ArticleAmerican journal of epidemiology2025
Racial disparities in maternal exposure to ambient air pollution during pregnancy and prevalence of congenital heart defects.
Article in American journal of epidemiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Breathing in harm: current insights into the effects of air pollution on cardiorespiratory health.Medical gas research · 2027Review
- Maternal Exposure to Air Pollution During Early Pregnancy and Congenital Heart Disease: An Exploratory Case-Control Analysis from Delhi NCR.Indian journal of pediatrics · 2026Article
- A nested case-control study of air pollution and congenital heart defects via circulating proteins.Nature communications · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
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.
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