COVID-19: a pandemic converged with global tobacco epidemic and widespread vaping-state of the evidence

Abstract

This review highlights the convergence of three global health challenges at a crossroad where the pandemic of coronavirus disease 2019 (COVID-19) meets the tobacco epidemic and vaping. It begins with an overview of the current knowledge on the biology, pathophysiology and epidemiology of COVID-19. It then presents the state of smoking and vaping during the pandemic by summarizing the published data on prevalence, use patterns, product availability/accessibility, sales records and motivation to quit before and after the start of the pandemic. It highlights the state of evidence on the association of tobacco product use with COVID-19 infection and transmission rates, symptom severity and clinical outcomes. Also discussed are proposed biological mechanisms and behavioral factors that may modulate COVID-19 risk in tobacco product users. Furthermore, competing hypotheses on the protective effect of nicotine against COVID-19 as well as the claimed 'smokers' paradox' are discussed. Considerations and challenges of COVID-19 vaccination in tobacco product users are underscored. Collectively, the present data show an 'incomplete' but rapidly shaping picture on the association of tobacco product use and COVID-19 infection, disease course and clinical outcomes. Evidence is also growing on the mechanisms by which tobacco product use may contribute to COVID-19 pathophysiology. Although we await definitive conclusions on the relative risk of COVID-19 infection in tobacco product users, compelling data confirm that many comorbidities associated with/caused by smoking predispose to COVID-19 infection, severe disease and poor prognosis. Additionally, it is becoming increasing clear that should smokers get the disease, they are more likely to have serious health consequences.

Graphical abstract

Figure 1.

The interplay of tobacco product use and COVID-19. Arrows indicate that comorbidities shown within circles are associated with tobacco product use (smoking). These comorbidities include COPD, cancer, CVD, chronic kidney disease, type 2 diabetes mellitus and obesity. The overlapping of ‘comorbidities’ with ‘COVID-19 risk and disease course and clinical outcomes’ represents ‘association’, not ‘causality’.

Figure 2.

Schematic diagram of SARS-CoV-2 lifecycle and host cell infection. The spike protein of SARS-CoV-2 binds to ACE2 receptors in host cells (i.e. attachment). The proteolytic function of transmembrane protease, serine 2 (TMPRSS2) cleaves the spike protein (i.e. activation), thus allowing entry and viral replication in the host cell, and subsequent release of the infectious virus into the intercellular milieu. This is a simplified diagram of the highly complex life cycle of SARS-CoV-2, which causes COVID-19; interested readers are referred to elegant references (12,40) for detailed information.