an assessment of methodology rather than a specific attempt to characterize the proportion of children at risk. The method could also be used to study possible combinations of residues for any class of chemicals believed to have a common adverse effect, including cancer, where the end point of concern is not a site-specific tumor but, rather, the probability of a tumor occurring.
Although it was not generally within the committee's charge to examine exposures to pesticides by routes other than dietary, the committee wishes to point out that infants and children are subject to such exposures from a variety of sources. These sources should not be overlooked when attempting to estimate the total exposure of infants and children to pesticides and are therefore briefly summarized in this section.
In January 1990 EPA published the Nonoccupational Pesticide Exposure Study (NOPES). One of the study's primary objectives was to assess the relative contribution of each source to overall exposure to certain pesticides. Among their findings, the NOPES researches concluded that (1) "house dust may be a source of exposure to pesticides via dermal contact, ingestion, and inhalation of suspended particulates, especially for infants and toddlers"; (2) "acute dermal exposures that occur during application events may contribute substantially to total exposure"; and (3) that, for the pesticides they examined, exposure from drinking water appeared to be minimal (EPA, 1990). Thus, exposure from all sources—not just ingestion—must be considered when estimating total exposure and risk to children.
The child's first exposure to pesticides begins in utero, where chemicals may cross over the mother's placenta. Several studies have suggested an association between parental exposure (occupational and otherwise) to pesticides and childhood cancers. Researchers from the Children's Cancer Study Group (a cooperative clinical trials group with approximately 100 members and affiliate institutions in the United States and Canada) conducted a case-control study of occupational and household exposures of parents of 204 children with acute nonlymphoblastic leukemia (ANLL) (Buckley et al., 1989). Their most consistent finding was an association of ANLL risk when both mother and father had been exposed to pesticides.
Human birth defects possibly associated with prenatal occupational exposure to the organophosphate oxydemeton-methyl were published in 1989 by Romero et al. (1989). Gordon and Shy (1981) used ecologic data