Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Hangkong Road 13, Wuhan 430030, Hubei, PR 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, Hangkong Road 13, Wuhan 430030, Hubei, PR China.
Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Hangkong Road 13, Wuhan 430030, Hubei, PR 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, Hangkong Road 13, Wuhan 430030, Hubei, PR China.
Ecotoxicol Environ Saf. 2018 Jan;147:1002-1009. doi: 10.1016/j.ecoenv.2017.09.058. Epub 2017 Oct 7.
Previous studies have reported an association of exposure to polycyclic aromatic hydrocarbons (PAHs) with lung function decline or cardiovascular diseases, or reduced lung function with 10-year cardiovascular (CV) risk. We analyzed risk factors for the 10-year Framingham CV risk using multiple logistic regression, and examined the mediational effect of reduced lung function on the association between exposure to PAHs and FRS using the post-exploratory structural equation modeling. Participants (n = 2268) were drawn from the Wuhan residents at baseline from the Wuhan-Zhuhai Cohort Study. They completed the physical examination, measurements of lung function and urinary monohydroxylated-PAHs (OH-PAHs). In all individuals, we found a dose-response relationship of PAHs exposure, forced expiratory volume in 1s (FEV1) or forced vital capacity (FVC) with the 10-year CV risk. The proportions of FEV1 and FVC mediation effects in association of PAH exposure with the10-year CV risk were 35% and 24%, respectively. The findings indicated that PAHs exposure or reduced lung function increased the 10-year CV risk. Impaired lung function may partly contribute to increase in the 10-year CV risk regarding exposure to PAHs.
先前的研究报告表明,多环芳烃(PAHs)暴露与肺功能下降或心血管疾病有关,或肺功能下降与 10 年心血管(CV)风险降低有关。我们使用多元逻辑回归分析了 10 年 Framingham CV 风险的危险因素,并使用探索性结构方程建模检查了肺功能降低对 PAHs 暴露与 FRS 之间关联的中介效应。参与者(n=2268)来自武汉-珠海队列研究的基线武汉居民。他们完成了体检、肺功能和尿液单羟基化多环芳烃(OH-PAHs)的测量。在所有个体中,我们发现 PAHs 暴露、1 秒用力呼气量(FEV1)或用力肺活量(FVC)与 10 年 CV 风险之间存在剂量反应关系。PAH 暴露与 10 年 CV 风险关联中 FEV1 和 FVC 中介效应的比例分别为 35%和 24%。研究结果表明,PAHs 暴露或肺功能降低会增加 10 年 CV 风险。受损的肺功能可能部分导致与 PAHs 暴露相关的 10 年 CV 风险增加。