ISEE-326 Introduction: A number of epidemiologic investigations have shown adverse effects of ambient air pollution on reproductive outcomes including spontaneous abortion, fetal growth, preterm delivery, and infant mortality. A southern California study found associations between carbon monoxide exposure and an increased risk for isolated ventricular septal defects, and ozone exposure and an elevated risk for isolated aortic artery and valve defects, pulmonary artery and valve defects, and conotruncal defects. Aim: Our population-based case-control study attempted to corroborate the results from the California study and expand the scope to include additional air pollutants and birth defects. We investigated the association between maternal exposures to carbon monoxide, nitrogen dioxide, ozone, sulphur dioxide, and PM10, during weeks three through eight of pregnancy, and the risk of selected cardiac birth defects and oral clefts among live births and foetal deaths between 1997 and 2000, in seven Texas counties. Methods: Cases were selected from the Texas Birth Defects Registry (n=4570). Non-malformed controls were sampled from vital records and frequency matched to cases on year of birth, vital status, and maternal county of residence at delivery (n=3667). Maternal address at delivery as reported in the vital record or Texas Birth Defects Registry was geocoded. Data from United States Environmental Protection Agency stationary monitors were used to estimate air pollution exposures. The risks for eight clinical diagnostic groupings and nine individual birth defects were analyzed. Unconditional binary and polytomous logistic regression models were used to adjust for covariates available in the vital record. Results: Comparing the highest quartile of exposure to the lowest, there were positive associations between carbon monoxide and tetralogy of Fallot (adjusted odds ratio (OR) = 2.04; 95% confidence interval (CI) 1.26, 3.29), PM10 and isolated atrial septal defects (OR = 2.27; 95% CI: 1.43, 3.60), and sulphur dioxide and isolated ventricular septal defects (OR = 2.16; 95% CI: 1.51, 3.09). Inverse associations were found between nitrogen dioxide and ventricular septal defects, and between sulphur dioxide and isolated atrial septal defects. The study provides limited evidence that air pollution exposure influences the risk of oral clefts. Conclusion: This study contributes to a growing body of epidemiologic literature on the adverse reproductive effects of ambient air pollution exposure, but does not provide strong evidence that air pollution influences the risk of birth defects. These results support one previously reported finding of an association between ozone exposure and pulmonary artery and valve defects. This is an abstract of a proposed presentation and does not necessarily reflect EPA policy.
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