Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 1.830
Filtrar
1.
BMC Public Health ; 21(1): 1633, 2021 09 07.
Artigo em Inglês | MEDLINE | ID: mdl-34493239

RESUMO

BACKGROUND: Waterpipe is one of the oldest methods of tobacco smoking, which has become the public health challenge, especially in the Eastern Mediterranean countries such as Iran. This study aimed to investigate the waterpipe smoking (WPS) in the young people of Kermanshah in 2020, using a qualitative method. METHODS: This was a qualitative study conducted with the approach of content analysis. Participants were young waterpipe user aged 17 to 25 years selected by purposeful sampling method in Kermanshah city, located in the west of Iran. Data were collected through semi-structured interviews in face-to-face and audio-recorded methods based on an interview guideline during June to August 2020. Then researchers transcribed verbatim and analyzed the content of the interviews thematically. RESULTS: In this study, 23 young people who were waterpipe users at the time of the study participated. The results showed that social aspects in three sub-categories were involved in WPS including "socio-cultural aspects", "socio-environmental aspects", and "social relations". Individual aspects of waterpipe use as second category also consisted of two sub-categories including "motivational aspects" and "lack of psycho-protective aspects". CONCLUSIONS: It seems that the implementation of the policy of reducing access to waterpipe in public environments is effective in reducing waterpipe consumption. It is suggested that educational and interventions, based on targeted models and theories be implemented in order to increase young people's belief and perception on dangers of WPS, and to improve their self-efficacy to smoking cessation.


Assuntos
Abandono do Hábito de Fumar , Fumar Cachimbo de Água , Adolescente , Humanos , Irã (Geográfico)/epidemiologia , Pesquisa Qualitativa , Fumar Tabaco , Fumar Cachimbo de Água/epidemiologia
2.
MMW Fortschr Med ; 163(16): 10-11, 2021 Sep.
Artigo em Alemão | MEDLINE | ID: mdl-34533704

Assuntos
Fumar , Fumar Tabaco , Humanos
4.
Sante Publique ; Vol. 33(1): 149-157, 2021 Jun 24.
Artigo em Francês | MEDLINE | ID: mdl-34372634

RESUMO

This article proposes a reflection on the policies of tobacco consumption regulation in the ECOWAS countries. The argument is built from a cost-benefit economic approach. It shows that, even if fiscal and pricing policies are necessary to reduce the demand for tobacco, they must make it possible to strengthen information and awareness policies for a comprehensive approach to the fight against smoking and passive smoking.New forms of regulation should be established, which are part of a logic of promotion and health education for dependent, and/or poor people because the latter have difficulty changing their behavior following an increase in drug prices.


Assuntos
Impostos , Tabaco , Humanos , Fumar , Prevenção do Hábito de Fumar , Fumar Tabaco , Uso de Tabaco
5.
Artigo em Inglês | MEDLINE | ID: mdl-34360367

RESUMO

BACKGROUND: The determination of the impact of risk factors such as smoking in periodontal disease development is of importance to better characterize the disease. However, its impact on host response remains unclear. This study aimed to evaluate the effects of tobacco smoking on GCF levels of neutrophil enzymes (myeloperoxidase (MPO), beta-glucuronidase (BGD), neutrophil elastase (NE) and periodontal parameters in healthy young adults with dental plaque biofilm-induced gingivitis. METHODS: The study population consisted of 60 systemically healthy young adults (39 smokers (Sm) and 21 non-smokers (n-Sm)) diagnosed with plaque-induced gingivitis. The periodontal examination consisted of a plaque index (PI); gingival index (GI); probing depth (PD); bleeding on probing (BoP), and clinical attachment level (CAL). GCF MPO, BGD, and NE levels were determined by means of an enzyme-linked immunosorbent assay (ELISA). RESULTS: PI, GI, and BoP were significantly increased in the Sm group (p < 0.05). PD and CAL showed no significant difference between Sm and n-Sm groups (p > 0.05). In GCF, MPO, BGD, and NE levels were significantly increased in Sm group (p < 0.05). NE levels showed a significant correlation with GI and BoP (p < 0.05 for both). Moreover, a positive correlation between BGD and NE levels (p < 0.05) was measured. CONCLUSIONS: It may be concluded that, even in young patients, tobacco consumption affects the host's immune response related to gingival inflammation. It is, therefore, mandatory to inform young patients about the risk related to tobacco consumption for their gingival health.


