Personal PM2.5 Elemental Components, Decline of Lung Function, and the Role of DNA Methylation on Inflammation-Related Genes in Older Adults: Results and Implications of the BAPE Study

Epidemiological evidence of the effects of PM2.5 elements on lung function and DNA methylation is limited. We conducted a longitudinal panel study of 76 healthy older adults aged 60–69 years in Jinan, China, from September 2018 to January 2019. We periodically measured individual 72 h PM2.5 and element concentrations, lung function, and DNA methylation levels of eight inflammation-related genes. We used linear mixed-effect models to investigate the effects of exposure to personal PM2.5 elements on the lung function and DNA methylation. Mediation analysis was used to investigate the underlying effect mechanism. Negative changes in the ratio of forced expiratory volume in 1 s to forced vital capacity, ranging from −1.23% [95% confidence interval (CI): −2.11%, −0.35%] to −0.77% (95% CI: −1.49%, −0.04%), were significantly associated with interquartile range (IQR) increases in personal PM2.5 at different lag periods (7–12, 13–24, 25–48, 0–24, 0–48, and 0–72 h). Arsenic (As), nickel, rubidium (Rb), selenium, and vanadium were significantly associated with at least three lung function parameters, and IQR increases in these elements led to 0.12–5.66% reductions in these parameters. PM2.5 elements were significantly associated with DNA methylation levels. DNA methylation mediated 7.28–13.02% of the As- and Rb-related reduced lung function. The findings indicate that exposure to elements in personal PM2.5 contributes to reduced lung function through DNA methylation.