Song Jie, Zhu Jingfang, Tian Ge, Li Haibin, Li Huijun, An Zhen, Jiang Jing, Fan Wei, Wang Gui, Zhang Yange, Wu Weidong
Henan International Collaborative Laboratory for Health Effects and Intervention of Air Pollution, School of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, China.
Henan International Collaborative Laboratory for Health Effects and Intervention of Air Pollution, School of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, China.
Environ Int. 2020 Apr;137:105579. doi: 10.1016/j.envint.2020.105579. Epub 2020 Feb 18.
The evidence that exposure to ambient ozone (O) causes acute cardiovascular effects appears inconsistent. A repeated-measure study with 61 healthy young volunteers was conducted in Xinxiang, Central China. Real-time concentrations of O were monitored. Cardiovascular outcomes including blood pressure (BP), heart rate (HR), serum levels of high sensitivity C-reactive protein (hs-CRP), 8-hydroxy-2'-deoxyguanosine (8-OHdG), tissue-type plasminogen activator (t-PA), and platelet-monocyte aggregation (PMA) were repeated measured. Linear mixed-effect models were used to analyze the association of ambient O with these cardiovascular outcomes. Additionally, the modifying effects of glutathione S-transferase mu 1 (GSTM1) and glutathione S-transferase theta 1 (GSTT1) polymorphisms were estimated to explore the potential mechanisms and role of the association between O exposure and the above cardiovascular outcomes. A 10 μg/m increase in O was associated with increases of 9.2 mmHg (95% confidence interval [CI]: 2.5, 15.9), 7.2 mmHg (95% CI: 0.8, 13.6), and 21.2 bpm (95% CI: 5.8, 36.6) in diastolic BP (DBP, lag1), mean arterial BP (MABP, lag1), and HR (lag01), respectively. Meanwhile, the serum concentrations of hs-CRP, 8-OHdG, and t-PA were all increased by O exposure, but the PMA level was decreased. Stratification analyses showed that the estimated effects of O on DBP, MABP, and HR in GSTM1-sufficient subjects were significantly higher than in GSTM1-null subjects. Moreover, GSTM1-null genotype enhanced O-induced increases, albeit insignificant, in levels of serum hs-CRP, 8-OHdG, and t-PA compared with GSTM1-sufficient genotype. Insignificant increases in hs-CRP and t-PA were also detected in GSTT1-null subjects. Taken together, our findings indicate that acute exposure to ambient O induces autonomic alterations, systemic inflammation, oxidative stress, and fibrinolysis in healthy young subjects. GSTM1 genotype presents the trend of modifying O-induced cardiovascular effects.
暴露于环境臭氧（O）会导致急性心血管效应，这一证据似乎并不一致。在中国中部的新乡，对61名健康年轻志愿者进行了一项重复测量研究。监测了O的实时浓度。重复测量了包括血压（BP）、心率（HR）、高敏C反应蛋白（hs-CRP）、8-羟基-2'-脱氧鸟苷（8-OHdG）、组织型纤溶酶原激活剂（t-PA）和血小板-单核细胞聚集（PMA）在内的心血管指标。使用线性混合效应模型分析环境O与这些心血管指标之间的关联。此外，评估了谷胱甘肽S-转移酶μ1（GSTM1）和谷胱甘肽S-转移酶θ1（GSTT1）基因多态性的修饰作用，以探讨O暴露与上述心血管指标之间关联的潜在机制和作用。O每增加10μg/m，舒张压（DBP，滞后1）、平均动脉压（MABP，滞后1）和心率（HR，滞后01）分别增加9.2mmHg（95%置信区间[CI]：2.5，15.9）、7.2mmHg（95%CI：0.8，13.6）和21.2次/分钟（95%CI：5.8，36.6）。同时，O暴露使hs-CRP、8-OHdG和t-PA的血清浓度均升高，但PMA水平降低。分层分析表明，在GSTM1充足的受试者中，O对DBP、MABP和HR的估计效应显著高于GSTM1缺失的受试者。此外，与GSTM1充足基因型相比，GSTM1缺失基因型增强了O诱导的血清hs-CRP、8-OHdG和t-PA水平的升高，尽管不显著。在GSTT1缺失的受试者中也检测到hs-CRP和t-PA有不显著的升高。综上所述，我们的研究结果表明，健康年轻受试者急性暴露于环境O会诱发自主神经改变、全身炎症、氧化应激和纤维蛋白溶解。GSTM1基因型呈现出修饰O诱导的心血管效应的趋势。
