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1.
Pathol Oncol Res ; 28: 1610495, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36091938

RESUMO

Aim: In this study, we aimed to evaluate the associations of vascular endothelial growth factor (VEGF) gene single nucleotide polymorphisms (SNPs) and its interaction with current smoking with gastric cancer (GC) risk in the Chinese Han population. Methods: We used logistic regression model to test the association between VEGF gene polymorphism and the risk of GC. The association strength was evaluated by odds ratio (OR) and 95% confidence interval (CI) calculated using logistic regression. Generalized multifactor dimensionality reduction (GMDR) was used to analyze the effect of the interaction between VEGF gene and current smoking on GC risk. Results: Logistic regression analysis showed that the risk of GC was significantly higher in rs10434 -G allele carriers than that in AA genotype carriers (AG + GG and AA), and the adjusted OR (95% CI) = 1.64 (1.24-2.08). In addition, we found a significantly higher GC risk in subjects with rs833061-T allele than those with CC allele (CT + TT and CC), adjusted or (95% CI) = 1.43 (1.10-1.87). We also found a statistically significant two- locus model (p = 0.018), including rs10434 and current smoking, indicating a significant interaction between rs10434 and current smoking on the risk of GC. Hierarchical analysis found that current smokers with AG or GG genotype have the highest GC risk, compared to never- smokers with AA genotype, OR (95% CI) = 2.43 (1.64-3.28). Conclusion: We found that rs10434 -G and rs833061-T alleles, gene- environment interaction between rs10434, and current smoking were all related to increased GC risk.


Assuntos
Neoplasias Gástricas , Fator A de Crescimento do Endotélio Vascular , China/epidemiologia , Predisposição Genética para Doença/genética , Humanos , Polimorfismo de Nucleotídeo Único/genética , Fumar/efeitos adversos , Fumar/genética , Neoplasias Gástricas/genética , Fator A de Crescimento do Endotélio Vascular/genética
2.
J Int Med Res ; 50(9): 3000605221123697, 2022 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-36112810

RESUMO

OBJECTIVE: To undertake a meta-analysis to investigate if there is an association between the glutathione S-transferase mu 1 (GSTM1) gene polymorphism, coronary artery disease (CAD) susceptibility and smoking. METHODS: Electronic databases, including PubMed®, Web of Science and Embase®, were searched for relevant case-control studies. Data were extracted and the odds ratio (OR) was calculated and appropriate statistical methods were used for the meta-analysis. RESULTS: The analysis included eight studies with a total of 1880 cases with CAD and 1758 control subjects. The results of this meta-analysis demonstrated that there is no association between the GSTM1 null and CAD (OR 1.24, 95% confidence interval [CI] 1.00, 1.55). An increased risk of CAD was observed in the smoking population with the GSTM1 null genotype (OR 1.48, 95% CI 1.02, 2.15). Subgroup analyses of geographical region, genotyping method and publication language category demonstrated potential relationships among gene polymorphism, smoking and CAD. CONCLUSIONS: Based on the current literature, the GSTM1 null genotype was associated to CAD in the smoking population. The interaction between smoking and GSTM1 polymorphism may contribute to the susceptibility of CAD.


Assuntos
Doença da Artéria Coronariana , Doença da Artéria Coronariana/etiologia , Doença da Artéria Coronariana/genética , Predisposição Genética para Doença , Glutationa Transferase/genética , Humanos , Polimorfismo Genético , Fatores de Risco , Fumar/efeitos adversos , Fumar/genética
3.
Respir Res ; 23(1): 247, 2022 Sep 16.
Artigo em Inglês | MEDLINE | ID: mdl-36114505

