Abstract:
Introduction
In 1993, the National Research Council (NRC) released a report, Pesticides in the Diet of Infants and Children (1), which raised the issue that children may be uniquely susceptible to harm from pesticide exposure. This idea arose from the fact that children have a higher metabolism than adults and immature nervous, reproductive, and immune systems (2). They also have unique diets and behavior patterns (1). Children are mainly exposed to pesticides indirectly through food residues (3). Recently, there has also been concern about children’s para-occupational exposure to pesticides (4).
At the time that the NRC report was published, the Environmental Protection Agency (EPA) did not consider infants and children to be sensitive sub-population. As a response to the NRC’s recommendations, Congress passed the Food Quality Protection Act (FQPA) on August 3, 1996. This act amended previous food and pesticide regulations. The FQPA called for: (1) consideration of multiple exposure routes when setting acceptable residue tolerance levels in food; (2) examination of the aggregate exposure and cumulative risk and (3) more complete exposure assessments for children (5).
Because organophosphate pesticides (OPs) are widely used in both agricultural and residential environments (6), this study focused on assessing children’s exposure to OPs. OPs can be acutely toxic. They inhibit the enzyme acetyl cholinesterase (AChE) (7) in the synapse between the nerve cells, causing adverse health effects in both the central and peripheral nervous system. The numerous symptoms of the resulting cholinergic intoxication (2) vary in severity from dizziness and headache to death (8).
There is also evidence that chronic exposure to OPs has adverse health impacts. Chronic exposure to OPs has been shown to adversely impact neurodevelopment. Studies done in adult humans have demonstrated that low level exposure results in decreased nerve conduction and decrease visuomotor speed. Animals that were chronically exposed to OPs have decreased body weight (9). In addition, several epidemiology studies have associated chronic OP pesticide exposure with elevated cancer incidence (10). Elevated leukemia risks and excess non-Hodgkin’s lymphomas were found among farmers using particular OPs. Studies in children have associated OP exposure to aplastic anemia and acute leukemia (10).
People generally metabolize OPs through oxidation and then excrete the metabolites in the urine within a few days (6) (11). OP pesticide metabolites can be classified as either diethyl or dimethyl metabolites (12). These characteristics make biomonitoring a good method for conducting OP exposure assessments (13). Biomonitoring measures the level of metabolites or parent compound in excretia (14), thereby accounting for all exposure pathways (15). Taking urine samples is less invasive than taking the blood samples that are required for cholinesterase monitoring. Biomonitoring is a sensitive biomarker of general OP pesticide exposure (16). This method cannot, however, detect the presence of specific organophosphate metabolites.