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1.
JAMA Netw Open ; 5(5): e2210029, 2022 May 02.
Artigo em Inglês | MEDLINE | ID: mdl-35503218

RESUMO

Importance: Menthol cigarettes were prohibited in England in May 2020 and nationally in Canada in October 2017 but remain permitted in the US. Evidence on the outcomes of menthol cigarette bans among youth outside of Canada, and the characteristics of youth smokers, is lacking. Objectives: To evaluate the outcomes of menthol cigarette bans on youth menthol cigarette smoking and to characterize youth menthol cigarette smokers in terms of demographics and cigarette consumption and dependence. Design, Setting, and Participants: This survey study uses data from online repeat cross-sectional International Tobacco Control Youth Tobacco and Vaping Surveys conducted in 2018, 2019, February 2020, and August 2020. Participants included past 30-day smokers aged 16 to 19 years. Data analysis was performed from March 2021 to January 2022. Main Outcomes and Measures: Usually smoke a brand of cigarettes that was menthol, including capsule. Exposures: Menthol cigarette ban, comparing 3 countries over time: Canada, where a ban already existed, England, where a ban was implemented during the study, and the US, where no national ban was present. Age, sex, race, and consumption and dependence were also examined by menthol smoking in each country, and in England before vs after the ban. Results: The analytical sample comprised 7067 participants aged 16 to 19 years, of whom 4129 were female and 5019 were White. In England, the weighted percentage of youth smokers who reported smoking a menthol or capsule cigarette brand was stable in the 3 survey waves before the menthol ban (2018 to February 2020, 9.4% vs 12.1%; adjusted odds ratio [AOR], 1.03; 95% CI, 0.99-1.06; P = .15) but decreased to 3.0% after the ban (February 2020 vs August 2020, AOR, 1.07; 95% CI, 1.04-1.10; P < .001). The decrease between February and August 2020 in England was similar across all demographic groups but was greater among youth who perceived themselves as addicted to cigarettes (AOR, 0.37; 95% CI, 0.41-0.97; P = .04). In the 2 comparison countries, menthol or capsule smoking was stable across all waves (2018 to August 2020: US, 33.6%-36.9%; Canada, 3.1%-2.3%) and was more prevalent in the US than in England (AOR, 5.58; 95% CI, 4.63-6.72; P < .001). Menthol or capsule smoking was also more prevalent among smokers in England who were female vs male (10.9% vs 7.2%; AOR, 1.04; 95% CI, 1.01-1.06; P = .002); among smokers in the US who identified as Black vs White (60.6% vs 31.9%; AOR, 1.33; 95% CI, 1.23-1.44; P < .001) or who were frequent smokers (AOR, 1.07; 95% CI, 1.01-1.13; P = .03), smoked more cigarettes per day (2-5 vs 1, AOR, 1.09; 95% CI, 1.02-1.15; P = .006; >5 vs 1, AOR, 1.10; 95% CI, 1.03-1.18; P = .007), or had urges to smoke every or most days (AOR, 1.08; 95% CI, 1.02-1.14; P = .006); and among smokers in Canada who perceived themselves as addicted to cigarettes (AOR, 1.02; 95% CI, 1.00-1.03; P = .01). Conclusions and Relevance: In this survey study, the proportion of youth smokers who smoke menthol (including capsule) cigarettes decreased substantially after the menthol ban in England. This association was consistent across all demographic groups. Perceived addiction among menthol smokers was also lower where menthol cigarettes were banned.


Assuntos
Fumar Cigarros , Abandono do Hábito de Fumar , Produtos do Tabaco , Adolescente , Canadá/epidemiologia , Fumar Cigarros/epidemiologia , Estudos Transversais , Inglaterra/epidemiologia , Feminino , Humanos , Masculino , Mentol , Tabaco
2.
BMJ Open ; 12(5): e058324, 2022 May 02.
Artigo em Inglês | MEDLINE | ID: mdl-35501081

RESUMO

OBJECTIVE: We sought to quantify the impact of vaping introduction on cigarette smoking across settings with varied regulatory approaches to vaping. DESIGN: Interrupted time series analysis, adjusted for cigarette tax levels. SETTING: Four Canadian provinces, UK and Australia. PARTICIPANTS: Entire population of smokers in each country. INTERVENTIONS: The year that vaping was widely introduced in each country. PRIMARY AND SECONDARY OUTCOME MEASURES: The primary outcome is cigarette consumption per adult, and the secondary outcome is smoking prevalence among young adults. RESULTS: Based on allowable nicotine levels, restrictions on e-cigarette advertising, sales and access, and taxation, the least to most restrictive jurisdictions were, in order, Alberta, Ontario, Quebec and British Columbia (all in Canada), UK and Australia. In most, but not all, settings where higher nicotine content was permitted in vaping products (66 mg/mL), vaping introduction led to a reduction in cigarette consumption per capita (Ontario: p=0.037, Quebec: p=0.007) or in smoking prevalence among young adults (Alberta men, p=0.027; Quebec men, p=0.008; Quebec women, p=0.008). In the UK, where the maximum permitted nicotine content in vaping products was 20 mg/mL, vaping introduction slowed the declining trend in cigarette smoking among men aged 16-24 years (p=0.031) and 25-34 years (p=0.002) but not in cigarette consumption per adult. In Australia, where nicotine was not permitted in e-cigarettes, e-cigarette introduction slowed the declining trend in cigarette consumption per capita and in smoking prevalence among men aged 18-24 years (cigarette consumption: p=0.015, prevalence: p=0.044). CONCLUSION: In environments that enable substitution of cigarettes with e-cigarettes, e-cigarette introduction reduces overall cigarette consumption. Thus, to reduce cigarette smoking, policies that encourage adults to substitute cigarette smoking with vaping should be considered.


