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      Editorial: Cigarette Smoke, E-Cigarette/E-Vaping and COVID-19: Risks and Implications in This New Era


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          In December 2019, a cluster of pneumonia was reported in Wuhan, China. The new disease, COVID-19, is caused by the novel coronavirus SARS-CoV-2 and rapidly spread to become pandemic in March 2020. Worldwide, on August 4, 2021, confirmed cases and deaths exceed 199 and 4 million, respectively, and there are 548,167 new cases and over 3 billion vaccine doses administrated (https://covid19.who.int). Cigarette smoking (CS) is a universal public health concern too. Because exposure to CS increases the incidence and mortality from infections (Jiang et al., 2020), CS could rise the risk for COVOD-19. Yet, the relationship between smoking and COVID-19 has been controversial. Lower prevalence in hospitalized COVID-19 patients (Goyal et al., 2020) and lower risk of SARS-CoV-2 infection (Lee et al., 2021) were reported among smokers. However, a meta-analysis (WHO, 2020) suggests an association between smoking and COVID-19 severity outcomes. The U.S. Centers for Disease Control and Prevention and the Food and Drug Administration list smoking as a factor likely to make COVID-19 worse. This Research Topic presents new findings and reviews evidence on the role of smoking/vaping on COVID-19 prognosis, diagnosis, and outcomes. Neither smoking tobacco nor vaping have health benefits. In fact, both damage the respiratory, cardiovascular, and other organ systems. Furthermore, smoking often occurs with drinking. About 15% of ingested alcohol is exhaled or metabolized in the lung where it impairs neutrophil recruitment and compromises epithelial barrier function (Sisson, 2007; Muthumalage et al., 2019). In a study of 1,500+ COVID-19 patients with smoking or alcohol consumption histories, Dai et al. show more severe COVID-19 and higher probability of death in smokers than non-smokers. While alcohol consumption is not associated with severity or mortality in this study, Wetzel and Wyatt find that e-cigarette users are at high risk for binge and chronic alcohol consumption. They postulate that dual vs. single substance use might promote tissue damage, decrease immune response and pathogen clearance, and increase IL-6 and IL-8 production and inflammation, which would elevate COVID-19 complications risk. Xie et al. highlight the importance of smokers' and alcohol consumers' behaviors that facilitate the spread of viruses. Peaks in COVID-19 cases and deaths in U.S. occurred after the (premature) opening in summer 2020 and the holidays in January 2021 (https://covidtracking.com/data/charts/2-metrics-7-day-average-curves). These events likely promoted physical closeness and crowding while drinking, hand-to-mouth contact, and smoke-induced lung insult that might increase susceptibility to COVID-19. This hypothesis could be tested by comparing with data during periods of lockdowns and social distancing. Xie et al. note that isolation and its negative effect on mental health make quitting smoking difficult and contribute to smoking and drinking. Some COVID-19 patients suffer long-COVID-19, which manifests as symptoms that last weeks or months after being infected with SARS-CoV-2 or can appear weeks after infection. The cause and role of smoking in long COVID-19 is unknown. Compared to non-smokers, Kaur et al. find persistent high levels and activity of ACE2, the SARS-CoV-2 receptor, and of eotaxin and monocyte chemoattractant protein-1 in the sera of COVID-19 patients with smoking history. The relevance of these alterations on long-COVID-19 deserves attention. Vaping, the inhalation of e-cigarette aerosols, associates with lung inflammation and injury. Teenagers and young adults who vape and/or smoke vs. non-users are 2.6–9 times more likely to obtain a COVID-19 test because of experiencing symptoms (Gaiha et al., 2020). Furthermore, youth who ever used e-cigarettes alone or plus conventional cigarettes are 5 or 6.8 times more likely, respectively, to receive a COVID-19 diagnosis than their peers who did not use. In this Research Topic, Masso-Silva et al. show changes in lung gene expression of mice exposed to e-cigarette aerosols that indicate neutrophil activation, a potential driver of acute lung injury in COVID-19. They also show vaping mint increases expression of ACE2. Moreover, Sivaraman et al. demonstrate that pre-exposure to vaped e-liquid vs. vehicle alone results in worse pulmonary inflammation and mortality in mice infected with the murine-tropic coronavirus MHV-A59. Together, these preclinical investigations indicate that vapers could have augmented