Smoking and the likelihood of contracting SARS-CoV-2 and COVID-19

The risk of respiratory infections such as colds, influenza, pneumonia, and tuberculosis is increased by smoking. Smoking may also contribute to complications of coronavirus disease 2019 (COVID-19).

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Numerous previous studies have confirmed that smoking is detrimental to the lungs. Both the epithelium and vascular endothelium of the lungs are affected by the carcinogens in tobacco smoke.

Specifically, it appears that these substances directly harm the epithelial cells, thereby affecting the epithelial barrier and mucociliary clearance. In addition to these direct effects, damaged cells also release modified molecules into the lungs, which stimulate specific receptors and ultimately activate innate and acquired immune responses.

Despite growing interest in determining the relationship between smoking and COVID-19, researchers have been unable to devote sufficient time to this investigation due to the overwhelming number of COVID-19 patients. In spite of this, a recent study published in The Lancet Respiratory Medicine investigates the potential effects of tobacco use on the transmission of severe acute respiratory virus coronavirus 2 (SARS-CoV-2), the pathophysiological changes caused by tobacco use, and the effects of tobacco on immune and inflammatory responses to COVID-19.

About the research
The purpose of this study was to determine whether tobacco users are more likely to develop symptomatic SARS-CoV-2 infection and whether this patient population is at a greater risk of severe COVID-19 or associated mortality, long COVID, or a different vaccination response.

The researchers investigated the behavioural mechanisms of tobacco use on COVID-19 and inflammatory immune responses. In addition, they screened risk factors for the development of public health policies and the delivery of patient care.

The researchers searched the PubMed and Embase databases for articles on COVID-19 and smoking. In addition to searching Web of Science, PsycINFO, CINAHL, and Sociological Abstracts, duplicates and opinion pieces were eliminated.

The databases PubMed, Web of Science, Embase, CINAHL, PsychINFO, and Sociological Abstracts were searched again for articles published between December 9, 2020 and August 30, 2021 on COVID-19 and tobacco use. In total, 2,151 articles were chosen for examination.

Research findings
Epidemiological studies examining the effect of cigarette smoking on SARS-CoV-2 infection have produced contradictory findings. Therefore, additional research is required to determine whether smoking or the use of other tobacco products contributes to COVID-19 susceptibility.

It appears that smokers are more likely to experience negative outcomes associated with COVID-19, such as hospitalisation and disease progression. Tobacco use is associated with the severity of COVID-19; however, additional research is necessary to determine whether nicotine and non-nicotine tobacco product ingredients contribute to disease susceptibility.

The association between cigarette smoking and severe COVID-19 may be mediated by upregulation of angiotensin-converting enzyme 2 (ACE2) receptors, immune suppression, oxidative stress, inflammation, and vascular damage. Cigarette smoking increases the risk of chronic lung disease, cardiovascular disease, and diabetes, all of which increase the risk of COVID-19 severity.

Tobacco products contain a wide variety of potentially toxic chemicals, and during the aerosolization process, caused by heating or combustion, additional harmful chemicals are produced. Tobacco use can result in significant harm; however, it remains unclear how specific chemicals and constituents contribute to these pathophysiological effects.

In addition to impaired mucociliary clearance in the lungs, smokers may be more susceptible to increased lung permeability, impaired immune function, increased expression of ACE2, cardiovascular dysfunction, viral infections, and severe diseases.

Nicotine exerts an anti-inflammatory effect in a variety of pathological conditions by stimulating the cholinergic response. However, its role within the context of these conditions’ complex environment is poorly understood. In addition, the risk of SARS-CoV-2 transmission is increased by the sharing of tobacco products, passive smoking, and inhalation of e-cigarette aerosols.

Conclusions
In comparison to non-smokers, smokers are more susceptible to COVID-19 complications. To better shape public health recommendations and enhance the care of individuals with a history of tobacco dependence, a deeper understanding of the relationship between tobacco use and disease risk is required.

It will be essential for future studies to collect adequate data on tobacco product use. In addition, the development of a validated and standardised method for assessing the effect of tobacco use on COVID-19 susceptibility, disease severity, and the risk of other infectious diseases will be essential.

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