Chronic Exposure to Bioaerosols in PM2.5 from Garbage Stations Accelerates Vascular Aging via the NF‐κB/NLRP3 Pathway

The fine particulate matter (PM2.5) in air pollution is a critical risk factor influencing human health. Our study included 8144 participants and showed that the risk of major adverse cardiovascular events increases by 35% (HR, 1.35; 95% CI, 1.14–1.60) for participants with the highest quartile to PM2.5 exposure as compared to those with lowest quartile. Bioaerosols, as an important environmental exposure in PM2.5, can induce systemic chronic inflammation leading to vascular aging. Thus, the effects of bioaerosols are investigated from household garbage stations in PM2.5 on vascular aging, and the underlying mechanisms are explored. In vivo, chronic exposure to bioaerosols upregulated senescence marker expression levels while causing vascular dysfunction and remodeling. In vitro, bioaerosol exposure induced decreased proliferation, G0/G1 arrest, and impaired migration of human umbilical vein endothelial cells (HUVECs). Furthermore, a single bacterium (AS22a) from the bioaerosol community was isolated and demonstrated that it upregulated inflammatory factors and accelerated cell senescence and vascular aging by activating the NF‐κB/NLRP3 signaling pathway, which may serve as a primary mechanism underlying vascular aging induced by bioaerosols in PM2.5. These findings suggest that high levels of bioaerosols in household garbage stations may adversely affect cardiovascular health. These findings indicate that the high concentrations of conditionally pathogenic bioaerosols in PM2.5 from garbage stations, may accelerate vascular aging. AS22a, as a bacterial component of bioaerosols, can stimulate vascular endothelial senescence via the NF‐κB/NLRP3 signaling pathway. This study first proves that bioaerosols in PM2.5 can accelerate vascular aging via the NF‐κB/NLRP3 signaling pathway.