UC Irvine

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental toxicants with deleterious effects on human health. Although many sources of exposure of PAHs have been identified, the contributions of specific PAHs within the sources to urinary metabolite biomarker concentrations are less well understood. Our study aims to quantify the relationship between specific urinary hydroxylated PAH metabolites and different sources of PAH exposure. We performed a cross-sectional data analysis of a longitudinal study of 51 women in Orange County California, all of whom were selected via convenience sampling. Nine different urinary monohydroxylated PAH metabolites were used as biomarkers of PAH exposure for each of the participants. Bivariate analyses were performed for each of the metabolites and the following potential explanatory variables: age, body mass index (BMI), ethnicity, Glutathione S-transferase Mu 1 (GSTM1) polymorphism status, Glutathione S-transferase theta-1 (GSTT1) polymorphism status, Cytochrome P450 Family 1 Subfamily B Member 1 (CYP1B1) polymorphism status, caffeinated coffee consumption, caffeinated tea consumption, commute time, cigarette smoking frequency, and ambient particulate matter. Particulate matter exposure was estimated using geospatial modeling for the participants home address. All associations with a p value of ≤ 0.2 were input into multiple linear regression models to achieve the highest adjusted R² value. The exposure source that had the most statistically significant associations with the metabolites was caffeinated coffee consumption; it was associated with 6 of the 9 metabolites. Of the particulate matter data, the strongest correlation observed was between the atmospheric organic carbon particulate matter less than 2.5 μm in aerodynamic diameter (PM2.5) concentrations, and the average 2-hydroxyfluorene concentrations, which had a Pearson’s correlation coefficient of 0.317. In conclusion, we were able to identify an association between coffee consumption and phenanthrene, pyrene, and fluorene urinary metabolites, and observed a small but statistically significant association between PM2.5 organic carbon exposure and a urinary metabolite of fluorene.