Fine particulate matter, its components and sources, and blood pressure: The perspective of DNA methylation

Limited studies focused on acute effects of PM2.5 components and sources exposure on blood pressure and the potential mediating role of DNA methylation. We conducted a repeated-measurement study design with 4 visits involving 64 participants to explore these underlying relationships. Ambient PM2.5 components were monitored at a fixed-site station and PMF was applied to perform source apportionment. DNA methylation levels at specific loci in the promoter region were detected by methyl-capture sequencing. We applied linear mixed-effects models to investigate these associations and conducted mediation analyses to assess the underlying effect patterns of DNA methylation changes. Exposure to PM2.5 at lag 1 day was most significantly associated with the elevation in blood pressure indicators. Specifically, SBP, MAP and PP increased by 0.79%, 0.53% and 1.70% per IQR increase in PM2.5 respectively. The carbonaceous components (EC and OC) and Ca, Cd, Cr, and Cl- were the major chemical components contributing to changes in blood pressure, corresponding to 0.87–1.71% increases in SBP and MAP. For the effect estimates of specific sources, combustion-derived PM2.5 showed robust positive associations with SBP and MAP. More differentially methylated CpG sites (DMCs) with hypomethylation were observed following PM2.5, its components as well as combustion-derived PM2.5 exposure, with 14 exerting the mediation effects. Furthermore, DMCs located in ACE, IL-6, IL-2 and NPPA genes mediated 9.2–34.7% of the PM2.5 and its component-related blood pressure changes. Our findings suggest that personal exposure to PM2.5 components may induce elevated blood pressure through hypomethylation of specific CpG sites.