Division of Cardiovascular Medicine, Department of Medicine
Cardiology | Cardiovascular Diseases | Pathological Conditions, Signs and Symptoms | Substance Abuse and Addiction
AIMS: Electronic (e)-cigarettes have been marketed as a 'healthy' alternative to traditional combustible cigarettes and as an effective method of smoking cessation. There are, however, a paucity of data to support these claims. In fact, e-cigarettes are implicated in endothelial dysfunction and oxidative stress in the vasculature and the lungs. The mechanisms underlying these side effects remain unclear. Here, we investigated the effects of e-cigarette vapour on vascular function in smokers and experimental animals to determine the underlying mechanisms.
METHODS AND RESULTS: Acute e-cigarette smoking produced a marked impairment of endothelial function in chronic smokers determined by flow-mediated dilation. In mice, e-cigarette vapour without nicotine had more detrimental effects on endothelial function, markers of oxidative stress, inflammation, and lipid peroxidation than vapour containing nicotine. These effects of e-cigarette vapour were largely absent in mice lacking phagocytic NADPH oxidase (NOX-2) or upon treatment with the endothelin receptor blocker macitentan or the FOXO3 activator bepridil. We also established that the e-cigarette product acrolein, a reactive aldehyde, recapitulated many of the NOX-2-dependent effects of e-cigarette vapour using in vitro blood vessel incubation.
CONCLUSIONS: E-cigarette vapour exposure increases vascular, cerebral, and pulmonary oxidative stress via a NOX-2-dependent mechanism. Our study identifies the toxic aldehyde acrolein as a key mediator of the observed adverse vascular consequences. Thus, e-cigarettes have the potential to induce marked adverse cardiovascular, pulmonary, and cerebrovascular consequences. Since e-cigarette use is increasing, particularly amongst youth, our data suggest that aggressive steps are warranted to limit their health risks.
Oxidative stress, Behavioural risk factor, E-cigarette vapour, Endothelial dysfunction, Lifestyle drug
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© The Author(s) 2019. Published by Oxford University Press on behalf of the European Society of Cardiology. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact firstname.lastname@example.org
DOI of Published Version
Kuntic M, Oelze M, Steven S, Kröller-Schön S, Stamm P, Kalinovic S, Frenis K, Vujacic-Mirski K, Bayo Jimenez MT, Kvandova M, Filippou K, Al Zuabi A, Brückl V, Hahad O, Daub S, Varveri F, Gori T, Huesmann R, Hoffmann T, Schmidt FP, Keaney JF, Daiber A, Münzel T. Short-term e-cigarette vapour exposure causes vascular oxidative stress and dysfunction: evidence for a close connection to brain damage and a key role of the phagocytic NADPH oxidase (NOX-2). Eur Heart J. 2020 Jul 7;41(26):2472-2483. doi: 10.1093/eurheartj/ehz772. PMID: 31715629; PMCID: PMC7340357. Link to article on publisher's site
European heart journal
Kuntic M, Keaney JF, Munzel T. (2020). Short-term e-cigarette vapour exposure causes vascular oxidative stress and dysfunction: evidence for a close connection to brain damage and a key role of the phagocytic NADPH oxidase (NOX-2). Open Access Publications by UMMS Authors. https://doi.org/10.1093/eurheartj/ehz772. Retrieved from https://escholarship.umassmed.edu/oapubs/4292
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial 4.0 License