Assuntos
Gengivite , Neutrófilos , Estudos de Casos e Controles , Líquido do Sulco Gengival , Humanos , Perda da Inserção Periodontal , Fumar/efeitos adversos , Fumar Tabaco , Adulto Jovem
7.
Ann Saudi Med ; 41(4): 191-197, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34420394

RESUMO

BACKGROUND: Tobacco smoking and its harmful health effects also increase economic burdens globally. Surprisingly, despite the detrimental health consequences of smoking, some studies have shown better survival among smokers compared with non-smokers, a phenomenon called "smoker's paradox". However, the impact of smoking status on clinical outcomes in severe calcified coronary artery disease (CAD) patients has yet to be reported. OBJECTIVES: Investigate the impact of smoking on clinical outcomes in calcified CAD receiving rotational atherectomy (RA). DESIGN: Retrospective review of medical records. SETTING: Multicenter registry in South Korea. PATIENTS AND METHODS: This multicenter registry included consecutive patients with calcified CAD who underwent RA at nine tertiary centers in Korea between January 2010 and October 2019. MAIN OUTCOME MEASURES: Target-vessel failure (TVF) which included the composite of cardiac death, target-vessel myocardial infarction (TVMI), and target-vessel revascularization (TVR). SAMPLE SIZE: 583 lesions in 540 patients followed for a median of 16.1 months. RESULTS: Lesions were divided into two groups: non-smokers (n=472, 81.0%) and smokers (n=111, 19.0%). TVF in the smoker group was significantly more frequent than in non-smoker group (log rank P=.016). The inverse probability of treatment weighting analysis also showed that smoking was significantly associated with a higher incidence of the primary outcome (HR: 1.617; 95% CI: 1.127-2.320; P=.009), cardiac death (HR 1.912; 95% CI: 1.105-3.311; P=.021), myocardial infarction (HR: 3.914; 95% CI: 1.884-8.132; P<.001), TVMI (HR: 3.234; 95% CI: 1.130-9.258; P=.029), and TVR (HR: 1.661; 95% CI: 1.043-2.643; P=.032). However, any bleeding was significantly observed less in the smokers. CONCLUSION: Smoking is significantly associated with adverse clinical outcomes in CAD patients requiring RA. LIMITATIONS: Retrospective design. CONFLICTS OF INTEREST: None.


Assuntos
Aterectomia Coronária , Doença da Artéria Coronariana , Intervenção Coronária Percutânea , Calcificação Vascular , Aterectomia Coronária/efeitos adversos , Angiografia Coronária , Doença da Artéria Coronariana/epidemiologia , Doença da Artéria Coronariana/cirurgia , Humanos , Sistema de Registros , República da Coreia/epidemiologia , Estudos Retrospectivos , Fatores de Risco , Fumar/efeitos adversos , Fumar/epidemiologia , Fumar Tabaco , Resultado do Tratamento , Calcificação Vascular/epidemiologia
8.
BMC Public Health ; 21(1): 1554, 2021 08 16.
Artigo em Inglês | MEDLINE | ID: mdl-34399729

RESUMO

BACKGROUND: Smoking impairs lung immune function and damages upper airways, increasing risks of contracting and severity of infectious diseases. This paper quantifies the association between smoking and COVID-19 disease progression. METHODS: We searched PubMed and Embase for studies published from January 1-May 25, 2020. We included studies reporting smoking behavior of COVID-19 patients and progression of disease, including death. We used random effects meta-analysis, meta-regression and locally weighted regression and smoothing to examine relationships in the data. RESULTS: We identified 46 peer-reviewed papers with a total of 22,939 COVID-19 patients, 5421 (23.6%) experienced disease progression and 2914 (12.7%) with a history of smoking (current and former smokers). Among those with a history of smoking, 33.5% experienced disease progression, compared with 21.9% of non-smokers. The meta-analysis confirmed an association between ever smoking and COVID-19 progression (OR 1.59, 95% CI 1.33-1.89, p = 0.001). Ever smoking was associated with increased risk of death from COVID-19 (OR 1.19, 95% CI 1.02-1.39, p = 0.003). We found no significant difference (p = 0.864) between the effects of ever smoking on COVID-19 disease progression between adjusted and unadjusted analyses, suggesting that smoking is an independent risk factor for COVID-19 disease progression. We also found the risk of having COVID-19 progression higher among younger adults (p = 0.001), with the effect most pronounced among younger adults under about 45 years old. CONCLUSIONS: Smoking is an independent risk for having progression of COVID-19, including mortality. The effects seem to be higher among young people. Smoking prevention and cessation should remain a priority for the public, physicians, and public health professionals during the COVID-19 pandemic.


