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

Limited studies focused on acute effects of PM 2.5 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 PM 2.5 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 PM 2.5 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 PM 2.5 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 PM 2.5 showed robust positive associations with SBP and MAP. More differentially methylated CpG sites (DMCs) with hypomethylation were observed following PM 2.5 , its components as well as combustion-derived PM 2.5 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 PM 2.5 and its component-related blood pressure changes. Our findings suggest that personal exposure to PM 2.5 components may induce elevated blood pressure through hypomethylation of specific CpG sites. • PM 2.5 and chemical components were associated with elevated blood pressure (BP). • The effect of PM 2.5 derived from the combustion source was more prominent. • More hypomethylated CpG sites were observed after exposure to PM 2.5 . • DNA methylation exerted mediation effects in PM 2.5 components on BP elevation.