organophosphate and carbamate exposure, is less well established, but is strongly suggestive. Similar to the data on lead, there is strong evidence that acute, high-level exposure results in severe systemic disease caused by biochemical mechanisms that affect the nervous system directly. In addition, the data suggest that more long-term effects may result from exposure and that low-level exposure may have subtle, but measurable, effects on neurologic function.
The emerging data suggest that neurotoxic and behavioral effects may result from low-level chronic exposure to some organophosphate and carbamate pesticides. Sophisticated methods will be required to pursue this line of research. For many other pesticides, the data are far less complete. However, when animal studies have shown that a pesticide functions by disrupting neurologic cellular function and when systemic toxic effects are known to occur after high-level acute exposures, the possibility of low-level chronic neurotoxic and behavioral effects must be considered.
In reviewing the data on the effects of pesticides, two questions must be addressed: Is there evidence that pesticides cause neurotoxic effects in children after acute exposure to high doses? Is there reason to suspect low-level, long-term developmental effects different from effects in adults?
Acute exposure of children to pesticides and resultant disease similar to neurotoxic effects in adults has been described for a range of pesticides, including organophosphate, carbamates, and organochlorines (Hayes 1970; Mortenson, 1986). Pediatric cases involving neurotoxic effects due to acute exposure continue to be reported for other pesticides (e.g., Roland et al., 1985, who reported on exposure to insect repellents and encephalopathy). Data on children as segments of larger exposed populations have also been reported (e.g., CDC, 1986).
Very few pesticides have been well studied for effects on neurologic development in humans and animals. Studies on polychlorinated biphenyls (PBBs) and polychlorinated biphenyls (PCBs) strongly suggest developmental effects from low-level exposures similar to the effects found for lead.
Data on exposure of humans were generated following a 1973–1974 exposure to PBBs in Michigan. Neuropsychological and developmental data were collected on children who were exposed in utero and during infancy. Physiological testing showed significant differences that were related to measures of body dose (Weil et al., 1981; Seagull, 1983).
In Taiwan, children exposed in utero to PCBs in contaminated cooking