Assuntos
COVID-19 , Pandemias , Adulto , Humanos , Pessoa de Meia-Idade , SARS-CoV-2 , Fumar/efeitos adversos , Fumar/epidemiologia , Fumar Tabaco , Adulto Jovem
9.
Artigo em Inglês | MEDLINE | ID: mdl-34360096

RESUMO

BACKGROUND: Little is known regarding long-term impacts of anti-tobacco media campaigns on youth smoking and related disparities in the United States. METHODS: We examined longitudinal cohort data from Monitoring the Future (MTF) between 2000 and 2017 in modified Poisson regression models to understand the long-term impacts of televised Truth and state-sponsored ad campaign exposure at baseline (age 18) on first cigarette and daily smoking initiation 1 to 2 years later (at modal ages 19/20). We also used additive interactions to test for potential effect modification between campaign exposure and smoking outcomes by sex, race/ethnicity, and parental educational attainment. RESULTS: We found no evidence for baseline media campaign exposure to be associated with first cigarette or daily smoking initiation at modal age 19/20. Further, results showed no evidence for effect modification between campaign exposure and first cigarette or daily smoking initiation. CONCLUSIONS: We found no evidence that baseline Truth and state-sponsored ad exposure was associated with first cigarette or daily smoking initiation at follow up, nor did we find any evidence for effect modification by sex, race/ethnicity, or parental education. We hypothesize that anti-tobacco media campaigns might have had a short-term impact on smoking behaviors, though these effects were not sustained long term.


Assuntos
Produtos do Tabaco , Tabaco , Adolescente , Adulto , Pré-Escolar , Promoção da Saúde , Humanos , Lactente , Meios de Comunicação de Massa , Fumar , Prevenção do Hábito de Fumar , Fumar Tabaco , Estados Unidos/epidemiologia , Adulto Jovem
10.
Curr Issues Mol Biol ; 43(2): 887-899, 2021 Aug 03.
Artigo em Inglês | MEDLINE | ID: mdl-34449539

RESUMO

BACKGROUND: Chronic Obstructive Pulmonary Disease (COPD) is an inflammatory disease characterized by airflow obstruction, commonly present in smokers and subjects exposed to noxious particles product of biomass-burning smoke (BBS). Several association studies have identified single-nucleotide polymorphisms (SNP) in coding genes related to the heat shock proteins family-genes that codify the heat shock proteins (Hsp). Hsp accomplishes critical roles in regulating immune response, antigen-processing, eliminating protein aggregates and co-activating receptors. The presence of SNPs in these genes can lead to alterations in immune responses. We aimed to evaluate the association of SNPs in the HSP90 gene complex and COPD. METHODS: We enrolled 1549 participants, divided into two comparison groups; 919 tobacco-smoking subjects (cases COPD-TS n = 294 and, controls SWOC n = 625) and 630 chronic exposed to BBS (cases COPD-BBS n = 186 and controls BBES n = 444). We genotyped 2 SNPs: the rs13296 in HSP90AB1 and rs2070908 in HSP90B1. RESULTS: Through the dominant model (GC + CC), the rs2070908 is associated with decreased risk (p < 0.01, OR = 0.6) to suffer COPD among chronic exposed BBS subjects. We found an association between rs13296 GG genotype and lower risk (p = 0.01, OR = 0.22) to suffer severe COPD-TS forms in the severity analysis. CONCLUSIONS: single-nucleotide variants in the HSP90AB1 and HSP90B1 genes are associated with decreased COPD risk in subjects exposed to BBS and the most severe forms of COPD in tobacco-smoking subjects.


