Oxidative damage mediates the association between polycyclic aromatic hydrocarbon exposure and lung function

Background: Exposure to polycyclic aromatic hydrocarbons (PAHs) is related to decreased lung function. However, whether oxidative damage is involved in this relationship remains unclear. This study was aimed to explore the potential mediating role of oxidative DNA or lipid damage in the association between PAH exposure and lung function. Methods: The urinary levels of monohydroxy polycyclic aromatic hydrocarbon metabolites (OH-PAHs) and lung function parameters were measured among 3367 participants from the baseline of the Wuhan-Zhuhai cohort. Urinary 8-hydroxy-2 '-deoxyguanosine (8-OHdG) and 8-isoprostane (8-iso-PGF2 alpha) were determined to evaluate the individuals' oxidative DNA and lipid damage degrees, respectively. Linear mixed models were used to investigate the associations of urinary OH-PAHs, 8-OHdG and 8-iso-PGF2 alpha with lung function parameters. Mediation analysis was further conducted to assess the potential role of oxidative damage in the association between urinary OH-PAHs and lung function. Results: Each one-percentage increase in the sum of urinary OH-PAHs, high-molecular-weight or low-molecular-weight OH-PAHs (Sigma OH-PAHs, Sigma HMW OH-PAH or Sigma LMW OH-PAHs, respectively) was associated with a 0.2152-, 0.2076- or 0.1985- ml decrease in FEV1, and a 0.1891-, 0.2195- or 0.1634- ml decrease in FVC, respectively. Additionally, significantly positive dose-response relationships of Sigma OH-PAHs, Sigma HMW OH-PAH and Sigma LMW OH-PAHs with urinary 8-OHdG or 8-iso-PGF2 alpha, as well as an inverse dose-response relationship between urinary 8-OHdG and FVC, were observed (allPfor trend < 0.05). Mediation analysis indicated that urinary 8-OHdG mediated 14.22% of the association between Sigma HMW OH-PAH and FVC. Conclusion: Higher levels of oxidative DNA damage might be involved in the decreased levels of FVC caused by high-molecular-weight PAH exposure.