Smoking is significantly associated with high mortality rates for infection or respiratory diseases, through a detrimental action on the immune system and direct lung injury. It could also have an impact on the ACE, implicated in COVID-19 (Berlin et al., 2020). In many lung cells, nicotinic receptors are co-expressed with most components of the RAS (Olds and Kabbani, 2020). ACE2-mediated activation drives epigenetic changes that underlie lung damage (Cai, 2020a). These pathways are also activated by nicotinic receptors. Thus, cigarette smoking induces a dose dependent up regulation of the natural SARS-CoV-2 receptor ACE2 in human cells (Cai et al., 2020), and increases the severity of COVID-19 associated inflammatory response (Ab et al., 2020). However, increased expression of ACE2 may also attenuate the risk of developing devastating lung and systemic injuries, characterizing severe and critical forms of COVID-19 (Lippi et al., 2020), and nicotine has also an anti-inflammatory potential (Polosa and Caci, 2020). There are few data concerning the sole effect of nicotine (substitute treatments) and its interaction with the ACE. Studies on the effects of e-cigarettes' electronic nicotine delivery systems
