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MODELING OF CHLORPYRIFOS EXPOSURE, DOSE, AND BIOMARKER USING NHEXAS MINNESOTA CHILDREN'S DATA
Citation:
Furtaw Jr., E J., M S. Okino, J J. Quackenboss, A. Roy, AND P. J. Lioy. MODELING OF CHLORPYRIFOS EXPOSURE, DOSE, AND BIOMARKER USING NHEXAS MINNESOTA CHILDREN'S DATA. Presented at ISEA 2000 Exposure Analysis in the 21st Century: Integrating Science, Policy and Quality of Life, Monterey Peninsula, CA, October 24-27, 2000.
Impact/Purpose:
The objectives for the current task are to 1) evaluate the utility of screening survey design and questionnaires for identifying households/individuals with higher exposures; and 2) compare estimates of dietary exposure derived from food consumption and residue databases with direct measurements of dietary exposure obtained in this study. (Results of the environmental, exposure, and biological measurements will be reported in collaboration with the other investigators.)
Description:
Data from the National Human Exposure Assessment Survey (NHEXAS) are now becoming available. For the organophosphorus insecticide chlorpyrifos, available data for NHEXAS Minnesota children include concentrations in air, food, beverages, water, house dust (transferable surface residues), soil, and hand rinses; and 3,5,6-trichloro-2-pyridinol (TCPy), a chlorpyrifos metabolite, in urine. To evaluate these data, we used the environmental measurements as inputs to a dynamic model of chlorpyrifos exposure and human pharmacokinetics. The model simulated the urinary TCPy concentration. Exposure factors were taken from EPA's Office of Pesticide Programs' Draft Standard Operating Procedures for Residential Exposure Assessments and from EPA's Exposure Factors Handbook. Non-dietary ingestion from hand-to-mouth activity, and dermal absorption, collectively accounted for over 84% of the modeled absorbed chlorpyrifos dose. Measured urinary TCPy concentrations exceeded modeled concentrations by a factor of about 6. Possible explanations for this disparity include: additional unmeasured exposure to chlorpyrifos occurred outside the home; actual exposure concentrations were different than those measured due to heterogeneity of residues; exposure factors are missing or incorrect; the pharmacokinetic model (which was based on adult male data) is inappropriate for children; and additional exposure to TCPy itself (which was not analyzed in environmental samples) may have occurred. Of these, the last explanation is supported by other research which has shown that TCPy occurs in agricultural products, and even more so in prepared foods, due to environmental degradation of chlorpyrifos. This possible explanation shows the importance of carefully selecting and matching environmental and biomarker measurements in exposure studies. When the chosen biomarker is a metabolite, consideration must be given to measuring the metabolite as well as the parent compound in environmental samples.
The U.S. EPA Office of Research and Development funded this research. The abstract was reviewed and approved. The presentation has not been reviewed.