While cigarette smoking still remains one of the most pressing global health issues of our time, newer forms of smoking device have been introduced across the globe in the last decade [1]. Electronic nicotine/non-nicotine delivery systems commonly known as electronic cigarettes (eCig) heat a solution (e-liquid) to create vapour [2]; the latest addition to this list is the introduction of heat-not-burn (HNBs) tobacco products branded as IQOS [3]. HNBs are hybrids between eCigs and traditional cigarettes i.e. they are equipped with a device that heats the product, without burning to generate aerosol and the product being heated is not a liquid but real tobacco [4, 5]. eCig vaping is comparatively new but its use is increasing at an alarming rate; it is believed it will surpass the use of traditional cigarettes in next 5 years, with global sales reaching US$10 billion [6]. Since its launch in Italy and Japan in 2014, IQOS has become the leader in the HNB market [4, 7]. To date, IQOS is available in 41 countries, including 22 from the WHO-European region, and its market share has now reached the level of cigars in Italy [4]. Emerging data shows that eCig use, particularly in the young, is associated with future cigarette use [8]. Similarly, over half of the people interested in IQOS are never-smokers [4]. Therefore, both eCigs and IQOS may represent a gateway for nicotine addiction among never-smokers rather than a substitute used for harm-reduction purposes in current smokers [4]. It is now clear that eCig vapour contains high levels of toxic compounds [9], which adversely affect respiratory, gastrointestinal and cardiovascular systems both in vitro and in vivo [10–12]. It is also important to recognise that IQOS products are comparatively new but emerging research suggests that IQOS emits substantially high levels of carbonyls [13]. There is as yet no published comparison between the effect of eCigs, IQOS and tobacco smoke on human lungs. Here, we examine whether exposure to IQOS has the same damaging effect on human airway epithelial and smooth muscle cells as traditional tobacco cigarette and eCigs in vitro.

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The COVID-19 pandemic has affected over 114 million people and has resulted in >2.5 million deaths so far. Some people have greater susceptibility which influences both SARS-CoV-2 infectivity and COVID-19 severity. Smoking is associated with increased ACE-2, the receptor for SARS-CoV-2, which facilitates its entry through the lung. However, despite the widespread use of e-cigarettes, also known as ‘vaping’, little is known regarding the effects of vaping on ACE-2 expression and how this affects SARS-CoV-2 infection. In addition, the added effect of nicotine in the vapor is also unknown. Thus, we tested whether vaping induces ACE-2 expression in the mouse lung. BALB/c mice exposed to e-cigarette vapor (±nicotine) resulted in a significant increase in peribronchiolar inflammation and influx of immune cells into the airways. Vapor increased monocyte chemoattractant protein-1, interleukin 1β, and KC levels in bronchoalveolar lavage fluid in both sexes, which were further enhanced by nicotine (whereas increase in interleukin 6 was sex and nicotine independent). The reduction in basal inspiratory capacity with vapor exposure occurred independent of sex or nicotine. The increase in methacholine-induced airway hyper-responsiveness was independent of sex; however, in female mice it was only significant in the nicotine-exposed group. Lung ACE-2 expression was increased in male mice in a nicotine-dependent manner as compared with female mice. Collectively, while vaping (±nicotine) induced airway inflammation and impaired lung function, the induction of lung ACE-2 occurred to a significantly greater degree in males exposed to vapor containing nicotine as compared with females. Thus, via these effects on ACE-2 expression in the lungs and airways, vaping itself may facilitate SARS-CoV-2 entry into the airways.