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A benefit from mechanistic research in toxicology.

Organophosphorus (OP) esters are encountered in the working environment in two forms. Certain widely used pesticides such as chlorpyriphos, dichlorvos, and demeton-S-methyl are OP esters designed to be toxic by virtue of their power to inhibit acetylcholinesterase with consequent disorganisation of the cholinergic nervous system. Within the molecular structure of such pesticides are features that enable man and other mammals to be more efficient than pests in disposing of moderate amounts of the agent which may be ingested unintentionally. A hazard to man most often arises from exposure to undiluted concentrates during the preparation of material for spraying or because of leakage from containers or from failure to dispose properly of "empty" containers. Massive quantities of a different class of OP esters are manufactured for use as plasticisers, flame proofing agents for fabrics, and as stable non-corroding non-inflammable hydraulic fluids: these are, typically, mixtures of triesters of phosphoric acid derived from various substituted phenols and, sometimes, higher alcohols. Gross exposure to hydraulic fluids due to poor work practices is not uncommon in some occupations. A minority of compounds in either class of OP esters have been found to produce a delayed onset polyneuropathy first characterised in thousands of people who, during the days of prohibition, drank "Ginger Jake" liquors adulterated with United States Pharmacopoeia extract of ginger mixed with triortho-cresyl phosphate.' Occasional neuropathies have been seen after accidental or deliberate ingestion of only a few OP pesticides,2 3 but many cases of severe OP pesticide intoxication have no apparent residual effects.2 For many years pesticides proposed for use in the United Kingdom have been subjected to single or double dose tests for their ability to cause organophosphate induced delayed polyneuropathy (OPIDP: often called delayed neurotoxicity) in the adult hen, the most convenient sensitive species.4 Similar tests, but often with repeated doses, may be applied to the OP plasticisers. The limitation of such tests is that their endpoints are virtually all or none, although some severity grading is possible of clinical ataxia or of degenerative lesions detected in the nerves by histopathology. In view of the largely irreversible nature of the neuropathy and the fact that it may be induced by a single exposure to some compounds, more discriminating tests are desirable which could be applicable (a) in evaluating new compounds or in re-evaluating currently used compounds and (b) in monitoring workers occupationally exposed to OP esters. Such tests are now available based on the identification of the cellular target and an understanding of the process of attack on this target developed in the Medical Research Council's Toxicology Unit at Carshalton.5 6 It is now known that the primary event in OPIDP is organophosphorylation of a single protein dubbed neuropathy target esterase (NTE) and that its molecular structure is modified by a subsequent intramolecular change. The cascade of events between initiation at the molecular level and clinical expression of OPIDP two or more weeks later is still largely unknown. The initiation event, however, may be monitored conveniently by determining the inhibition of the esterase catalytic activity of NTE in necropsy samples taken from dosed animals.7 For the dialkyl phosphate esters, which constitute most of the tonnage ofOP pesticides used, and for the plasticisers the essential secondary intramolecular change ("aging") is virtually instantaneous and so may be assumed to have occurred in test samples but this may not be so for some more complex OP molecules.