RESUMO

BACKGROUND: The club cell secretory protein (CC16) has anti-inflammatory and antioxidant effects, and low CC16 serum levels have been associated with both risk and progression of COPD, yet the interaction between smoking and CC16 on lung function outcomes remains unknown. METHODS: Utilizing cross-sectional data on United States veterans, CC16 serum concentrations were measured by ELISA and log transformed for analyses. Spirometry was conducted and COPD status was defined by post-bronchodilator FEV1/FVC ratio < 0.7. Smoking measures were self-reported on questionnaire. Multivariable logistic and linear regression were employed to examine associations between CC16 levels and COPD, and lung function with adjustment for covariates. Unadjusted Pearson correlations described relationships between CC16 level and lung function measures, pack-years smoked, and years since smoking cessation. RESULTS: The study population (N = 351) was mostly male, white, with an average age over 60 years. An interaction between CC16 and smoking status on FEV1/FVC ratio was demonstrated among subjects with COPD (N = 245, p = 0.01). There was a positive correlation among former smokers and negative correlation among current or never smokers with COPD. Among former smokers with COPD, CC16 levels were also positively correlated with years since smoking cessation, and inversely related with pack-years smoked. Increasing CC16 levels were associated with lower odds of COPD (ORadj = 0.36, 95% CI 0.22-0.57, Padj < 0.0001). CONCLUSIONS: Smoking status is an important effect modifier of CC16 relationships with lung function. Increasing serum CC16 corresponded to increases in FEV1/FVC ratio in former smokers with COPD versus opposite relationships in current or never smokers. Additional longitudinal studies may be warranted to assess relationship of CC16 with smoking cessation on lung function among subjects with COPD.


Assuntos
Doença Pulmonar Obstrutiva Crônica , Uteroglobina , Anti-Inflamatórios/metabolismo , Antioxidantes/metabolismo , Broncodilatadores/metabolismo , Estudos Transversais , Feminino , Humanos , Pulmão/metabolismo , Masculino , Pessoa de Meia-Idade , Doença Pulmonar Obstrutiva Crônica/diagnóstico , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Doença Pulmonar Obstrutiva Crônica/metabolismo , Fumaça , Fumar/efeitos adversos , Fumar/epidemiologia , Tabaco , Uteroglobina/metabolismo
4.
BMC Oral Health ; 22(1): 372, 2022 09 02.
Artigo em Inglês | MEDLINE | ID: mdl-36056338

RESUMO

BACKGROUND: This study aims to evaluate the association between smoking habits and dental care utilization and cost in individuals registered with the Japan Health Insurance Association, Osaka branch. METHODS: We used the administrative claims database and specific medical check-up data and included 226,359 participants, who visited dental institutions, underwent dental examinations, and underwent specific medical checkups, with smoking data from April 2016 to March 2017. We calculated propensity scores with age, gender, exercise, eating habits, alcohol intake, and sleep. We also compared dental care utilization with the total cost of each procedure. RESULTS: According to propensity score matching, 62,692 participants were selected for each group. Compared to non-smokers, smokers were younger, and a higher proportion were men. Smokers tended to skip breakfast, have dinner just before bed, and drink alcohol. After adjusting for potential confounding factors with propensity score matching, the mean annual dental cost among smokers was significantly higher than non-smokers. The prevalence of pulpitis, missing teeth, and apical periodontitis were higher among smokers than non-smokers, while inlay detachment, caries, and dentine hypersensitivity were higher among non-smokers. CONCLUSION: This study suggests that smokers have higher dental cost consisted of progressive dental caries, missing teeth, and uncontrolled acute inflammation that necessitated the use of medications. It is suggested that smokers tend to visit the dentist after their symptoms become severe.


Assuntos
Cárie Dentária , Consumo de Bebidas Alcoólicas/efeitos adversos , Consumo de Bebidas Alcoólicas/epidemiologia , Assistência Odontológica , Cárie Dentária/epidemiologia , Feminino , Humanos , Masculino , Fumantes , Fumar/efeitos adversos , Fumar/epidemiologia
5.
Front Cell Infect Microbiol ; 12: 939910, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36061871

RESUMO

Objective: The pathogenesis of chronic pancreatitis (CP) is not completely clear. With further studies, smoking is toxic to the pancreas. This study classified smoking-related CP as a new etiology of CP and defined the cutoff of smoking. Design: Patients with CP admitted from January 2000 to December 2013 were included in the study. The characteristics were compared between smoking patients, drinking patients, and a group of patients who never smoke or drink (control group). The cumulative rates of steatorrhea, diabetes mellitus (DM), pancreatic pseudocyst (PPC), pancreatic stone, and biliary stricture after the onset of CP were calculated, respectively. Results: A total of 1,324 patients were included. Among them, 55 were smoking patients, 80 were drinking patients, and 1,189 were controls. The characteristics of smokers are different from the other two groups, especially in age at the onset and diagnosis of CP, initial manifestation, and type of pain. The development of DM (P = 0.011) and PPC (P = 0.033) was significantly more common and earlier in the smokers than in the other two groups. Steatorrhea also developed significantly more in the smokers than in the controls (P = 0.029). Smokers tend to delay the formation of pancreatic stones and steatorrhea. Conclusion: The clinical characteristics of smoking-related CP is different from CP of other etiologies. A new type of CP, smoking-related CP, was put forward. Smoking-related CP should be separated from idiopathic CP and defined as a new independent subtype of CP different from alcoholic CP or idiopathic CP.


