Over the last few years, new tobacco or nicotine presentations such as electronic cigarettes, heated tobacco products or nicotine sachets for oral use have been introduced in our environment. The use of these new products does not require them to be subjected to temperatures as high as those produced by smoking a conventional cigarette and are therefore often advertised with the promise of generating non-combustion emissions, containing mainly harmless substances such as water vapour, or posing up to 95% less health risk compared to conventional tobacco use.

The recently published study assessed different epigenetic changes in samples from the mouth, cervix and blood of people who had reported a previous history of using smoked tobacco, e-cigarettes or oral tobacco products such as snus. The authors found a higher frequency of DNA alterations associated with the development of different forms of cancer in samples from smokers, which were attenuated in samples from those who had quit smoking. Epigenetic changes were also found in samples from non-smokers who had used e-cigarettes or oral tobacco products, suggesting that continued use of these products has some of the carcinogenic effects of tobacco on DNA.   

Although further research is needed to complement the results of this observational study, these new findings show possible carcinogenic effects of e-cigarettes and complement a recent review that showed that continued use is associated with an increase in cardiovascular disease and metabolic disease similar to that caused by conventional cigarettes, and a substantial increase in respiratory and oral pathologies somewhat less than that seen among those who exclusively smoke tobacco. The health harms associated with dual use of e-cigarettes and conventional cigarettes have also been shown to be even greater than those caused by the use of each of these products separately.  

The accumulated evidence on the health effects of the use of e-cigarettes justifies the convenience of reinforcing the control of their advertising, sale and consumption, in order to protect young people and adolescents, their main users. E-cigarettes are not a safe tool to quit smoking or reduce the risks of tobacco use. 

This interesting study shows e-cigarette use is associated with similar damaging changes in methylation in human cells as smoking. Although it doesn’t show a direct causal effect, this study shows that further research must be done to understand the effects of e-cigarettes on human health and whether they could be linked to an increased risk of cancer.

This international study used a relatively large number of samples (N>3,500), collected from different sites (saliva, blood, cervix) and comprising different cell types (epithelial, immune and lymphoid), to assess epigenetic changes that may be associated with cancer development. The study included current, ex- and never smokers, and also included a subsample of vapers (N=116) who had never regularly smoked cigarettes. 
This comprehensive analysis confirms well-known epigenetic changes associated with smoking observed in blood, extending this to saliva and specific cell types, as well as identifying novel associations with cigarette smoking, which are also seen in separate cancer tissue and early lesion samples. Crucially, some of the epigenetic changes were also observed in saliva samples from vapers, albeit to a lesser extent and not across all cell types.
While this study provides useful information about potential corollaries of e-cigarette use also seen with cigarettes, which need to be studied further, in my mind this does not provide proof that e-cigarettes cause cancer for several reasons: 

1. It is difficult to assess the extent to which the changes seen here translate into actual cancer development. Most cancers involve complex multicellular and multistep processes involving different biological systems, which can include epigenetic changes. However, these alone are unlikely to tell the whole story. 
2. The changes reported here are based on differences seen in smokers, some of which are also replicated in a smaller group of vapers. However, such similarities could be the result of confounding (e.g., if vapers are more likely to engage in a variety of unmeasured harmful behaviours that may drive epigenetic change seen in smokers). This study did not assess or control for this kind of confounding, which is compounded by the fact that the participants from the different datasets used here provided samples from different sites and likely varied in important characteristics. 
3. Because the group of vapers studied was relatively small, it was not possible to link epigenetic changes to vaping exposure in a clear dose-response manner. While the authors looked at vaping duration, there is only limited evidence that longer duration was associated with greater changes. 
4. The paper does not assess epigenetic changes unique to e-cigarettes but looked at those seen in smokers. This is of importance as we already know that e-cigarettes, compared with cigarettes, expose users to much lower levels of known tobacco-related carcinogens that drive cancer (in part because e-cigarettes do not involve combustion, which generates high levels of harmful chemicals seen in tobacco smoke). This means that the health consequences (and underlying causative processes) of e-cigarette use may be quite distinct from those of cigarettes use. These e-cigarette-specific changes need to be investigated in their own right.

Notwithstanding these limitations, the findings in this paper highlight the continued need to elucidate the potential impact of vaping on disease, including assessing effects distinct from tobacco exposure. It is important to remember that e-cigarettes are a harm reduction product, not a risk-free product, aimed at those using uniquely harmful cigarettes. This paper does not change this risk calculus and serves to underscore the CMO's advice: ‘if you smoke, vaping is much safer; if you don't smoke, don't vape’.