COVID-19 and tobacco use

It is generally accepted that tobacco products are linked to a higher incidence of respiratory symptoms, heart disease and cancers. During the pandemic a smoking habit can be an additional compromise on the body’s immune and respiratory systems.


The hand to mouth direct contact in substance abusers, augmented salivary secretion, the sharing of a cigarette and, in some cases, constant spitting during chewing and expectoration,  can offer a portal of entry for the virus. The chemical carcinogens in tobacco affect the lining oral epithelium and the excretory ducts of the salivary glands. The excretory ducts of the salivary glands can be infected by SARS-CoV-2 and can be a reservoir for the virus in saliva.1,2


Tobacco induced hyposalivation can decrease the antiviral salivary action, compromise the innate immune system and be a risk factor for respiratory infections, including COVID-19. Smokers harbour constantly higher levels of the SARS-CoV-2 receptor ACE2 in their respiratory tracts due to chronic smoke exposure. This contributes to the up-regulation of inflammatory signalling linked to ACE2 expression and expansion of the population of secretory (goblet) cells.3


The byproducts of the tobacco flame can injure the endothelial cells and disrupt the lung cell homeostasis. The emission of aerosols from E-cigarettes that burn at a lower temperature is a conducive environment for the virus.4 The hand to mouth practice and the aerosols generated during smoking are likely to make an individual more susceptable to the virus. The need  to smoke and, in some communities, the practice of manual grinding and placing betel quid into the gingivobuccal sulcus may result in minimal use of a face mask.


The proclivity of the virus to the ACE2 receptor which is widely expressed in multiple tissue and organ systems may explain its manifold attack. During lockdown, stress and loss of jobs, means that people engage in altered lifestyles and risky behaviours, such as substance abuse. COVID-19 data attests quite equitably that tobacco smoking may significantly add to the expression of angiotensin-converting enzyme 2 (ACE2), the primary receptor of the novel coronavirus at the surface of many cell types, including respiratory epithelia. A seminal study by Sama et al (2020) found that circulating ACE2 is higher in men than in women and patients with diabetes or cardiovascular diseases.5


Smokers should be encouraged and supported to quit, particularly during the COVID-19 pandemic.



1. Xu R, Cui B, Duan X et al. Saliva: potential diagnostic value and transmission of 2019-nCoV. Int J Oral Sci. 2020;12(1):1-6 doi:10.1038/s41368-020-0080-z

2. Fini MB. Oral saliva and COVID-19. Oral Oncol. 2020; 27:104821.

3. Smith JC, Sausville EL, Girish V et al. Cigarette smoke exposure and inflammatory signaling increase the expression of the SARS-CoV-2 receptor ACE2 in the respiratory tract. Dev Cell. 2020;53(5):514-529.

4. Thorne D, Dalrymple A, Dillon D et al. A comparative assessment of cigarette smoke aerosols using an in vitro air–liquid interface cytotoxicity test. Inhalation toxicol. 2015;27(12):629-640.

5.Sama IE, Ravera A, Santema BT et al. Circulating plasma concentrations of angiotensin-converting enzyme 2 in men and women with heart failure and effects of renin–angiotensin–aldosterone inhibitors. European Heart J. 2020;41(19):1810-1817.




Manipal College of dental sciences

Light house, Hill Road ,Mangalore

Manipal academy of higher education. A constituent of MAHE




School of dentistry, Tehran University of Medical sciences, Tehran, Iran

Master of Health Promotion

Oklahoma State University Stillwater, OK, USA




Dept. of Head and Neck Oncology,

Health Care Global Enterprises Ltd, Bangalore, India




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