Organophosphate poisoning, humans

Inns RH, Tuckwell NJ, Bright JE et al. (1990). Histochemical demonstration of calcium accumulation in muscle fibres after experimental organophosphate poisoning. Human Exp Toxicol, 9, 245-250. 

Varmeste, Y. and Lison, D., 1993, Biochemical changes associated with muscle fibre necrosis after experimental organophosphate poisoning. Human Exper. Toxicol 12 365. 

Peter, J.V., Moran, J.L., Graham, P. (2006). Oxime therapy and outcomes in human organophosphate poisoning an evaluation using meta-analytic techniques. Crit. Care Med. 34(2) 502-10. 

Evron, T., Geyer, B.C., Chemi, I., Muralidharan, M., Kilboume, J., Fletcher, S.P., Soreq, H., Mor, T.S. (2007a). Plant-derived human acetylcholinesterase-R provides protection from lethal organophosphate poisoning and its chronic aftermath. FASEB J. 21 2961-9. 

Levy, A., Cohen, G., Gilat, E., Kapon, J., Dachir, S., Abraham, S., Herskovitz, M., Teitelbaum, Z., Raveh, L. (2007). Extrapolation from animal studies to the efficacy in humans of a pretreatment combination against organophosphate poisoning. Arch. Toxicol. 81 353-9. 

Stevens, R.C., Suzuki, S.M., Cole, T.B., Park, S.S., Richter, R.T., Furlong, C.E. (2008). Engineered recombinant human paraoxonase 1 (rHuPONl) purified from Escherichia coli protects against organophosphate poisoning. Proc. Natl. Acad. Sci. USA 105 12780-4. 

See also Anticholinergics Carbamate Pesticides Organophosphate Poisoning, Intermediate Syndrome Organophosphates Poisoning Emergencies in Humans. 

Karademir M, Erturk E, and Kocak R (1990) Two cases of organophosphate poisoning with development of intermediate syndrome. Human Experimental Toxicology 9 187-189. 

Organophosphates. The acute toxicity of organophosphate pesticides is basically derived from the anticholinesterase property of these chemicals. This property, which results in accumulation of acetylcholine at synapses and myoneural junctions, is responsible for both the insecticidal activity and mammalian toxicity. Early symptoms of organophosphate poisoning in humans include, among others, miosis (pinpoint pupils) and blurred vision, and a response known as the SLUD (salivation, lacrimation, urination, and diarrhea) syndrome all of these are the result of muscarinic effects (12-15). Clinical manifestations of more severe poisoning involve predominantly nicotinic and central effects which include convulsions, paralysis, depressed respiration and cardiovascular functions, and coma (12-15). Death is usually due to respiratory failure, accompanied by cardio-vascular failure (13). 

K21. Khan, S., Hemalatha, R., Jeyaseelan, L., Oomen, A., and Zachariah, A., Neuroparalysis and oxime efficacy in organophosphate poisoning A study of butyrylcholinesterase. Human Exp. Toxicol. 20,169-174 (2001). 

As noted earlier, all pesticides are toxic to humans. Different classes of pesticides, however, poison by different mechanisms. Organophosphates poison insects and animals primarily by phosphorylation of the acetylcholinesterase enzyme (AChE) at nerve endings, thus interfering with normal nerve impulse transmission. A-Methyl carbamates also poison by attacking the AChE and interfering with nerve transmissions. The other major class of pesticides, the organochlorines, are not cholinesterase... 

Huang, Y.S., Huang, Y., Baldasssarre, H., et al., 2007. Recombinant human butyr-ylcholinesterase from milk of transgenic animals to protect against organophosphate poisoning. Proc. Natl Acad. Sci. USA 104, 13603-13608. 

Organophosphate Ester Hydraulic Fluids. Human studies of exposure to organophosphates are primarily those of acute, accidental poisonings with tricresyl phosphate (Goldstein et al. 1988 Senayanake and Jeyaratnam 1981 Srivastava et al. 1990). 

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. 

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