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. 2025 May 28;11(1):dvaf013.
doi: 10.1093/eep/dvaf013. eCollection 2025.

Prenatal ambient air pollution associations with DNA methylation in asthma- and allergy-relevant genes: findings from ECHO

Meredith Palmore  1 , Emma E Thompson  2 , Fang Fang  3 , Theresa M Bastain  4 , Carrie Breton  4 , Scott Collingwood  5 , Frank D Gilliland  4 , Diane R Gold  6   7 , Rima Habre  8 , Tina Hartert  9 , Gurjit K Khurana Hershey  10   11 , Daniel J Jackson  12   13 , Rachel Miller  14 , Patrick Ryan  11   15 , Lyndsey Shorey-Kendrick  16 , Eliot R Spindel  16 , Joseph Stanford  17 , James Gern  12   13 , Chris McKennan  18 , Carole Ober  2 , Christine Ladd-Acosta  1
Affiliations

Prenatal ambient air pollution associations with DNA methylation in asthma- and allergy-relevant genes: findings from ECHO

Meredith Palmore et al. Environ Epigenet. .

Abstract

Prenatal exposure to air pollution is an important risk factor for child health outcomes, including asthma. Identification of DNA methylation changes associated with air pollutant exposure can provide new intervention targets to improve children's health. The aim of this study is to test the association between prenatal air pollutant exposure and DNA methylation in developmental and asthma-/allergy-relevant biospecimens (placenta, buccal, cord blood, nasal mucosa, and lavage). A subset of 2294 biospecimens collected from 1906 child participants enrolled in the Environmental Influences on Child Health Outcomes program with prenatal air pollutant and high-quality Illumina Asthma&Allergy DNA methylation array measures (n = 37 197 probes) were included. Prenatal ozone, nitrogen dioxide, and fine particulate matter were derived using residential history during pregnancy and spatiotemporal models. For each pollutant, biospecimen type, and prenatal exposure window, we estimated the effects of air pollution on gene DNA methylation levels. We compared results across pollutants, biospecimen types, and trimesters and tested for critical months of exposure using distributed lag models. DNA methylation levels at 154 out of 4746 tested genes were associated with air pollution; over 95% were exposure window, pollutant, and biospecimen-type specific. The fewest gene associations were detected in trimester 2, relative to other exposure windows. A variety of trends in methylation patterns were observed in response to lagged monthly pollution levels. Child DNA methylation changes at specific respiratory- and immune-relevant genes are associated with prenatal air pollutant exposures. Future studies should examine the relationship between these pollution-sensitive genes and child health.

Keywords: DNA methylation; Environmental influences on Child Health Outcomes (ECHO); prenatal air pollution.

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Conflict of interest statement

Dr C.L.-A. reports consulting fees from the University of Iowa for providing expertise on autism epigenetics, outside the scope of this work. All other authors have no conflicts to declare.

Figures

Figure 1.
Figure 1.
Total number of genes in each exposure window showing significant methylation changes associated with prenatal exposure to (a) O3, (b) NO2, and (c) PM2.5 levels. The right side of each panel shows the number of gene associations with the pollutant in bar plots. Genes in the bar plots are not mutually exclusive across time periods. Patterns in the bar charts denote each biospecimen source. On the left of each panel is a Venn diagram comparing overlap across time periods within a biospecimen type.
Figure 2.
Figure 2.
Conceptual overview of how genes were categorized into distributed lag result types. (a) Serpentine trend where the coefficient for the third-order polynomial was negative. (b) Serpentine trend where the coefficient for the third-order polynomial was positive. (c) U-shaped trend where the coefficient for the second-order polynomial was negative. (d) U-shaped trend where the coefficient for the second-order polynomial was positive. (e) Linear trend where the coefficient for the first-order polynomial was negative. (f) Linear trend where the coefficient for the first-order polynomial was positive.
See this image and copyright information in PMC

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