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3.
Int J Environ Res Public Health ; 17(15)2020 07 25.
Article in English | MEDLINE | ID: covidwho-670800

ABSTRACT

Combustible tobacco users appear to be at greater risk for serious complications from COVID-19. This study examined cigar smokers' perceived risk of COVID-19, quit intentions, and behaviors during the current pandemic. We conducted an online study between 23 April 2020 to 7 May 2020, as part of an ongoing study examining perceptions of different health effects of cigars. All participants used cigars in the past 30 days (n = 777). Three-quarters of the sample (76.0%) perceived they had a higher risk of complications from COVID-19 compared to non-smokers. The majority of participants (70.8%) intended to quit in the next six months due to COVID-19, and almost half of the sample (46.5%) reported making a quit attempt since the start of the COVID-19 pandemic. Far more participants reported increasing their tobacco use since COVID-19 started (40.9%) vs. decreasing their tobacco use (17.8%). Black or African American participants, participants who reported using a quitline, and participants with higher COVID-19 risk perceptions had higher intentions to quit using tobacco due to COVID-19, and higher odds of making a quit attempt since COVID-19 started. More research is needed to understand how tobacco users are perceiving COVID-19 risks and changing their tobacco use behaviors.


Subject(s)
Coronavirus Infections/psychology , Pneumonia, Viral/psychology , Smokers/psychology , Tobacco Use Cessation/psychology , Adult , African Americans , Betacoronavirus , Cigar Smoking , Coronavirus Infections/ethnology , Cross-Sectional Studies , Female , Health Knowledge, Attitudes, Practice , Humans , Intention , Male , Middle Aged , Pandemics , Pneumonia, Viral/ethnology , Tobacco , Tobacco Products , Tobacco Use , Tobacco Use Cessation/ethnology , United States
5.
Nitric Oxide ; 103: 1-3, 2020 10 01.
Article in English | MEDLINE | ID: covidwho-611235

ABSTRACT

It has long been suggested that NO may inhibit an early stage in viral replication. Furthermore, in vitro tests have shown that NO inhibits the replication cycle of severe acute respiratory syndrome coronavirus. Despite smoking being listed as a risk factor to contract Covid-19, only a low proportion of the smokers suffered from SARS-corona infection in China 2003, and from Covid-19 in China, Europe and the US. We hypothesize, that the intermittent bursts of high NO concentration in cigarette smoke may be a mechanism in protecting against the virus. Mainstream smoke from cigarettes contains NO at peak concentrations of between about 250 ppm and 1350 ppm in each puff as compared to medicinal use of no more than 80 to a maximum of 160 ppm. The diffusion of NO through the cell wall to reach the virus should be significantly more effective at the very high NO concentration in the smoke, according to classic laws of physics. The only oxide of nitrogen in the mainstream smoke is NO, and the NO2 concentration that is inhaled is very low or undetectable, and methemoglobin levels are lower in smokers than non-smokers, reasonably explained by the breaths of air in between the puffs that wash out the NO. Specialized iNO machines can now be developed to provide the drug intermittently in short bursts at high concentration dose, which would then provide both a preventative drug for those at high risk, as well as an effective treatment, without the health hazards associated with smoking.


Subject(s)
Betacoronavirus/drug effects , Coronavirus Infections/prevention & control , Nitric Oxide/pharmacology , Pandemics/prevention & control , Pneumonia, Viral/prevention & control , Protective Agents/pharmacology , Administration, Inhalation , Coronavirus Infections/drug therapy , Female , Humans , Male , Nitric Oxide/administration & dosage , Protective Agents/administration & dosage , Smokers , Smoking
6.
JMIR Mhealth Uhealth ; 8(6): e19494, 2020 06 11.
Article in English | MEDLINE | ID: covidwho-605405