Assuntos
Biomassa , Proteínas de Choque Térmico HSP90/genética , Pulmão/metabolismo , Glicoproteínas de Membrana/genética , Doença Pulmonar Obstrutiva Crônica/genética , Fumaça/efeitos adversos , Fumar Tabaco/efeitos adversos , Idoso , Estudos de Casos e Controles , Feminino , Humanos , Pulmão/patologia , Masculino , Pessoa de Meia-Idade , Polimorfismo de Nucleotídeo Único , Doença Pulmonar Obstrutiva Crônica/metabolismo , Doença Pulmonar Obstrutiva Crônica/patologia
11.
Am J Public Health ; 111(9): 1661-1672, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-34410826

RESUMO

The topic of e-cigarettes is controversial. Opponents focus on e-cigarettes' risks for young people, while supporters emphasize the potential for e-cigarettes to assist smokers in quitting smoking. Most US health organizations, media coverage, and policymakers have focused primarily on risks to youths. Because of their messaging, much of the public-including most smokers-now consider e-cigarette use as dangerous as or more dangerous than smoking. By contrast, the National Academies of Science, Engineering, and Medicine concluded that e-cigarette use is likely far less hazardous than smoking. Policies intended to reduce adolescent vaping may also reduce adult smokers' use of e-cigarettes in quit attempts. Because evidence indicates that e-cigarette use can increase the odds of quitting smoking, many scientists, including this essay's authors, encourage the health community, media, and policymakers to more carefully weigh vaping's potential to reduce adult smoking-attributable mortality. We review the health risks of e-cigarette use, the likelihood that vaping increases smoking cessation, concerns about youth vaping, and the need to balance valid concerns about risks to youths with the potential benefits of increasing adult smoking cessation.


Assuntos
Fumar Cigarros/prevenção & controle , Sistemas Eletrônicos de Liberação de Nicotina/estatística & dados numéricos , Prevenção do Hábito de Fumar/métodos , Fumar Tabaco/terapia , Vaping/prevenção & controle , Adolescente , Adulto , Humanos , Estados Unidos
12.
Epidemiol Health ; 43: e2021046, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34265892

RESUMO

OBJECTIVES: Tobacco smoking is classified as carcinogenic to humans (International Agency for Research on Cancer Group 1). We aimed to estimate the percentage and number of incident cancer cases diagnosed in Texas in 2015 that were attributable to tobacco smoking, and we examined differences in the proportions of smoking-attributable cancers between the major racial/ethnic subgroups of the population. METHODS: We calculated population-attributable fractions for cancers attributable to tobacco smoking using prevalence data from the Texas Behavioral Risk Factor Surveillance System and relative risks associated with smoking status from pooled analyses of cohort studies or meta-analyses. Cancer incidence data were collected from the Texas Cancer Registry. RESULTS: We estimated that 19,000 excess cancer cases or 18.4% of all cancers diagnosed in 2015 in Texans aged ≥ 25 years were caused by tobacco smoking. Males had a higher overall proportion of cancers attributable to tobacco smoking than females (male, 23.3%, 11,993 excess cases; female, 13.5%, 7,006 cases). Approximately 20% of cancer cases in non-Hispanic Whites and non-Hispanic Blacks were attributable to tobacco smoking compared to 12.8% among Hispanics. CONCLUSIONS: Despite ongoing public health campaigns combatting tobacco use, this preventable behavior still contributes significantly to cancer incidence in Texas. Racial/ethnic differences in smoking prevalence and smoking-attributable cancer incidence should be considered when designing cancer prevention programs.


Assuntos
Grupos de Populações Continentais/estatística & dados numéricos , Grupos Étnicos/estatística & dados numéricos , Neoplasias/etnologia , Fumar Tabaco/etnologia , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Feminino , Disparidades nos Níveis de Saúde , Humanos , Masculino , Pessoa de Meia-Idade , Neoplasias/etiologia , Neoplasias/prevenção & controle , Sistema de Registros , Fatores de Risco , Texas/epidemiologia , Fumar Tabaco/efeitos adversos , Adulto Jovem
13.
Carcinogenesis ; 42(8): 1009-1022, 2021 08 19.
Artigo em Inglês | MEDLINE | ID: mdl-34223886

RESUMO

This review highlights the convergence of three global health challenges at a crossroad where the pandemic of coronavirus disease 2019 (COVID-19) meets the tobacco epidemic and vaping. It begins with an overview of the current knowledge on the biology, pathophysiology and epidemiology of COVID-19. It then presents the state of smoking and vaping during the pandemic by summarizing the published data on prevalence, use patterns, product availability/accessibility, sales records and motivation to quit before and after the start of the pandemic. It highlights the state of evidence on the association of tobacco product use with COVID-19 infection and transmission rates, symptom severity and clinical outcomes. Also discussed are proposed biological mechanisms and behavioral factors that may modulate COVID-19 risk in tobacco product users. Furthermore, competing hypotheses on the protective effect of nicotine against COVID-19 as well as the claimed 'smokers' paradox' are discussed. Considerations and challenges of COVID-19 vaccination in tobacco product users are underscored. Collectively, the present data show an 'incomplete' but rapidly shaping picture on the association of tobacco product use and COVID-19 infection, disease course and clinical outcomes. Evidence is also growing on the mechanisms by which tobacco product use may contribute to COVID-19 pathophysiology. Although we await definitive conclusions on the relative risk of COVID-19 infection in tobacco product users, compelling data confirm that many comorbidities associated with/caused by smoking predispose to COVID-19 infection, severe disease and poor prognosis. Additionally, it is becoming increasing clear that should smokers get the disease, they are more likely to have serious health consequences.


