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Racial Disparities in Maternal Exposure to Ambient Air Pollution During Pregnancy and Prevalence of Congenital Heart Defects.
Arogbokun Knutson, Olufunmilayo C; Luben, Thomas J; Stingone, Jeanette A; Engel, Lawrence S; Martin, Chantel L; Olshan, Andrew F.
Afiliação
  • Arogbokun Knutson OC; Department of Health and Exercise Science, Morrison Family College of Health, University of St. Thomas, St. Paul, Minnesota, United States.
  • Luben TJ; United States Environmental Protection Agency, Office of Research and Development, Center for Public Health and Environmental Assessment, Research Triangle Park, North Carolina, United States.
  • Stingone JA; Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York, United States.
  • Engel LS; Department of Epidemiology, Gillings School of Global Public Health University of North Carolina, Chapel Hill, North Carolina, United States.
  • Martin CL; Department of Epidemiology, Gillings School of Global Public Health University of North Carolina, Chapel Hill, North Carolina, United States.
  • Olshan AF; Department of Epidemiology, Gillings School of Global Public Health University of North Carolina, Chapel Hill, North Carolina, United States.
Am J Epidemiol ; 2024 Aug 06.
Article em En | MEDLINE | ID: mdl-39108168
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 2003-2015 (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 micrometers in diameter (PM2.5) and ozone during weeks 3-9 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.

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Am J Epidemiol Ano de publicação: 2024 Tipo de documento: Article País de afiliação: Estados Unidos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Am J Epidemiol Ano de publicação: 2024 Tipo de documento: Article País de afiliação: Estados Unidos