Tobacco smoking in the age of COVID-19
COVID-19 is predominantly a disease of the respiratory tract, with emerging evidence indicating that cellular entry, viral replication and virion shedding occur within the respiratory tract, more specifically in mucosal epithelial cells and the lung alveolar tissue.
A Chinese study published in The New England Journal of Medicine in February 2020 and based on a sample of 1,099 confirmed cases of COVID-19 reported that 12.4% (17/137) of smokers, who had a severe clinical outcome, required intensive care or mechanical ventilation, compared with 4.7% (44/927) of non-smokers.
Definitive evidence that current smokers are at increased risk of disease, morbidity and mortality from COVID-19 is not yet available, but further consideration on this matter would be necessary and useful.
Several studies conducted in the past have shown that smokers are prone to a greater number and severity of viral infections, including respiratory syncytial virus infections. The mechanism for this increased susceptibility is not fully known, but several researches indicate that, in viral infections, cigarette smoke causes cellular necrosis rather than apoptosis, leading to increased inflammation and viral replication.
It is worth remembering that apoptosis, or programmed cell death, is a host cell mechanism that limits viral replication. Therefore, the type of cell death that occurs in response to viral infection (apoptosis versus necrosis) is an important determinant of viral survival, replication and inflammation. Compared to necrosis, apoptosis is an efficient way to rid the airway of virally infected cells, and is associated with a less significant inflammatory response. Indeed, when necrotic cells burst, the virus is released and not contained as is the case in apoptosis.
In this respect, several studies have shown that cigarette smoke causes necrosis rather than apoptosis, and that this is associated with increased viral replication. Cigarette smoke contains thousands of compounds and many of its harmful effects have been attributed to unsaturated aldehydes, such as acrolein, and nitrogen monoxide. These effects include inhibiting neutrophil activation and apoptosis and converting lymphocyte apoptosis to necrosis. However, it is has been proved that cigarette smoke components can alter apoptosis in various ways, depending on the specific component and cell type.
With regard to a potential increased risk among smokers of becoming infected with SARS-CoV-2 (the virus responsible for COVID-19), it is important to remember that smoking involves repetitive hand-to-face movements, which also provide a route of entry for the virus.
- Article “Clinical Characteristics of Coronavirus Disease 2019 in China” published in The New England Journal of Medicine in February 2020
- Pages of the ISS website dedicated to the Anti-smoking toll-free number (TVF) 800 554088 of the National Observatory for Smoking, Alcohol and Drugs (in Italian)