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.
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 Jan 1;340(Pt 1):122801. doi: 10.1016/j.envpol.2023.122801. Epub 2023 Oct 25.
To quantify the association of polycyclic aromatic hydrocarbons (PAHs) and the polygenic risk score (PRS) with lung function decline, we developed a repeated-measures study with 4681 observations from baseline and 6-year follow-up of the Wuhan-Zhuhai cohort. Lung function and urinary monohydroxylated PAH metabolites (OH-PAHs) were measured for each observation. The PRS was derived from 246 lung function-associated genetic variants weighted by the effect size of the decreasing ratio of forced expiratory volume in 1 s by forced vital capacity (FEV1/FVC). Linear mixed models were used to estimate the longitudinal exposure-response relationships between OH-PAHs and lung function, and to evaluate the interactions between OH-PAHs and PRS on the longitudinal change of lung function. We found that each 1-unit increase in log-transformed values of 9-hydroxyfluorene, 2-hydroxyfluorene, 4-hydroxyphenanthrene, 9-hydroxyphenanthrene, 2-hydroxyphenanthrene, 1-hydroxyphenanthrene, 1-hydroxypyrene, low molecular weight OH-PAHs (ΣLMW-OH-PAHs), and total OH-PAHs (ΣOH-PAHs) was associated with an annual change in FEV1/FVC of -0.140, -0.112, -0.260, -0.300, -0.159, -0.220, -0.145, -0.156, and -0.177 %/year, respectively. Interactions on the annual decline of FEV1/FVC were detected between ΣLMW-OH-PAHs and PRS (-0.010 %/year, 95% confidence interval -0.018 to -0.001, P = 0.0228), and between ΣOH-PAHs and PRS (-0.010 %/year, -0.018 to -0.001, P = 0.0203). These results indicated that specific and total urinary OH-PAHs were associated with the longitudinal FEV1/FVC decline, and ΣLMW-OH-PAHs as well as ΣOH-PAHs interacted with PRS on the annual decline of FEV1/FVC.
为了量化多环芳烃（PAHs）和多基因风险评分（PRS）与肺功能下降的关联，我们对武汉-珠海队列的 4681 次观测值进行了重复测量研究，包括基线和 6 年随访。对每次观测值都进行了肺功能和尿液单羟基化多环芳烃代谢物（OH-PAHs）的测量。PRS 是由 246 个与肺功能相关的遗传变异加权得到的，权重为 1 秒用力呼气量（FEV1）与用力肺活量（FVC）的比值下降率。采用线性混合模型来估计 OH-PAHs 与肺功能之间的纵向暴露-反应关系，并评估 OH-PAHs 和 PRS 之间的相互作用对肺功能的纵向变化的影响。我们发现，9-羟基芴、2-羟基芴、4-羟基菲、9-羟基菲、2-羟基菲、1-羟基菲、1-羟基芘、低分子量 OH-PAHs（ΣLMW-OH-PAHs）和总 OH-PAHs（ΣOH-PAHs）的 log 转换值每增加 1 个单位，FEV1/FVC 的年变化率分别为-0.140、-0.112、-0.260、-0.300、-0.159、-0.220、-0.145、-0.156 和-0.177%/年。在 FEV1/FVC 的年下降率方面，ΣLMW-OH-PAHs 和 PRS 之间（-0.010%/年，95%置信区间为-0.018 至-0.001，P=0.0228），以及 ΣOH-PAHs 和 PRS 之间（-0.010%/年，-0.018 至-0.001，P=0.0203）均检测到了相互作用。这些结果表明，特定和总尿 OH-PAHs 与 FEV1/FVC 的纵向下降有关，ΣLMW-OH-PAHs 以及 ΣOH-PAHs 与 PRS 对 FEV1/FVC 的年下降率有交互作用。
