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1.
Acta Biomed ; 94(2): e2023114, 2023 04 24.
Article in English | MEDLINE | ID: covidwho-2322532

ABSTRACT

BACKGROUND: The recent pandemic has led to major lifestyle changes, especially in women, changes that will impact cardiovascular risk. The aim of the present observational study was to evaluate changes occurred during pandemic in coffee and caffeine intake in a group of adult women and compare changes in smoking versus non-smoking women. METHODS: A web questionnaire was sent through a online survey platform to a group of unselected adult women. The consumption of coffee and caffeine were investigated in 2 groups of women by comparing smokers and non-smokers. RESULTS: A total of 435 adult women (256 non-smokers and 179 smokers) answer to all questions. Smokers increase the number of cigarette/days (mean + 3.4 cig/day). Coffee intake was significantly increase in smokers compared to non-smokers (3.1+1.0 versus 1.5+0.6 cups/day p<0.01). In smokers, self-perception of increase stress was related to increased coffee intake (r = 0.84; p <0.001), increased sugar- rich foods (r=0.81; p<0.001), increased chocolate rich snacks (r=0.72; p<0.01), increased sitting time (r=0.79; p<0.01). CONCLUSIONS: These preliminary data must suggest to undertake social campaigns aimed at encouraging a return to a healthy lifestyle that certainly includes a healthy diet but also the suspension of smoking. These observational results need further evaluation with prospective studies in order to quantify the effects of pandemic-induced changes in lifestyle on cardiovascular risk in women.


Subject(s)
Cardiovascular Diseases , Coffee , Adult , Humans , Female , Caffeine , Prospective Studies , Non-Smokers , Pandemics , Risk Factors , Cardiovascular Diseases/epidemiology , Cardiovascular Diseases/prevention & control
2.
J Emerg Manag ; 21(7): 307-313, 2023.
Article in English | MEDLINE | ID: covidwho-2296472

ABSTRACT

INTRODUCTION: Fear of COVID-19 may differ for individuals with compromised health and those with unhealthy behaviors, placing them at greater risk. Based on previous analysis of academic medical center faculty and staff, the authors predicted that workers who were smokers/previous smokers would express the greater fear of COVID-19 relative to nonsmokers. METHODS: The present study used the Fear of COVID-19 Scale to assess fear among nonsmokers (n = 1,489) and smokers/previous smokers (n = 272) from a larger population of academic medical center members (N = 1,761). This study assessed nonsmokers' and smokers/previous smokers' demographic and background variables on Fear of COVID-19 scores. RESULTS: In this academic community, smokers/previous smokers had higher fear of COVID-19 scores than did nonsmokers (p < 0.05). Smokers/previous smokers differed from nonsmokers on three Fear of COVID-19 scale items (most afraid of COVID-19, fear of losing life, and physiological fear of COVID-19). DISCUSSION/CONCLUSIONS: These results provide a better understanding of how fear of COVID-19 can differ based on one's smoking status. These findings inform public health smoking cessation efforts aimed at reducing morbidity and mortality, both in response and secondary to COVID-19 exposure.


Subject(s)
COVID-19 , Smokers , Humans , Non-Smokers , Fear , Health Promotion
3.
Arch Razi Inst ; 77(1): 449-459, 2022 02.
Article in English | MEDLINE | ID: covidwho-1744447

ABSTRACT

Cigarette smoking is a risk factor associated with different diseases, claiming millions of lives annually. Smoking status has been studied for a long time and proved to be a major cause of smokers' decreased immunity. In the present pandemic COVID-19 disease, there was an unclear belief about the effect of smoking on patients with COVID-19. Therefore, the current cross-sectional study aimed to evaluate the effect of cigarette smoking on the sequelae of COVID-19. This cross-sectional study involved 200 COVID-19 patients (114 males and 86 females) aged 13-77 years. A number of 87 patients were smokers, and the rest of them were non-smokers. All patients underwent a comprehensive laboratory assessment and diagnosis by full medical history by the physicians. The results indicated a significant difference (P<0.001) between smokers and non-smokers in terms of hypertension, anticoagulant, steroid therapy, pulmonary lesion, oxygen saturation, and duration of disease. As an overall conclusion, it can be stated that COVID-19 is less severe in smokers and they require less intensive treatment.