Assuntos
Diabetes Mellitus , Pancreatite Crônica , Esteatorreia , Humanos , Pancreatite Crônica/complicações , Pancreatite Crônica/diagnóstico , Fatores de Risco , Fumar/efeitos adversos , Esteatorreia/etiologia
6.
Can Respir J ; 2022: 6810745, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36051533

RESUMO

Objective: The aim of the study was to explore the relevance of CD40, CD86, and GSTO1 with the pathogenesis of COPD. Methods: Patients with acute exacerbation of COPD were contrasted with the healthy and nonsmoking ones and smoking but without COPD ones. The changes of CD40, CD86, and GSTO1 in the peripheral blood, collected from different groups, were detected by flow cytometry and western blotting, respectively. Results: Compared with the nonsmoking group and smoking but without the COPD group, the expression of CD40 and CD86 of the patients with COPD increased significantly, but the expression of GSTO1 decreased. CD40 and CD86 were negatively correlated with FEV1%, while GSTO1 was positively correlated with FEV1% and negatively correlated with CD40 and CD86. Conclusion: CD40, CD86, and GSTO1 may play a role in the pathogenesis of COPD, and they are related to the severity of COPD and the degree of changes in the lung function.


Assuntos
Antígeno B7-2/metabolismo , Antígenos CD40/metabolismo , Glutationa Transferase/metabolismo , Doença Pulmonar Obstrutiva Crônica , Citometria de Fluxo , Humanos , Doença Pulmonar Obstrutiva Crônica/etiologia , Fumar/efeitos adversos
7.
Artigo em Inglês | MEDLINE | ID: mdl-36078612

RESUMO

Chronic obstructive pulmonary disease (COPD) was the third leading cause of death worldwide in 2019, with a significant disease burden. We conducted a nested case-control study using data from the China Metal-Exposed Workers Cohort Study (Jinchang Cohort) and assessed the associations of exposure to metals and tobacco smoking with the risk of COPD. We used the logistic regression model and the interaction multiplication model to assess the independent and combined effects of heavy metal and smoke exposure on COPD. The cumulative incidence of COPD was 1.04% in 21,560 participants during a median of two years of follow-up. The risk of COPD was significantly elevated with an increase in the amount of tobacco smoked daily (p < 0.05), the number of years of smoking (ptrend < 0.05), and the number of packs of cigarettes smoked per year (ptrend < 0.01). Compared with the low metal exposure group, the adjusted OR was 1.22 (95% CI: 0.85-1.76) in the medium exposure group (mining/production workers) and 1.50 (95% CI: 1.03-2.18) in the high exposure group; smoking and metal exposure had a combined effect on the incidence of COPD (pinteraction < 0.01), with an OR of 4.60 for those with >40 pack-years of smoking who also had the highest metal exposures. Both exposures to metals and smoking were associated with the risk of COPD, and there was an interaction between the two exposures for the risk of COPD.


Assuntos
Metais Pesados , Exposição Ocupacional , Doença Pulmonar Obstrutiva Crônica , Estudos de Casos e Controles , Estudos de Coortes , Humanos , Metais Pesados/toxicidade , Exposição Ocupacional/efeitos adversos , Exposição Ocupacional/análise , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Doença Pulmonar Obstrutiva Crônica/etiologia , Fatores de Risco , Fumar/efeitos adversos , Fumar/epidemiologia , Fumar Tabaco
8.
Sci Rep ; 12(1): 15041, 2022 Sep 03.
Artigo em Inglês | MEDLINE | ID: mdl-36057695