susceptibility to SARS-CoV-2 infection and be at higher risk of developing severe COVID-19. The presence of comorbidities and the relatively small studies' sample size had limited the generation of robust conclusions about COVID-19 and smoking association. Our Research Topic contains four reports with variable number of patients. In a study of 622 COVID-19 patients at an academic hospital in China, Peng et al. find that smokers have higher mortality risk than non-smokers after adjusting for age, sex, and underlying diseases. Smokers exhibit greater levels of leucocytes, hemoglobin and creatinine, and lower erythrocyte sedimentation rate than non-smokers. Zhong et al. study 91 patients between 3 months and 76 years of age in a tertiary hospital in China during the first 3 months of the outbreak. Severe disease occurs in people 65 or older, married, and with or below primary school education. While smoking, drinking, or betel quid chewing have no significant relationship with disease severity, diabetes and being retired/unemployed associate with worse COVID-19. In a longitudinal study of 10 controls and 25 COVID-19 adults with no comorbidities in Brazil, Alberca et al. show no difference in the number of leucocytes among current or former smokers and COPD patients during the hospital stay. However, smokers and COPD patients are at risk of kidney injury, and death occurs only among smokers. Although small, this study shows that, in the absence of comorbidities, smoking or COPD influences COVID-19 course. Replicating these results in larger populations and different demographics would be compelling. Together, these studies reveal that COVID-19 might present differently in distinct settings or countries or phases of the pandemic. Children carry and transmit SARS-CoV-2. Compared to adults, COVID-19 in children is milder with lower hospitalization rates and death in U.S. and Europe. Potential protective factors are the transfer of maternal antibodies and antiviral proteins in the milk (Root-Bernstein, 2020a), administration of certain vaccines (Root-Bernstein, 2020b), lower ACE2 expression (Molloy and Bearer, 2020), and absence of underlying diseases in general. However, children are exposed to secondhand or direct CS, which may deteriorate pre-existing conditions or lead to respiratory problems and infections in at-risk patients. Schiliro et al. review that pediatric COVID-19 cases continue to increase, its symptoms are non-specific, and about 50% of cases happen with respiratory coinfections. While 80% of North America's pediatric intensive care unit admissions have developmental delay and/or genetic anomalies, only 4% suffer from chronic lung disease such as asthma. Nevertheless, multisystem inflammatory syndrome in children resembling Kawasaki disease can develop after COVID-19 diagnosis. The course of the pandemic will shift toward improved outcomes as more people worldwide are vaccinated, effective therapies developed, and the mechanisms of disease understood. Unfortunately, new virus variants emerge, and old and new inhalation modalities are adopted with unknown health consequences. Thirupathi et al. show that physical exercise attenuates lung and muscle inflammation and histopathology in mice chronically exposed to hand-rolled cornhusk cigarette smoke. Elegant pre-clinical studies by Tian et al. elucidate the role of the CD73/adenosine A2B receptor/PKCa/ERK pathway in cigarette smoke-mediated airway epithelial injury. In conclusion, this Research Topic provides a view on how cigarette smoke, e-cigarette, or vaping can predispose and worsen COVID-19 and the negative effect of dual use of smoking with alcohol on this disease. Gaps in knowledge will close as preclinical and clinical investigations are completed and new studies implemented. ClinicalTrials.gov lists seven interventional or behavioral studies on COVID-19 and either smoking or tobacco use or nicotine. No study on COVID-19 and e-cigarette/vaping is registered. A study on immune senescence association with prior smoking as a susceptibility factor in COVID-19 is underway (NCT04403386), Longitudinal studies are necessary to understand long-COVID and develop appropriate treatments. Success of COVID-19 vaccination globally will reduce the risk of SARS-CoV-2 infection and spread of COVID-19 and improve long-COVID-19 symptoms. Because achievement of these goals will take months if not years, every effort to quit smoking and vaping should be a priority. Author Contributions All authors contributed to the manuscript and read and approved it for publication. Conflict of Interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Publisher's Note All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

