Short-term Exposure to PM2.5 and Epigenetic Aging: A Quasi-Experimental Study

BACKGROUND AND AIM: Fine particulate matter 2.5μm in aerodynamic diameter (PM2.5), has been considered a global threat to accelerated biological aging. DNA methylation age (DNAmAge) is one of the most studied forms age, its discrepancy with chronological (i.e. acceleration, AA) was associated multiple aging-related health outcomes and had positive associations long-term PM2.5 exposure. However, AAs short-term exposure are still partly understood. In order elucidate causal between DNAmAge, we performed quasi-experiment social experiment design 26 healthy adults. We aimed understand whether via pollution waves (PPWs, ambient concentration 75 μg/m3 for 2 or more days) could accelerate AAs. METHODS: conducted three visits participants: pre-PPW (baseline), during-PPW (1st follow-up), post-PPW (2nd follow-up). isolated from collected peripheral CD4+ T-helper cells used detect levels. Seven including Horvath’s, Hannums’, PhenoAge, GrimAge, DunedinPoAm, mortality risk score, epiTOC were estimated. RESULTS:Comparing baseline, first observed that all increased during PPWs considerably declined after PPWs, albeit not statistically significant. further tested change two follow-ups average personal 0-24h 24-48h prior blood collection. found z-scored GrimAge DunedinPoAm significantly elevated by 0.097 0.081-unit 5 increase Such acute effects mediated several oxidative inflammation biomarkers up 18% proportions. CONCLUSIONS:This exhibited exposures high levels moderately aging, which be captured responses stress. KEYWORDS: Air pollution, PM2.5, aging