RESUMO

Smoking, inflammation and depression commonly co-occur and may be mechanistically linked. However, key questions remain around the direction of association and the influence of residual confounding. We aimed to characterize the association between lifetime smoking and depression, as well as to assess the role that genetically-predicted C-reactive protein (CRP) level, (an archetypal generalized inflammatory marker) and/or IL-6 activity, as a potential explanation for this association. We performed inverse variance weighted Mendelian randomization (MR) analyses using recently published summary-level GWAS data for lifetime smoking index, CRP levels, and depression. A subset of inflammatory-related genetic variants from the lifetime smoking GWAS were also used to assess the potential inflammatory causal pathways between smoking and depression. The analysis indicated reciprocal relationships of lifetime smoking with depression (ORSmk-Dep = 2.01, 95% CI 1.71-2.37, p < 0.001; ORDep-Smk = 1.09, 95% CI 1.06-1.13, p < 0.001), CRP levels and IL-6 activity (ORSmk-CRP = 1.40, 95% CI 1.21-1.55, p < 0.001; ORCRP-Smk = 1.03, 95% CI 1.02-1.05, p < 0.001, ORIL-6/CRP-Smk = 1.06 (1.03-1.09), p < 0.001). These associations were also supported by the majority of the robust MR methods performed. We did not find evidence for a reciprocal relationship between CRP levels (using > 500 genetic instruments for CRP) and depression (ORCRP-Dep = 1.01, 95% CI 0.99-1.04; ORDep-CRP = 1.03, 95% CI 0.99-1.07). We observed little variation in the IVW estimates between smoking and depression when we limited the genetic variants assessed to those related to measures of generalized inflammation, but we found evidence for an attenuation of the smoking-depression association in multivariable mendelian randomization when adjusting for IL-6 activity, suggesting that the IL-6 pathway may be at least in part responsible for the association of smoking and depression. Our study supports potential bidirectional causal associations between lifetime smoking and depression which may be at least in part explained by the IL-6 signalling pathway. The IL-6 pathway may represent a putative therapeutic target for smoking and to mitigate the effects of smoking on depression.


Assuntos
Análise da Randomização Mendeliana , Fumar , Depressão/epidemiologia , Depressão/genética , Estudo de Associação Genômica Ampla , Humanos , Inflamação/genética , Interleucina-6/genética , Análise da Randomização Mendeliana/métodos , Polimorfismo de Nucleotídeo Único , Fumar/efeitos adversos , Fumar/genética
9.
Zhonghua Yi Xue Za Zhi ; 102(35): 2774-2778, 2022 Sep 20.
Artigo em Chinês | MEDLINE | ID: mdl-36124349

RESUMO

Objective: To explore the alterations of cerebral cortical thickness in severe nicotine addicts by using surface-based morphology (SBM) method and further analyzing the association of these changes with smoking-related characteristics. Methods: Data were retrospectively collected from August 2014 to August 2019 from severe nicotine addicts [aged 25 to 52(38±8)years] and 56 non-smokers healthy volunteers [aged 22 to 51(36±8)years]. All subjects underwent 3.0 T magnetic resonance scans, and FreeSurfer software was used to analyze the difference in cortical thickness between the two groups, and Pearson correlation analysis was used to explore the correlation between the nicotine dependence group and smoking-related characteristics. Results: Compared to control group, the severe nicotine dependence group had a significant reduction in the cortical thickness in 9 areas of the brain, the left cerebral cortex, including: middletemporal, precentral, superiorfrontal, insula [(2.78±0.10) mm vs (2.92±0.17) mm, (2.57±0.15) mm vs (2.70±0.14) mm, (2.63±0.18) mm vs (2.76±0.15) mm, (3.01±0.10) mm vs (3.13±0.13) mm, all P<0.01, respectively], and the right cerebral cortex including: temporalpole, rostralmiddlefrontal, superiorfrontal, postcentral, parsopercularis [(3.12±0.14) mm vs (3.26±0.19) mm, (2.71±0.16) mm vs (2.87±0.18) mm, (2.96±0.15) mm vs (3.10±0.20) mm, (2.57±0.15) mm vs (2.71±0.15) mm, (2.54±0.11) mm vs (2.65±0.15) mm, all P<0.05, respectively]. The cortical thickness of left insular was positively correlated with the initial smoking age (r=0.403,P=0.009), while the cortical thickness of the other brain regions had no significant correlation with smoking-related characteristics (all P>0.05). Conclusion: Significant alterations were observed in cortical thickness in severe nicotine addicts, and there is a correlation between the thickness of the left insular cortex and the age of initial smoking.


