The number of studies addressing the possible effects of air pollutants on human reproduction, especially prenatal outcomes, has grown extensively. However, the plausible biological mechanisms by which air pollutants influence prenatal outcomes remain unclear. The aims of this dissertation are (1) to determine whether ambient air pollution exposure (including particles of less than 10 µm (PM10) and less than 2.5 µm diameter (PM2.5), carbon monoxide, nitrogen dioxide, sulfur dioxide, and ozone) contributes to increased inflammatory response by measuring C-reactive protein (CRP) concentrations during early pregnancy, and (2) to examine associations between ambient air pollution exposures and blood pressure changes during pregnancy. In addition, because smoking during pregnancy is a risk factor for some adverse birth outcomes such as preterm delivery, and inflammation has been suggested to increase the risk of preterm delivery, the other aim of this dissertation was to examine whether systemic inflammation mediates the link between smoking and preterm delivery. The study population was selected from the Prenatal Exposures and Preeclampsia Prevention study (PEPP) conducted in Pittsburgh, PA between 1997 and 2001. Space-time Kriging interpolation for ambient station measures at the maternal ZIP code was performed to estimate maternal air pollution exposure. Multiple linear and logistic regressions were employed to evaluate associations between air pollution, CRP concentrations, and blood pressure changes during pregnancy. Positive associations between particulate (both PM2.5 and PM10) and ozone air pollution and elevated CRP concentrations in non-smoking women during early pregnancy were observed. For blood pressure changes, we found that first trimester exposure to PM10 and ozone air pollution was associated to increases in mean systolic and diastolic blood pressure changes during pregnancy. For smoking and preterm study, no evidence that systemic inflammation mediates this association was found. Our findings provide some new evidence that associations between particulate air pollution and adverse birth outcomes may be mediated by systemic inflammation and blood pressure changes. These findings have considerable public health significance to further prevent the adverse birth outcomes associated with air pollution exposure