Assuntos
Fumar Cigarros , Sistemas Eletrônicos de Liberação de Nicotina , Vaping , Fumar Cigarros/epidemiologia , Feminino , Humanos , Análise de Séries Temporais Interrompida , Masculino , Nicotina , Ontário , Vaping/epidemiologia , Adulto Jovem
3.
Front Immunol ; 13: 887681, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35514978

RESUMO

There is a high incidence of tobacco use among intravenous opioid drug users. It is well established that opioids and tobacco smoke induce a degree of immune activation, and recent work suggests that the combination of these drugs promotes further activation of the immune system. Our approach involved the treatment of wild-type mice with cigarette smoke (SM) for a period of eight weeks, and the chronic continuous administration of morphine (M) via mini-pumps for the final four weeks. In an effort to examine the responses of CD4+CD25highCD127low regulatory T (Treg) cells, the major immune suppressive cell type, to the combined chronic administration of SM and M, we determined the frequency of these cells in the spleen, lymph nodes and lungs. Flow cytometric analyses showed that SM and M individually, and the combination (SM + M) have differential effects on the numbers of Treg in the spleen, lymph node, and lung. Either SM or M alone increased Treg cell numbers in the spleen, but SM+M did not. Furthermore, SM + M decreased Treg cell numbers in the lymph node and lung. We then performed RNA-Seq on Treg cells from mice treated with SM, M, or SM + M, and we found that the S + M induced a number of significant changes in the transcriptome, that were not as apparent following treatment with either SM or M alone. This included an activation of TWEAK, PI3K/AKT and OXPHOS pathways and a shift to Th17 immunity. Our results have provided novel insights on tissue Treg cell changes, which we suggest are the result of transcriptomic reprogramming induced by SM, M, and SM + M, respectively. We believe these results may lead to the identification of novel therapeutic targets for suppressing smoke and opioid induced Treg cell impairment.


Assuntos
Fumar Cigarros , Linfócitos T Reguladores , Analgésicos Opioides/farmacologia , Animais , Camundongos , Morfina/farmacologia , Fosfatidilinositol 3-Quinases/metabolismo , Transcriptoma
4.
Braz Dent J ; 33(2): 99-108, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35508042

RESUMO

Considering that smoking is a public health problem that has been growing among adolescents, the aim of this study was to investigate the impact of cigarette smoke on osteogenic and osteoclastogenic signaling in middle palatal suture of rats. Male Wistar rats exposed (n = 30) or not to cigarette smoke (n = 30) were used. Exposure to smoke was carried out for two daily periods of 3 minutes each, with an interval of 12 hours between exposures. After the experimental periods of 3, 7, 14 and 21 days, the animals were euthanized. The collected tissues were analyzed using light microscopy and real-time RT-PCR was performed to investigate gene expression. The data obtained were compared using the Kruskal Wallis and Dunn tests (⍺ = 5%). Morphologically, there were no significant changes in the middle palatal suture of rats exposed or not to cigarette smoke during 3, 7, 14 and 21 days (p> 0.05). On the other hand, osteoclastogenic signaling was increased in animals exposed to smoke and was characterized by a higher production of RANKL at 3 and 14 days (p <0.05), with no change in the synthesis of RANK and osteoprotegerin (p> 0.05). Interestingly, in the exposed animals, an early increase in the synthesis of osteocalcin, bone sialoprotein and osteopontin was also identified at 3 days of exposure (p <0.05), not sustained over time (p> 0.05). Cigarette smoke modulates osteogenic and osteoclastogenic signaling in the middle palatal suture of young rats, although morphological changes have not been evidenced.