ABSTRACT

BACKGROUND: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak may motivate smokers to attempt to stop in greater numbers. However, given the temporary closure of UK stop smoking services and vape shops, smokers attempting to quit may instead seek out mobile health support, such as smartphone apps. OBJECTIVE: We examined, using an interrupted time series approach, whether the SARS-CoV-2 outbreak has been associated with a step change or increasing trend in UK downloads of an otherwise popular smoking cessation app, Smoke Free. METHODS: Data were from daily and nondaily adult smokers in the United Kingdom who had downloaded the Smoke Free app between January 1, 2020, and March 31, 2020 (primary analysis), and January 1, 2019, and March 31, 2020 (secondary analysis). The outcome variable was the number of downloads aggregated at the 12-hourly (primary analysis) or daily level (secondary analysis). The explanatory variable was the start of the SARS-CoV-2 outbreak, operationalized as March 1, 2020 (primary analysis), and January 15, 2020 (secondary analysis). Generalized additive mixed models adjusted for relevant covariates were fitted. RESULTS: Data were collected on 45,105 (primary analysis) and 119,881 (secondary analysis) users. In both analyses, there was no evidence for a step change or increasing trend in downloads attributable to the start of the SARS-CoV-2 outbreak. Calculation of Bayes factors (BFs) indicated that the data for the primary analysis favored the null hypothesis compared with large associations (for level, BF=0.25; for slope, BF=0.26) but were insensitive to the detection of small associations (for level, BF=0.78; for slope, BF=1.35). CONCLUSIONS: In the United Kingdom, between January 1, 2020, and March 31, 2020, and between January 1, 2019, and March 31, 2020, there was no evidence that the SARS-CoV-2 outbreak has been associated with a large step change or increasing trend in downloads of a popular smoking cessation app. Findings on the association of the SARS-CoV-2 outbreak with a small step change or increasing trend were inconclusive.


Subject(s)
Coronavirus Infections/epidemiology , Disease Outbreaks , Mobile Applications/statistics & numerical data , Pneumonia, Viral/epidemiology , Smokers/psychology , Smoking Cessation/psychology , Adult , Humans , Interrupted Time Series Analysis , Motivation , Pandemics , Smokers/statistics & numerical data , United Kingdom/epidemiology
7.
Immunol Lett ; 224: 28-29, 2020 08.
Article in English | MEDLINE | ID: covidwho-548688

ABSTRACT

Statistical surveys of COVID-19 patients indicate, against all common logic, that people who smoke are less prone to the infection and/or exhibit less severe respiratory symptoms than non-smokers. This suggests that nicotine may have some preventive or modulatory effect on the inflammatory response in the lungs. Because it is known that the response to, and resolution of the SARS-CoV-2 infection depends mainly on the lung macrophages, we discuss the recent scientific findings, which may explain why and how nicotine may modulate lung macrophage response during COVID-19 infection.


Subject(s)
Anti-Inflammatory Agents/administration & dosage , Betacoronavirus/pathogenicity , Coronavirus Infections/prevention & control , Cytokine Release Syndrome/prevention & control , Cytokines/immunology , Lung/drug effects , Nicotine/administration & dosage , Nicotinic Agonists/administration & dosage , Pandemics/prevention & control , Pneumonia, Viral/prevention & control , Smokers , Administration, Inhalation , Betacoronavirus/drug effects , Coronavirus Infections/diagnosis , Coronavirus Infections/immunology , Coronavirus Infections/virology , Cytokine Release Syndrome/diagnosis , Cytokine Release Syndrome/immunology , Cytokine Release Syndrome/virology , Host-Pathogen Interactions , Humans , Lung/immunology , Lung/virology , Macrophages/drug effects , Macrophages/immunology , Macrophages/virology , Pneumonia, Viral/diagnosis , Pneumonia, Viral/immunology , Pneumonia, Viral/virology , Protective Factors , Receptors, Nicotinic/drug effects , Receptors, Nicotinic/immunology , Risk Factors , Severity of Illness Index , alpha7 Nicotinic Acetylcholine Receptor/agonists , alpha7 Nicotinic Acetylcholine Receptor/immunology
8.
Biochem Biophys Res Commun ; 528(3): 413-419, 2020 07 30.
Article in English | MEDLINE | ID: covidwho-436643

