Department of Occupational & Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Environ Health. 2020 Jul 2;19(1):75. doi: 10.1186/s12940-020-00621-x.
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.
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-PGF2α) 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-PGF2α 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.
Each one-percentage increase in the sum of urinary OH-PAHs, high-molecular-weight or low-molecular-weight OH-PAHs (ƩOH-PAHs, ƩHMW OH-PAH or ƩLMW OH-PAHs, respectively) was associated with a 0.2152-, 0.2076- or 0.1985- ml decrease in FEV, and a 0.1891-, 0.2195- or 0.1634- ml decrease in FVC, respectively. Additionally, significantly positive dose-response relationships of ƩOH-PAHs, ƩHMW OH-PAH and ƩLMW OH-PAHs with urinary 8-OHdG or 8-iso-PGF2α, as well as an inverse dose-response relationship between urinary 8-OHdG and FVC, were observed (all P for trend < 0.05). Mediation analysis indicated that urinary 8-OHdG mediated 14.22% of the association between ƩHMW OH-PAH and FVC.
Higher levels of oxidative DNA damage might be involved in the decreased levels of FVC caused by high-molecular-weight PAH exposure.
多环芳烃（PAHs）暴露与肺功能下降有关。然而，氧化损伤是否参与其中尚不清楚。本研究旨在探讨 PAH 暴露与肺功能之间关联的潜在中介作用，即氧化 DNA 或脂质损伤。
在武汉-珠海队列的基线中，对 3367 名参与者进行了尿液中单羟基多环芳烃代谢物（OH-PAHs）水平和肺功能参数的测量。分别测定尿 8-羟基-2'-脱氧鸟苷（8-OHdG）和 8-异前列腺素（8-iso-PGF2α）以评估个体的氧化 DNA 和脂质损伤程度。采用线性混合模型探讨尿 OH-PAHs、8-OHdG 和 8-iso-PGF2α 与肺功能参数之间的关联。进一步进行中介分析以评估氧化损伤在尿 OH-PAHs 与肺功能之间的关联中的潜在作用。
尿 OH-PAHs 总量、高分子量或低分子量 OH-PAHs（ƩOH-PAHs、ƩHMW OH-PAH 或 ƩLMW OH-PAHs）每增加一个百分点，FEV 分别降低 0.2152、0.2076 或 0.1985ml，FVC 分别降低 0.1891、0.2195 或 0.1634ml。此外，还观察到 ƩOH-PAHs、ƩHMW OH-PAH 和 ƩLMW OH-PAHs 与尿 8-OHdG 或 8-iso-PGF2α 之间呈显著正剂量-反应关系，以及尿 8-OHdG 与 FVC 之间呈负剂量-反应关系（所有趋势 P 值均<0.05）。中介分析表明，尿 8-OHdG 介导了 ƩHMW OH-PAH 与 FVC 之间 14.22%的关联。
较高水平的氧化 DNA 损伤可能参与了高分子量 PAH 暴露导致的 FVC 降低。
