711 yarrow, 624-625 prunasin, 48 kava, 528 yellow bird-of-paradise, 749 daffodils and other emetic bulbs Laetrile", 763 yellow oleander, 854 galanthamine, 704 lavender, 534 yew, 899 dogbane family and cardenolides licorice Abrin,729-731 common oleander, 849 glycyrrhetinic acid, 540 camphor yellow oleander, 855-856 limonene, 639 cinnamomin, 409 domoic acid, 214 rna huang ricin, 409, 723, 730 ephedra alkaloids, 547 ephedra alkaloids, 548 Absorption, xvii erythrosine, 29 ephedrine, 547, 549 aloe vera, 380 garlic mayapple amatoxin-containing mushrooms S-allyl cysteine, 473 podophyllotoxin, 789 amatoxin poisoning, 273-275, gastrointestinal viruses milk thistle 279 viral gastroenteritis, 205 silibinin, 555 aspartame, 24 ginger, 485 mistletoe, 793 Medical Toxicology ofNatural Substances, by Donald G.
    [Show full text]
  • Adverse Health Effects of Heavy Metals in Children
    TRAINING FOR HEALTH CARE PROVIDERS [Date …Place …Event …Sponsor …Organizer] ADVERSE HEALTH EFFECTS OF HEAVY METALS IN CHILDREN Children's Health and the Environment WHO Training Package for the Health Sector World Health Organization www.who.int/ceh October 2011 1 <<NOTE TO USER: Please add details of the date, time, place and sponsorship of the meeting for which you are using this presentation in the space indicated.>> <<NOTE TO USER: This is a large set of slides from which the presenter should select the most relevant ones to use in a specific presentation. These slides cover many facets of the problem. Present only those slides that apply most directly to the local situation in the region. Please replace the examples, data, pictures and case studies with ones that are relevant to your situation.>> <<NOTE TO USER: This slide set discusses routes of exposure, adverse health effects and case studies from environmental exposure to heavy metals, other than lead and mercury, please go to the modules on lead and mercury for more information on those. Please refer to other modules (e.g. water, neurodevelopment, biomonitoring, environmental and developmental origins of disease) for complementary information>> Children and heavy metals LEARNING OBJECTIVES To define the spectrum of heavy metals (others than lead and mercury) with adverse effects on human health To describe the epidemiology of adverse effects of heavy metals (Arsenic, Cadmium, Copper and Thallium) in children To describe sources and routes of exposure of children to those heavy metals To understand the mechanism and illustrate the clinical effects of heavy metals’ toxicity To discuss the strategy of prevention of heavy metals’ adverse effects 2 The scope of this module is to provide an overview of the public health impact, adverse health effects, epidemiology, mechanism of action and prevention of heavy metals (other than lead and mercury) toxicity in children.
    [Show full text]
  • The Deactivation of Industrial SCR Catalysts—A Short Review
    energies Review The Deactivation of Industrial SCR Catalysts—A Short Review Agnieszka Szymaszek *, Bogdan Samojeden * and Monika Motak * Faculty of Energy and Fuels, AGH University of Science and Technology, Al. Mickiewicza 30, 30-059 Kraków, Poland * Correspondence: [email protected] (A.S.); [email protected] (B.S.); [email protected] (M.M.) Received: 2 July 2020; Accepted: 24 July 2020; Published: 29 July 2020 Abstract: One of the most harmful compounds are nitrogen oxides. Currently, the common industrial method of nitrogen oxides emission control is selective catalytic reduction with ammonia (NH3-SCR). Among all of the recognized measures, NH3-SCR is the most effective and reaches even up to 90% of NOx conversion. The presence of the catalyst provides the surface for the reaction to proceed and lowers the activation energy. The optimum temperature of the process is in the range of 150–450 ◦C and the majority of the commercial installations utilize vanadium oxide (V2O5) supported on titanium oxide (TiO2) in a form of anatase, wash coated on a honeycomb monolith or deposited on a plate-like structures. In order to improve the mechanical stability and chemical resistance, the system is usually promoted with tungsten oxide (WO3) or molybdenum oxide (MoO3). The efficiency of the commercial V2O5-WO3-TiO2 catalyst of NH3-SCR, can be gradually decreased with time of its utilization. Apart from the physical deactivation, such as high temperature sintering, attrition and loss of the active elements by volatilization, the system can suffer from chemical poisoning. All of the presented deactivating agents pass for the most severe poisons of V2O5-WO3-TiO2.
