Personal PM2.5 exposure and lung function: Potential mediating role of systematic inflammation and oxidative damage in urban adults from the general population

Short-term effects of fine particulate matter (PM2.5) exposure on lung function have been reported. However, few studies have assessed PM2.5 exposure on the personal level, and the mechanism underlying the effects of PM2.5 exposure on lung function remains less clear. To evaluate the association between personal PM2.5 exposure and lung function alteration in general population and to explore the roles of systematic inflammation and oxidative damage in this association. A total of 7685 lung function tests were completed among 4697 urban adults in Wuhan, China. Plasma C-reactive protein (CRP), urinary 8-iso-prostaglandin-F2α (8-iso-PGF2α) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels were measured. Personal PM2.5 exposure levels were estimated using an estimation model from the actual measurements of individual PM2.5 levels in 191 participants. Mixed linear models were used to evaluate the association between personal PM2.5 exposure and lung function. Mediation analyses were conducted to investigate the roles of CRP, 8-iso-PGF2α and 8-OHdG in above associations. After adjusting for confounders, each 10 μg/m3 increase in the previous-day personal PM2.5 exposure was associated with 2.94 mL, 2.02 mL and 16.14 mL/s decreases in forced vital capacity (FVC), forced expiration volume in 1 s (FEV1) and peak expiratory flow, respectively. The associations were more obvious among never smokers compared with current smokers. Cumulative 7-day exposure to PM2.5 led to the strongest adverse effects on lung function. Among never smokers with high PM2.5 exposure levels, a positive relationship was observed between personal PM2.5 level and urinary 8-iso-PGF2α, and 8-iso-PGF2α meditated 4.69% and 12.30% of the association between the 7-day moving PM2.5 concentration and FVC and FEV1, respectively. We did not observe a significant positive association between PM2.5 exposure and plasma CRP or urinary 8-OHdG. Short-term personal exposure to PM2.5 is associated with reduced pulmonary ventilation function. Urinary 8-iso-PGF2α partly mediates these associations.