Smoking is a worldwide healthy issue, concerning millions of people including youth individuals with a serious impact 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 subjects to quit. In order to minimize
smoking-related damages, modern strategies essentially based on surrogates of traditional tobacco products, have been developed.
Accordingly, Electronic Cigarettes (EC), a technological surrogate of traditional tobacco cigarettes (TC) has been firtly marketed in 2004. As EC employ heat to convert nicotine or flavored nicotine-free solutions into vapour avoiding combustion, in theory they should represent a much less harmful alternative to TC. Despite this apparent advantage, the harmlessness of EC is still to be fully proven. In 2016 an improvement of these devices has been launched on the market as I-Quit-Ordinary-Smoking (iQOS 2.2, by Philip Morris). However little independent research on the heat-not-burn Tobacco Heating System 2.2 (THS2.2, IQOS) has been reported. Since 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, in particular on oxidative stress and on endothelial function, we aim to compare in a new randomized controlled clinical trial the in vivo effects on cardiovascular and pulmonar function of TC, EC or iQOS.
Our study may provide new biological insights into the cardiovascular effects of both iQOS and EC 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 of every country (1).
Furthermore, 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 solution in order to prevent CV tobacco related diseases. 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 or as an alternative, less harmful 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 missing, as this topic is also strictly related to tobacco industry 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 cardiovascular system.
Our original recent publication in Chest has suggested that EC negatively influence the cardiovascular system, 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
response. Accordingly, we already demonstrated that both EC and TC similarly reduce FMD and that EC is able to increase oxidative
stress, therefore contributing to vascular damage (4). Nevertheless, this supposed similarity will not necessarily reflect the deeper
modifications into biological mechanisms altered by the new smoking devices, especially those related to cardiovascular epigenetic
modifications, which represent a key imprinting on the genome of individuals in the long term. In fact, so far our preliminary data show
that TC alters the expression of specific cardiac-related circulating miRNAs in acute phase response to smoking. However, angiogenic
and epigenetic biological changes in iQOS devices have been never verified. Accordingly, a very recent report has highlighted the need
to revoke information about the new iQOS device, which is profoundly questioned regarding potential toxic compounds released even
in presence of incomplete combustion (pyrolysis) (5), which seems not to guarantee the safety of the device.
Besides, our study will verify the effects of a single nicotine containing TC, EC and iQOS, without discriminating among additives
and/or flavours, as a deeper understanding of the real negative impact of smoking on vascular function can be achieved only if we examine the smoking devices in their entirely. In fact, the synergic effects of nicotine and other hazardous products during smoking could be far more important than the effects of single products on the cardiovascular function.
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