Assuntos
COVID-19/epidemiologia , SARS-CoV-2/isolamento & purificação , Fumar Tabaco/epidemiologia , Vaping/epidemiologia , COVID-19/complicações , COVID-19/patologia , COVID-19/virologia , Saúde Global , Humanos , Fumar Tabaco/patologia , Vaping/patologia
14.
Clin Immunol ; 229: 108798, 2021 08.
Artigo em Inglês | MEDLINE | ID: mdl-34280578

RESUMO

Inflammatory response in patients with COPD secondary to organic dust exposure (OD-COPD) is poorly understood. We therefore aimed to characterize inflammatory and immune profile from peripheral blood mononuclear cells (PBMC) in a group of patients with mild-to-moderate COPD secondary to organic dust exposure (OD-COPD), tobacco smoking (T-COPD), or both. We compared T, B and NK cells distribution and inflammatory (TNF-α, Il-1ß, IL-6), type 1 (IFN-γ), type 2 (IL-4, IL-13) and type 3 (IL-17) immunity related cytokines at baseline, and after stimulation with LPS, flagellin and CD3/CD28 beads in all COPD groups. OD-COPD displayed significantly lower NK cells and CD8+ T cells compared with controls. After flagellin stimulation, T-COPD had significantly lower IL-13 levels than OD-COPD and controls (p < 0.05) whereas IFN-γ tended to be lower in OD-COPD. All COPD groups displayed higher IL-1ß and IL-17 than controls after CD3/CD28 stimulation. Inflammatory responses in OD-COPD were different from T-COPD. OD-COPD displayed higher levels of type 2 immunity related cytokines.


Assuntos
Poeira/imunologia , Compostos Orgânicos/toxicidade , Doença Pulmonar Obstrutiva Crônica/imunologia , Idoso , Agricultura , Linfócitos B/imunologia , Linfócitos B/patologia , Estudos de Casos e Controles , Citocinas/biossíntese , Feminino , Humanos , Inflamação/etiologia , Inflamação/imunologia , Inflamação/patologia , Células Matadoras Naturais/imunologia , Células Matadoras Naturais/patologia , Leucócitos Mononucleares/imunologia , Leucócitos Mononucleares/patologia , Masculino , Pessoa de Meia-Idade , Exposição Ocupacional/efeitos adversos , Doença Pulmonar Obstrutiva Crônica/etiologia , Doença Pulmonar Obstrutiva Crônica/patologia , Linfócitos T/imunologia , Linfócitos T/patologia , Fumar Tabaco/efeitos adversos
16.
Pak J Pharm Sci ; 34(1(Supplementary)): 321-325, 2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34275857

RESUMO

The study was aimed to mention the epidemiology of smoking in Pakistani COVID-19 infected patients along with the disease severity, oxygen dependency and fatality rate. A cross sectional epidemiological study was carried out on 555 confirmed cases of COVID-19 infection. The median age was 47±16 years. 59% were male and 41% were female. Most of the patients (97.5%) survived, while only 2.5% expired. 25.6% patients required the oxygen. Total 17 (3%) COVID-19 patients with age 20-75 years were identified as smokers. No mortality was observed in smokers. The 1.4% smokers presented with mild disease, 1.2% with moderate disease and 0.4% had severe disease. According to Chi-Square test, there existed an insignificant difference (p-value: 0.38649) between smokers and non-smokers in disease severity levels. Smoking is a precursor for countless diseases, but it behaved differently in COVID-19 infected patients, as its prevalence was significantly low. We found no significant variation of the disease severity among the smokers and non-smokers. Profound experiments should be conducted to recommend whether nicotine can be used as a protective agent to negate COVID-19 infection.