Assuntos
Fumar Cigarros , Osteoclastos , Animais , Masculino , Ratos , Ratos Wistar , Suturas
5.
Respir Res ; 23(1): 110, 2022 May 04.
Artigo em Inglês | MEDLINE | ID: mdl-35509068

RESUMO

BACKGROUND: Retinoid-related orphan receptor-α (RORα) and autophagy dysregulation are involved in the pathophysiology of chronic obstructive pulmonary disease (COPD), but little is known regarding their association. We investigated the role of RORα in COPD-related autophagy. METHODS: The lung tissues and cells from a mouse model were analyzed for autophagy markers by using western blot analysis and transmission electron microscopy. RESULTS: Cigarette smoke increased the LC3-II level and decreased the p62 level in whole lung homogenates of a chronic cigarette smoking mouse model. Although cigarette smoke did not affect the levels of p62 in Staggerer mutant mice (RORαsg/sg), the baseline expression levels of p62 were significantly higher than those in wild type (WT) mice. Autophagy was induced by cigarette smoke extract (CSE) in Beas-2B cells and in primary fibroblasts from WT mice. In contrast, fibroblasts from RORαsg/sg mice failed to show CSE-induced autophagy and exhibited fewer autophagosomes, lower LC3-II levels, and higher p62 levels than fibroblasts from WT mice. Damage-regulated autophagy modulator (DRAM), a p53-induced modulator of autophagy, was expressed at significantly lower levels in the fibroblasts from RORαsg/sg mice than in those from WT mice. DRAM knockdown using siRNA in Beas-2B cells inhibited CSE-induced autophagy and cell death. Furthermore, RORα co-immunoprecipitated with p53 and the interaction increased p53 reporter gene activity. CONCLUSIONS: Our findings suggest that RORα promotes autophagy and contributes to COPD pathogenesis via regulation of the RORα-p53-DRAM pathway.


Assuntos
Fumar Cigarros , Doença Pulmonar Obstrutiva Crônica , Animais , Autofagia , Fumar Cigarros/efeitos adversos , Camundongos , Membro 1 do Grupo F da Subfamília 1 de Receptores Nucleares/genética , Membro 1 do Grupo F da Subfamília 1 de Receptores Nucleares/metabolismo , Doença Pulmonar Obstrutiva Crônica/metabolismo , Tabaco , Proteína Supressora de Tumor p53/efeitos adversos
6.
Open Biol ; 12(4): 210310, 2022 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-35472288

RESUMO

Cigarette smoke significantly induces oxidative stress, resulting in cardiovascular disease. NRF2, a well-known antioxidative stress response factor, is generally considered to play protective roles in cardiovascular dysfunction triggered by oxidative stress. Interestingly, recent studies reported adverse effects of NRF2 on the cardiovascular system. These unfavourable pathogenic effects of NRF2 need to be further investigated. Our work shows that cigarette smoke extract (CSE)-induced oxidative stress disturbs fibronectin (FN) assembly during angiogenesis. Furthermore, this effect largely depends on hyperactive NRF2-STAT3 signalling, which consequently promotes abnormal FN deposition. Consistently, disruption of this pathway by inhibiting NRF2 or STAT3 prevents CSE-induced FN disorganization and vasculature disruption in human umbilical vein endothelial cells or zebrafish. Taken together, these findings demonstrate the cardiovascular dysfunction caused by CSE from a novel perspective that NRF2-dependent signalling engages in FN disorganization.


Assuntos
Fumar Cigarros , Fator 2 Relacionado a NF-E2 , Animais , Células Endoteliais/metabolismo , Fibronectinas/metabolismo , Fibronectinas/farmacologia , Fator 2 Relacionado a NF-E2/genética , Fator 2 Relacionado a NF-E2/metabolismo , Estresse Oxidativo , Tabaco , Peixe-Zebra/metabolismo
7.
Hum Exp Toxicol ; 41: 9603271221088996, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35382644

RESUMO

With the development of the times, electronic cigarettes (e-cigarettes) are being received by more and more people. We compared the different effects of e-cigarettes and tobacco cigarettes on human umbilical vein endothelial cells (HUVECs) treated with the typical e-cigarette aerosol extracts (ECA) and cigarette smoking extracts (CS) sourced from commercial retail stores. HUVECs were treated with different kinds of ECA or CS with different nicotinic concentrations (0.03125, 0.125, 0.5, 2, 8, or 32 µg/mL). Cell viability was examined by the MTT assay. The cell apoptosis was investigated by acridine orange (AO) and Hoechst 33258 staining. The RT-PCR and western blot assays were used to analyze the adhesion molecules and inflammation cytokines released by HUVECs. Furthermore, the intracellular reactive oxygen species (ROS) was observed by fluorescence microscopy. Our data showed that the CS (nicotine concentration at 0.125 µg/mL could decrease the viability of HUVECs by 71%, but not the four kinds of ECA. The apoptotic ratio was about 32.5% in the CS group. No matter the levels of adhesion molecules, inflammation cytokines or ROS, they were higher in CS groups than in ECA groups. Overall, the four kinds of e-cigarettes induced significantly less cytotoxicity than the commercially available tobacco cigarettes in HUVECs. The CS showed the most severe impact on HUVECs. ECA might provide a harm reduction measure, especially in cardiovascular risk, after people switch from tobacco cigarettes to e-cigarettes.


