The Roles of Aging Signs in the Effect of Environmental Polycyclic Aromatic Hydrocarbon Exposure on Liver Fibrosis Risk: Results From Population‐Based Study and In Vitro Study

Aging and polycyclic aromatic hydrocarbon (PAH) exposure are linked to chronic liver disease. However, the potential mechanisms and roles of aging in the effect of PAHs on liver fibrosis are unclear. A subpopulation ( n = 2537) was derived from the Henan Rural Cohort study. Plasma PAHs and telomere length (TL) were measured by the GC‐MS and RT‐PCR methods. The impacts of TL and PAH exposure on liver fibrosis were assessed. Furthermore, the potential mechanisms of PAH exposure–induced aging were explored in vitro. Several PAHs and 10‐PAH mixture were positively related to liver fibrosis, particularly in smoking and cooking participants. Joint effects of shortened TL and high PAH exposure on increased liver fibrosis risk were observed. Compared to the solvent control group, increased ROS generation of intracellular and mitochondria, upregulation of expression of inflammation‐related genes ( cGAS and STING ), senescence‐related modulation genes of p53 , p21 , p16 , and SASPs ( IL-6 and IL-8 ) at RNA levels and AST/ALT ratio, and downregulation of albumin were found in cells treated with 300.00 μ M Phe plus 0.30 μ M BaP groups. The findings indicated that aging may aggravate PAH exposure–related liver fibrosis via inducing inflammation‐ and senescence‐related pathways, suggesting that delaying the aging process may be an effective measure to reduce the negative effect of PAH exposure. Trial Registration ClinicalTrials.gov identifier: ChiCTR‐OOC‐15006699