and neurochemical disturbances (Otto and Reiter, 1984; Alfano and Petit, 1985; Otto et al., 1985; Moore et al., 1986) have supported the findings of toxic effects from exposure to low lead levels in humans (<30 µg/dl) and in animals. By testing for subtle neurologic, cognitive, and behavioral effects in children, these investigators elucidated neurodevelopmental toxic effects of lead.
The research that produced these findings was characterized by a variety of methodological approaches:
Multifaceted approaches included a range of methods for biochemical and neurophysiologic measurements in animals and (where ethically possible) humans.
Studies to evaluate subtle neurologic and developmental effects of lead included innovative methods that combined extensive batteries of different psychologic tests and rigorous statistical design focusing on various constructs to control confounding variables.
Investigators looking for lead toxicity did not assume safe levels of exposure or protective effects. When biochemical alteration in function was found at what was considered to be subclinical levels of exposure, researchers looked for methods that would measure subtle functional changes.
Many classes of compounds are used as pesticides. Some of them are known neurotoxicants. Important subclasses of the substances in use are known to have neurotoxic effects. Organophosphates and carbamates are used for demonstration purposes in this section of the extensive data—not because they present greater potential risk than other compounds.
Data suggest that in addition to short-term effects, there are other neurologic effects of a long-term nature in adult humans. For example, symptoms of organophosphate-induced delayed neurotoxicity have been found several weeks after acute exposure and have continued for many months (Whorton and Obrinsky, 1983; Vasilesque et al., 1984; Cherniak, 1988). An intermediate syndrome starts several days after acute exposure and involves paralytic symptoms for many days (Senanayake and Karalliedde, 1987). Abnormal nerve conduction velocities have also been observed in some settings involving low-level, long-term exposure (Misra et al., 1988). Neurobehavioral and psychiatric effects have been reported in some epidemiologic studies of adult populations (Maizlish et al., 1987) and in studies of adult animals (Overstreet, 1984).
The evidence on chronic effects, particularly neurobehavioral effects of