Subject(s)
COVID-19 , Non-Smokers , Smokers , Adolescent , Adult , Aged , COVID-19/diagnosis , COVID-19/epidemiology , Cross-Sectional Studies , Female , Humans , Male , Middle Aged , Risk Factors , Smoking/epidemiology , Young Adult
4.
Nicotine Tob Res ; 24(3): 413-415, 2022 02 14.
Article in English | MEDLINE | ID: covidwho-1684758

ABSTRACT

INTRODUCTION: The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the virus responsible for the COVID-19 pandemic, gains entry into the host cell when its Spike protein is cleaved by host proteases TMPRSS2 and furin, thereby markedly increasing viral affinity for its receptor, angiotensin-converting enzyme-2 (ACE2). In rodent and diseased human lungs, tobacco cigarette (TCIG) smoke increases ACE2, but the effect of electronic cigarette vaping (ECIG) is unknown. It is unknown whether nicotine (in both TCIGs and ECIGs) or non-nicotine constituents unique to TCIG smoke increase expression of key proteins in COVID-19 pathogenesis. METHODS: Immune (CD45+) cells collected before the pandemic in otherwise healthy young people, including TCIG smokers (n = 9), ECIG vapers (n = 12), or nonsmokers (NS) (n = 12), were studied. Using flow cytometry, expression of key proteins in COVID-19 pathogenesis were compared among these groups. RESULTS: TCIG smokers and ECIG vapers had similar smoking or vaping burdens as indicated by similar plasma cotinine levels. TCIG smokers compared with NS had a significantly increased percentage of cells that were positive for ACE2 (10-fold, p < .001), TMPRSS2 (5-fold, p < .001), and ADAM17 (2.5-fold, p < .001). Additionally, the mean fluorescence intensity (MFI) consistently showed greater mean ACE2 (2.2-fold, p < .001), TMPRSS2 (1.5-fold, p < .001), furin (1.1-fold, p < .05), and ADAM17 (2-fold, p < .001) in TCIG smokers compared with NS. In ECIG vapers, furin MFI was increased (1.15-fold, p < .05) and TMPRSS2 MFI tended to be increased (1.1-fold, p = .077) compared with NS. CONCLUSIONS: The finding that key instigators of COVID-19 infection are lower in ECIG vapers compared with TCIG smokers is intriguing and warrants additional investigation to determine if switching to ECIGs is an effective harm reduction strategy. However, the trend toward increased proteases in ECIG vapers remains concerning. IMPLICATIONS: (1) This is the first human study to report a marked increase in proteins critical for COVID-19 infection, including ACE2, TMPRSS2, and ADAM17, in immune cells from healthy tobacco cigarette smokers without lung disease compared with e-cigarette vapers and nonsmokers. (2) These findings warrant additional investigation to determine whether switching to electronic cigarettes may be an effective harm reduction strategy in smokers addicted to nicotine who are unable or unwilling to quit. (3) The increase in proteases in electronic cigarette vapers remains concerning.


Subject(s)
COVID-19 , Electronic Nicotine Delivery Systems , Tobacco Products , Vaping , Adolescent , Humans , Non-Smokers , Pandemics , SARS-CoV-2 , Smokers , Tobacco
5.
BMC Public Health ; 21(1): 1972, 2021 11 01.
Article in English | MEDLINE | ID: covidwho-1496161

