Organophosphate neuropathy and biomarkers of exposure.
McConnell-R; Godbold-J; Simpson-D; Wolff-M; Cuadra-R; Delgado-E; Miranda-J; Torres-E; Lundberg-I
NIOSH 1997 Dec; :1-45
A case of acute methamidophos poisoning followed from the time of hospital admission with serial measurements of lymphocyte neuropathy target esterase and erythrocyte cholinesterase, and dynanometric measurement of pinch and grip strength, quantitatively determined vibrotactile threshold, and nerve conduction studies of ulnar motor and sensory, tibial and sural nerves demonstrated the appropriateness of these methods for evaluating the organophosphate induced delayed polyneuropathy (OPIDP) which developed two weeks after acute cholinergic poisoning. Final analysis of data from a retrospective cohort study of Nicaraguan workers previously poisoned with methamidophos demonstrated elevated vibrotactile threshold, compared with an age and sex matched community comparison group. Preliminary results from this study formed the basis for the project proposal. In a prospective study a cohort of 50 Nicaraguan patients acutely poisoned with neuropathic organophosphate insecticides (methamidophos and chlorpyrifos) and a comparison group of 22 patients poisoned with other organophosphates were examined after recovery from acute cholinergic poisoning but prior to the time when OPIDP might be expected to develop (at the time of hospital discharge). These patients were re-examined 6 weeks after poisoning) and two years after poisoning. Thirty-nine adults from a community comparison group also were examined (at the same intervals). Analysis of results from the first two examinations demonstrated no significant differences between the three study groups in the mean change in quantitatively measured vibrotactile threshold, dynanometrically measured grip or pinch strength, or in action potential amplitudes or in nerve conduction velocity of ulnar nerves or sural nerve, after controlling for age and severity of poisoning. A decrease in tibial nerve conduction velocity in the group poisoned with neuropathic pesticides may have been a chance statistically significant finding resulting from the multiple comparisons made, given that there was not a corresponding decrease in amplitude of the tibial nerve compound muscle action potential. There was no evidence for an interactive effect of age or severity of poisoning with neuropathic exposure. One would have expected sensory deficits, at least, in the prospectively evaluated cohort, given the deficit in vibrotactile threshold measured in the preliminary study. The prospective design and better exposure evaluation would have increased statistical power in the prospective study. It is possible that the project cohort did not suffer any neuropathic effect of poisoning, that subtle neuropathy appears earlier after poisoning than reported for clinical neuropathy (and thus was already present at the time of the first evaluation), or that the onset of subtle neuropathy reported in the literature (and thus had not yet appeared at the time of the second examination). The results of the examinations two years after poisoning of the patients in this cohort, which will be completed in 1988, may clarify this point.
Organo-phosphorus-pesticides; Pesticides-and-agricultural-chemicals; Insecticides; Insecticide-poisoning; Pesticides; Neuropathy;
Division of Environmental and Occupational Medicine, Mount Sinai School of Medicine, New York, New York
Final Grant Report
NTIS Accession No.
Exposure Assessment Methods; Work Environment and Workforce
National Institute for Occupational Safety and Health
Division of Environmental and Occupational Medicine, Department of Community Medicine, Mount Sinai School of Medicine, New York, New York