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Racial Disparities in Maternal Exposure to Ambient Air Pollution During Pregnancy and Prevalence of Congenital Heart Defects
Citation:
Luben, Tom, O. Arogbokun Knutson, J. Stingone, L. Engel, C. Martin, AND A. Olshan. Racial Disparities in Maternal Exposure to Ambient Air Pollution During Pregnancy and Prevalence of Congenital Heart Defects. Society for Epidemiologic Research, Portland, OR, June 13 - 16, 2023.
Impact/Purpose:
Evaluate racial disparities in the association between gestational exposure to ambient air pollution and congenital heart defects
Description:
Background: Birth defects are the primary cause of infant mortality in the United States. However, the causes of birth defects are largely unknown. Environmental factors, such as air pollution, are among potential causes. Racial disparities in pollution exposure and congenital heart defects (CHDs) have been identified, but disparities in their association have not been explored. Methods: We conducted a case-control study to investigate the relationship between air pollutants and CHDs using North Carolina birth certificate and birth defect registry data from 2003 – 2015 (N=1,225,285). Maternal air pollution exposure was determined using the Environmental Protection Agency’s CMAQ Downscaler Model. A 7-week average of particulate matter <2.5 microns (PM2.5) and ozone exposure at the geocoded address at birth was estimated for each pregnancy during weeks 3-9. CHDs included were pulmonary valve atresia/stenosis, Tetralogy of Fallot (TOF), and atrioventricular septal defects. Single-pollutant and co-pollutant log-binomial models were created for the entire study population and stratified by race, limited to non-Hispanic Black and non-Hispanic White women to investigate disparities. Results: Positive associations between both pollutants and CHDs were observed in adjusted co-pollutant categorical models not stratified by race. An increasing concentration-response association was found for PM2.5 and TOF (Quartile 4 aPR: 1.46; 95% CI: 1.06, 2.03). Elevated aPRs were present in the pulmonary valve atresia/stenosis model as well; however, there was no increasing concentration-response trend. The pattern of association for PM2.5 and pulmonary atresia/stenosis was stronger for infants of non-Hispanic Black women. Conclusion: PM2.5 and ozone exposure early in pregnancy may increase the prevalence of certain CHDs. Air pollution exposure may impact non-Hispanic Black and non-Hispanic White pregnancies differently, though more epidemiologic studies are needed to confirm findings.