    [Show full text]
  • A Case of Mushroom Poisoning with Russula Subnigricans: Development of Rhabdomyolysis, Acute Kidney Injury, Cardiogenic Shock, and Death
    CASE REPORT Nephrology http://dx.doi.org/10.3346/jkms.2016.31.7.1164 • J Korean Med Sci 2016; 31: 1164-1167 A Case of Mushroom Poisoning with Russula subnigricans: Development of Rhabdomyolysis, Acute Kidney Injury, Cardiogenic Shock, and Death Jong Tae Cho and Jin Hyung Han Mushroom exposures are increasing worldwide. The incidence and fatality of mushroom poisoning are reported to be increasing. Several new syndromes in mushroom poisoning Department of Internal Medicine, College of have been described. Rhabdomyolytic mushroom poisoning is one of new syndromes. Medicine, Dankook University, Cheonan, Korea Russula subnigricans mushroom can cause delayed-onset rhabdomyolysis with acute Received: 17 April 2015 kidney injury in the severely poisoned patient. There are few reports on the toxicity of R. Accepted: 6 June 2015 subnigricans. This report represents the first record of R. subnigricans poisoning with rhabdomyolysis in Korea, describing a 51-year-old man who suffered from rhabdomyolysis, Address for Correspondence: Jong Tae Cho, MD acute kidney injury, severe hypocalcemia, respiratory failure, ventricular tachycardia, Department of Internal Medicine, College of Medicine, cardiogenic shock, and death. Mushroom poisoning should be considered in the evaluation Dankook University, 201 Manghyang-ro, Dongnam-gu, Cheonan 31116, Korea of rhabdomyolysis of unknown cause. Furthermore, R. subnigricans should be considered E-mail: [email protected] in the mushroom poisoning with rhabdomyolysis. Keywords: Mushroom Poisoning; Rhabdomyolysis; Acute Kidney Injury; Respiratory Failure; Cardiogenic Shock INTRODUCTION in August, 2010 at the Jujak mountain located on the province of Jeollanam­do, the southern area of Korea. He was a bus driv­ More leisure time for hobbies, hiking, and trekking has led to er.
    [Show full text]
  • Detection,Prevention and Management of Arsenicosis in India
    Detection,Prevention and Management of Arsenicosis in India A Field Guide Directorate General of Health Services Ministry of Health and Family Welfare Government of India 1 FOREWORD Arsenicosis has been known to be a health problem in some parts of our country. It occurs mainly by drinking Arsenic contaminated ground water and also through contaminated food chain or Industrial pollution for prolonged period. It results in skin manifestations such as Kerotosis, Melanosis and may also affect lungs, liver or lead to various types of cancers. The condition is preventable if measures are taken to provide safe drinking water to the community, promotion of nutrition and also if diagnosed early. With a view to formulate Guidelines for prevention, control and management of Arsenicosis, an Expert Group was constituted under my Chairmanship. After detailed round of discussions and subsequent exchange of communications, these Guidelines have now been finalized. I am sure that these Guidelines shall be very useful for sensitizing the Health Programme Managers and for training of Medical & Paramedical personnel in the field. I compliment the officials of the Nutrition & IDD Cell of the Dte. General of Health Services for facilitating in preparation and finalization of these Guidelines. It is hoped that these Guidelines shall be helpful in prevention and control of Arsenicosis in the affected areas of the country. Dr. Jagdish Prasad Director General of Health Services, Ministry of Health & Family Welfare, Government of India. 2 CONTENTS 1. Preamble 2. Health Impacts of exposure 3. Detection and Management of Arsenicosis Goal and Objectives Components Linkages & Coordination mechanism Recording and Reporting Review and Evaluation 4.
