Logo image
The association of prenatal ambient air pollution with placental epigenetic gestational age at birth
Journal article   Open access   Peer reviewed

The association of prenatal ambient air pollution with placental epigenetic gestational age at birth

Zhengting He, Ashley Y Song, Rose Schrott, Jason I Feinberg, Kelly M Bakulski, Kelly S Benke, Lisa A Croen, Irva Hertz-Picciotto, Rebecca J Schmidt, Kristen Lyall, …
Environmental epidemiology, v 9(3), e384
Jun 2025
PMID: 40331055
url
https://doi.org/10.1097/EE9.0000000000000384View
Published, Version of Record (VoR) Open

Abstract

DNA methylation Epigenetic aging Air Pollution Placenta
Prenatal air pollutants have been associated with adverse birth outcomes, and DNA methylation (DNAm) changes in placenta may contribute to these associations. DNAm-based epigenetic gestational age (GA) estimators are emerging biomarkers for aging/biological age that can reflect early-life exposures and predict long-term health outcomes. We leveraged 103 mother-offspring pairs from the Early Autism Risk Longitudinal Investigation cohort to assess associations between prenatal air pollution and placental epigenetic GA at birth. Prenatal air pollution concentrations (NO , O , PM , and PM ) were estimated from weekly data from monitoring stations near maternal residence and calculated for preconception and pregnancy periods. DNAm from fetal-side placenta samples was measured on Illumina HumanMethylation450 BeadChip. Epigenetic GA was computed using Lee's robust placenta clock algorithm. GA acceleration/deceleration was the residual of predicted epigenetic GA on chronologic GA, adjusted (intrinsic) or unadjusted (extrinsic) for cell type proportions. We used linear regressions to examine associations between average air pollution levels in each period and GA acceleration/deceleration, and weekly distributed lag models to examine critical exposure windows. Higher pregnancy average O and PM exposures were associated with decelerated intrinsic (β = -0.65 and -0.79) and extrinsic GA (β = -0.69 and -0.74) at birth (per 10-unit increment). Trimester-specific analyses revealed higher O and PM exposures in trimesters 2 to 3 associated with decelerated GA at birth. Weekly distributed lag models suggested pregnancy weeks 21 to 31 and 21 to 29 were critical windows of O and PM exposures, respectively. Prenatal air pollution exposures, especially during mid- to late-pregnancy, were associated with lower biological maturity at birth.

Metrics

5 Record Views
1 citations in Scopus

Details

UN Sustainable Development Goals (SDGs)

This publication has contributed to the advancement of the following goals:

#3 Good Health and Well-Being

Source: SDGs in the Output

InCites Highlights

Data related to this publication, from InCites Benchmarking & Analytics tool:

Collaboration types
Domestic collaboration
Web of Science research areas
Environmental Sciences
Public, Environmental & Occupational Health
Logo image