ABSTRACT

Coronavirus disease 2019 (COVID-19) is a worldwide pandemic. It has a high transmission rate among humans, and is a threat to global public health. However, there are no effective prophylactics or therapeutics available. It is necessary to identify vulnerable and susceptible groups for adequate protection and care against this disease. Recent studies have reported that COVID-19 has angiotensin-converting enzyme 2 (ACE2) as a functional receptor, which may lead to the development of severe cerebrovascular diseases (CVD), including strokes, in patients with risk factors for CVD such as diabetes and smoking. Thus, the World Health Organization (WHO) advised caution against COVID-19 for smokers and patients with underlying clinical symptoms, including cardiovascular diseases. Here, we observed ACE2 expression in the brain of rat middle cerebral artery occlusion (MCAO) model and evaluated the effects of cigarette smoke extract (CSE) and diabetes on ACE2 expression in vessels. We showed that the levels of ACE2 expression was increased in the cortex penumbra after ischemic injuries. CSE treatment significantly elevated ACE2 expression in human brain vessels. We found that ACE2 expression was upregulated in primary cultured human blood vessels with diabetes compared to healthy controls. This study demonstrates that ACE2 expression is increased in ischemic brains and vessels exposed to diabetes or smoking, makes them vulnerable to COVID-19 infection.


Subject(s)
Betacoronavirus/metabolism , Brain Ischemia/virology , Brain/blood supply , Diabetes Mellitus , Peptidyl-Dipeptidase A/biosynthesis , Receptors, Virus/biosynthesis , Smokers , Stroke/virology , Up-Regulation , Animals , Betacoronavirus/pathogenicity , Brain/drug effects , Brain Ischemia/genetics , Brain Ischemia/metabolism , Coronavirus Infections/genetics , Coronavirus Infections/metabolism , Coronavirus Infections/virology , Diabetes Mellitus/genetics , Diabetes Mellitus/metabolism , Disease Models, Animal , Disease Susceptibility , Infarction, Middle Cerebral Artery/complications , Male , Mice , Mice, Inbred C57BL , Pandemics , Peptidyl-Dipeptidase A/genetics , Pneumonia, Viral/genetics , Pneumonia, Viral/metabolism , Pneumonia, Viral/virology , Rats , Rats, Sprague-Dawley , Receptors, Virus/genetics , Smoke/adverse effects , Stroke/genetics , Stroke/metabolism , Up-Regulation/drug effects
18.
Mol Pharmacol ; 97(5): 351-353, 2020 05.
Article in English | MEDLINE | ID: covidwho-27322

ABSTRACT

COVID19 is a devastating global pandemic with epicenters in China, Italy, Spain, and now the United States. While the majority of infected cases appear mild, in some cases, individuals present serious cardiorespiratory complications with possible long-term lung damage. Infected individuals report a range of symptoms from headaches to shortness of breath to taste and smell loss. To that end, less is known about how the virus may impact different organ systems. The SARS-CoV2 virus, which is responsible for COVID19, is highly similar to SARS-CoV. Both viruses have evolved an ability to enter host cells through direct interaction with the angiotensin converting enzyme (ACE) 2 protein at the surface of many cells. Published findings indicate that SARS-CoV can enter the human nervous system with evidence from both postmortem brains and detection in cerebrospinal fluid of infected individuals. Here, we consider the ability of SARS-CoV2 to enter and infect the human nervous system based on the strong expression of the ACE2 target throughout the brain. Moreover, we predict that nicotine exposure through various kinds of smoking (cigarettes, electronic cigarettes, or vape) can increase the risk for COVID19 neuroinfection based on known functional interactions between the nicotinic receptor and ACE2. We advocate for higher surveillance and analysis of neurocomplications in infected cases. SIGNIFICANCE STATEMENT: The COVID19 epidemic has spurred a global public health crisis. While many of the cases requiring hospitalization and intensive medical care center on cardiorespiratory treatment, a growing number of cases present neurological symptoms. Viral entry into the brain now appears a strong possibility with deleterious consequences and an urgent need for addressing.


Subject(s)
Betacoronavirus/pathogenicity , Brain/virology , Coronavirus Infections/virology , Pneumonia, Viral/virology , Smoking/adverse effects , Humans , Pandemics , Risk , Smokers
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