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          Most cited references9

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          Clinical Characteristics of Covid-19 in New York City

          To the Editor: The world is in the midst of the coronavirus disease 2019 (Covid-19) pandemic, 1,2 and New York City has emerged as an epicenter. Here, we characterize the first 393 consecutive patients with Covid-19 who were admitted to two hospitals in New York City. This retrospective case series includes adults 18 years of age or older with confirmed Covid-19 who were consecutively admitted between March 3 (date of the first positive case) and March 27, 2020, at an 862-bed quaternary referral center and an affiliated 180-bed nonteaching community hospital in Manhattan. Both hospitals adopted an early-intubation strategy with limited use of high-flow nasal cannulae during this period. Cases were confirmed through reverse-transcriptase–polymerase-chain-reaction assays performed on nasopharyngeal swab specimens. Data were manually abstracted from electronic health records with the use of a quality-controlled protocol and structured abstraction tool (details are provided in the Methods section in the Supplementary Appendix, available with the full text of this letter at NEJM.org). Among the 393 patients, the median age was 62.2 years, 60.6% were male, and 35.8% had obesity (Table 1). The most common presenting symptoms were cough (79.4%), fever (77.1%), dyspnea (56.5%), myalgias (23.8%), diarrhea (23.7%), and nausea and vomiting (19.1%) (Table S1 in the Supplementary Appendix). Most of the patients (90.0%) had lymphopenia, 27% had thrombocytopenia, and many had elevated liver-function values and inflammatory markers. Between March 3 and April 10, respiratory failure leading to invasive mechanical ventilation developed in 130 patients (33.1%); to date, only 43 of these patients (33.1%) have been extubated. In total, 40 of the patients (10.2%) have died, and 260 (66.2%) have been discharged from the hospital; outcome data are incomplete for the remaining 93 patients (23.7%). Patients who received invasive mechanical ventilation were more likely to be male, to have obesity, and to have elevated liver-function values and inflammatory markers (ferritin, d-dimer, C-reactive protein, and procalcitonin) than were patients who did not receive invasive mechanical ventilation. Of the patients who received invasive mechanical ventilation, 40 (30.8%) did not need supplemental oxygen during the first 3 hours after presenting to the emergency department. Patients who received invasive mechanical ventilation were more likely to need vasopressor support (95.4% vs. 1.5%) and to have other complications, including atrial arrhythmias (17.7% vs. 1.9%) and new renal replacement therapy (13.3% vs. 0.4%). Among these 393 patients with Covid-19 who were hospitalized in two New York City hospitals, the manifestations of the disease at presentation were generally similar to those in a large case series from China 1 ; however, gastrointestinal symptoms appeared to be more common than in China (where these symptoms occurred in 4 to 5% of patients). This difference could reflect geographic variation or differential reporting. Obesity was common and may be a risk factor for respiratory failure leading to invasive mechanical ventilation. 3 The percentage of patients in our case series who received invasive mechanical ventilation was more than 10 times as high as that in China; potential contributors include the more severe disease in our cohort (since testing and hospitalization in the United States is largely limited to patients with more severe disease) and the early-intubation strategy used in our hospitals. Regardless, the high demand for invasive mechanical ventilation has the potential to overwhelm hospital resources. Deterioration occurred in many patients whose condition had previously been stable; almost a third of patients who received invasive mechanical ventilation did not need supplemental oxygen at presentation. The observations that the patients who received invasive mechanical ventilation almost universally received vasopressor support and that many also received new renal replacement therapy suggest that there is also a need to strengthen stockpiles and supply chains for these resources.
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            Association Between Youth Smoking, Electronic Cigarette Use, and Coronavirus Disease 2019

