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Are Smoking, Environmental Pollution, and Weather Conditions Risk Factors for COVID-19? José Miguel Chatkin1a, Irma Godoy2a

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Are Smoking, Environmental Pollution, and Weather Conditions Risk Factors for COVID-19? José Miguel Chatkin1a, Irma Godoy2a J Bras Pneumol. 2020;46(5):e20200183 https://dx.doi.org/10.36416/1806-3756/e20200183 REVIEW ARTICLE Are smoking, environmental pollution, and weather conditions risk factors for COVID-19? José Miguel Chatkin1a, Irma Godoy2a 1. Departamento de Medicina Interna ABSTRACT e Pneumologia, Escola de Medicina, Pontifícia Universidade Católica do Rio Coronavirus disease 2019 (COVID-19), caused by the highly contagious severe acute Grande do Sul, Porto Alegre (RS) Brasil. respiratory syndrome coronavirus 2 (SARS-CoV-2), is probably systemic, has a major 2. Disciplina de Pneumologia, respiratory component, and is transmitted by person-to-person contact, via airborne Departamento de Clínica Médica, droplets or aerosols. In the respiratory tract, the virus begins to replicate within cells, Faculdade de Medicina de Botucatu, after which the host starts shedding the virus. The individuals recognized as being at risk Universidade Estadual Paulista, Botucatu (SP) Brasil. for an unfavorable COVID-19 outcome are those > 60 years of age, those with chronic diseases such as diabetes mellitus, those with hypertension, and those with chronic lung Submitted: 20 April 2020. diseases, as well as those using chemotherapy, corticosteroids, or biological agents. Accepted: 27 May 2020. Some studies have suggested that infection with SARS-CoV-2 is associated with other Study carried out at the Escola de risk factors, such as smoking, external environmental pollution, and certain climatic Medicina, Pontifícia Universidade Católica conditions. The purpose of this narrative review was to perform a critical assessment of do Rio Grande do Sul, Porto Alegre (RS) the relationship between COVID-19 and these potential risk factors. and at the Faculdade de Medicina de Botucatu, Universidade Estadual Paulista, Keywords: Coronavirus infections; COVID-19; Air pollution; Smoking; Tobacco use Botucatu (SP) Brasil. disorder. INTRODUCTION SMOKING In recent decades, life-threatening viral epidemics Smoking has been associated with unfavorable outcomes have emerged in various regions of the world. Serious in COVID-19.(5,6) Smokers, who are more vulnerable to outbreaks of Ebola virus disease, severe acute respiratory respiratory viruses than are nonsmokers, have a greater syndrome coronavirus (SARS-CoV), and Middle Eastern risk of severe influenza infection and more severe clinical respiratory syndrome coronavirus (MERS-CoV), as well conditions. Therefore, smokers, when compared with as outbreaks of influenza, particularly more severe types nonsmokers, have a higher risk of hospitalization (OR of influenza, such as H1N1.(1) = 1.5; 95% CI: 1.3-1.7) and ICU admission (OR = 2.2; (7) Because of the severity and worldwide dissemination of 95% CI: 1.4-3.4) after having influenza infections. In the current outbreak of the new coronavirus (designated addition, during the MERS-CoV outbreak, smokers had SARS-CoV-2) infection, the World Health Organization higher mortality rates than did nonsmokers.(8,9) The use (WHO) has stated that the coronavirus disease 2019 of electronic cigarettes and heated tobacco devices have (COVID-19) has become a pandemic. On April 16, 2020, also been related to a higher frequency of respiratory COVID-19 had reached 210 countries and territories, having infections, especially viral ones.(10-15) caused over 100,000 deaths and infected approximately The mechanism of this increased susceptibility appears 2 million people, the overall fatality rate being 3.4%. to be multifactorial, including structural changes, such as Previous case-fatality rates for SARS-CoV and MERS-CoV increased permeability of the bronchial mucosa, impaired epidemics were 10% and 37%, respectively.(1) mucociliary clearance, greater pathogen adherence, COVID-19, Caused by a highly contagious virus,(2) is rupture of the respiratory epithelium, peribronchial probably systemic, has a major respiratory component, inflammation, and fibrosis. There is also a decrease in and is transmitted by person-to-person contact, via the production of antibodies and defense immune cells. airborne droplets or aerosols. In the respiratory tract, (10,16) In addition to those mechanisms, the association the virus begins to replicate within cells, after which the between SARS-CoV-2 and smoking can be facilitated by host starts shedding the virus.(3,4) the rituals of smoking, involving repeated hand-to-face (17) The role of smoking has been little remembered and movements. even less discussed in this current public health situation. Studies on respiratory syncytial virus, which has a Other factors, such as environmental pollution and similar structure to that of SARS-CoV-2, have shown climatic conditions, also need to be understood better. that inhaling tobacco smoke increases the rate of viral The purpose of this narrative review was to perform an transmission and the severity of infections, confirming assessment of the current knowledge about these risk the association between tobacco smoke and some viral factors and their importance in the COVID-19 pandemic. infections and possibly explaining the severity of COVID-19 Correspondence to: José Miguel Chatkin. Avenida Ipiranga, 6690, Sala 501, CEP 90610-000, Porto Alegre, RS, Brasil. Tel.: 55 51 3320-3378. Fax: 55 51 3320-3316. E-mail: [email protected] Financial support: None. 1/6 © 2020 Sociedade Brasileira de Pneumologia e Tisiologia ISSN 1806-3713 Chatkin JM, Godoy I in certain groups of individuals. Tobacco use has been order to clarify the association between the severity considered a risk factor for MERS-CoV.