ABSTRACT

BACKGROUND: The COVID-19 pandemic has affected all aspects of human society, including education, culture, and the economy, and has also introduced changes in people's health behaviors such as drinking alcohol, nutrition intake, and practicing healthy living. This study conducted qualitative research in the Korean context to examine the changes in the smoking behavior of smokers and secondhand smoke exposure of non-smokers during the COVID-19 pandemic. METHODS: Focus group interviews were conducted with 36 Korean participants (18 men and 18 women). The groups were composed of cigarette smokers, e-cigarette users, heated tobacco product users, and non-smokers. RESULTS: During the pandemic, it was found that there was an increase in the frequency of use, irrespective of the tobacco product, in users who refrained from social interaction and worked or studied from home. Users who continued to be socially active increased the amount used with each usage. Smokers showed a tendency to avoid smoking rooms and to smoke alone in places unoccupied by people. In addition, non-smokers' exposure to secondhand smoke did not decrease, but since non-smokers used masks, they reported more relief from the risk of exposure to secondhand smoke than before. CONCLUSIONS: Despite smokers being a high-risk group for COVID-19, the risk did not result in smoking cessation among smokers. Therefore, policies and educational campaigns to raise awareness about the dangers of smoking and to encourage smoking cessation are needed in the future.


Subject(s)
COVID-19 , Electronic Nicotine Delivery Systems , Tobacco Smoke Pollution , Attitude , Female , Humans , Male , Non-Smokers , Pandemics , Qualitative Research , Republic of Korea/epidemiology , SARS-CoV-2 , Smokers
6.
Respir Med Res ; 80: 100844, 2021 Nov.
Article in English | MEDLINE | ID: covidwho-1260852

ABSTRACT

Recent data show an interaction between COVID-19 and nicotine and indicate the need for an assessment of transdermal nicotine use in non-smokers. Assessments have been conducted into the short-term cognitive effects of nicotine and into diseases such as Parkinson's, Tourette syndrome, ADHD or ulcerative colitis. METHODS: Analyses of nicotine administration protocols and safety were conducted after reviewing Medline and Science Direct databases performing a search using the words [transdermal nicotine] AND [non-smoker] AND selected diseases. RESULTS: Among 298 articles identified, there were 35 reviewed publications reporting on 33 studies of non-smokers receiving transdermal nicotine for >48hours. In the 16 randomized trials, 7 crossover, 1 case/control and 9 open studies patients received an initial nicotine dose of between 2.5mg and 15mg/day. In 22 studies, daily doses increased by 2 to 7 steps in 3 to 96 days until the dose was between 5mg and 105mg/day. The target nicotine dose was 19.06±20.89mg/day. The 987 non-smokers (534 never-smokers, 326 ex-smokers and 127 classified as "non-smokers") received or did not receive nicotine. The most common side-effects were nausea and skin itching. Forty-three (7.1%) non-smokers stopped treatment because of an adverse event of nicotine. No hospitalization related to nicotine side-effects were reported. CONCLUSION: Despite a relatively safe tolerance profile, transdermal nicotine therapy in non-smokers can only be used in clinical trials. There is a lack of formal assessment of the potential risk of developing a tobacco addiction. This review offers baseline data to set a transdermal nicotine protocol for non-smokers with a new purpose.


Subject(s)
COVID-19 , Colitis, Ulcerative , Humans , Nicotine/adverse effects , Non-Smokers , SARS-CoV-2
8.
Chem Biol Interact ; 335: 109370, 2021 Feb 01.
Article in English | MEDLINE | ID: covidwho-1014379

ABSTRACT

The aberrant expression level of SARS-CoV-2 cell receptor gene ACE2 was reported in lung adenocarcinoma (LUAD) comorbidity of COVID-19. However, the association of ACE2 expression levels with immunosuppression and metabolic reprogramming in LUAD remains lacking. We investigated the expression level of ACE2, an association of ACE2 expression level with various types of immune signatures, immune ratios, and pathways. We employed a weighted gene co-expression network analysis (WGCNA) R package to identify the gene modules and investigated prognostic roles of hub genes in LUAD. Overexpression of ACE2 level was found in LUAD and ACE2 expression was negatively associated with various types of immune signatures including CD8+ T cells, CD4+ regulatory T cells, NK cells, and T cell activation. Besides, ACE2 upregulation was not only associated with CD8+ T cell/CD4+ regulatory T cell ratios but also linked with downregulation of immune-markers including CD8A, KLRC1, GZMA, GZMB, NKG7, CCL4, and IFNG. Moreover, the ACE2 expression level was found to be associated with the enrichment level of various metabolic pathways and it was also found that the metabolic pathways are directly positively correlated with the increased expression levels of ACE2, indicating that the overexpression of ACE2 is associated with metabolic reprogramming in LUAD. Furthermore, WGCNA based analysis revealed the gene modules in the high-ACE2-expression-level group of LUAD and identified GCLC and SLC7A11 hub genes which are not only highly expressed in lung adenocarcinoma but also correlated with the poor survival prognosis. Our analysis of ACE2 in LUAD tissues suggests that ACE2 is not only a receptor but is also associated with immunosuppression and metabolic reprogramming. This study underlines the clue for understanding the clinical significance of ACE2 in COVID-19 patients with LUAD comorbidity.


