PuSH - Publication Server of Helmholtz Zentrum München: Long-term exposure to traffic-related air pollution is associated with epigenetic age acceleration.

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Yao,Y. ; Wolf, K. ; Breitner-Busch, S. ; Zhang, S. ; Waldenberger, M. ; Winkelmann, J. ; Schneider, A.E. ; Peters, A.

Long-term exposure to traffic-related air pollution is associated with epigenetic age acceleration.

Environ. Res. 288:123284 (2026)

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Epigenetic aging biomarkers, predicted by selected Cytosine-phosphate-Guanine (CpG) sites, might be influenced by air pollution exposure. However, evidence from longitudinal studies is still limited. To determine the associations between long-term exposure to air pollution and epigenetic aging biomarkers and identify vulnerable subgroups. Data was collected from the German population-based Cooperative Health Research in the Region of Augsburg (KORA) S4 survey (1999-2001) and two follow-up examinations (F4: 2006-08 and FF4: 2013-14). We measured DNA methylation (DNAm) in blood samples and calculated DNAm Age and DNAm-based telomere length (DNAmTL). We only included participants with at least two repeated measurements. Annual average concentrations of ultrafine particles (PNC), particulate matter (PM) less than 10 μm (PM₁₀), fine particles (PM_2.5), coarse particles (PM_coarse), soot (PM_2.5abs), nitrogen oxides (NO₂ and NO_x) and ozone (O₃) were estimated by land-use regression models. We applied linear mixed-effect regression models to assess the associations between air pollutants and epigenetic aging biomarkers, and further performed a limited epigenome-wide association study (EWAS) to examine whether air pollution influences individual CpGs. We included 4,105 observations from 1,651 KORA participants. In clinical models, interquartile range (IQR) increases in all air pollutants except O₃ were positively associated with accelerated DNAmGrimAge and DNAmPhenoAge. Moreover, all air pollutants showed negative associations with DNAmTL. Specifically, in ever smokers, the air pollutants were positively associated with the age acceleration of DNAmHorvathAge and DNAmPhenoAge, and inversely associated with DNAmTL with the largest effect estimates observed for PM_2.5abs. We identified two exposure-related CpGs with PM_coarse at a Benjamini-Hochberg false discovery rate corrected p-value < 0.05 in ever smokers. Our findings suggest a robust association between long-term exposure to traffic-related air pollution with epigenetic age acceleration, especially in ever smokers. These results imply that air pollution is augmenting the negative impact of smoking on biological ageing.

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