Evidence map›Paper›PMID 39108168›Full record

ArticleAmerican journal of epidemiology2025

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

Olufunmilayo C Arogbokun Knutson, Thomas J Luben, Jeanette A Stingone, Lawrence S Engel, Chantel L Martin, Andrew F Olshan

Abstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Olufunmilayo C Arogbokun KnutsonDepartment of Health and Exercise Science, Morrison Family College of Health, University of St. Thomas, St. Paul, MN, United States.ORCID 0000-0002-4401-5381
Thomas J LubenUnited States Environmental Protection Agency, Office of Research and Development, Center for Public Health and Environmental Assessment, Research Triangle Park, NC, United States.ORCID 0000-0002-7867-5126
Jeanette A StingoneDepartment of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, United States.ORCID 0000-0003-3508-8260
Lawrence S EngelDepartment of Epidemiology, Gillings School of Global Public Health University of North Carolina, Chapel Hill, NC, United States.ORCID 0000-0001-9268-4830
Chantel L MartinDepartment of Epidemiology, Gillings School of Global Public Health University of North Carolina, Chapel Hill, NC, United States.ORCID 0000-0003-1907-0810
Andrew F OlshanDepartment of Epidemiology, Gillings School of Global Public Health University of North Carolina, Chapel Hill, NC, United States.ORCID 0000-0001-9115-5128

Funding

Bill and Melinda Gates FoundationCDC HHS U50CCU422096Intramural EPA EPA999999
6 · The paper itself

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.

Indexed as

Air PollutionHealth Status DisparitiesHeart Defects, CongenitalMaternal ExposureRacial GroupsAdultAir PollutantsFemaleHumansNorth CarolinaOzoneParticulate MatterPregnancyPrevalenceYoung AdultAir PollutantsOzoneParticulate Matterair pollutionbirth defectscongenital heart defectsozoneparticulate matterpregnancyracial disparities

Identifiers

PMID39108168
PMCPMC11955996

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.