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    Man smoking E-Cigarette.

    Do a few puffs on an e-cigarette raise your risk of heart disease?

    6 December 2016

    It has been claimed that just 10 puffs on an e-cigarette is enough to trigger physiological changes that can lead to heart disease (but see our analysis below).

    Researchers from the Karolinska Institute in Stockholm say that inhaling e-cig vapour leads to a ‘rapid rise’ in levels of endothelial progenitor cells (EPC), which is indicative of damage to the inner lining of blood vessels, which can cause hardening of the arteries.

    During the study, which has been published in the journal Atherosclerosis, the researchers examined 16 ‘occasional smokers’ of traditional cigarettes as they took 10 puffs on an e-cigarette.

    Within an hour the rise in EPC levels had been observed. EPC levels were found to remain higher than normal for 24 hours.

    The study’s authors acknowledge the limitations of their research, saying: ’While it is an important finding that only few puffs of an electronic cigarette can induce a biological response that appears qualitatively similar to cigarette smoke, it is not clear how dangerous this is and whether this response is due to nicotine or other factors associated with the electronic cigarette use.

    ‘Therefore, it is one of the major limitations of the article that no “nicotine free” control was used to dissect the effects of nicotine from the effects of electronic cigarette vapour, including components in the liquid other than nicotine or particulate matter.’

    Instant analysis
    This was a small study of 16 healthy volunteers to assess possible harms of using electronic cigarettes on blood vessels. There were two groups, randomly allocated by chance, and both groups were exposed to 10 puffs of an electronic cigarette. Researchers then measured levels of different cells that play key roles in the regeneration of the lining of blood vessels, called endothelial progenitor cells (EPCs), and can lead to atherosclerosis — that is, the build-up of fatty plaques.

    It was demonstrated that such exposure to electronic cigarette smoke did indeed increase the levels of EPCs measured at one hour. (At 24 hours they had fallen back to normal levels.)

    However, it is not clear why. Is this simply due to nicotine, and therefore would also be found with other harm reduction strategies such as nicotine patches or gum? Or is it due to other constituents in the vapour? Is this more or less than found with traditional cigarettes?

    Such findings would also need replicating in groups several magnitudes of order greater before we can apply these results to the real world. And they may still be due to chance. Indeed, tobacco and e-cigarette smoke, both active and passive, would need to be compared to see which causes more harm. But obtaining ethical approval for such a study would be challenging.

    Finally, the possible harms of cigarette smoking — atherosclerosis, high blood pressure, heart attacks, stroke and death — accrue over months to years, not minutes to hours. This is something this research cannot address.

    Based on this study, e-cigarettes still represent the lesser of two evils when compared to the evidence of overwhelming harm from tobacco smoke. But more research is needed on the long-term harms of e-cigarettes, both to the cardiovascular and respiratory systems. Furthermore, it remains difficult to say if e-cigarettes or other forms of nicotine replacement are safer than another.
    DW
    Research score: 2/5