Assuntos
Espessura Cortical do Cérebro , Tabagismo , Humanos , Nicotina , Estudos Retrospectivos , Fumar/efeitos adversos , Tabagismo/complicações
10.
BMC Med ; 20(1): 345, 2022 Sep 21.
Artigo em Inglês | MEDLINE | ID: mdl-36127702

RESUMO

BACKGROUND: Employment disruptions can impact smoking and alcohol consumption. During the COVID-19 pandemic, many countries implemented furlough schemes to prevent job loss. We examine how furlough was associated with smoking, vaping and alcohol consumption in the UK. METHODS: Data from 27,841 participants in eight UK adult longitudinal surveys were analysed. Participants self-reported employment status and current smoking, current vaping and alcohol consumption (>4 days/week or 5+ drinks per typical occasion) both before and during the early stages of the pandemic (April-July 2020). Risk ratios were estimated within each study using modified Poisson regression, adjusting for a range of potential confounders, including pre-pandemic behaviour. Findings were synthesised using random effects meta-analysis. RESULTS: Compared to stable employment and after adjustment for pre-pandemic characteristics, furlough was not associated with smoking (ARR = 1.05; 95% CI: 0.95-1.16; I2: 10%), vaping (ARR = 0.89; 95% CI: 0.74-1.08; I2: 0%) or drinking (ARR = 1.03; 95% CI: 0.94-1.13; I2: 48%). There were similar findings for no longer being employed, and stable unemployment, though this varied by sex: stable unemployment was associated with smoking for women (ARR = 1.35; 95% CI: 1.00-1.82; I2: 47%) but not men (0.84; 95% CI: 0.67-1.05; I2: 0%). No longer being employed was associated with vaping among women (ARR = 2.74; 95% CI: 1.59-4.72; I2: 0%) but not men (ARR = 1.25; 95% CI: 0.83-1.87; I2: 0%). CONCLUSIONS: We found no clear evidence of furlough or unemployment having adverse impacts on smoking, vaping or drinking behaviours during the early stages of the COVID-19 pandemic in the UK. Differences in risk compared to those who remained employed were largely explained by pre-pandemic characteristics.


Assuntos
COVID-19 , Vaping , Adulto , Consumo de Bebidas Alcoólicas/epidemiologia , COVID-19/epidemiologia , COVID-19/prevenção & controle , Feminino , Humanos , Estudos Longitudinais , Pandemias , Fumar/efeitos adversos , Fumar/epidemiologia , Reino Unido/epidemiologia , Vaping/epidemiologia
11.
PLoS One ; 17(9): e0272202, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36129905

RESUMO

BACKGROUND: More deprived populations typically experience higher cancer incidence rates and smoking prevalence compared to less deprived populations. We calculated the proportion of cancer cases attributable to smoking by socio-economic deprivation in England and estimated the impact smoking has on the deprivation gap for cancer incidence. METHODS: Data for cancer incidence (2013-2017), smoking prevalence (2003-2007) and population estimates (2013-2017) were split by sex, age-group and deprivation quintile. Relative risk estimates from meta-analyses were used to estimate the population attributable fraction (PAF) for 15 cancer types associated with smoking. The deprivation gap was calculated using age-specific incidence rates by deprivation quintile. RESULTS: Smoking-related cancer PAFs in England are 2.2 times larger in the most deprived quintile compared to the least deprived quintile (from 9.7% to 21.1%). If everyone had the same smoking prevalence as the least deprived quintile, 20% of the deprivation gap in cancer incidence could have been prevented. If nobody smoked, 61% of the deprivation gap could have been prevented. CONCLUSIONS: The majority of the deprivation gap in cancer incidence could have been prevented in England between 2013-2017 if nobody had smoked. Policy makers should ensure that tobacco control policies reduce overall smoking prevalence by tackling smoking inequalities.