Assuntos
Fumar Cigarros , Sistemas Eletrônicos de Liberação de Nicotina , Aerossóis , Células Endoteliais da Veia Umbilical Humana , Humanos , Inflamação , Tabaco/toxicidade
8.
Artigo em Inglês | MEDLINE | ID: mdl-35378837

RESUMO

Background: Prohibitin has been identified to play roles in cell survival and apoptosis. Here, this study aimed to clarify the role of prohibitin in cigarette smoke extract (CSE)-induced endothelial cell apoptosis. Methods: The protein level of prohibitin was assessed by Western blot in lung tissues from emphysema and control mice. CSE-induced human pulmonary microvascular endothelial cells (hPMECs) were applied to mimic smoke-related cell apoptosis in vitro. Prohibitin was overexpressed in hPMECs with or without CSE. Mitochondrial function was analyzed by JC-1 staining and ATP assay kits. Oxidative stress was assessed by flow cytometry, fluorescence staining and immunocytochemistry. Apoptosis was analyzed by flow cytometry, Western blot and caspase-3 activity assays. In addition, the expression of inflammatory markers was assessed by Western blot and real-time polymerase chain reaction (PCR). The secretion of inflammatory cytokines was measured by ELISA. Results: Prohibitin was downregulated in emphysema mouse tissues compared with control experiments. Consistently, CSE inhibited both the protein and RNA levels of prohibitin in hPMECs in a dose-dependent manner. Gain-of-function experiments indicated that CSE induced collapse of mitochondrial membrane potential (MMP) and loss of ATP, while prohibitin improved mitochondrial function. CSE induced robust ROS production and oxidative DNA damage, while prohibitin decreased this damage. Upregulation of prohibitin protected the apoptosis of hPMECs from CSE. Overexpression of prohibitin significantly reduced the levels of the main proinflammatory cytokines. Finally, prohibitin inhibited nuclear factor-kappa B (NF-κB) p65 accumulation and IκBα degradation induced by CSE. Conclusion: The current findings suggest that CSE-mediated mitochondrial dysfunction, oxidative stress, cell apoptosis and inflammation in hPMECs were reduced by overexpression of prohibitin. We identified prohibitin as a novel regulator of endothelial cell apoptosis and survival in the context of CSE exposure.


Assuntos
Fumar Cigarros , Doença Pulmonar Obstrutiva Crônica , Animais , Apoptose , Células Endoteliais/metabolismo , Humanos , Inflamação/metabolismo , Inflamação/prevenção & controle , Pulmão/metabolismo , Camundongos , Doença Pulmonar Obstrutiva Crônica/metabolismo
9.
Medicina (Kaunas) ; 58(4)2022 Mar 31.
Artigo em Inglês | MEDLINE | ID: mdl-35454341

RESUMO

Background and Objectives: Cigarette smoking among the youth population has increased significantly in developing countries, including Bosnia and Herzegovina. However, no extant literature assesses the prevalence of tobacco use, nor identifies factors associated with smoking. This study determined the prevalence of cigarette smoking among a specific cohort of students and assessed factors related to tobacco use in this population. Materials and Methods: This cross-sectional study included 1200 students at all faculties of Banja Luka University. Data were collected from questionnaires adapted from the Global Youth Tobacco Survey (GYTS) and the Global Health Professional Student Survey (GHPSS) standardized questionnaires and were analyzed using descriptive statistics, Pearson's χ2 test, and logistic regression. Results: When the prevalence of cigarette smoking within the last thirty days was recorded, we found that 34.1% of students smoked within this period. Nearly three-quarters (74.9%) of the student population had smoked or experimented with cigarette smoking. However, medical students were 27.2% less likely to smoke than their counterparts from other faculties. Overall, 87% of all students were aware of the harmful effects of cigarette smoking, 79% were aware of the harmful effects of secondhand smoke, and 65% reported that it was difficult to quit. Increased spending of personal money was associated with a higher probability of smoking, while exposure to secondhand smoke increased the odds of smoking by 62%. Conclusion: Policies, strategies, and action plans should be introduced in order to reduce the prevalence of smoking among university students and to create a smoke-free environment at the various universities involved.


Assuntos
Fumar Cigarros , Estudantes de Medicina , Poluição por Fumaça de Tabaco , Adolescente , Fumar Cigarros/epidemiologia , Estudos Transversais , Humanos , Prevalência , Inquéritos e Questionários , Tabaco
10.
BMC Pulm Med ; 22(1): 139, 2022 Apr 11.
Artigo em Inglês | MEDLINE | ID: mdl-35410206

RESUMO

BACKGROUND: Mesenchymal stem cells (MSCs) have shown therapeutic potential for engraftment to, differentiation into, endothelial cells (ECs). However, low-efficiency yields hinder their use as ECs for therapeutic vascularization. METHODS: The Notch1 signaling pathway is key to optimal pulmonary development. Recent evidence has shown that this pathway participated in angiogenesis. Herein, we found that in MSCs, Jagged1 was a target for Notch 1, resulting in a positive feedback loop that propagated a wave of ECs differentiation. RESULTS: In vitro, Jagged1 was found to be activated by Notch1 in MSCs, resulting in the RBP-Jκ-dependent expression of Jagged1 mRNA, a response that was blocked by Notch1 inhibition. Notch1 promoted the formation of cord-like structures on Matrigel. However, cigarette smoke extract inhibited this process, compared to that in control groups. Moreover, Notch1-overexpressing cells upregulated the expressing of HIF-1α gene. The HIF-1α was an angiogenic factor that clustered with Notch1, underscoring the critical role of Notch1 pathway in vessel assembly. Interestingly, this was abrogated by incubation with Notch1 shRNA. CONCLUSIONS: Notch signaling pathway promotes differentiation of MSCs in to ECs. It also regulates angiogenesis and transcription of specific markers on ECs. These results provide a mechanism that regulates differentiation of MSCs into ECs phenotypes.


