OBJECTIVES. This work was undertaken to determine whether there are any chronic neurological sequelae to acute organophosphate pesticide poisoning. METHODS. California surveillance data were used in a study of neurological function among 128 men poisoned by organophosphate pesticides in California from 1982 to 1990 and 90 referents. Tests included a neurological physical examination, 5 nerve conduction tests, 2 vibrotactile sensitivity tests, 10 neurobehavioral tests, and 1 postural sway test. RESULTS. After correcting for confounding, the poisoned group performed significantly worse than the referent group on two neurobehavioral tests (sustained visual attention and mood scales). When the data were restricted to men with documented cholinesterase inhibition (n = 83) or to men who had been hospitalized (n = 36), the poisoned subjects also showed significantly worse vibrotactile sensitivity of finger and toe. Significant trends of increased impairment were found with increased days of disability on a wide spectrum of tests of both central and peripheral nerve function. CONCLUSIONS. While these findings are limited by low response rates and by small sample sizes for specific pesticides, this study was based on a large surveillance database and is the largest study to date of the chronic effects of organophosphate pesticide poisoning. The evidence of some long-term effects of poisoning is consistent with two prior studies.

Chlorpyrifos is a moderately toxic organophosphate pesticide. Houses and lawns in the United States receive a total of approximately 20 million annual chlorpyrifos treatments, and 82% of U.S. adults have detectable levels of a chlorpyrifos metabolite (3,5, 6-trichloro-2-pyridinol; TCP) in the urine. The U.S. Environmental Protection Agency has estimated that there are 5,000 yearly reported cases of accidental chlorpyrifos poisoning, and approximately one-fourth of these cases exhibit symptoms. Organophosphates affect the nervous system, but there are few epidemiologic data on chlorpyrifos neurotoxicity. We studied neurologic function in 191 current and former termiticide applicators who had an average of 2.4 years applying chlorpyrifos and 2.5 years applying other pesticides, and we compared them to 189 nonexposed controls. The average urinary TCP level for 65 recently exposed applicators was 629.5 microg/L, as compared to 4.5 microg/L for the general U.S. population. The exposed group did not differ significantly from the nonexposed group for any test in the clinical examination. Few significant differences were found in nerve conduction velocity, arm/hand tremor, vibrotactile sensitivity, vision, smell, visual/motor skills, or neurobehavioral skills. The exposed group did not perform as well as the nonexposed group in pegboard turning tests and some postural sway tests. The exposed subjects also reported significantly more symptoms, including memory problems, emotional states, fatigue, and loss of muscle strength; our more quantitative tests may not have been adequate to detect these symptoms. Eight men who reported past chlorpyrifos poisoning had a pattern of low performance on a number of tests, which is consistent with prior reports of chronic effects of organophosphate poisoning. Overall, the lack of exposure effects on the clinical examination was reassuring. The findings for self-reported symptoms raise some concern, as does the finding of low performance for those reporting prior poisoning. Although this was a relatively large study based on a well-defined target population, the workers we studied may not be representative of all exposed workers, and caution should be exercised in generalizing our results.

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To test the hypothesis that chronic neurologic sequelae are associated with cholinesterase depression short of frank organophosphate poisoning, we compared 45 male subjects who had a history of moderate cholinesterase inhibition with 90 male subjects who had neither past cholinesterase inhibition nor current pesticide exposure. Cholinesterase-inhibited subjects were defined as having had a history of (a) red blood cell cholinesterase at 70% or less of baseline or (b) plasma cholinesterase at 60% or less of baseline absent symptoms of frank poisoning. In the subject comparison evaluation, only 1 of 27 neurologic tests (i.e., serial digit performance) was significant statistically, but it was opposite of the direction hypothesized. In a companion study for which the same battery of neurologic tests and the same subjects were used, neurologic sequelae were related to high exposures among subjects who sought treatment for organophosphate poisoning. The data in the current study, in which the subjects experienced lower exposures short of frank poisoning, provide some evidence that preventing acute organophosphate poisoning also prevents neurologic sequelae.

This study demonstrates a method for linking independently obtained health and job characteristic data based on occupational code.