Association between indoor PM2.5 components and accelerated biological aging in schizophrenia patients: Evidence from multi-omics mechanisms

Indoor fine particulate matter (PM2.5) poses a considerable hazard to the aging process, particularly in vulnerable populations such as schizophrenia patients who frequently spend extended periods in indoor environments. Currently, the evidence on which PM2.5 components contribute to accelerated aging remains unclear. To address these issues, we conducted a prospective, repeated-measurement study on 104 schizophrenia patients. Our findings indicated that exposure to PM2.5 components was significantly associated with accelerated biological aging in schizophrenia patients. Notably, the most prominent effects were observed for thallium (1.303, 95 % CI: 0.481-2.125), chromium (1.029, 95 % CI: 0.303-1.756), lead (1.021, 95 % CI: 0.296-1.746), antimony (0.915, 95 % CI: 0.233-1.597), selenium (0.854, 95 % CI: 0.209-1.499), and manganese (0.833, 95 % CI: 0.186-1.480). Multivariate analysis revealed that PM2.5 components predominantly induced alterations in serum glycerophospholipid metabolites, accelerating the aging process. This intricate connection was closely linked to the gut microbiota, particularly to species such as Dorea and Blautia. Mediation analysis showed that the Blautia-PC (16:0/0:0) pathway mediated the largest proportion (30.69 %) of the effect of manganese exposure on accelerating immune biological aging in schizophrenia patients, as measured using the Klemera-Doubal method. These results underscore the need to address pollution sources that harm health, and provide new evidence for improving regional air quality.