35 to 40 days for both sexes. Detailed experiments were conducted to determine the influence of aging on metabolic activation of the two compounds, as well as on detoxification systems (e.g., aryl esterase-catalyzed hydrolysis, glutathione-dependent dearylation and dealkylation, and binding in the liver and plasma). Benke and Murphy (1975) concluded that increased detoxification of the active oxygen analogues of parathion and parathion-methyl was largely responsible for the lower acute toxicity of the two insecticides in adult animals. Murphy (1982) subsequently pointed to two other factors that contributed to the lower sensitivity of adult rats to organophosphates: greater binding to noncritical tissue constituents and more rapid catabolism of the parent compounds.

The limited information available suggests that immature humans also experience greater susceptibility to organophosphate- and carbamate-induced cholinesterase inhibition and related effects. In 1976 in Jamaica, 79 people were acutely poisoned as a result of eating parathion-contaminated flour (Diggory et al., 1977). Seventeen of the patients died. Case-fatality ratios were highest (i.e., 40%) among children ranging from newborns to 4 years of age. Zwiener and Ginsburg (1988) presented the clinical histories of 37 infants and children exhibiting moderate to severe organophosphate and carbamate toxicity. Although most of these patients ingested the pesticides, six became intoxicated after playing on sprayed surfaces. Zwiener and Ginsburg (1988) noted that 76% of their subjects were younger than 3 years old. The investigators found there was a paucity of information in the literature on the toxicity of cholinesterase inhibitors in infants and children.

Parathion contamination of stored foodstuffs (Diggory et al., 1977) and aldicarb contamination of crops (Goldman et al., 1990) have resulted in the most widespread outbreaks of foodborne pesticide toxicity in North America. Goldman and co-workers investigated more than 1,000 cases of illness caused by consumption of aldicarb-contaminated watermelons and cucumbers. Unfortunately, infants and children were not studied as a subpopulation at risk. The investigators did calculate doses of aldicarb sulfoxide that produced illness in the general population and estimated that a 10-kg child could readily consume enough of the pesticide on watermelons to experience toxicity. The U.S. Environmental Protection Agency (EPA, 1988) concluded that infants and children are at the greatest risk of acute aldicarb toxicity. This conclusion was based on dietary consumption and contamination patterns, however, rather than on the greater sensitivity of infants and children to this potent cholinesterase inhibitor.

Although immature humans appear to be more susceptible than adults to the acute effects of cholinesterase inhibitors, the age-dependency of this phenomenon is not entirely clear. Some of the most applicable information has been provided by a study of the perinatal development of

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