Background:

Tobacco smoking represents a major cardiovascular risk factor and consequently causes serious illness and premature death. In the past few years, several “healthier” alternatives, e.g. e-cigarettes or heat-not-burn tobacco products have been developed, the effects of which cannot yet be predicted. We used a mouse model in combination with a translational human study to characterize the underlying mechanisms of vascular dysfunction, oxidative stress and inflammation caused by short-term exposure with e-cigarettes and heat-not-burn tobacco products (HTP).

Methods and Results:

Acute e-cigarette and HTP exposure caused impairment of endothelial function in chronic smokers determined by flow-mediated dilation. In mice, e-cigarette vapour with and without nicotine caused detrimental effects on endothelial function, markers of oxidative stress, inflammation, and lipid peroxidation. These effects of e-cigarette vapour were largely absent in mice lacking phagocytic NADPH oxidase (NOX-2). We also established that the e-cigarette product acrolein, a reactive aldehyde, recapitulated many of the NOX-2-dependent effects of e-cigarette vapour. Also, short-term exposure to heat-not-burn tobacco vapour caused cardiovascular complications.

Conclusions:

E-cigarette vapour exposure increases vascular, cerebral, and pulmonary oxidative stress via a NOX-2-dependent mechanism. With regard to the human endothelial function, analogous effects were observed for the various tobacco products (conventional cigarettes, e-cigarettes and HTP). Since the use of alternative tobacco products is increasing, particularly amongst youth, our data suggest that more experimental and human studies are required as well as aggressive steps are warranted to limit their health risks.

Support or Funding Information: 

Stiftung Mainzer Herz and Boehringer Ingelheim Stiftung.