Assuntos
Fumar Cigarros , Células-Tronco Mesenquimais , Diferenciação Celular , Células Endoteliais/metabolismo , Humanos , Neovascularização Patológica/genética , Receptor Notch1/genética
11.
BMJ Open ; 12(3): e049646, 2022 Mar 31.
Artigo em Inglês | MEDLINE | ID: mdl-35361635

RESUMO

OBJECTIVES: The relationship between smoking and ovarian reserve markers is inconclusive. The primary objective of our study was to assess the effect of cigarette smoking on the quantitative ovarian reserve parameters, serum anti-Mullerian hormone (AMH) and antral follicle count (AFC) as relevant to prediction of fertility outcomes in women seeking fertility treatment. Our secondary aims were to validate self-reported smoking behaviour using biomarkers and evaluate the association between biomarkers of ovarian reserve (serum AMH and AFC) with biomarkers of smoking exposure (breath carbon monoxide (CO) and urine cotinine levels). DESIGN: Prospective, cross-sectional study. SETTING: Single tertiary care fertility centre. PARTICIPANTS: Women ≤35 years seeking fertility treatment. PRIMARY OUTCOME MEASURES: Serum AMH and AFC. RESULTS: Significant differences were found among current smokers, ex-smokers and never smokers for breath CO (F(2,97)=33.32, p<0.0001) and urine cotinine levels (p<0.001). However, no significant differences were found either for serum AMH (F(2,91)=1.19, p=0.309) or total AFC (F(2,81)=0.403, p=0.670) among the three groups. There was no significant correlation between pack years of smoking and serum AMH (r=-0.212, n=23, p=0.166) or total AFC (r=-0.276, n=19, p=0.126). No significant correlation was demonstrated between breath CO and serum AMH (r=0.082, n=94, p=0.216) or total AFC (r=0.096, n=83, p=0.195). Similarly, no significant correlation was demonstrated between urine cotinine levels and serum AMH (r=0.146, n=83, p=0.095) or total AFC (r=-0.027, n=77, p=0.386). CONCLUSION: We did not find a statistically significant difference in quantitative ovarian reserve markers between current smokers, ex-smokers and never smokers which would be clinically meaningful in our study population. We confirmed that self-reported smoking correlates well with quantitatively measured biomarkers of smoking. This validated the self-reported comparison groups to ensure a valid comparison of outcome measures. There was no significant association between biomarkers of smoking and biomarkers of ovarian reserve. We were also unable to demonstrate a correlation between the lifetime smoking exposure and ovarian reserve.


Assuntos
Hormônio Antimülleriano , Fumar Cigarros , Infertilidade Feminina , Folículo Ovariano , Adulto , Hormônio Antimülleriano/sangue , Fumar Cigarros/efeitos adversos , Estudos Transversais , Feminino , Humanos , Infertilidade Feminina/terapia , Folículo Ovariano/diagnóstico por imagem , Estudos Prospectivos
12.
COPD ; 19(1): 206-215, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35416743

RESUMO

A high smoking-independent chronic obstructive pulmonary disease (COPD) prevalence is observed in lung cancer patients. However, the underlying connection between these two diseases still remains unclear. Cigarette smoking and ambient air pollution are common risk factors for COPD and lung cancer. In this study, we established rat COPD model through exposure to cigarette smoke (CS) or motor vehicle exhaust (MVE). The model rats developed COPD-like phenotypes, manifested as lung functions decline, lung inflammation, emphysema-like alveolar enlargement and airway remodeling. The programmed death-ligand 1 (PD-L1), a factor contributing to immune escape of tumor cells, was overexpressed in lungs from COPD model rats, though more severe COPD phenotypes did not bring with further PD-L1 overexpression in lung. The upregulations of proinflammatory cytokines and PD-L1 were also observed in cultured human bronchial epithelial cells BEAS-2B upon treatment with cigarette smoke extract (CSE) or diesel-related particulate matter 2.5 (PM2.5, SEM1650b). The inflammatory cytokines produced in BEAS-2B cells reflected the PD-L1 levels. Furthermore, ERK1/2, a kinase mediating PD-L1 upregulation in premalignant bronchial cells or NSCLC cells, and STAT1/3, which was reportedly associated with PD-L1 expression in lung tumors, were activated in COPD rats' lungs or in BEAS-2B cells treated with CSE or PM2.5. Therefore, we proposed that inflammation associated PD-L1 overexpression in airway epithelial cells could be the underlying factor facilitating lung cancer incidence in COPD.


