Air pollution and particulate matter composition in relation to epigenetic age

OPS 48: Air pollution and epigenetics, Room 417, Floor 4, August 26, 2019, 4:30 PM - 5:30 PM Background. Air pollution is associated with numerous adverse health outcomes. Advanced epigenetic age, estimated using DNA methylation, may be a marker of biological consequences of prolonged air pollution exposure. Methods. In a sample of non-Hispanic white women ages 35-74 living in the contiguous U.S. (n=2,764), we estimated annual average ambient residential levels of PM2.5, PM10 and NO2 using a model combining land-use regression and kriging fit to regulatory monitoring data. Predictive k-means was used to assign participants to one of 7 clusters that corresponded to different relative combinations of PM2.5 components. We measured DNA methylation (DNAm) in blood samples using the Illumina’s Infinium HumanMethylation450 BeadChip and calculated DNAm age using the Levine/PhenoAge clock. Age acceleration was derived by regressing DNAm age on chronological age and calculating the residuals. Using linear regression models accounting for blood cell composition, we estimated adjusted associations between an interquartile range (IQR) increase in pollutants and age acceleration. We stratified the associations for PM2.5 by component cluster membership. Results. Higher age acceleration was observed for PM10 (β=0.24, 95% CI: 0.03, 0.46) but not for NO2. For PM2.5, we observed heterogeneity by component cluster membership (p for interaction=0.001). PM2.5 was associated with an almost 4-year higher age acceleration in a cluster characterized by higher relative fractions of crustal elements Si, Ca, K and Al (β=3.96, 95% CI: 0.72, 7.20), and an almost 2-year higher age acceleration in a cluster characterized by low sulfur fractions relative to overall PM2.5 (β=1.94, 95% CI: 0.41, 3.46). In contrast, PM2.5 was inversely associated with age acceleration in a cluster distinguished by low relative nitrite concentrations (β=-1.84, 95% CI: -3.19, -0.48). Conclusions. Air pollution was associated with epigenetic age, a marker of mortality and disease risk, with heterogeneity in the association between PM2.5 and epigenetic age acceleration by particulate matter composition.