Prenatal Air Pollution Exposure and Early Cardiovascular Phenotypes in Young Adults
Open accessAbstract
Exposure to ambient air pollutants increases risk for adverse cardiovascular health outcomes in adults. We aimed to evaluate the contribution of prenatal air pollutant exposure to cardiovascular health, which has not been thoroughly evaluated. The Testing Responses on Youth (TROY) study consists of 768 college students recruited from the University of Southern California in 2007-2009. Participants attended one study visit during which blood pressure, heart rate and carotid artery arterial stiffness (CAS) and carotid artery intima-media thickness (CIMT) were assessed. Prenatal residential addresses were geocoded and used to assign prenatal and postnatal air pollutant exposure estimates using the U.S. Environmental Protection Agency's Air Quality System (AQS) database. The associations between CAS, CIMT and air pollutants were assessed using linear regression analysis. Prenatal PM10 and PM2.5 exposures were associated with increased CAS. For example, a 2 SD increase in prenatal PM2.5 was associated with CAS indices, including a 5% increase (β = 1.05, 95% CI 1.00-1.10) in carotid stiffness index beta, a 5% increase (β = 1.05, 95% CI 1.01-1.10) in Young's elastic modulus and a 5% decrease (β = 0.95, 95% CI 0.91-0.99) in distensibility. Mutually adjusted models of pre- and postnatal PM2.5 further suggested the prenatal exposure was most relevant exposure period for CAS. No associations were observed for CIMT. In conclusion, prenatal exposure to elevated air pollutants may increase carotid arterial stiffness in a young adult population of college students. Efforts aimed at limiting prenatal exposures are important public health goals.
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Current studies support measurable biological embedding during fetal life, but they do not yet provide validated causal or prognostic markers for adult disease.
“Current studies support measurable biological embedding during fetal life [73,80,115], but they do not yet provide validated causal or prognostic markers for adult disease.”
From Placental Pathophysiology and Developmental Programming of Adult Cardiometabolic Risk: A Narrative Review of Pregnancy Exposures (2026) · cites this paper as [80]
The Discussion (page not provided) reports that prenatal PM2.5 and PM10 exposure was associated with greater carotid artery stiffness measured in college students, supporting a measurable later-life correlate of prenatal exposure. It does not measure biological changes during fetal life, so that part of the cited claim is more specific than the evidence. The Discussion also says the implications for adult cardiovascular disease remain unclear. (LLM, conf=0.84)
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Prenatal particulate air pollution exposure predicts arterial stiffness in childhood
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Exposition prénatale à la pollution atmosphérique extérieure et grossesse
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- Authors
- Breton, C. V., Mack, W. J., Yao, J., Berhane, K., Amadeus, M., Lurmann, F., Gilliland, F., McConnell, R., Hodis, H. N., Künzli, N., & Avol, E.
- Affiliations
- University of Southern California (US)
- Sonoma Technology (United States) (US)
- Swiss Tropical and Public Health Institute (CH)
- Corresponding author
- Breton, Carrie V.
- ORCID
- Venue
- PLOS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2016-03-07
- Volume
- 11
- Issue
- 3
- Pages
- e0150825
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC4780745
- OpenAlex
- W2295473583
- Cited by
- 53
- References
- 45
- Citations by year
- 2026: 1 · 2025: 6 · 2024: 8 · 2023: 3 · 2022: 6 · 2021: 7 · 2020: 7 · 2019: 3 · 2018: 4 · 2017: 7 · 2016: 1
- FWCI
- 3.14
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Funders
- U.S. Department of Veterans Affairs (RD83 1861-01)
- National Institutes of Health
- U.S. Public Health Service (R826708-01)
- National Institute of Environmental Health Sciences (R01ES014708, P01ES022845, P01ES009581, K01ES017801, P30ES007048)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Social Sciences › Sociology and Political Science › Environmental Justice and Health Disparities
- Keywords
- prenatal air pollution exposure, ambient particulate matter, PM2.5, PM10, carotid artery stiffness, carotid intima-media thickness, cardiovascular health, young adults, university students, blood pressure, heart rate, distensibility, elastic modulus, developmental origins of health and disease
- MeSH terms
- Air Pollution, Blood Pressure, Cardiovascular System, Carotid Arteries, Child, Female, Heart Rate, Humans, Male, Phenotype, Pregnancy, Prenatal Exposure Delayed Effects, Particulate Matter, Young Adult, Carotid Intima-Media Thickness, Vascular Stiffness
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