Essentially all women are exposed to polycyclic aromatic hydrocarbons (PAHs), formed during incomplete combustion of organic materials, including fossil fuels, wood, foods, and tobacco. PAHs are ovarian toxicants in rodents, and cigarette smoking is associated with reproductive abnormalities in women. Biomonitoring of hydroxylated PAH (OH-PAH) metabolites in urine provides an integrated measure of exposure to PAHs via multiple routes and has been used to characterize exposure to PAHs in humans. We hypothesized that concentrations of OH-PAHs in urine are associated with reproductive function in women. We recruited women 18-44years old, living in Orange County, California to conduct daily measurement of urinary luteinizing hormone (LH) and estrone 3-glucuronide (E₁3G) using a microelectronic fertility monitor for multiple menstrual cycles; these data were used to calculate endocrine endpoints. Participants also collected urine samples on cycle day 10 for measurement of nine OH-PAHs. Models were constructed for eight endpoints using a Bayesian mixed modeling approach with subject-specific random effects allowing each participant to act as a baseline for her set of measurements. We observed associations between individual OH-PAH concentrations and follicular phase length, follicular phase LH and E₁3G concentrations, preovulatory LH surge concentrations, and periovulatory E₁3G slope and concentration. We have demonstrated the feasibility of using urinary reproductive hormone data obtained via fertility monitors to calculate endocrine endpoints for epidemiological studies of ovarian function during multiple menstrual cycles. The results show that environmental exposure to PAHs is associated with changes in endocrine markers of ovarian function in women in a PAH-specific manner.