Smoking is a worldwide healthy issue, affecting millions of people including youth individuals with profound repercussions on National Health Systems. Although international recommendations encourage smoking cessation, relapses always occur due to the variety of known and unknown biological mechanisms underlying smoking addiction, which hamper the subject to quit. In order to minimize smoking-related damages, modern strategies essentially based on substitutes of tobacco smoking cessation, have been developed such as the Electronic cigarettes (EC), a technological surrogate of traditional tobacco cigarettes (TC) marketed in 2004. As EC employ heat to convert nicotine or flavored nicotine-free solutions into vapour avoiding combustion, they represent a much less harmful alternative than TC. Despite this apparent advantage, the harmlessness of EC is still to be fully proven. In 2016 an improvement of the heating-not-burning device has been launched on the market as I-Quit-Ordinary-Smoking (iQOS, by Philip Morris). Although iQOS seem less harmful than TC, skepticism still remains as no study on proper comparison among TC, EC and iQOS devices is currently available to prove similarities or differences.
Recently, we have firstly conducted in literature a cross-over single-blind study on the impact of EC vs. TC, demonstrating an equal and unfavourable influence on the cardiovascular function parallel to increased oxidative stress and impaired endothelial function.
Here, we aim to compare in a new randomized controlled clinical trial the in vivo effects on cardiovascular function in TC, EC or iQOS users and to evaluate their potential biological effects on the angiogenic, epigenetic and oxidative-related profile by employing the in vitro model of circulating endothelial progenitor cells (EPCs) obtained from recruited subjects. Our study may provide new biological insights into the cardiovascular effects of both iQOS and EC also with high clinical and social relevance.
Tobacco-related diseases exert a tremendous and worldwide impact on individuals including young generations, therefore with huge consequences on the National Health System in every country (1).
The influence of tobacco on heart diseases is incontrovertible (2). The Word Heart Federation has reported that smoking increases the risk of stroke and coronary heart disease by 100% and the risk of death from undiagnosed coronary heart disease by 300% (3).
Among all potential cardiovascular associated-risk factors, smoking represents one of the most totally avoidable and preventable habit. Consequently, smoking cessation is the only gold standard solution. Yet, the scenario is more complicated, as tobacco addiction is based on multiple mechanisms of dependence. These latter are essentially related to the effects of nicotine itself on the vascular endothelial function in the whole body system, to the myriad of harmful products derived from the combustion of TC, but also to the combination of genetic background and epigenetic variations that affect cognitive responses to nicotine receptors. Accordingly, most smokers do not quit, although aware of long term detrimental effects of tobacco.
Nowadays, the control and the targeting of all biological and physiopathological mechanisms altered by smoking have not been efficiently achieved yet. Thus, the recommendation to stop smoking has been reinterpreted as a smoking-reduction approach. To date, this strategy seems more achievable. Our proposal is in line with this concept.
Since there is still a lack of evidence on both acute and chronic effects of novel marketed devices such as EC and iQOS on human health, the clarification of health risks associated, appears to be critical. Besides, it is noteworthy to highlight that independent studies on the use of EC and specifically on iQOS are infrequent (if not missing), as this topic is also strictly related to tobacco industry's interests and different smoking worldwide policies/bans. This could justify a discrete amount of conflicting data existing in literature.
Notably, our study will compare for the first time the acute effects of TC, EC and iQOS on the cardiovascular system in smokers. Results generated will be useful to provide a classification in accordance to the harmfulness of the specific device and in strict association with the circulatory system.
Our original recent publication in Chest has suggested that EC negatively influence the acute cardiovascular response, showing comparable effects for some extent to those induced by TC (4). Considering that iQOS contains a certain amount of nicotine, we predict a significant degree of difference between groups, likely to be TC
Finally, our proposal will only assess acute effects. However, our results will represent a first significant platform to explore chronic effects in future, but also to understand the modality by which these novel marketed devices may predispose to the progression of CV-associated health consequences.
References
1. Hecht 55. Nat Rev Cancer. 2003;3:733-744.
2. Robertson JO et al. JACC Cardiovasc lnterv. 2014;7(4):372-379
3.www.wordl-heartfederation.org
4. Carnevale R, et al. Chest. 2016 150:606-612
5. Auer R et al. JAMA Intern Med 2017