Assuntos
Fumar Cigarros , Neoplasias Pulmonares , Doença Pulmonar Obstrutiva Crônica , Animais , Antígeno B7-H1/genética , Antígeno B7-H1/metabolismo , Fumar Cigarros/efeitos adversos , Citocinas/metabolismo , Células Epiteliais/metabolismo , Humanos , Pulmão/patologia , Neoplasias Pulmonares/complicações , Camundongos , Camundongos Endogâmicos C57BL , Veículos Automotores , Material Particulado/toxicidade , Doença Pulmonar Obstrutiva Crônica/metabolismo , Ratos , Tabaco/metabolismo , Tabaco/toxicidade , Regulação para Cima
13.
Lancet Respir Med ; 10(5): 485-496, 2022 May.
Artigo em Inglês | MEDLINE | ID: mdl-35427534

RESUMO

Chronic obstructive pulmonary disease (COPD) is a deadly and highly morbid disease. Susceptibility to and heterogeneity of COPD are incompletely explained by environmental factors such as cigarette smoking. Family-based and population-based studies have shown that a substantial proportion of COPD risk is related to genetic variation. Genetic association studies have identified hundreds of genetic variants that affect risk for COPD, decreased lung function, and other COPD-related traits. These genetic variants are associated with other pulmonary and non-pulmonary traits, demonstrate a genetic basis for at least part of COPD heterogeneity, have a substantial effect on COPD risk in aggregate, implicate early-life events in COPD pathogenesis, and often involve genes not previously suspected to have a role in COPD. Additional progress will require larger genetic studies with more ancestral diversity, improved profiling of rare variants, and better statistical methods. Through integration of genetic data with other omics data and comprehensive COPD phenotypes, as well as functional description of causal mechanisms for genetic risk variants, COPD genetics will continue to inform novel approaches to understanding the pathobiology of COPD and developing new strategies for management and treatment.


Assuntos
Fumar Cigarros , Doença Pulmonar Obstrutiva Crônica , Estudos de Associação Genética , Predisposição Genética para Doença , Humanos , Pulmão , Fenótipo , Doença Pulmonar Obstrutiva Crônica/genética
14.
BMJ Open ; 12(4): e056209, 2022 Apr 29.
Artigo em Inglês | MEDLINE | ID: mdl-35487748

RESUMO

OBJECTIVE: To evaluate smoking status and its influencing factors in high-income areas of China. DESIGN: Cross-sectional. SETTING: High-income areas in China. PARTICIPANTS: 4064 persons aged 15 years or older from the survey results in Global Adult Tobacco Survey-China 2018. METHODS: Gross national income data were used to determine China's high-income economic regions, and the results of the survey in Global Adult Tobacco Survey-China 2018 were used for statistical analysis. RESULTS: A total of 4064 people were included in our study, including 881 current smokers, 2884 who had never smoked and 299 who had quit smoking. Using the standardised rate method, the standardised smoking rates in high-income and non-high-income areas in China were calculated to be 23.56% and 27.77%, respectively. Men, high school education or below, knowledge of e-cigarette information, permission to smoke at home and people with poor smoking health literacy are the main influencing factors of smokers in high-income areas of China. CONCLUSION: The smoking rate of people in China's high-income areas is lower than the overall smoking rate in China, and we should increase the public awareness that smoking is harmful to health, encourage the prohibition of smoking at home, increase investment in higher education and improve residents' smoking health literacy level. The purpose of this study was to encourage reduction in the rate of smoking and better control the prevalence of smoking.


Assuntos
Fumar Cigarros , Sistemas Eletrônicos de Liberação de Nicotina , Adulto , China/epidemiologia , Fumar Cigarros/epidemiologia , Estudos Transversais , Humanos , Masculino , Tabaco
15.
Sci Rep ; 12(1): 5446, 2022 03 31.
Artigo em Inglês | MEDLINE | ID: mdl-35361852

RESUMO

We report cessation behaviors, reasons for use of electronic cigarettes (EC) and heated tobacco products (HTP) and association of their use with quit attempts and smoking intensity using Romania Global Adult Tobacco Survey 2018. Weighted estimates of EC and HTP by cigarette smoking (CS) status were assessed. Quit attempts, intention to quit, reasons for lack of intention to quit among current CS, and reasons for current use of EC and HTP were estimated. The association of 'ever use' of EC and HTP with cigarette smoking intensity and quit attempts was explored using binary logistic regression. Of the total 4571 surveyed, 1243 (27.3%) were current CS, 300 (24.4%) made quit attempts in the past 12 months. Only 38 (12.5%) and 26 (8.6%) had used EC and HTP as an aid to quit. Among current CS, 512 (41.2%) had no intention to quit. Reasons for this were, 'enjoy smoking' (86.1%), 'reduce stress' (65.9%), and 'staying alert' (46.3%). Awareness and use of EC and HTP were significantly higher among current CS. 'Dual use' of EC and HTP with CS was manifolds higher than stand-alone use. Reasons for current use of EC and HTP were 'enjoyment', and 'use in places where smoking was prohibited'.


