Zhang Qingli, Du Xihao, Li Huichu, Jiang Yixuan, Zhu Xinlei, Zhang Yang, Niu Yue, Liu Cong, Ji John, Chillrud Steven N, Cai Jing, Chen Renjie, Kan Haidong
School of Public Health, Key Lab of Public Health Safety of the Ministry of Education and NHC Key Lab of Health Technology Assessment, Fudan University, Shanghai 200032, China.
Department of Environmental Health, Harvard TH Chan School of Public Health, Boston, MA, USA.
J Hazard Mater. 2022 Aug 5;435:129031. doi: 10.1016/j.jhazmat.2022.129031. Epub 2022 Apr 29.
A system-wide cardiovascular response to traffic-related air pollution (TRAP) has been rarely described. To systemically understand the mechanisms underlying cardiovascular effects of TRAP, we conducted a randomized, crossover trial in 56 young adults, who engaged in two 4-hour exposure sessions on a main road and in a park, alternately. We measured personal exposures to traffic-related air pollutants (TRAPs), including fine and ultrafine particulate matter, black carbon, nitrogen dioxide, and carbon monoxide. Lipidomics, targeted proteomics, urine metabolomics, targeted biomarkers, ambulatory blood pressure and electrocardiogram were measured. We used linear mixed-effects models to estimate the associations. The exposures to TRAPs except for fine particulate matter in the road session were 2-3 times higher. We observed elevated blood pressure and decreased heart rate variability (HRV) after TRAP exposure, accompanied by dozens of molecular alterations involving systemic inflammation, oxidative stress, endothelial dysfunction, coagulation, and lipid metabolism. Pathways like vascular smooth muscle cell proliferation and biomarkers like trimethylamine N-Oxide might also be disturbed. Some of these TRAP-related molecular biomarkers were also associated with changes of blood pressure or HRV. Our results provided systematical mechanistic profiling for the cardiovascular effects of TRAP using multi omics, which may have implications in TRAP control.
目前很少有研究描述交通相关空气污染（TRAP）对全系统心血管的影响。为了系统地了解TRAP对心血管产生影响的潜在机制，我们对56名年轻人进行了一项随机交叉试验，他们在主干道和公园交替进行了两次4小时的暴露实验。我们测量了与交通相关的空气污染物（TRAPs）的个人暴露情况，包括细颗粒物和超细颗粒物、黑碳、二氧化氮和一氧化碳。我们还测量了脂质组学、靶向蛋白质组学、尿液代谢组学、靶向生物标志物、动态血压和心电图。我们使用线性混合效应模型来估计两者之间的关联。除了在道路环境中暴露的细颗粒物外，其他TRAPs的暴露量高出2至3倍。我们观察到，暴露于TRAP后血压升高、心率变异性（HRV）降低，同时伴随着数十种分子变化，涉及全身炎症、氧化应激、内皮功能障碍、凝血和脂质代谢。血管平滑肌细胞增殖等通路以及氧化三甲胺等生物标志物也可能受到干扰。其中一些与TRAP相关的分子生物标志物也与血压或HRV的变化有关。我们的研究结果使用多组学方法为TRAP对心血管的影响提供了系统的机制分析，这可能对控制TRAP具有重要意义。
