Dietary exposure to chlorpyrifos and levels of 3,5,6-trichloro-2-pyridinol in urine

Abstract

Information on associations between chlorpyrifos residues in food and personal exposure to chlorpyrifos would be valuable for evaluating the relationship between personal exposure and possible health effects. We used food consumption records, chlorpyrifos levels in duplicate plates, and measures of 3,5,6-trichloro-2-pyridinol (TCPy) in urine obtained from human volunteers in the National Human Exposure Assessment Survey in Maryland (NHEXAS-MD) to evaluate a food consumption–chemical residue model for estimating dietary intake of chlorpyrifos. Model inputs were the NHEXAS-MD food consumption records and chlorpyrifos residues in specific foods measured in the U.S. Food and Drug Administration Total Diet Study (TDS) market baskets from 1993 to 1997. The estimated mean and standard deviation of chlorpyrifos concentration (μg/kg) in duplicate plates (n=203) were within 20% and 50%, respectively, of the corresponding parameters of measured chlorpyrifos levels. However, predicted and measured concentrations in the 78 duplicate plates with detectable levels of chlorpyrifos were not significantly associated according to Spearman correlation analysis (r=0.04, p=0.7667) and linear regression (p=0.2726). Measured and estimated chlorpyrifos intakes for observations with non-zero values for each intake measure (n=71) were moderately associated on a rank (Spearman's r=0.24, p=0.0462) and linear basis (regression r²=0.07, p=0.0242). Measured intakes of chlorpyrifos from food and urinary TCPy were significantly correlated in rank order (n=87, Spearman's r=0.30, p=0.0041) and linear (n=87, Pearson's r=0.22, p=0.0409) analyses. Correlation coefficients between estimated intake of chlorpyrifos from food and TCPy were significantly different from zero (n=87; Spearman's r=0.22, p=0.0393; Pearson's r=0.21, p=0.0479). Comparing mean measured chlorpyrifos intake from food (0.46 μg/day) to mean estimated TCPy excretion via urine (6.3 μg/day), dietary intake of chlorpyrifos accounted for approximately 7% of TCPy in this population. These findings suggest the food consumption–chemical residue model can yield reasonably accurate estimates of the population distribution of dietary chlorpyrifos intake, but has little ability to predict dietary exposure for individuals; and that intake of chlorpyrifos from food is a minor contributor to TCPy in urine.