Department of Occupational & Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, 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, Hubei, 430030, China.
Hubei Provincial Key Laboratory for Applied Toxicology, Hubei Provincial Center for Disease Control and Prevention, Wuhan, Hubei, 430079, China.
Environ Pollut. 2024 Nov 1;360:124664. doi: 10.1016/j.envpol.2024.124664. Epub 2024 Aug 5.
A few studies found polycyclic aromatic hydrocarbons (PAHs) were associated with serum uric acid (SUA) or hyperuricemia (HUA). However, the longitudinal study is vacant, and the underlying mechanisms remain unclear. We aimed to assess the cross-sectional and longitudinal associations of urinary PAHs metabolites with SUA levels and HUA risk, and explore the mediating effects of oxidative stress and inflammation. 10 urinary mono-hydroxylated PAHs metabolites and SUA levels were measured among 4047 Chinese urban residents at baseline and 1496 individuals at 6-year follow-up. Biomarkers of oxidative damage and inflammation in urine/plasma were determined at baseline. We adopted generalized linear mixed models and logistic regression to assess the associations of PAHs metabolites with SUA and HUA, weighted quantile sum regression and adaptive elastic net regression to evaluate the overall effects of multi-PAHs mixture, and mediation analysis to estimate the mediating roles of the biomarkers. In the cross-sectional study, each 1-unit increase in the ln-transformed values of 2-OHNa, 2-OHFlu, 4-OHPh, 9-OHPh, 3-OHPh, 2-OHPh, ΣOHNa, ΣOHPh, and ΣOHPAHs was associated with a 4.10-, 3.90-, 6.42-, 7.33-, 4.85-, 5.43-, 4.47-, 7.67-, and 5.22-μmol/L increase in SUA, respectively. Meanwhile, each 1-unit increase in the ln-transformed values of 1-OHNa, 2-OHNa, 4-OHPh, 9-OHPh, 3-OHPh, 2-OHPh, ΣOHNa, ΣOHPh, and ΣOHPAHs was associated with a 17, 14, 15, 22, 14, 19, 18, 27, and 21% increment in HUA risk, respectively. After 6 years, individuals with persistent high level of 9-OHPh had a 12.5 μmol/L increase in SUA compared with those with persistent low level. The overall effects of multi-PAHs mixture on SUA and HUA remain positive. 8-hydroxy-deoxyguanosine mediated the associations of PAHs metabolites with SUA and HUA, and the mediated proportion ranged from 5.39% to 15.34%. PAHs exposure was associated with the elevated SUA levels and increased HUA risk, and oxidative DNA damage may be one of the underlying mechanisms.
一些研究发现多环芳烃（PAHs）与血清尿酸（SUA）或高尿酸血症（HUA）有关。然而，纵向研究仍然空缺，其潜在机制尚不清楚。我们旨在评估尿中多环芳烃代谢物与 SUA 水平和 HUA 风险的横断面和纵向关联，并探讨氧化应激和炎症的介导作用。在基线时，对 4047 名中国城市居民和 1496 名居民测量了 10 种尿单羟基化 PAHs 代谢物和 SUA 水平。在基线时测定尿液/血浆中的氧化损伤和炎症生物标志物。我们采用广义线性混合模型和逻辑回归来评估 PAHs 代谢物与 SUA 和 HUA 的关联，加权分位数总和回归和自适应弹性网回归来评估多 PAHs 混合物的总体效应，以及中介分析来估计生物标志物的介导作用。在横断面研究中，ln 转换值每增加 1 单位，2-OHNa、2-OHFlu、4-OHPh、9-OHPh、3-OHPh、2-OHPh、ΣOHNa、ΣOHPh 和 ΣOHPAHs 与 SUA 分别增加 4.10、3.90、6.42、7.33、4.85、5.43、4.47、7.67 和 5.22μmol/L。同时，ln 转换值每增加 1 单位，1-OHNa、2-OHNa、4-OHPh、9-OHPh、3-OHPh、2-OHPh、ΣOHNa、ΣOHPh 和 ΣOHPAHs 与 HUA 风险分别增加 17、14、15、22、14、19、18、27 和 21%。6 年后，与持续低水平相比，9-OHPh 持续高水平的个体的 SUA 增加了 12.5μmol/L。多 PAHs 混合物对 SUA 和 HUA 的总体影响仍然是积极的。8-羟基脱氧鸟苷介导了 PAHs 代谢物与 SUA 和 HUA 的关联，介导比例范围为 5.39%至 15.34%。PAHs 暴露与 SUA 水平升高和 HUA 风险增加有关，氧化 DNA 损伤可能是其潜在机制之一。
