Personal PM 2.5 -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 (PM _2.5 ) exposure. Limited studies have explored the association between PM _2.5 -bound polycyclic aromatic hydrocarbons (PAHs) and lung function, but studies at the personal level in healthy young adults are scarce. Here, we assessed personal PM _2.5 and PM _2.5 -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 PM _2.5 and PAHs had the greatest negative effect on forced expiratory volume in 1 s (FEV ₁ ), peak expiratory flow rate (PEF) and forced expiratory flow between 25% and 75% vital capacity (FEF _25-75 ) at lag 3 days. An IQR increase in personal PM _2.5 exposure was associated with a change of 0.35% (95% CI: 0.27%, 0.42%) in FEV ₁ , 0.39% (95% CI: 0.29%, 0.47%) in PEF and 0.36% (95% CI: 0.27%, 0.45%) in FEF _25-75 . An IQR increase in personal PAH exposure was associated with a decrease of 0.63% (95% CI: 0.55%, 0.69%) in FEV ₁ , 0.69% (95% CI: 0.61%, 0.75%) in PEF and 0.66% (95% CI: 0.57%, 0.72%) in FEF _25-75 . Additionally, exposure to PM _2.5 and PAHs resulted in the strongest positive effects on urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) and 8-iso-prostaglandin-F _2α (8-iso-PGF _2α ). Of these, 8-OHdG mediated 10.33%, 8.87% and 9.45% of the associations of personal PM _2.5 exposure with FEV ₁ , PEF and FEF _25-75 , respectively. Our results revealed that personal exposure to PM _2.5 and PAHs was associated with lung function decline in healthy young adults, and urinary 8-OHdG mediated the association between personal PM _2.5 and lung function.
(Copyright © 2021. Published by Elsevier Ltd.)