Personal PM2.5-bound PAH exposure, oxidative stress and lung function: The associations and mediation effects in healthy young adults

Decreased lung function is an early hazard of respiratory damage from fine particulate matter (PM2.5) exposure. Limited studies have explored the association between PM2.5-bound polycyclic aromatic hydrocarbons (PAHs) and lung function, but studies at the personal level in healthy young adults are scarce. Here, we assessed personal PM2.5 and PM2.5-bound PAH levels in a panel of 45 healthy young adults by a time-weighted model. The aims were to investigate the relationship between personal exposure and lung function by a linear mixed effect model, and to explore the mediating effects of oxidative stress in this association. The results showed that personal exposure to PM2.5 and PAHs had the greatest negative effect on forced expiratory volume in 1 s (FEV1), peak expiratory flow rate (PEF) and forced expiratory flow between 25% and 75% vital capacity (FEF25-75) at lag 3 days. An IQR increase in personal PM2.5 exposure was associated with a change of 0.35% (95% CI: 0.27%, 0.42%) in FEV1, 0.39% (95% CI: 0.29%, 0.47%) in PEF and 0.36% (95% CI: 0.27%, 0.45%) in FEF25-75. An IQR increase in personal PAH exposure was associated with a decrease of 0.63% (95% CI: 0.55%, 0.69%) in FEV1, 0.69% (95% CI: 0.61%, 0.75%) in PEF and 0.66% (95% CI: 0.57%, 0.72%) in FEF25-75. Additionally, exposure to PM2.5 and PAHs resulted in the strongest positive effects on urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) and 8-iso-prostaglandin-F2α (8-iso-PGF2α). Of these, 8-OHdG mediated 10.33%, 8.87% and 9.45% of the associations of personal PM2.5 exposure with FEV1, PEF and FEF25-75, respectively. Our results revealed that personal exposure to PM2.5 and PAHs was associated with lung function decline in healthy young adults, and urinary 8-OHdG mediated the association between personal PM2.5 and lung function.