Assuntos
COVID-19/epidemiologia , COVID-19/etiologia , Fumar/epidemiologia , Adolescente , Adulto , Distribuição por Idade , Idoso , Idoso de 80 Anos ou mais , Estudos Transversais , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Paquistão/epidemiologia , Índice de Gravidade de Doença , Distribuição por Sexo , Fumar Tabaco/epidemiologia , Adulto Jovem
17.
Redox Biol ; 45: 102055, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-34214709

RESUMO

BACKGROUND: Chronic lung diseases, such as chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF) are linked to several mitochondrial alterations. Cigarette smoke (CS) alters the structure and function of mitochondria. OPA1 is the main inner mitochondrial GTPase responsible for the fusion events. OPA1 undergoes proteolytic cleavage from long to short forms during acute stress and mitophagy. However, the exact role of OPA1 isoforms and related proteins during CS-induced mitophagy and COPD is not clear. METHODS: Lung tissues from non-smokers, smokers, COPD and IPF were used to determine the relative expression of OPA1 and related proteins. Additionally, we used mouse lungs from chronic (6 months) CS exposure to evaluate the status of OPA1. Primary lung fibroblasts from normal and COPD patients and naked mole rat (NMR) lung fibroblasts, human fetal lung fibroblast (HFL1), mouse embryonic fibroblast from wild type (WT), OPA1-/-, MFN1 and MFN2-/- were used to determine the effect of CS on OPA1 isoforms. Various mitochondrial fusion promoters/activators (BGP-15, leflunomide, M1) and fission inhibitor (DRP1) were used to determine their effect on OPA1 status and cigarette smoke extract (CSE)-induced lung epithelial (BEAS2B) cell damage, respectively. Seahorse flux analyzer was used to determine the effect of these compounds in BEAS2B cells with and without CSE exposure. FINDINGS: Short OPA1 isoforms were predominantly detected and significantly increased in COPD subjects. Acute CSE treatment in various cell lines except NMR was found to increase the conversion of long to short OPA1 isoforms. CSE treatment significantly increased mitochondrial stress-related protein SLP2 in all the cells used. OPA1 interacting partners like prohibitins (PHB1 and 2) were also altered depending on the CS exposure. Finally, BGP-15 and leflunomide treatment were able to preserve the long OPA1 isoform in cells treated with CSE. INTERPRETATION/CONCLUSION: The long OPA1 isoform along with SLP2 and prohibitins play a crucial role in CS-induced lung damage, causing mitophagy/mitochondrial dysfunction in COPD, which may be used as a novel therapeutic target in COPD.


Assuntos
Proteínas Mitocondriais , Doença Pulmonar Obstrutiva Crônica , Animais , Fibroblastos , GTP Fosfo-Hidrolases/genética , GTP Fosfo-Hidrolases/metabolismo , Humanos , Pulmão/metabolismo , Camundongos , Mitocôndrias , Proteínas Mitocondriais/genética , Proteínas Mitocondriais/metabolismo , Doença Pulmonar Obstrutiva Crônica/genética , Doença Pulmonar Obstrutiva Crônica/metabolismo , Fumaça/efeitos adversos , Tabaco , Fumar Tabaco
18.
Elife ; 102021 07 06.
Artigo em Inglês | MEDLINE | ID: mdl-34227468

RESUMO

Background: To understand a causal role of modifiable lifestyle factors in angiotensin-converting enzyme 2 (ACE2) expression (a putative severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2] receptor) across 44 human tissues/organs, and in coronavirus disease 2019 (COVID-19) susceptibility and severity, we conducted a phenome-wide two-sample Mendelian randomization (MR) study. Methods: More than 500 genetic variants were used as instrumental variables to predict smoking and alcohol consumption. Inverse-variance weighted approach was adopted as the primary method to estimate a causal association, while MR-Egger regression, weighted median, and MR pleiotropy residual sum and outlier (MR-PRESSO) were performed to identify potential horizontal pleiotropy. Results: We found that genetically predicted smoking intensity significantly increased ACE2 expression in thyroid (ß=1.468, p=1.8×10-8), and increased ACE2 expression in adipose, brain, colon, and liver with nominal significance. Additionally, genetically predicted smoking initiation significantly increased the risk of COVID-19 onset (odds ratio=1.14, p=8.7×10-5). No statistically significant result was observed for alcohol consumption. Conclusions: Our work demonstrates an important role of smoking, measured by both status and intensity, in the susceptibility to COVID-19. Funding: XJ is supported by research grants from the Swedish Research Council (VR-2018-02247) and Swedish Research Council for Health, Working Life and Welfare (FORTE-2020-00884).


