Previous studies have suggested that traffic-related air pollution is associated with adverse fertility outcomes, such as reduced fecundability and subfertility. The purpose of this research is to investigate if PM_2.5 exposure prior to conception or traffic-related exposures (traffic density and distance to nearest major roadway) at birth address is associated with fertility-assisted births. We obtained all live and still births from the Massachusetts state birth registry with an estimated conception date between January 2002 through December 2008. All births requiring fertility drugs or assisted reproductive technology were identified as cases. We randomly selected 2000 infants conceived each year to serve as a common control group. PM_2.5 exposure was assessed using 4 km spatial satellite remote sensing, meteorological and land use spatiotemporal models at geocoded birth addresses for the year prior to conception. The mean PM_2.5 level was 9.81 µg m^-3 (standard deviation = 1.70 µg m^-3), with a maximum of 14.27 µg m^-3. We calculated crude and adjusted fertility treatment odds ratios (ORs) and 95% confidence intervals (CI) per interquartile range of 1.72 µg m^-3 increase in PM_2.5 exposure. Our final analyses included 10 748 fertility-assisted births and 12 225 controls. After adjusting for parental age, marital status, race, maternal education, insurance status, parity, and year of birth, average PM_2.5 exposure during the year prior to conception was weakly associated with fertility treatment (OR: 1.01; 95% CI: 0.97, 1.05). Fertility-assisted births were inversely associated with traffic density (highest quartile compared to lowest quartile, OR: 0.92; 95% CI: 0.83, 1.02) and positively associated with distance from major roadway (OR per 100 m: 1.01; 95% CI: 1.00, 1.02) in adjusted analyses. We did not find strong evidence to support an adverse relationship between traffic-related air pollution exposure and fertility-assisted births.

Environmental factors have been linked to many diseases and health conditions, but reliable assessment of environmental exposures is challenging. Developing biomarkers of environmental exposures, rather than relying on self-report, will improve our ability to assess the association of such exposures with disease. Epigenetic markers, most notably DNA methylation, have been identified for some environmental exposures, but identification of markers for additional exposures is still needed. The rationale behind the Markers for Environmental Exposures (MEE) Study was to (1) identify biomarkers, especially epigenetic markers, of environmental exposures, such as pesticides, air/food/water contaminants, and industrial chemicals that are commonly encountered in the general population; and (2) support the study of potential relationships between environmental exposures and health and health-related factors. The MEE Study is a cross-sectional study with potential for record linkage and follow-up. The well-characterized cohort of 400 postmenopausal women has generated a repository of biospecimens, including blood, urine, and saliva samples. Paired data include an environmental exposures questionnaire, a breast health questionnaire, dietary recalls, and a food frequency questionnaire. This work describes the rationale, study design, and cohort characteristics of the MEE Study. In addition to our primary research goals, we hope that the data and biorepository generated by this study will serve as a resource for future studies and collaboration.