Assuntos
Neoplasias , Pobreza , Inglaterra/epidemiologia , Humanos , Incidência , Neoplasias/epidemiologia , Neoplasias/etiologia , Fumar/efeitos adversos , Fumar/epidemiologia , Fatores Socioeconômicos
12.
Am J Otolaryngol ; 43(5): 103555, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36037765

RESUMO

PURPOSE: To characterize the significance of patient-level influences, including smoking history, on oncologic outcomes in human papillomavirus (HPV)-mediated oropharyngeal cancer (OPC). MATERIALS AND METHODS: A bi-institutional retrospective cohort study of previously untreated, HPV+ OPC patients who underwent curative treatment from 1/1/2008 to 7/1/2018 was performed. The primary outcome was disease-free survival (DFS) and the primary exposure was ≤10 versus >10-pack-year (PY)-smoking history. RESULTS: Among 953 OPC patients identified, 342 individuals with HPV+ OPC were included. The median patient age was 62 years, 33.0% had a > 10-PY-smoking history, 60.2% had AJCC8 stage I disease, and 35.0% underwent primary surgery. The median follow-up was 49 months (interquartile range [IQR] 32-75 months). Four-year DFS-estimates were similar among patients with ≤10-PY-smoking history (78.0%, 95% CI:71.7%-83.1%) compared to >10-PYs (74.8%; 95% CI:65.2%-82.0%; log-rank:p = 0.53). On univariate analysis, >10-PY-smoking history did not correlate with DFS (hazard ratio[HR]:1.15;95% CI:0.74-1.79) and remained nonsignificant when forced into the multivariable model. On adjusted analyses, stage, treatment paradigm, and age predicted DFS. Neither >10-PYs, nor any other definition of tobacco use (e.g., current smoker or > 20-PYs) was predictive of DFS, overall survival, or disease-specific survival. Conversely, age nonsignificantly and significantly predicted adjusted DFS (adjusted HR[aHR]:1.02,95% CI:0.997-1.05, p = 0.08), overall survival (aHR 1.05; 95% CI: 1.02-1.08; p = 0.002) and disease-specific survival (aHR 1.04;95% CI: 0.99-1.09;p = 0.09). CONCLUSION: Other than age, patient-level influences may not be primary drivers of HPV+ OPC outcomes. Although limited by its modest sample size, our study suggests the significance of smoking has been overstated in this disease. These findings and the emerging literature collectively do not support risk-stratification employing the >10-PY threshold. LEVEL OF EVIDENCE: Level 4.


Assuntos
Alphapapillomavirus , Neoplasias Orofaríngeas , Infecções por Papillomavirus , Humanos , Pessoa de Meia-Idade , Neoplasias Orofaríngeas/cirurgia , Papillomaviridae , Infecções por Papillomavirus/complicações , Prognóstico , Estudos Retrospectivos , Fumar/efeitos adversos , Fumar/epidemiologia
15.
Front Public Health ; 10: 945955, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35991047

RESUMO

Genetic polymorphisms may contribute to individual susceptibility to DNA damage induced by environmental exposure. In this study, we evaluate the effects of co-exposure to PAHs, smoking and XPC polymorphisms, alone or combined, on damage in exons. A total of 288 healthy male coke oven workers were enrolled into this study, and urinary 1-hydroxypyrene (1-OH-Pyr) was detected. Base modification in exons of KRAS and BRAF gene, and polymorphisms of XPC were determined in plasma by real-time PCR. We observed 1-OH-Pyr was positively related to damage in exon 2 of KRAS (KRAS-2) and in exon 15 of BRAF (BRAF-15), respectively, and KRAS-2 and BRAF-15 were significantly associated with increased 1-OH-Pyr. A stratified analysis found 1-OH-Pyr was significantly associated with KRAS-2 in both smokers and non-smokers, while 1-OH-Pyr was significantly associated with BRAF-15 only in smokers. Additionally, individuals carrying both rs2228001 G-allele (GG+GT) and rs3731055 GG homozygote (GG) genotype appeared to have more significant effect on KRAS-2. The high levels of 1-OH-Pyr were associated with KRAS-2 only in rs2228001 GG+GT genotype carriers and the high levels of 1-OH-Pyr were associated with KRAS-2 only in rs3731055 GG genotype carriers and the most severe KRAS-2 was observed among subjects carrying all four of the above risk factors. Our findings indicated the co-exposure effect of PAHs and smoking could increase the risk of KRAS-2 by a mechanism partly involving XPC polymorphisms.