    [Show full text]
  • Pattern and Epidemiology of Poisoning in the East African Region: a Literature Review
    Hindawi Publishing Corporation Journal of Toxicology Volume 2016, Article ID 8789624, 26 pages http://dx.doi.org/10.1155/2016/8789624 Review Article Pattern and Epidemiology of Poisoning in the East African Region: A Literature Review Dexter Tagwireyi,1 Patience Chingombe,1 Star Khoza,2 and Mandy Maredza3 1 Drug and Toxicology Information Service (DaTIS), School of Pharmacy, College of Health Sciences, University of Zimbabwe, P.O. Box A178, Avondale, Harare, Zimbabwe 2Department of Clinical Pharmacology, College of Health Sciences, University of Zimbabwe, P.O. Box A178, Avondale, Harare, Zimbabwe 3School of Public Health, Faculty of Health Sciences, University of Witwatersrand, Johannesburg, South Africa Correspondence should be addressed to Dexter Tagwireyi; [email protected] Received 19 July 2016; Accepted 19 September 2016 Academic Editor: Steven J. Bursian Copyright © 2016 Dexter Tagwireyi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The establishment and strengthening of poisons centres was identified as a regional priority at the first African regional meeting on the Strategic Approach to International Chemicals Management (SAICM) in June 2006. At this meeting, the possibility of a subregional poisons centre, that is, a centre in one country serving multiple countries, was suggested. The WHO Headquarters following consultation with counterparts at the WHO Regional Office for Africa (AFRO) and the SAICM Africa Regional Focal Point successfully submitted a proposal to the SAICM Quick Start Programme (QSP) Trust Fund Committee for a feasibility study into a subregional poisons centre in the Eastern Africa subregion.
    [Show full text]
  • N-Acetylcysteine in the Treatment of Human Arsenic Poisoning
    J Am Board Fam Pract: first published as 10.3122/jabfm.3.4.293 on 1 October 1990. Downloaded from N-Acetylcysteine In The Treatment Of Human Arsenic Poisoning Debra S. Martin, M.D., Stephen E. Willis, M.D., and David M. Cline, M.D. Abstract: A 32-year-old man was brought to the emergency department 5 1/2 hours after ingesting a potentiaIly lethal dose (900 mg) of sodium arsenate ant poison in a suicide attempt. The patient deteriorated progressively for 27 hours. After intramuscular dimercaprol and supportive measures failed to improve his condition, he was given N-acetylcysteine intravenously. The patient showed remarkable clinical improvement during the following 24 hours and was discharged from the hospital several days later. (J Am Board Fam Pract 1990; 3:293-6.) Arsenic has been used since medieval times, known use of intravenous NAC in a patient with both as medicine and poison. Although its me­ arsenic poisoning. dicinal use has declined, arsenic can still be found as an ingredient in certain homeopathic Case Report formulas, I which are available in some health A 32-year-old man was brought to the emer­ food stores. Arsenic also is present in high con­ gency department by ambulance 5 hours after centrations in many easily obtainable ant kill­ he ingested approximately 900 mg of sodium ers, and this source is responsible for most toxic arsenate - five times the lethal doseJ,6 - in a human ingestions. 2 Other sources include in­ suicide attempt. He was lethargic but arousable secticides, herbicides, and rodenticides. Com­ by voice and answered questions appropriately.