Assuntos
Fumar Cigarros , Sistemas Eletrônicos de Liberação de Nicotina , Abandono do Hábito de Fumar , Produtos do Tabaco , Adulto , Humanos , Romênia
16.
BMC Med Genomics ; 15(1): 76, 2022 04 03.
Artigo em Inglês | MEDLINE | ID: mdl-35369880

RESUMO

BACKGROUND: Acute exposure to cigarette smoke alters gene expression in several biological pathways such as apoptosis, immune response, tumorigenesis and stress response, among others. However, the effects of electronic nicotine delivery systems (ENDS) on early changes in gene expression is relatively unknown. The objective of this study was to evaluate the early toxicogenomic changes using a fully-differentiated primary normal human bronchial epithelial (NHBE) culture model after an acute exposure to cigarette and ENDS preparations. RESULTS: RNA sequencing and pathway enrichment analysis identified time and dose dependent changes in gene expression and several canonical pathways when exposed to cigarette preparations compared to vehicle control, including oxidative stress, xenobiotic metabolism, SPINK1 general cancer pathways and mucociliary clearance. No changes were observed with ENDS preparations containing up to 28 µg/mL nicotine. Full model hierarchical clustering revealed that ENDS preparations were similar to vehicle control. CONCLUSION: This study revealed that while an acute exposure to cigarette preparations significantly and differentially regulated many genes and canonical pathways, ENDS preparations containing the same concentration of nicotine had very little effect on gene expression in fully-differentiated primary NHBE cultures.


Assuntos
Fumar Cigarros , Sistemas Eletrônicos de Liberação de Nicotina , Células Epiteliais , Expressão Gênica , Humanos , Nicotina/metabolismo , Nicotina/farmacologia , Tabaco , Inibidor da Tripsina Pancreática de Kazal/metabolismo , Inibidor da Tripsina Pancreática de Kazal/farmacologia
17.
Artigo em Inglês | MEDLINE | ID: mdl-35409765

RESUMO

Carcinogenic effects of tobacco smoke may affect breast tumorigenesis. To assess whether cigarette smoking is associated with breast cancer characteristics, we investigated the relationships between smoking, pathological characteristics, and outcomes in 2153 women diagnosed with breast cancer 2001-2016. Patients were classified as never, former, or current smokers at the time of diagnosis. Logistic regression and multivariable Cox proportional hazards analysis were performed to determine whether smoking was associated with tumor characteristics. Multivariable Cox proportional hazards analysis was conducted to compare former or current smokers to never smokers in survival with adjustment for the potential confounders. The majority of women (61.8%) never smoked, followed by former smokers (26.2%) and current smokers (12.0%). After adjustment for demographic variables, body mass index, and comorbidities, tumor characteristics were not significantly associated with smoking status or pack-years smoked. Ten-year overall survival was significantly lower for former and current smokers compared to never smokers (p = 0.0105). However, breast cancer specific survival did not differ significantly between groups (p = 0.1606). Although cigarette smoking did not alter the underlying biology of breast tumors or breast cancer-specific survival, overall survival was significantly worse in smokers, highlighting the importance of smoking cessation in the recently diagnosed breast cancer patient.


Assuntos
Neoplasias da Mama , Fumar Cigarros , Abandono do Hábito de Fumar , Neoplasias da Mama/diagnóstico , Fumar Cigarros/efeitos adversos , Fumar Cigarros/epidemiologia , Comorbidade , Feminino , Humanos , Fatores de Risco , Tabaco
18.
Tomography ; 8(2): 1024-1032, 2022 04 03.
Artigo em Inglês | MEDLINE | ID: mdl-35448716

RESUMO

PURPOSE: The aim of this study was to evaluate the role of Pi10 in patients with fibrotic interstitial lung abnormality (fibrotic ILA) in a chest CT, according to cumulative cigarette smoking. METHODS: We retrospectively assessed 54 fibrotic ILA patients and 18 healthy non-smokers (control) who underwent non-enhanced CT and pulmonary function tests. We quantitatively analyzed airway changes (the inner luminal area, airway inner parameter, airway wall thickness, Pi10, skewness, and kurtosis) in the chest CT of fibrotic ILA patients, and the fibrotic ILA patients were categorized into groups based on pack-years: light, moderate, heavy. Airway change data and pulmonary function tests among the three groups of fibrotic ILA patients were compared with those of the control group by one-way ANOVA. RESULTS: Mean skewness (2.58 ± 0.36) and kurtosis (7.64 ± 2.36) in the control group were significantly different from those of the fibrotic ILA patients (1.89 ± 0.37 and 3.62 ± 1.70, respectively, p < 0.001). In fibrotic ILA group, only heavy smokers had significantly increased Pi10 (mean increase 0.04, p = 0.013), increased airway wall thickness of the segmental bronchi (mean increase 0.06 mm, p = 0.005), and decreased lung diffusing capacity for carbon monoxide (p = 0.023). CONCLUSION: Pi10, as a biomaker of quantitative CT in fibrotic ILA patients, can reveal that smoking affects airway remodeling.


