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As part of the Children's Total Exposure to Persistent Pesticides and Other Persistent Organic Pollutants (CTEPP) study, we investigated the exposures of preschool children to chlorpyrifos and its degradation product 3,5,6-trichloro-2-pyridinol (TCP) in their everyday environments. During this study, the participants were still able to purchase and apply chlorpyrifos at their homes or day care centers. Participants were recruited randomly from 129 homes and 13 day care centers in six North Carolina counties. Monitoring was performed over a 48-h period at the children's homes and/or day care centers. Samples that were collected included duplicate plate, indoor and outdoor air, urine, indoor floor dust, play area soil, transferable residues (PUF roller), and surface wipes (hand, food preparation, and hard floor). The samples were extracted and analyzed by gas chromatography/mass spectrometry. Chlorpyrifos was detected in 100% of the indoor air and indoor floor dust samples from homes and day care centers. TCP was detected at homes and day care centers in 100% of the indoor floor dust and hard floor surface wipe, in >97% of the solid food, and in >95% of the indoor air samples. Generally, median levels of chlorpyrifos were higher than those of TCP in all media, except for solid food samples. For these samples, the median TCP concentrations were 12 and 29 times higher than the chlorpyrifos concentrations at homes and day care centers, respectively. The median urinary TCP concentration for the preschool children was 5.3 ng/ml and the maximum value was 104 ng/ml. The median potential aggregate absorbed dose (ng/kg/day) of chlorpyrifos for these preschool children was estimated to be 3 ng/kg/day. The primary route of exposure to chlorpyrifos was through dietary intake, followed by inhalation. The median potential aggregate absorbed dose of TCP for these children was estimated to be 38 ng/kg/day, and dietary intake was the primary route of exposure. The median excreted amount of urinary TCP for these children was estimated to be 117 ng/kg/day. A full regression model of the relationships among chlorpyrifos and TCP for the children in the home group explained 23% of the variability of the urinary TCP concentrations by the three routes of exposure (inhalation, ingestion, dermal absorption) to chlorpyrifos and TCP. However, a final reduced model via step-wise regression retained only chlorpyrifos through the inhalation route and explained 22% of the variability of TCP in the children's urine. The estimated potential aggregate absorbed doses of chlorpyrifos through the inhalation route were low (median value, 0.8 ng/kg/day) and could not explain most of the excreted amounts of urinary TCP. This suggested that there were other possible sources and pathways of exposure that contributed to the estimated potential aggregate absorbed doses of these children to chlorpyrifos and TCP. One possible pathway of exposure that was not accounted for fully is through the children's potential contacts with contaminated surfaces at homes and day care centers. In addition, other pesticides such as chlorpyrifos-methyl may have also contributed to the levels of TCP in the urine. Future studies should include additional surface measurements in their estimation of potential absorbed doses of preschool children to environmental pollutants. In conclusion, the results showed that the preschool children were exposed to chlorpyrifos and TCP from several sources, through several pathways and routes. .

In the summer of 1997, we measured the aggregate exposures of nine preschool children, aged 2-5 years, to a suite of organic pesticides and other persistent organic pollutants that are commonly found in the home and school environment. The children attended either of two child day care centers in the Raleigh-Durham-Chapel Hill area of North Carolina and were in day care at least 25 h/week. Over a 48-h period, we sampled indoor and outdoor air, play area soil and floor dust, as well as duplicate diets, hand surface wipes, and urine for each child at day care and at home. Our target analytes were several polycyclic aromatic hydrocarbons (PAH), organochlorine pesticides, and polychlorinated biphenyls (PCB); two organophosphate pesticides (chlorpyrifos and diazinon), the lawn herbicide 2,4-dichlorophenoxyacetic acid (2,4-D), three phenols (pentachlorophenol (PCP), nonyl phenols, and bisphenol-A), 3,5,6-trichloro-2-pyridinol (TCP), and two phthalate esters (benzylbutyl and dibutyl phthalate). In urine, our target analytes were hydroxy-PAH, TCP, 2,4-D, and PCP. To allow estimation of each child's aggregate exposures over the 48-h sampling period, we also used time-activity diaries, which were filled out by each child's teacher at day care and the parent or other primary caregiver at home. In addition, we collected detailed household information that related to potential sources of exposure, such as pesticide use or smoking habits, through questionnaires and field observation. We found that the indoor exposures were greater than those outdoors, that exposures at day care and at home were of similar magnitudes, and that diet contributed greatly to the exposures. The children's potential aggregate doses, calculated from our data, were generally well below established reference doses (RfDs) for those compounds for which RfDs are available.