The SARS-CoV-2 virus that causes COVID-19 has been the paramount topic in the news, in family discussions, and around the water cooler (if people are still able to go to work and/or congregate around the water cooler). One important question is whether or not smoking and vaping increase someone’s risk of being infected by the virus and what effects can occur if that person is infected. The novel coronavirus is just that—very new. The fact that it is so new means there are very few peer-reviewed studies that can argue any side of the topic.
The goals of this article are to give a brief background on what has been found in regards to COVID-19 and its receptor sites in the lungs and to review what has been found with smoking and vaping in relation to the virus.
The respiratory system is a complex and sensitive set of structures that allow for transportation, filtration, and humidification of air. The upper airway protects against microorganisms and toxins that could potentially cause harm to the individual. To this end, they have a complex structure with cartilaginous elements anteriorly for structural support and a collapsing posterior wall to enable high airspeed velocity during coughing, nervous system innervation, a smooth muscle layer to facilitate bronchoconstriction, glands and surface epithelia that produce a mucous layer that hydrates the underlying epithelium and traps microbes, cilia that transport mucus away from the alveolar space, and extensive lymphatics (Gotts). In contrast, the alveoli are delicate structures lined by thin alveolar type 1 epithelial cells and surfactant producing alveolar type 2 cells, along with alveolar macrophages (Gotts). A single fused basement membrane separates the alveolar epithelium and capillary endothelium, yielding a remarkably thin alveolar-capillary barrier of approximately 5 μm to facilitate gas diffusion (Tsunoda).
The term “coronaviruses” arose from their crown-like appearance when imaged, the Latin for crown being corona (Brake). The distinguishing crown-like feature of coronaviruses is attributed to the presence of large type 1 transmembrane spike (S) glycoproteins (Brake). This heavily glycosylated cell surface protein contains 2 distinct functional domains (S1 and S2), which are thought to mediate host cell entry by the virus (Brake). The S1 domain contains the angiotensin-converting enzyme-2 (ACE2) receptor-binding domain and is responsible for first-stage host cell entry (Li). The ACE2 receptor provides a human cell-binding site for the S protein for the SARS-coronavirus (SARS-CoV) (a virus that was first identified in 2003 in a southern province of China), the coronavirus NL63, and now SARS-CoV-2 (NCBI).
The attachment of the virus to cell surface ACE2 protects them from immune surveillance mechanisms, leaving them tagged to the host for relatively longer periods, thus making them an efficient carrier and vulnerable host for future infections and spread (Brake). The eventual engulfment of ACE2 further provides the virus access to the host cells system, thus providing a flourishing environment, not just to sustain and proliferate but also to mutate and modify host evasion mechanisms (Brake).
The ACE2 protein is expressed on the surface of lung type-2 pneumocytes, and it could thus act as a novel adhesion molecule for Covid-19 and be a potential therapeutic target for the prevention of fatal microbial infections in the community (Brake).
In summary, the ACE2 receptor sites are responsible for the attachment of the virus in the lungs and protect the virus once attached. This enables the virus to replicate and evade the host’s natural immune system. Further research could determine if the ACE2 receptor could be an area to prevent virus attachment and proliferation.
An early suggestion is that ACE2 is upregulated on the airway epithelium of smokers (Brake). ACE2 is expressed explicitly in type-2 pneumocytes, in which genes regulating viral reproduction and transmission are highly expressed, and this indicates that smokers may be more susceptible to infection by SARS-CoV-2, and possibly Covid-19 (Zhao). In one study, smoke-induced changes in ACE2 expression correlated with essential biological processes including viral processes and immune response, indicating that ACE2 is involved in virus infection and immune response (Wang).
Analysis of deaths from coronavirus in China shows that men are more likely to die than women, something that may be related to the fact that many more Chinese men smoke than women (Glantz). Among Chinese patients diagnosed with COVID-19-associated pneumonia, the odds of disease progression (including to death) were 14 times higher among people with a history of smoking compared to those who did not smoke (Glantz). Wang reported that cigarette smoke could induce elevated ACE2 expression in the respiratory tract, indicating that smokers have a higher susceptibility to COVID-19 than non-smokers.
Smokers, as a vulnerable group, must be supported to quit and should be advised to avoid areas where they may be liable to be exposed to Covid-19, especially smokers with pre-existing respiratory health concerns. Smokers should be prioritized for vaccination when a vaccine is developed, particularly if it is found they are a key transmission source (Brake).
The increase seen in smokers further raises the question of whether this is also true for people engaged in waterpipe smoking (Meo) and those switching over to the more recent alternatives such as electronic cigarettes and “heat-not-burn” IQOS devices (Brake). It is essential to recognize that these devices are not “safer,” they are still a tobacco product that produces vapor or smoke and similarly could cause infectious lung damage as we see with traditional cigarettes (Sohal).
Emerging evidence suggests that exposure to aerosols from e-cigarettes harms the cells of the lung and diminishes the ability to respond to infection (Glantz). Nasal scrape biopsies from non-smokers, smokers, and vapers showed extensive immunosuppression at the gene level with e-cigarette use (Martin). Healthy non-smokers were exposed to e-cigarette aerosol, and bronchoalveolar lavage was obtained to study alveolar macrophages (Staudt). The expression of more than 60 genes was altered in e-cigarette users’ alveolar macrophages after just 20 puffs, including genes involved in inflammation (Glantz).
Even though it may seem like common sense that vaping is as dangerous as smoking, the proper studies have not been done to prove that statement. To date, no long-term vaping toxicological/safety studies have been done in humans; without these data, saying with certainty that e-cigarettes are safer than combustible cigarettes is impossible (Gotts). Given the survey data showing increased symptoms of respiratory disease and the many lines of human, animal, and in vitro experimental evidence that e-cigarette aerosol can negatively affect multiple aspects of lung cellular and organ physiology and immune function, e-cigarettes will likely prove to have at least some pulmonary toxicity with chronic and possibly even short-term use (Gotts).
An important question to answer right now is whether or not vapers have a higher risk of infection with SARS-CoV-2 virus, and once infected, is their disease progression any different than a smoker’s, non-smoker’s, or never-smoker’s? The answer could help stop the spread of COVID-19 by individuals who think they are not at any higher risk than non-smokers.
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Dan Bunker DNAP, MSNA, CRNA—Dan has worked in the healthcare industry for nearly 30 years. He worked as a registered nurse in the Coronary Care ICU for 7 years and was a flight nurse with Intermountain’s Life Flight for nearly 10 years. He has been a Certified Registered Nurse Anesthetist (CRNA) for 11 years working in the hospital settings as well as maintaining his own private practice. In addition, he is a professor in the nurse anesthesia program at Westminster College in Salt Lake City, Utah. He has served in various leadership roles within the Utah Association of Nurse Anesthetists (UANA) and current president-elect.