Long-term exposure to ambient air pollution and epigenetic age acceleration in children.

Abstract

Long-term exposure to ambient air pollution has been associated with epigenetic age acceleration (EAA) in adults, but its impact on children remains less understood. We analyzed data from 457 children (mean age: 7.9 years) in the Project Viva cohort (2007-2010, eastern Massachusetts, USA). We calculated the following EAAs from leukocytes: Horvath's epigenetic age acceleration (HorvathEAA), intrinsic epigenetic age acceleration (IEAA), and skin and blood epigenetic age acceleration (Skin&BloodEAA). We applied generalized additive models to evaluate associations of prior-365-day average and lifetime average exposure to fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3), as well as the distance to major roadways, with EAA. Results indicated that each IQR increase (1.9 μg m-3) in the prior-365-day average of PM2.5 was associated with 0.26 years (95% CI, -0.49 to -0.03) lower HorvathEAA, although it did not survive multiple testing adjustment. Similar patterns but with wider CIs were observed for IEAA (-0.22; 95% CI, -0.44 to 0.01) and Skin&BloodEAA (-0.04; 95% CI, -0.19 to 0.11). No associations were observed of exposure to lifetime average PM2.5, prior-365-day or lifetime average NO2 or O3, or distance to major roadways with EAA. These findings suggest higher prior-365-day average PM2.5 exposure may relate to lower HorvathEAA in children.