Assuntos
Fumar Cigarros , Doenças Pulmonares Intersticiais , Humanos , Pulmão/diagnóstico por imagem , Doenças Pulmonares Intersticiais/diagnóstico por imagem , Estudos Retrospectivos , Tomografia Computadorizada por Raios X
19.
JAMA ; 327(16): 1566-1576, 2022 04 26.
Artigo em Inglês | MEDLINE | ID: mdl-35471512

RESUMO

Importance: Tobacco use is highly concentrated in persons with mental illness. Objectives: To assess trends in past-month prevalence of cigarette smoking among adults with vs without past-year depression, substance use disorders (SUDs), or both, using nationally representative data. Design, Setting, and Participants: Exploratory, serial, cross-sectional study based on data from 558 960 individuals aged 18 years or older who participated in the 2006-2019 US National Surveys on Drug Use and Health. Exposure: Past-year major depressive episode (MDE) and SUD using Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition, Text Revision) criteria. Main Outcomes and Measures: Past-month self-reported cigarette use, adjusted for sociodemographic characteristics. Results: Of the sampled 558 960 adults, 41.4% (unweighted) were aged 18 to 25 years, 29.8% (unweighted) were aged 26 to 49 years, and 53.4% (unweighted) were women. From 2006 to 2019, the past-month self-reported cigarette smoking prevalence declined significantly among adults with MDE from 37.3% to 24.2% for an average annual percent change of -3.2 (95% CI, -3.5 to -2.8; P < .001), adults with SUD from 46.5% to 35.8% for an average annual percent change of -1.7 (95% CI, -2.8 to -0.6; P = .002), and adults with co-occurring MDE and SUD from 50.7% to 37.0% for an annual average annual percent change of -2.1 (95% CI, -3.1 to -1.2; P < .001). The prevalence declined significantly for each examined age, sex, and racial and ethnic subgroup with MDE and with SUD (all P < .05), except for no significant changes in American Indian or Alaska Native adults with MDE (P = .98) or with SUD (P = .46). Differences in prevalence of cigarette smoking between adults with vs without MDE declined significantly for adults overall from 11.5% to 6.6%, for an average annual percent change of -3.4 (95% CI, -4.1 to -2.7; P < .001); significant average annual percent change declines were also seen for men (-5.1 [95% CI, -7.2 to -2.9]; P < .001); for women (-2.7 [95% CI, -3.9 to -1.5]; P < .001); for those aged 18 through 25 years (-5.2 [95% CI, -7.6 to -2.8]; P < .001); for those aged 50 years or older (-4.7 [95% CI, -8.0 to -1.2]; P = .01); for Hispanic individuals (-4.4 [95% CI, -8.0 to -0.5]; P = .03), and for White individuals (-3.6 [95% CI, -4.5 to -2.7]; P < .001). For American Indian or Alaska Native adults, prevalence did not significantly differ between those with vs without MDE during 2006-2012 but was significantly higher for those with MDE during 2013-2019 (difference, 11.3%; 95% CI, 0.9 to 21.7; P = .04). Differences among those with vs without SUD declined for women for an average annual percent change of -1.8 (95% CI, -2.8 to -0.9; P = .001). Conclusions and Relevance: In this exploratory, serial, cross-sectional study, there were significant reductions in the prevalence of self-reported cigarette smoking among US adults with major depressive episode, substance use disorder, or both, between 2006 and 2019. However, continued efforts are needed to reduce the prevalence further.


Assuntos
Fumar Cigarros , Transtorno Depressivo Maior , Transtornos Relacionados ao Uso de Substâncias , Adolescente , Adulto , Fumar Cigarros/epidemiologia , Estudos Transversais , Depressão/epidemiologia , Transtorno Depressivo Maior/epidemiologia , Feminino , Humanos , Masculino , Prevalência , Transtornos Relacionados ao Uso de Substâncias/epidemiologia , Adulto Jovem
20.
Front Immunol ; 13: 846605, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35386685

RESUMO

Cigarette smoking is reported in about one third of adults worldwide. A strong relationship between cigarette smoke exposure and chronic obstructive pulmonary disease (COPD) as well as lung cancer has been proven. However, about 15% of lung cancer cases, and between one fourth and one third of COPD cases, occur in never-smokers. The effects of cigarette smoke on the innate as well as the adaptive immune system have been widely investigated. It is assumed that certain immunologic features contribute to lung cancer and COPD development in the absence of smoking as the major risk factor. In this article, we review different immunological aspects of lung cancer and COPD with a special focus on non-smoking related risk factors.


Assuntos
Fumar Cigarros , Neoplasias Pulmonares , Doença Pulmonar Obstrutiva Crônica , Adulto , Causalidade , Fumar Cigarros/efeitos adversos , Humanos , Neoplasias Pulmonares/complicações , Doença Pulmonar Obstrutiva Crônica/etiologia , Fatores de Risco , Tabaco
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