    [Show full text]
  • CHAPTER E49 Heavy Metal Poisoning
    discussion with respect to the four most hazardous toxicants (arsenic, CHAPTER e49 cadmium, lead, and mercury). Arsenic, even at moderate levels of exposure, has been clearly linked with increased risks for cancer at a number of different tissue Heavy Metal Poisoning sites. These risks appear to be modified by smoking, folate and selenium status, and other factors. Evidence is also emerging that low-level arsenic may cause neurodevelopmental delays in children Howard Hu and possibly diabetes, but the evidence (particularly for diabetes) remains uneven. Metals pose a significant threat to health through low-level environ- Serious cadmium poisoning from the contamination of food mental as well as occupational exposures. One indication of their and water by mining effluents in Japan contributed to the 1946 CHAPTER e49 importance relative to other potential hazards is their ranking by outbreak of “itai-itai” (“ouch-ouch”) disease, so named because the U.S. Agency for Toxic Substances and Disease Registry, which of cadmium-induced bone toxicity that led to painful bone frac- maintains an updated list of all hazards present in toxic waste sites tures. Modest exposures from environmental contamination have according to their prevalence and the severity of their toxicity. The recently been associated in some studies with a lower bone density, first, second, third, and seventh hazards on the list are heavy metals: a higher incidence of fractures, and a faster decline in height in lead, mercury, arsenic, and cadmium, respectively (http://www. both men and women, effects that may be related to cadmium’s atsdr.cdc.gov/cercla/07list.html) . Specific information pertaining calciuric effect on the kidney.
    [Show full text]
  • Phalloidin, Amanita Phalloides
    Phalloidin, Amanita phalloides sc-202763 Material Safety Data Sheet Hazard Alert Code EXTREME HIGH MODERATE LOW Key: Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION PRODUCT NAME Phalloidin, Amanita phalloides STATEMENT OF HAZARDOUS NATURE CONSIDERED A HAZARDOUS SUBSTANCE ACCORDING TO OSHA 29 CFR 1910.1200. NFPA FLAMMABILITY1 HEALTH4 HAZARD INSTABILITY0 SUPPLIER Company: Santa Cruz Biotechnology, Inc. Address: 2145 Delaware Ave Santa Cruz, CA 95060 Telephone: 800.457.3801 or 831.457.3800 Emergency Tel: CHEMWATCH: From within the US and Canada: 877-715-9305 Emergency Tel: From outside the US and Canada: +800 2436 2255 (1-800-CHEMCALL) or call +613 9573 3112 PRODUCT USE Toxic bicyclic heptapeptide (a member of the family of phallotoxins) isolated from the green mushroom, Amanitra phalloides Agaricaceae (the green death cap or deadly agaric). Binds to polymeric actin, stabilising it and interfering with the function of endoplasmic reticulum and other actin-rich structures. NOTE: Advice physician prior to working with phallotoxins. Prepare Emergency procedures. SYNONYMS C35-H48-N8-O11-S, phalloidine, "Amanita phalloides Group I toxin", "Amanita phalloides Group I toxin", "mushroom (green death cap/ deadly agaric) phallotoxin/ peptide", "cyclopeptide/ bicyclic bioactive heptapeptide" Section 2 - HAZARDS IDENTIFICATION CANADIAN WHMIS SYMBOLS EMERGENCY OVERVIEW RISK Very toxic by inhalation, in contact with skin and if swallowed. POTENTIAL HEALTH EFFECTS ACUTE HEALTH EFFECTS SWALLOWED ■ Severely toxic effects may result from the accidental ingestion of the material; animal experiments indicate that ingestion of less than 5 gram may be fatal or may produce serious damage to the health of the individual. ■ At sufficiently high doses the material may be hepatotoxic(i.e.
