Smoking and COVID-19: What we know so far

Shastri, Madhur D.; Shukla, Shakti D.; Chong, Wai Chin; Kc, Rajendra; Dua, Kamal; Patel, Rahul P.; Peterson, Gregory M.; O'Toole, Ronan

doi:10.1016/j.rmed.2020.106237

Cited by 100 publications

(85 citation statements)

References 96 publications

(97 reference statements)

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“…In fact, cigarette smoking promotes alterations in the respiratory tract that might increase the risk of viral infections through multiple mechanisms such as impairment of mucociliary clearance, mucus hypersecretion, fibrosis, and dysfunction of the epithelial barrier. These mechanisms are accompanied by alterations in the immune response, eventually harming the function of the lungs, including gas exchange ( 82 – 86 ).…”

Section: Differential Response To Covid-19 Could Be Related To Ace2 Ementioning

confidence: 99%

Combination of Angiotensin (1-7) Agonists and Convalescent Plasma as a New Strategy to Overcome Angiotensin Converting Enzyme 2 (ACE2) Inhibition for the Treatment of COVID-19

et al. 2021

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Coronavirus disease-2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is currently the most concerning health problem worldwide. SARS-CoV-2 infects cells by binding to angiotensin-converting enzyme 2 (ACE2). It is believed that the differential response to SARS-CoV-2 is correlated with the differential expression of ACE2. Several reports proposed the use of ACE2 pharmacological inhibitors and ACE2 antibodies to block viral entry. However, ACE2 inhibition is associated with lung and cardiovascular pathology and would probably increase the pathogenesis of COVID-19. Therefore, utilizing ACE2 soluble analogs to block viral entry while rescuing ACE2 activity has been proposed. Despite their protective effects, such analogs can form a circulating reservoir of the virus, thus accelerating its spread in the body. Levels of ACE2 are reduced following viral infection, possibly due to increased viral entry and lysis of ACE2 positive cells. Downregulation of ACE2/Ang (1-7) axis is associated with Ang II upregulation. Of note, while Ang (1-7) exerts protective effects on the lung and cardiovasculature, Ang II elicits pro-inflammatory and pro-fibrotic detrimental effects by binding to the angiotensin type 1 receptor (AT1R). Indeed, AT1R blockers (ARBs) can alleviate the harmful effects associated with Ang II upregulation while increasing ACE2 expression and thus the risk of viral infection. Therefore, Ang (1-7) agonists seem to be a better treatment option. Another approach is the transfusion of convalescent plasma from recovered patients with deteriorated symptoms. Indeed, this appears to be promising due to the neutralizing capacity of anti-COVID-19 antibodies. In light of these considerations, we encourage the adoption of Ang (1-7) agonists and convalescent plasma conjugated therapy for the treatment of COVID-19 patients. This therapeutic regimen is expected to be a safer choice since it possesses the proven ability to neutralize the virus while ensuring lung and cardiovascular protection through modulation of the inflammatory response.

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Section: Differential Response To Covid-19 Could Be Related To Ace2 Ementioning

confidence: 99%

Combination of Angiotensin (1-7) Agonists and Convalescent Plasma as a New Strategy to Overcome Angiotensin Converting Enzyme 2 (ACE2) Inhibition for the Treatment of COVID-19

et al. 2021

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“…Cigarette smoking is associated with underlying chronic inflammation, oxidative stress, and epithelial and immune dysfunction that may also contribute to COVID-19 progression ( Gulsen et al, 2020 ; Shastri et al, 2021 ). Even if not extensively tested, the same increased risk may apply to SHS and nicotine vapers.…”

Section: Pathophysiologic Insights Of Cigarette Smoke‐ and Sars-cov-2-induced Lung Inflammationmentioning

confidence: 99%

Cigarette Smoke Exposure, Pediatric Lung Disease, and COVID-19

et al. 2021

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The detrimental effects of tobacco exposure on children’s health are well known. Nonetheless, the prevalence of secondhand or direct cigarette smoke exposure (CSE) in the pediatric population has not significantly decreased over time. On the contrary, the rapid incline in use of e-cigarettes among adolescents has evoked public health concerns since increasing cases of vaping-induced acute lung injury have highlighted the potential harm of these new “smoking” devices. Two pediatric populations are especially vulnerable to the detrimental effects of cigarette smoke. The first group is former premature infants whose risk is elevated both due to their prematurity as well as other risk factors such as oxygen and mechanical ventilation to which they are disproportionately exposed. The second group is children and adolescents with chronic respiratory diseases, in particular asthma and other wheezing disorders. Coronavirus disease 2019 (COVID-19) is a spectrum of diseases caused by infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that has spread worldwide over the last year. Here, respiratory symptoms ranging from mild to acute respiratory distress syndrome (ARDS) are at the forefront of COVID-19 cases among adults, and cigarette smoking is associated with worse outcomes in this population, and cigarette smoking is associated with worse outcomes in this population. Interestingly, SARS-CoV-2 infection affects children differently in regard to infection susceptibility, disease manifestations, and complications. Although children carry and transmit the virus, the likelihood of symptomatic infection is low, and the rates of hospitalization and death are even lower when compared to the adult population. However, multisystem inflammatory syndrome is recognized as a serious consequence of SARS-CoV-2 infection in the pediatric population. In addition, recent data demonstrate specific clinical patterns in children infected with SARS-CoV-2 who develop multisystem inflammatory syndrome vs. severe COVID-19. In this review, we highlight the pulmonary effects of CSE in vulnerable pediatric populations in the context of the ongoing SARS-CoV-2 pandemic.

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“…Recent literature reviews found that tobacco use is associated with poor disease progression ( 32 ), and that severe COVID-19 outcomes among tobacco users are further perpetuated among those with these pre-existing conditions ( 33 ). One study found patients with a smoking history were over 14 times more likely to experience disease progression than patients with no smoking history after adjustment for important factors including patient age ( 27 ).…”

Section: Tobacco Use and Covid-19mentioning

confidence: 99%