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.