We hypothesized that exposure to the PAH, derived from local emissions from diesel and non-diesel motor vehicles, as well as residential heating, power generation, tobacco smoking, and other combustion sources, is associated with adverse respiratory outcomes such as asthma symptoms in young children. We chose to focus on prenatal exposure to PAH because growing evidence suggests that the prenatal period may represent a window when the impact of inhaled environmental agents on respiratory outcomes is heightened. For example, the offspring of mice exposed either to allergens or residual oil fly ash (consisting of heavy metals, PAH) during pregnancy have been found to develop airway hyperreactivity and increased airway eosinophilia.11–12 In light of studies13–15 demonstrating that environmental tobacco smoke (ETS) exposure is associated with abnormal lung function in infancy that persists through adolescence, we also hypothesized that additional exposure to ETS may worsen respiratory outcomes beyond that observed following PAH alone. To test our hypotheses, we recruited a cohort of pregnant women from northern Manhattan, collected 48-h personal PAH exposure measurements in the third trimester of pregnancy, and monitored their children prospectively for the onset of respiratory symptoms. Our results suggest that the interaction of prenatal exposure to PAH and postnatal exposure to ETS leads to increased respiratory symptoms and probable diagnosis of asthma by age 12 to 24 months.