ArticleClinical epigenetics2025
An epigenome-wide analysis of DNA methylation, racialized and economic inequities, and air pollution.
Article in Clinical epigenetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Epigenetic age and telomere length correlations in pediatric-onset multiple sclerosis.Multiple sclerosis (Houndmills, Basingstoke, England) · 2025Article
- Analyzing multiple types of discrimination using implicit and explicit measures, comparing target vs. Dominant groups, in a study of smoking/vaping among community health center members in Boston, Massachusetts (2020-2022).International journal for equity in health · 2025Article
- Nutritional status, body indices, and somatotype in Aymara and Quechua children from high Andean areas of Peru.Journal of nutritional science · 2025Article
- Exposure to air pollution increases susceptibility to ulcerative colitis through epigenetic alterations in CXCR2 and MHC class III region.EBioMedicine · 2024Article
- Familial Loss of a Loved One and Biological Aging: NIMHD Social Epigenomics Program.JAMA network open · 2024Article
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13 authors.
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Abstract
backgroundDNA methylation (DNAm) provides a plausible mechanism by which adverse exposures become embodied and contribute to health inequities, due to its role in genome regulation and responsiveness to social and biophysical exposures tied to societal context. However, scant epigenome-wide association studies (EWAS) have included structural and lifecourse measures of exposure, especially in relation to structural discrimination. Our study tested the hypothesis that DNAm is a mechanism by which racial discrimination, economic adversity, and air pollution become biologically embodied, via a series of cross-sectional EWAS, conducted in two population-based samples of US-born Black non-Hispanic (Black NH), white non-Hispanic (white NH), and Hispanic individuals (My Body My Story:: n = 224 Black NH and 69 white NH;; and the Multi-Ethnic Study of Atherosclerosis:: n = 229 Black NH, n = 555 white NH and n = 191 Hispanic). Genome-wide changes in DNAm were measured using the Illumina EPIC BeadChip (MBMS; using frozen blood spots) and Illumina 450 k BeadChip (MESA; using purified monocytes).
resultsWe observed the strongest associations with traffic-related air pollution (between 0 and 22 DNAm sites associated at p < 2.4e-07, measured via black carbon and nitrogen oxides exposure), with evidence from both studies suggesting that air pollution exposure may induce epigenetic changes related to inflammatory processes. However, we did not replicate previous air pollution EWAS findings. We also found suggestive associations of DNAm variation with measures of structural racial discrimination (e.g. for Black NH participants, in MBMS born in a Jim Crow state associates with a DNAm site in ZNF286B at p = 8.43E-08; and in MESA adult exposure to racialized economic residential segregation associates with a DNAm site in FUT6 at p = 4.05E-08) situated in genes with plausible links to effects on health.
conclusionsOverall, this work suggests that DNAm is a biological mechanism through which structural racism and air pollution (of which distribution of exposure is inequitable) become embodied and may lead to health inequities. Due to the extensive range of exposures we tested, further replication in additional studies and other tissues is warranted.
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