Department of Environmental Health Sciences, Columbia University Mailman School of Public Health, 722 W 168th Street, New York, NY, 10032, USA.
Department of Environmental Health and Engineering, Johns Hopkins University, Baltimore, MD, USA.
Curr Environ Health Rep. 2020 Dec;7(4):353-361. doi: 10.1007/s40572-020-00297-y. Epub 2020 Nov 26.
Electronic cigarettes (e-cigs) are a source of metals. Epidemiologic and experimental evidence support that metals are toxic to the cardiovascular system. Little is known, however, about the role that e-cig metals may play as toxicants for the possible cardiovascular effects of e-cig use. The goal of this narrative review is to summarize the evidence on e-cig use and metal exposure and on e-cig use and cardiovascular toxicity and discuss the research needs.
In vitro studies show cytotoxicity and increased oxidative stress in myocardial cells and vascular endothelial cells exposed to e-liquids and e-cig aerosols, with effects partially reversed with antioxidant treatment. There is some evidence that the heating coil plays a role in cell toxicity. Mice exposed to e-cigs for several weeks showed higher levels of oxidative stress, inflammation, platelet activation, and thrombogenesis. Cross-over clinical experiments show e-cig use alters nitric oxide-mediated flow-mediated dilation, endothelial progenitor cells, and arterial stiffness. Cross-sectional evidence from large nationally representative samples in the USA support that e-cig use is associated with self-reported myocardial infarction. Smaller studies found associations of e-cig use with higher oxidized low-density protein and heart variability compared to healthy controls. Numerous studies have measured elevated levels of toxic metals in e-cig aerosols including lead, nickel, chromium, and manganese. Arsenic has been measured in some e-liquids. Several of these metals are well known to be cardiotoxic. Numerous studies show that e-cigs are a source of cardiotoxic metals. Experimental studies (in vitro, in vivo, and clinical studies) show acute toxicity of e-cigs to the vascular system. Studies of long-term toxicity in animals and humans are missing. Longitudinal studies with repeated measures of metal exposure and subclinical cardiovascular outcomes (e.g., coronary artery calcification) could contribute to determine the long-term cardiovascular effects of e-cigs and the potential role of metals in those effects.
电子烟（e-cig）是金属的来源。流行病学和实验证据支持金属对心血管系统有毒。然而，对于电子烟使用可能作为有毒物质对心血管的潜在影响，电子烟金属可能扮演的角色知之甚少。本综述的目的是总结电子烟使用和金属暴露与电子烟使用和心血管毒性的证据，并讨论研究需求。
体外研究表明，暴露于电子烟液和电子烟气溶胶的心肌细胞和血管内皮细胞存在细胞毒性和氧化应激增加，抗氧化治疗可部分逆转这些作用。有一些证据表明，加热线圈在细胞毒性中起作用。暴露于电子烟数周的小鼠表现出更高水平的氧化应激、炎症、血小板激活和血栓形成。交叉临床实验表明，电子烟使用改变了一氧化氮介导的血流介导的扩张、内皮祖细胞和动脉僵硬。来自美国全国代表性大样本的横断面证据支持电子烟使用与自我报告的心肌梗死相关。较小的研究发现，与健康对照组相比，电子烟使用与较高的氧化型低密度脂蛋白和心脏变异性相关。许多研究已经测量了电子烟气溶胶中包括铅、镍、铬和锰在内的有毒金属的升高水平。一些电子烟液中检测到砷。其中一些金属是众所周知的心脏毒性物质。许多研究表明电子烟是心脏毒性金属的来源。实验研究（体外、体内和临床研究）表明电子烟对血管系统有急性毒性。动物和人类长期毒性的研究缺失。具有金属暴露和亚临床心血管结局（例如冠状动脉钙化）重复测量的纵向研究可能有助于确定电子烟的长期心血管影响以及金属在这些影响中的潜在作用。