(18) of COVID-19 and current smoking. The need for clarification of that association was The possibility of this association has been investigated reinforced by the fact that the highest proportion of regarding biological aspects. The angiotensin-converting deaths from COVID-19 occurred in males in China.(19) enzyme 2 (ACE2) is likely to be related to the severity These finding might be related to the fact that the of symptoms and unfavorable outcomes of COVID-19. number of smokers, as well as their smoking history, SARS-CoV-2 penetrates human cells by binding to is a lot greater among males than among females in the extracellular domain of the ACE2 receptor. (31,32) (20) that country (288 million vs. 12.6 million in 2018). This enzyme acts on the renin-angiotensin system, This fact is likely to be at least a cofactor that increases fragmenting the molecule of angiotensin 2, a the chance of males to develop pulmonary, heart, and potent inflammatory and vasoconstrictor agent, and neoplastic diseases. These data are in line with the producing angiotensin-(1-7), which has a significant findings of the WHO-China Joint Mission on Coronavirus anti-inflammatory action.(33,34) Therefore, anti-ACE2 Disease 2019, which has reported higher case-fatality antibodies or the blockade of their receptor prevent the rates in men than in women (4.7% vs. 2.8%).(21-23) virus from binding, contributing to a greater severity Other studies have also reported a higher prevalence of the disease in the elderly, as well as in those with (24) of COVID-19 in men. Guan et al., evaluating 1,099 diabetes or hypertension.(35) In those groups of patients, critical patients with COVID-19 in 552 hospitals in 30 there is a clear decrease in the expression of ACE2, provinces in China, found a proportion of 58.1% of making it difficult to form degradation products, which (25) male patients. In addition, Yang et al. found that have anti-inflammatory action, whereas there would males accounted for 67% of the patients in their be greater amounts of ACE2, which is an inflammatory (26) sample. Liu et al. identified that tobacco use was agent. These two mechanisms could partially explain more frequent in the group of patients with unfavorable the greater severity of the clinical course of the outcomes when compared with nonsmokers (27.3% disease. Younger patients have a higher expression vs. 3.0%, p = 0.018).However, Zhang et al.,(27) of angiotensin-(1-7), which has anti-inflammatory evaluating 140 patients with COVID-19 in China, action, and tend to present with less severe disease, found no differences regarding gender. In that same although much more frequently.(35,36) publication, the authors reported only 1.4% of male patients as current smokers, although the proportion Smith & Sheltzer(37) found that samples of lung of cases with COPD included in the sample was much tissue collected from smokers had 40-50% more ACE2 higher. Guan et al.(24) showed a greater number of receptors than did those collected from nonsmokers, current smokers (12.6%) and former smokers (1.9%) even when the analysis was controlled for age, sex, in their study. Nevertheless, the authors could point race, and body mass index. Smokers with a history out that being a current smoker was significantly of > 80 pack-years showed a 100% increase in ACE2 related to presenting with more severe symptoms. The receptors when compared with smokers with a history small proportion of smokers in those two studies,(24,27) of < 20 pack-years. In that same study,(37) the authors when compared with the high prevalence of smoking found that smoking cessation led to decreased levels of in China (50.5%),(22) might indicate a smaller chance ACE2 in the lungs, i.e., the increase in the expression of an association of smoking with the incidence and of ACE2 was shown to be potentially reversible. severity of COVID-19.(20) This type of upregulation of ACE2 was also found in Two meta-analyses reached contradictory results. patients with idiopathic pulmonary fibrosis, but not Lippi et al.(28) identified no association between smoking in those with asthma, sarcoidosis, or cystic fibrosis, and disease severity. However, Vardavas & Nikitara(29) which reinforces the association of smoking with the showed that current smoking was associated with a upregulation of ACE2, but this association does not risk of developing more severe symptoms 1.4 (95% occur in other respiratory diseases.(38) CI: 0.98-2.00) times greater and a risk of needing The greater amount of ACE2 receptors in the lungs mechanical ventilation 2.4 (95% CI: 1.43-4.04) times of smokers, possibly induced by nicotine itself, would greater.
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