key: cord-260402-9b1ltcf1
authors: Lang, Adam Edward; Yakhkind, Aleksandra
title: More Than Meets the Eye: The Similarities Between COVID-19 and Smoking
date: 2020-08-11
journal: Mayo Clin Proc
DOI: 10.1016/j.mayocp.2020.08.008
sha: 
doc_id: 260402
cord_uid: 9b1ltcf1

nan

To the Editor: Research shows that cigarette smoking upregulates ACE2, the receptor by which SARS-CoV-2 gains entry to the host resulting in COVID-19, in the lungs and therefore potentially leads to increased morbidity [1] . However, the virus and smoking share far more similarities than meet the eye.

As part of a tobacco treatment campaign implemented at the beginning of the pandemic at McDonald Army Health Center, the authors performed a literature search and found that SARS-CoV-2 and smoking both contribute to myocarditis, thrombosis, immune impairment, and increased inflammation. SARS-CoV-2 leads to an increase NF-κB, TNF-alpha, and lymphocyte dysregulation. Smoking leads to an increase of neutrophil counts and can cause neutrophil-to-lymphocyte ratio elevation. Together, this can contribute to the development of and worse outcomes in patients with ARDS [2] .

Fibrin deposition in pulmonary vasculature, which is increased in both COVID-19 and smoking, is thought to contribute to the development of ARDS. Tissue Factor (TF), which initiates the extrinsic coagulation cascade, is expressed highly by alveolar macrophages and epithelial cells. Inflammatory cytokines and regulators including TNF-α and NF-κB upregulate TF expression, leading to fibrin deposition, further inflammation and microvascular permeability in the lungs [3] . SARS-CoV-2 and smoking upregulate this cytokine release and lead to an increased risk of coagulopathy [4, 5] .

The upregulation of ACE2 in smokers may predispose this population to an increased risk of SARS-CoV-2 infection. The host cell transmembrane protease, serine 2 (TMPSRSS2), which primes the SAR-CoV-2 S protein for entry, may also be upregulated in smokers [6] , which would further increase the odds of viral infectivity.

From a cardiovascular perspective, NT-proBNP, LDH and ferritin have been shown to be predictors of poor outcomes and cardiac tissue damage in those with COVID-19 [7] . Smoking has been shown to cause elevations in all of these parameters, potentially contributing to the detrimental impact of SARS-CoV-2 on the myocardium [8] [9] [10] .

While the lungs are a gateway to the body for both tobacco smoke and SARS-CoV-2, they each exhibit harmful systemic effects throughout the body. Our goal is to bring awareness to the similar and potentially synergistic ways in which smoking and SARS-CoV-2 cause harm in order to guide research and work towards a better understanding of both conditions. 

ACE-2 expression in the small airway epithelia of smokers and COPD patients: implications for COVID-19

COVID-19 and Smoking: How and Why We Implemented a Tobacco Treatment Campaign

Therapeutic modulation of coagulation and fibrinolysis in acute lung injury and the acute respiratory distress syndrome

ISTH interim guidance on recognition and management of coagulopathy in COVID-19

Acute effects of cigarette smoking on platelet-dependent thrombin generation

Smoking-Mediated Upregulation of the Androgen Pathway Leads to Increased SARS-CoV-2 Susceptibility

Mild versus severe COVID-19: Laboratory Markers

Serum and Salivary Lactate Dehydryogenase Levels as Biomarkers of Tissue Damage Among Cigarette Smokers

Association of serum ferritin levels with smoking and lung function in the Korean adult population: analysis of the fourth and fifth Korean National Health and Nutrition Examination Survey

Relation of Smoking Status to Serum Levels of N-Terminal Pro-Brain Natriuretic Peptide in Middle-Aged Men Without Overt Cardiovascular Disease

J o u r n a l P r e -p r o o f 
