Toxicological Screening For Organophosphorus Induced Delayed Neurotoxicity: Complications In Toxicity Testing.
Abstract
Organophosphorus induced delayed neurotoxicity (OPIDN) is discussed. The clinical signs of OPIDN are temporally distinct from the acute anti/acetylcholinesterase (AChE) effect and the syndrome of motor end plate inhibition. OPIDN occurs 6 to 21 days after oral, inhalation, or dermal exposure and its development is independent of an acute cholinergic reaction. The clinical signs include progressive weakness and ataxia beginning distally in the hind or lower limbs and may evolve into a flaccid paralysis that may also extend to the forelimbs. Persistent spinal cord damage may occur as spasticity, ataxia, or quadriplegia. Unlike the acute enzyme inhibition of AChE, OPIDN is either irreversible or resolves only gradually. Human cases of OPIDN are described. Organophosphorus pesticides that can cause OPIDN are enumerated. The role of toxicology and possible addenda to current screening procedures for detecting OPIDN are discussed. It is concluded that the range and prevalence of neurotoxic effects of organophosphorus pesticides are greater than expected, when considered from the standpoint of current regulatory and surveillance efforts. As a minimum, every organophosphorus ester that is in commercial use should be characterized as to its ability to induce OPIDN.
Keywords
NIOSH-Author; Pesticides-and-agricultural-chemicals; Organophosphorous-compounds; Biological-effects; Hazardous-materials; Enzyme-activity; Clinical-symptoms; Health-standards; Regulations; Health-protection;
NTIS Accession No.
PB86-107703
Source Name
NIOSH, U.S. Department of Health and Human Services, Cincinnati, Ohio, 46 pages, 113 references
