Racial disparities in maternal exposure to ambient air pollution during pregnancy and prevalence of congenital heart defects

• Arogbokun Knutson, Olufunmilayo C ^[1] ; Luben, Thomas J ^[3] ; Stingone, Jeanette A ^[2] ; Engel, Lawrence S ^[4] ; Martin, Chantel L ^[4] ; Olshan, Andrew F ^[4]
  1. [1] University of St. Thomas

     University of St. Thomas

     City of Saint Paul, Estados Unidos

     
  2. [2] Columbia University

     Columbia University

     Estados Unidos

     
  3. [3] United States Environmental Protection Agency, Office of Research and Development, Center for Public Health and Environmental Assessment, Research Triangle Park , NC ,
  4. [4] Department of Epidemiology, Gillings School of Global Public Health University of North Carolina , Chapel Hill, NC ,

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• Localización: American journal of epidemiology, ISSN-e 1476-6256, ISSN 0002-9262, Vol. 194, Nº. 3, 2025, págs. 709-721
• Idioma: inglés
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  • Abstract Air pollution may be a potential cause of congenital heart defects (CHDs), but racial disparities in this association are unexplored. We conducted a statewide population-based cohort study using North Carolina birth data from 2003 to 2015 (n = 1 225 285) to investigate the relationship between air pollution and CHDs (specifically pulmonary valve atresia/stenosis, tetralogy of Fallot [TOF], and atrioventricular septal defect [AVSD]). Maternal exposure to particulate matter ≤ 2.5 μm in diameter (PM2.5) and ozone during weeks 3 to 9 of pregnancy were estimated using the Environmental Protection Agency’s Downscaler Model. Single- and co-pollutant log-binomial models were created for the entire population and stratified by race to investigate disparities. Positive associations between PM2.5 and CHDs were observed. An increasing concentration-response association was found for PM2.5 and TOF in adjusted, co-pollutant models (quartile 4 prevalence ratio: 1.46; 95% CI, 1.06-2.03). Differences in the effect of PM2.5 on CHD prevalence were seen in some models stratified by race, although clear exposure-prevalence gradients were not evident. Positive associations were also seen in adjusted, co-pollutant models of ozone and AVSD. Study results suggest that prenatal PM2.5 and ozone exposure may increase the prevalence of certain CHDs. A consistent pattern of differences in association by race/ethnicity was not apparent. This article is part of a Special Collection on Environmental Epidemiology.