Subject(s)
Adenocarcinoma of Lung/metabolism , Angiotensin-Converting Enzyme 2/metabolism , Immunity, Cellular/genetics , Immunity, Innate/genetics , Lung Neoplasms/metabolism , Adenocarcinoma of Lung/epidemiology , Amino Acid Transport System y+/genetics , Angiotensin-Converting Enzyme 2/genetics , COVID-19/epidemiology , Comorbidity , Computational Biology , Databases, Genetic/statistics & numerical data , Female , Gene Expression Regulation, Neoplastic , Glutamate-Cysteine Ligase/genetics , Humans , Lung Neoplasms/epidemiology , Lymphocyte Activation/genetics , Male , Non-Smokers , Protein Interaction Maps/genetics , SARS-CoV-2 , Smokers , T-Lymphocytes/metabolism , Transcriptome , Up-Regulation
9.
J Intern Med ; 289(4): 574-583, 2021 04.
Article in English | MEDLINE | ID: covidwho-955543

ABSTRACT

BACKGROUND: COVID-19 is a new pneumonia. It has been hypothesized that tobacco smoking history may increase severity of this disease in the patients once infected by the underlying coronavirus SARS-CoV-2 because smoking and COVID-19 both cause lung damage. However, this hypothesis has not been tested. OBJECTIVE: Current study was designed to focus on smoking history in patients with COVID-19 and test this hypothesis that tobacco smoking history increases risk for severe COVID-19 by damaging the lungs. METHODS AND RESULTS: This was a single-site, retrospective case series study of clinical associations, between epidemiological findings and clinical manifestations, radiographical or laboratory results. In our well-characterized cohort of 954 patients including 56 with tobacco smoking history, smoking history increased the risk for severe COVID-19 with an odds ratio (OR) of 5.5 (95% CI: 3.1-9.9; P = 7.3 × 10-8 ). Meta-analysis of ten cohorts for 2891 patients together obtained an OR of 2.5 (95% CI: 1.9-3.3; P < 0.00001). Semi-quantitative analysis of lung images for each of five lobes revealed a significant difference in neither lung damage at first examination nor dynamics of the lung damage at different time-points of examinations between the smoking and nonsmoking groups. No significant differences were found either in laboratory results including D-dimer and C-reactive protein levels except different covariances for density of the immune cells lymphocyte (P = 3.8 × 10-64 ) and neutrophil (P = 3.9 × 10-46 ). CONCLUSION: Tobacco smoking history increases the risk for great severity of COVID-19 but this risk is achieved unlikely by affecting the lungs.


Subject(s)
COVID-19 , Lung , Pneumonia, Viral , Tobacco Smoking , C-Reactive Protein/analysis , COVID-19/diagnosis , COVID-19/epidemiology , COVID-19/physiopathology , COVID-19/psychology , China/epidemiology , Correlation of Data , Ex-Smokers/statistics & numerical data , Female , Fibrin Fibrinogen Degradation Products/analysis , Humans , Leukocyte Count/methods , Leukocyte Count/statistics & numerical data , Lung/diagnostic imaging , Lung/physiopathology , Male , Middle Aged , Non-Smokers/statistics & numerical data , Pneumonia, Viral/diagnostic imaging , Pneumonia, Viral/etiology , Retrospective Studies , Risk Assessment/methods , Risk Assessment/statistics & numerical data , SARS-CoV-2 , Severity of Illness Index , Tobacco Smoking/blood , Tobacco Smoking/epidemiology , Tobacco Smoking/pathology
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