Prolonged Exposure to Particulate Air Pollution and Decreased DNA Methylation

Abstract

ISEE-0332 Background and Objective: Acute and chronic exposure to particulate air pollution is associated with increased cardiovascular morbidity and mortality. Epigenetic mechanisms are a potential pathway linking environmental exposures to disease. Lower blood DNA methylation, an epigenetic mechanism, has been found in processes related to cardiovascular disease. Recently, acute air pollution exposure has been associated with changes in DNA methylation in heavily methylated sequences with high representation throughout the human genome. We hypothesized that prolonged exposure to particulate pollution might also modify DNA methylation and be a potential mechanism by which chronic air pollution exposure adversely affects health. Methods: We measured DNA methylation of LINE-1 and Alu repetitive elements by quantitative PCR-Pyrosequencing of 985 blood samples from 680 elderly participants in the Boston Normative Aging Study. We used covariate-adjusted mixed models to account for repeated measures. We estimated effects on DNA methylation of ambient pollutants (black carbon, PM2.5, and sulfate) in multiple exposure windows (ranging from 1 month to 1 year) prior to the examination. Results: We found that a 1μg/m3 increase in black carbon over a 60-day period was associated with a 0.8% (95% CI: 0.004%, 1.6%) decrease in methylation of LINE-1 repetitive elements. A 1 μg/m3 increase in black carbon over a 90-day period was associated with a 0.6% (0.001%, 1.1%) decrease in Alu repetitive elements. A 1 μg/m3 increase in sulfate over a 90-day period was associated with 0.3% (0.02%, 0.6%) decrease in LINE-1 repetitive elements. The association with longer exposure windows persisted when we fit models simultaneously adjusting for 1-week moving averages of pollutant exposure. There was no association with PM2.5. Conclusion: Exposure to particulates over 2 to 3 months is associated with decreased repetitive element methylation. This may be a mechanism by which chronic exposure to air pollution increases risk of morbidity and mortality.