            Purpose This study aimed to assess whether youth cigarette and electronic cigarette (e-cigarette) use are associated with coronavirus disease 2019 (COVID-19) symptoms, testing, and diagnosis. Methods An online national survey of adolescents and young adults (n = 4,351) aged 13–24 years was conducted in May 2020. Multivariable logistic regression assessed relationships among COVID-19–related symptoms, testing, and diagnosis and cigarettes only, e-cigarettes only and dual use, sociodemographic factors, obesity, and complying with shelter-in-place. Results COVID-19 diagnosis was five times more likely among ever-users of e-cigarettes only (95% confidence interval [CI]: 1.82–13.96), seven times more likely among ever-dual-users (95% CI: 1.98–24.55), and 6.8 times more likely among past 30-day dual-users (95% CI: 2.40–19.55). Testing was nine times more likely among past 30-day dual-users (95% CI: 5.43–15.47) and 2.6 times more likely among past 30-day e-cigarette only users (95% CI: 1.33–4.87). Symptoms were 4.7 times more likely among past 30-day dual-users (95% CI: 3.07–7.16). Conclusions COVID-19 is associated with youth use of e-cigarettes only and dual use of e-cigarettes and cigarettes, suggesting the need for screening and education.
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              Alcohol and airways function in health and disease.

              The volatility of alcohol promotes the movement of alcohol from the bronchial circulation across the airway epithelium and into the conducting airways of the lung. The exposure of the airways through this route likely accounts for many of the biologic effects of alcohol on lung airway functions. The effect of alcohol on lung airway functions is dependent on the concentration, duration, and route of exposure. Brief exposure to mild concentrations of alcohol may enhance mucociliary clearance, stimulates bronchodilation, and probably attenuates the airway inflammation and injury observed in asthma and chronic obstructive pulmonary disease (COPD). Prolonged and heavy exposure to alcohol impairs mucociliary clearance, may complicate asthma management, and likely worsens outcomes including lung function and mortality in COPD patients. Nonalcohol congeners and alcohol metabolites act as triggers for airway disease exacerbations especially in atopic asthmatics and in Asian populations who have a reduced capacity to metabolize alcohol. Research focused on the mechanisms of alcohol-mediated changes in airway functions has identified specific mechanisms that mediate alcohol effects within the lung airways. These include prominent roles for the second messengers calcium and nitric oxide, regulatory kinases including PKG and PKA, alcohol- and acetaldehyde-metabolizing enzymes such as aldehyde dehydrogenase 2. The role alcohol may play in the pathobiology of airway mucus, bronchial blood flow, airway smooth muscle regulation, and the interaction with other airway exposure agents, such as cigarette smoke, represents opportunities for future investigation.

                Author and article information

                Front Physiol
                Front Physiol
                Front. Physiol.
                Frontiers in Physiology
                Frontiers Media S.A.
                09 September 2021
                09 September 2021
                : 12
                [1] 1Department of Internal Medicine, Morsani College of Medicine, University of South Florida , Tampa, FL, United States
                [2] 2Huan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University , Changsha, China
                [3] 3Department of Pharmaceutical Sciences, USF Health Taneja College of Pharmacy, University of South Florida , Tampa, FL, United States
                Author notes

                Edited by: Sharon Glynn, National University of Ireland Galway, Ireland

                Reviewed by: John Laffey, National University of Ireland Galway, Ireland

                *Correspondence: Blanca Camoretti-Mercado bcamoret@ 123456usf.edu
                Diane Allen-Gipson dallengi@ 123456usf.edu

                This article was submitted to Redox Physiology, a section of the journal Frontiers in Physiology

                Copyright © 2021 Camoretti-Mercado, Liao, Tian and Allen-Gipson.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 10, Pages: 3, Words: 2016

                Anatomy & Physiology

                tobacco smoking, covid-19, alcohol, inflammation, sars-cov-2, vaping, electronic cigarette, ace2


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