Assuntos
Enzima de Conversão de Angiotensina 2/metabolismo , COVID-19/patologia , Análise da Randomização Mendeliana , SARS-CoV-2/fisiologia , Fumar Tabaco/efeitos adversos , Tecido Adiposo/metabolismo , Consumo de Bebidas Alcoólicas/genética , Enzima de Conversão de Angiotensina 2/genética , Encéfalo/metabolismo , COVID-19/virologia , Causalidade , Colo/metabolismo , Regulação da Expressão Gênica , Humanos , Fígado/metabolismo , Polimorfismo de Nucleotídeo Único , Glândula Tireoide/metabolismo
19.
Artigo em Inglês | MEDLINE | ID: mdl-34205612

RESUMO

Heated tobacco products (HTP) are a form of nicotine delivery intended to be an alternative to traditional cigarettes. HTP tobacco products are sold to consumers as a less harmful alternative to traditional cigarettes, both for users and bystanders. The actual impact of HTP on the health of users and its overall impact on public health is still not fully known. A systematic search of the literature was carried out to identify relevant studies published in English from 2015 to February 2021. The following databases were used: PubMed, Scopus, Elsevier and ClinicalKey. 25 studies (independent and sponsored by the tobacco industry) were considered. The analysis of exposure biomarkers and cardiovascular and respiratory biomarkers showed differences between smokers and people using heated tobacco products. Improvements in clinically relevant risk markers, especially cholesterol, sICAM-1, 8-epi-PGF2α, 11-DTX-B2, HDL and FEV1, were observed compared to persistent cigarette smokers. On the other hand, exposure to IQOS has been reported to alter mitochondrial function, which may further exaggerate airway inflammation, airway remodeling and lung cancer. These products have the potential to increase oxidative stress and increase respiratory tract infections by increasing microbial adherence to the respiratory tract. Our review suggests that HTP products may be products with a reduced risk of chronic diseases, including respiratory and cardiovascular diseases and cancer compared to traditional smoking, although in the case of non-smokers so far, they may pose a risk of their occurrence. Research seems to be necessary to assess the frequency of HTP use and its potential negative health effects.


Assuntos
Sistemas Eletrônicos de Liberação de Nicotina , Produtos do Tabaco , Humanos , Nicotina , Fumantes , Tabaco , Fumar Tabaco
20.
Artigo em Inglês | MEDLINE | ID: mdl-34200773

RESUMO

OBJECTIVES: We aimed to examine patterns in smoking and electronic nicotine delivery system (ENDS) use over an extended period of time (up to 20 weeks) in people who smoked and who had never previously made a successful quit attempt using an ENDS. DESIGN AND SETTING: We conducted a longitudinal mixed-methods study in Dunedin, New Zealand, during 2018 and 2019. PARTICIPANTS: Purposively selected participants (N = 45; age (≥18 years), gender, ethnicities, cigarettes/day) who wished to quit smoking. INTERVENTIONS: Participants were provided with a second-generation ENDS device (vape pen or starter "tank" device) at the start of their quit attempt, and asked to complete smartphone-based daily diary surveys assessing smoking and ENDS use. OUTCOME MEASURES: Sunburst plots and a sequence plot were used to describe weekly and daily patterns of smoking and ENDS use (smoking only, ENDS use only, dual use, abstinent). RESULTS: The most frequently reported movements among participants, classified according to their study week behaviour, occurred between dual use and exclusive ENDS use (and vice versa). A smaller group reported moving from dual use to exclusive smoking (and often back to dual use), and a small number reported moving between abstinence and different ENDS and smoked tobacco usage behaviours. Data visualisations focussing on those participants who had provided data during each of weeks 9-12 indicate that only a minority reported sustained dual use; instead, most participants indicated varied smoked tobacco and ENDS use, which included periods of dual use. CONCLUSIONS: The considerable variety observed within and between study participants suggests that high variability is typical rather than exceptional. Transitions from smoking to ENDS use may involve considerable periods of dual use, which is likely to be dynamic and potentially sustained over several months.


Assuntos
Sistemas Eletrônicos de Liberação de Nicotina , Abandono do Hábito de Fumar , Vaping , Adolescente , Humanos , Nova Zelândia/epidemiologia , Fumar , Fumar Tabaco
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...