Short-Term Exposure of PM2.5 and Epigenetic Aging: A Quasi- Experimental Study

Epigenetic age (EA) is an emerging DNA methylation-based biomarker of biological aging, but whether EA is causally associated with short-term PM2.5 exposure remains unknown. We conducted a quasi-experimental study of 26 healthy adults to test whether short-term PM2.5 exposure accelerates seven EAs with three health examinations performed before, during, and after multiple PM2.5 pollution waves. Seven EAs were derived from the DNA methylation profiles of the Illumina HumanMethylationEPIC BeadChip from CD4+ T-helper cells. We found that an increase of 10 mu g/m3 in the 0-24 h personal PM2.5 exposure prior to health examinations was associated with a 0.035, 0.035, 0.050, 0.055, 0.052, and 0.037-unit increase in the changes of z-scored DNA methylation age acceleration (AA,Horvath), AA (Hannum), AA (GrimAge), DunedinPoAm, mortality risk score (MS), and epiTOC, respectively (p-values < 0.05). The same increase in the 24-48 h average personal PM2.5 exposure yielded smaller effects but was still robustly associated with the changes in AA (GrimAge), DunedinPoAm, and MS. Such acute aging effects of PM2.5 were mediated by the changes in several circulating biomarkers, including EC-SOD and sCD40L, with up to -,28% mediated proportions. Our findings demonstrated that short-term PM2.5 exposure could accelerate aging reflected by DNA methylation profiles via blood coagulation, oxidative stress, and systematic inflammation.

Automated summary

This study found that short-term exposure to PM2.5 can accelerate the aging process reflected by DNA methylation profiles. The findings suggest that PM2.5 plays an important mediating role in the changes in blood coagulation, oxidative stress, and systemic inflammation.