Early on during the coronavirus pandemic, an interesting, counterintuitive hypothesis emerged that nicotine may prevent symptomatic COVID-19 infection from worsening.
A June 2020 study co-authored by French researchers concluded, “Based on the current scientific literature and on new epidemiological data … reveal that current smoking status appears to be a protective factor against the infection by SARS-CoV-2.”
Really … smoking is good for you, at least when it comes to preventing severe COVID-19 symptoms?
Unfortunately for smokers, one year later, the nicotinic hypothesis may prove to be wrong. While isolating the nicotine chemical compound may prove to be beneficial in treating respiratory distress, smoking, according to a new study, increases the ability of the SARS-CoV-2 spike protein to bind to the ACE2 receptor. The ACE2 receptor is the host cell site where the potentially damaging spike protein first tries to enter the cells.
Despite the early so-called nicotinic hypothesis, the latest research demonstrates a solid association between smoking and symptomatic COVID-19. This is true for both combustible nicotine (regular cigarettes) and e-cigarettes (vaping).
The researchers observed that both smoking and vaping increases the risk for influenza and other respiratory viruses, and that smokers have higher levels of ACE2, News-Medical.net reports.
Some people may incorrectly believe that vaping is healthier than inhaling nicotine via combustible cigarettes. However, electronic nicotine delivery, the researchers note, causes toxicity in the lung tissue via the synthesis of noxious proteins as well as through immunologic alterations.
Smokers, traditional and vape enthusiasts alike, showed markedly higher levels of ACE2 as compared to non-smokers of the same age, according to the study. Furthermore, cell cultures revealed that exposure to cigarette smoke for just one day led to a significant increase in levels of ACE2. And the higher levels of ACE2, the more entry points the spike protein has to infect human cells.
The researchers were able to create cell cultures that simulated human lung tissue. In these synthetic respiratory cell lines, the researchers exposed a pseudovirus to cigarette smoke. The observation that smoking leads to increased levels of ACE2 was replicated when the cells were exposed to the e-liquid (vape juice) from JUUL Virginia Tobacco-flavored vapes, which contains 5% nicotine benzoate.