![]() A single drop on the skin can be rapidly fatal.Īccording to the World Health Organization (WHO), there are about 1 million people a year admitted to hospital with accidental poisoning and 2 million with suicidal intent. One was in Matsumoto in 1994 and the other was in the Tokyo subway in 1995. Sarin is an OP poison and there are two recorded episodes of deliberate release - both in Japan. ![]() Fortunately, terrorist or warfare use of OP is rare but the potential exists to expose a great many people at once.Intentional self-harm tends to involve much higher doses than accidental exposure. Hospital admissions for intentional OP poisoning are twice as numerous as for accidental poisoning.There is a much higher incidence in rural areas of the third world. The vast majority of cases are accidental from the use of pesticides.There are no accurate figures kept about the incidence of OP poisoning. This is a significant problem which may also affect children and further research in this field is necessary. This is supported by a case control study which reported that chronic exposure to OP pesticides can lead both to depressive and anxiety disorders and also to cognitive defects (unrelated to psychiatric disorders). ![]() The syndrome is inconsistent in those affected but is neither simply a post-traumatic stress disorder nor the result of acute OP poisoning and is likely to represent low-level chronic toxicity. Certainly, insecticides were freely used, as were many other chemicals. There is some suggestion that the use of OP pesticides may have caused some neurotoxicity and be responsible for 'Gulf War syndrome'. This is prohibited under the Geneva Convention but could be used by terrorists or rogue regimes. They are used as pesticides but can also be used as 'nerve gas'. Hence, acetylcholine accumulates at nerve synapses and neuromuscular junctions, stimulating muscarinic and nicotinic receptors and the central nervous system. Possible lines of future investigations are indicated.The organophosphate (OP) pesticides inhibit acetylcholinesterase. A brief account is given of the range of compounds for which PAM has been shown to be a successful antidote in intact animals and of the ability of PAM to overcome the signs and symptoms of poisoning both in animals and in man. Pyridine-2-aldoxime methiodide and methanesulphonate have been by far the most successful as reactivators and in the treatment of poisoned animals. Types of compounds with either or both of these properties are o-dihydroxybenzene derivatives, metal chelates, hydroxylamine, hydroxamic acids, and oximes. In both cases essentially the same type of compound is needed, namely, one with a high intrinsic reactivity with organophosphoryl compounds, in (a) with the inhibitor itself or in (b) with the phosphorylated enzyme. ![]() Consequently two rational lines of treatment are: (a) To find some compound which could be phosphorylated as rapidly as the enzyme and which, if introduced into the body, would protect the enzyme from inhibition by competing with it for the organophosphate, or (b) to find a compound which would restore the activity of the inhibited enzyme by dephosphorylating it. Organophosphates are lethal because they inactivate cholinesterase due to phosphorylation of the enzyme's active centre. This paper reviews historically the researches which led to the development of pyridine-2-aldoxime methiodide (PAM) and its corresponding methane-sulphonate (P2S), the two most successful oximes yet tried, and summarizes the theoretical back-ground to their rational use. The discovery of the nature of the biochemical lesion in organophosphate poisoning has permitted the design of drugs to repair specifically this particular lesion. Oximes (with or without atropine as an adjunct) have recently been used successfully in the treatment of humans poisoned by organophosphate anticholinesterases. ![]()
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