Organophosphates toxicity/poisoning

Farm workers are especially susceptible to organophosphate insecticide poisoning. Unsafe spraying conditions can lead to accumulated toxicity and chronic symptoms. Since there are many enzymes in the body which are in the serine esterase family along with Achase and can complex... 

Prevention of organophosphate toxicity is aimed at protecting the acetylcholine receptor and/or acetylcholinesterase itself. Atropine can be used to prevent as well as to treat organophosphate poisonings. In addition, use of reversible inhibitors of acetylcholinesterase has been used to prevent organophosphate... 

Mutch E, Blain PG, Williams FM Interindividual variations in enzymes controlling organophosphate toxicity in man. Hum Exp Toxicol 11 109-116,1992 Nalin DR Epidemic of suicide by malathion poisoning in Guyana. Tropical and Geographical Medicine 25 8-14,1973... 

Mutch E, Blain PG, Williams FM Interindividual variations in enzymes controlling organophosphate toxicity in man. Hum Exp Toxicol 11 109-116, 1992 Noyes H Internet telemedicine saves woman s life (news). The Mercury (U.S. Army Medical Department, Houston, TX) 24 6,1996 Prick JJG, Smitt WGS, Muller L Thallium Poisoning. Amsterdam, Elsevier, 1955 Reed D, Crawley J, Faro SN, et al Thallotoxicosis acute manifestations and sequelae. JAMA 183 516-522,1963... 

List the major signs and symptoms of (1) organophosphate insecticide poisoning and (2) acute nicotine toxicity. 

Doctor, B.R, Raveh, L., Wolfe, A.D., et al., 1991. Enzymes as pretreatment drugs for organophosphate toxicity. Neurosci. Biobehav. Rev. 15 (1), 123-128. Eddleston, M., Dawson, A.H., 2012. Triage and clinical management of patients with acute pesticide self-poisoning presenting to small rural hospitals. Clin. Toxicol. (Phila) 50 (6), 455-457. 

Nosocomial Poisoning Associated with Emergency Department Treatment of Organophosphate Toxicity - Georgia, 2000. Morbidity Mortality Weekly Rep. 2001,49, 1156-1158. 

Irreversible anticholinesterases include the organophosphorus inhibitors and ambenonium, which irreversibly phosphorylate the esteratic site. Such drugs have few clinical uses but have been developed as insecticides and nerve gases. Besides blocking the muscarinic receptors with atropine sulphate in an attempt to reduce the toxic effects that result from an accumulation of acetylcholine, the only specific treatment for organopho-sphate poisoning would appear to be the administration of 2-pyridine aldoxime methiodide, which increases the rate of dissociation of the organophosphate from the esteratic site on the enzyme surface. 

Merrill DG, Mihm EG Prolonged toxicity of organophosphate poisoning. Grit Care Med 10 5 50-551, 1982... 

Malathion is an organophosphate cholinesterase inhibitor. Up to 8% of the topically applied dose may be absorbed. Malathion is used as a treatment for head lice, body lice and scabies. It effectively kills both the eggs and the adult lice. Malathion is an insecticide of relatively low human toxicity. However if malathion is used in an indoor environment, as it breaks down into malaoxon, it can be seriously and chronically poisonous. The safety of malathion in pregnancy and in lactating women and in children has not been established. 

All the organophosphates except echothiophate are distributed to all parts of the body, including the central nervous system. Therefore, central nervous system toxicity is an important component of poisoning with these agents. 

Esterase activity is important in both the detoxication of organophosphates and the toxicity caused by them. Thus brain acetylcholinesterase is inhibited by organophosphates such as paraoxon and malaoxon, their oxidized metabolites (see above). This leads to toxic effects. Malathion, a widely used insecticide, is metabolized mostly by carboxylesterase in mammals, and this is a route of detoxication. However, an isomer, isomalathion, formed from malathion when solutions are inappropriately stored, is a potent inhibitor of the carboxylesterase. The consequence is that such contaminated malathion becomes highly toxic to humans because detoxication is inhibited and oxidation becomes important. This led to the poisoning of 2800 workers in Pakistan and the death of 5 (see chap. 5 for metabolism and chap. 7 for more details). 

In California, mixer-loaders and spray applicators who work with toxicity category I and II organophosphates or N-methyl carbamates more than 30 hours per 30-day period are required to have medical supervision. Supervision consists of an interview and a medical examination to determine if a medical condition exists which would make the worker unusually susceptible to poisoning due to cholinesterase inhibition, and to caution the individual about the use of certain drugs such as the pheno-thiazine tranquilizers vdtich potentiate the effects of cholinesterase (ChE) inhibition. Two blood samples, taken several days apart, are analyzed to determine the individual s preexposure plasma and red blood cell (RBC) ChE activity (baseline value). The physician arranges a routine ChE testing program and provides for extra ChE tests should the worker be accidently exposed to OP s. If ChE activity is depressed to 50 percent of the baseline value, the physician may ask the employer to place the worker on... 

Examination of the mouth provides evidence of exposure to some toxicants. Caustic acids and bases cause a moist condition of the mouth. Other toxicants that cause the mouth to be moister than normal include mercury, arsenic, thallium, carbamates, and organophosphates. A dry mouth is symptomatic of poisoning by tricyclic antidepressants, amphetamines, antihistamines, and glutethimide. 

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