Why the study?
Data supporting claims that e-cigarettes are a healthy alternative to combustible cigarettes are lacking, and the mechanisms underlying e-cigarette-induced endothelial dysfunction and oxidative stress remain unclear.
Does acute e-cigarette vapour exposure cause vascular oxidative stress and endothelial dysfunction in smokers and experimental models?
Does acute e-cigarette vapour exposure cause vascular oxidative stress and endothelial dysfunction in smokers and experimental models?
E-cigarette vapour induces significant vascular oxidative stress and endothelial dysfunction via a NOX-2-dependent pathway mediated by acrolein, highlighting potential cardiovascular risks.
May caution e-cigarette use in smokers; leaves open whether nicotine-free vapour poses greater human vascular risk.
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.
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Kuntić et al. (2019) studied this question.
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