    [Show full text]
  • Arsenic Poisoning
    From the Toxipedia website in original form. Last updated by Toxipedia in 2014. Sean Foley, author. Arsenic Poisoning Background and History Arsenic has a long and diverse history of use. It is most famous for its use as a poison from Roman times to the mid-nineteenth century. Its lack of color, odor, and taste made it a favored poison. When ingested in high quantities, arsenic causes severe abdominal cramps, diarrhea, vomiting, and eventually, death. When ingested in small doses, symptoms mimic those of chronic illnesses, disguising the assassin's intent. Arsenic poisoning was such a widespread concern that the Roman Consul Lucius Cornelius Sulla issued the Lex Cornelia in 82 B.C. outlawing arsenic poisoning. However, The Borgias, led by Cesare Borgia and his father Pope Alexander VI, assassinated numerous wealthy cardinals and popes and, by church law, acquired holdings and money of the deceased. The Borgias became some of the richest men in all of Italy, but they themselves succumbed to the poison. Napoleon is also rumored to have died of arsenic poisoning, though the debate is highly contentious and continues to this day. (See Napoleon's Death by Arsenic Exposure...? for a detailed description of the debate.) The use of arsenic as a poison began decreasing in the 18th century, when English chemist James Marsh developed a chemical test that identifies arsenic in the body. The use of arsenic as a pesticide began in the late nineteenth century. Though the majority of arsenic- based pesticides are no longer used in agriculture or horticulture in the U.S., arsenic-based wood preservatives are still used in nonresidential construction.
    [Show full text]
  • Addressing Toxic Smoke Particulates in Fire Restoration
    Addressing Toxic Smoke Particulates in Fire Restoration By: Sean M. Scott In the restoration industry today, a lot of attention testing laboratory or industrial hygienist provides an is given to the testing and abatement of air clearance test to certify that the abatement or microscopic hazardous materials. These include remediation process was successful. Upon receipt asbestos, lead, mold, bacteria, bloodborne of the clearance, people can then reenter the pathogens, and all sorts of bio-hazards fall into this remediated area, rooms, or building. However, category. If these contaminants are disturbed, when the structural repairs are completed after a treated, or handled improperly, all of them can fire, an air clearance test is rarely ever performed. cause property damage and serious harm to the How then can consumers be assured or restoration health and welfare of those living or working in or companies guarantee that the billions of toxic near the areas where they’re present. However, particulates and VOC’s generated by the fire have there are other hazardous toxins that commonly been removed? Is there cause for concern or is a present themselves in restoration projects, that simple “sniff” test or wiping a surface with a Chem- seem to go unnoticed. These are the toxic smoke sponge sufficient? Why is it so common to hear particulates and volatile organic compounds customers complain of smelling reoccurring smoke (VOC’s) created during structure fires. odor long after the restoration is completed? What measures are being taken to protect workers and When a building is abated from asbestos, lead, or their families from toxic ultra-fine particulate matter mold, special care is given to be sure every or VOC’s? microscopic fiber, spore, and bacteria is removed.
    [Show full text]
  • Mushroom Poisoning
    CHAPTER Mushroom Poisoning 114 Bhupen Barman, KG Lynrah, Iadarilang Tiewsoh INTRODUCTION Acute gastroenteritis – A wide variety of non eatable Mushroom poisoning among other forms of poisoning mushrooms when consumed causes nausea, vomiting, contributes to high morbidity and mortality in the diarrhea and abdominal cramps within one to three country. In certain ethnic populations of India, mushroom hours of consumption. These symptoms are caused most is an important constituent of their diet. The incidence of commonly by the chlorophyllum molybdites species are mushroom poisoning in India in the recent years has been also called “backyard mushrooms”. recognized due to increasing awareness and the affected NEUROTOXIC SYNDROMES individuals seeking health care at the earliest. The tropical a. The hallucinogenic effects are produced by the belt of the country with its biodiversity is a mother load ingestion of mushroom containing psilocybin of different fungal mushroom species. As per studies and psilocin. They are known to be abused for conducted in India, there are 1200 species with only 50 recreational purposes. to 100 species known to be poisonous. Twelve groups of the identified mushroom toxins have been identified b. CNS excitation and depression: This syndrome responsible for 14 described clinical syndromes. is caused by Amanita species containing toxins muscimol and ibotenic acid. Muscimol is a CNS EPIDEMIOLOGY depressant whereas ibotenic acid has excitatory From the studies conducted the 50-100 toxic mushrooms effects at glutamic acid receptors in the CNS. produces the mycotoxins responsible for different clinical Symptoms include somnolence, dizziness, syndromes which are described below. In the United hallucination, dysphoria, bizarre behavior and States the North American mycological association seizures.
    [Show full text]