Assuntos
Coque , Exposição Ocupacional , Hidrocarbonetos Policíclicos Aromáticos , Coque/efeitos adversos , Coque/análise , Proteínas de Ligação a DNA , Éxons , Humanos , Masculino , Exposição Ocupacional/efeitos adversos , Exposição Ocupacional/análise , Hidrocarbonetos Policíclicos Aromáticos/efeitos adversos , Hidrocarbonetos Policíclicos Aromáticos/análise , Polimorfismo Genético , Proteínas Proto-Oncogênicas B-raf , Proteínas Proto-Oncogênicas p21(ras) , Fumar/efeitos adversos
16.
Trials ; 23(1): 717, 2022 Aug 29.
Artigo em Inglês | MEDLINE | ID: mdl-36038883

RESUMO

BACKGROUND: At present, effectively implementing smoking cessation programs in the health care system constitutes a major challenge. A unique opportunity to initiate smoking cessation focuses on smokers scheduled for surgery. These patients are not only highly motivated to quit smoking but also likely to benefit from a reduction in postoperative complications which may translate into a decrease of costs. Nevertheless, surgical patients are not routinely informed about the benefits of preoperative smoking cessation. Potential reasons for this missed opportunity may be the lack of time and training of surgeons and anaesthesiologists. We therefore aim to analyse the impact of a preoperative high-intensity smoking cessation intervention on surgical complications up to a 90-day postoperative period in patients of various surgical disciplines. The hypothesis is that a preoperative smoking cessation program improves outcomes in smokers undergoing intermediate to high-risk surgery. METHODS: The present study is a single-centre, randomized trial with two parallel groups of smokers scheduled for surgery comparing surgery alone and surgery with preoperative smoking cessation. We plan to randomize 251 patients. The primary objective is to compare complications between patients with an institutional multifaceted smoking cessation intervention starting 4 weeks before surgery compared to patients in the advice-only group (control group) within a 90-day postoperative period. The primary endpoint is the Comprehensive Complication Index (CCI®) within 90 days of surgery. Secondary outcomes include the length of hospital stay, cost of care, quality of life, smoking abstinence, and reduction in nicotine consumption. DISCUSSION: The hypothesis is that a preoperative smoking cessation program improves outcomes in smokers undergoing surgery. TRIAL REGISTRATION: BASEC #2021-02004; ClinicalTrials.gov: NCT05192837 . Registered on January 14, 2022.


Assuntos
Abandono do Hábito de Fumar , Atenção à Saúde , Humanos , Nicotina , Qualidade de Vida , Fumar/efeitos adversos
17.
BMC Med ; 20(1): 276, 2022 08 16.
Artigo em Inglês | MEDLINE | ID: mdl-35971150

RESUMO

BACKGROUND: Smoking is a major risk factor for cardiovascular disease and smoking cessation reduces excess risk. E-cigarettes are popular for smoking cessation but there is little evidence on their cardiovascular health effect. Our objective was to compare the medium- and longer-term cardiovascular effects in smokers attempting to quit smoking using e-cigarettes with or without nicotine or prescription nicotine replacement therapy (NRT). METHODS: This was a single-center, pragmatic three-arm randomized (1:1:1) controlled trial, which recruited adult smokers (≥ 10 cigarettes/day), who were willing to attempt to stop smoking with support (n = 248). Participants were randomized to receive behavioral support with either (a) e-cigarettes with 18 mg/ml nicotine, (b) e-cigarettes without nicotine, and (c) NRT. Flow-mediated dilation (%FMD) and peak cutaneous vascular conductance (CVCmax) responses to acetylcholine (ACh) and sodium nitroprusside (SNP), mean arterial pressure (MAP), and other outcomes were recorded at baseline, 3, and 6 months after stopping smoking. Data were analyzed using generalized estimating equations (GEE). RESULTS: At 3- and 6-month follow-up, %FMD showed an improvement over baseline in all three groups (e.g., p < 0.0001 at 6 months). Similarly, ACh, SNP, and MAP improved significantly over baseline in all groups both at 3 and 6 months (e.g., ACh: p = 0.004, at 6 months). CONCLUSIONS: Smokers attempting to quit experienced positive cardiovascular impact after both a 3- and 6-month period. None of the groups (i.e., nicotine-containing and nicotine-free e-cigarettes or NRT) offered superior cardiovascular benefits to the others. TRIAL REGISTRATION: ClinicalTrials.gov NCT03061253 . Registered on 17 February 2017.


Assuntos
Sistemas Eletrônicos de Liberação de Nicotina , Abandono do Hábito de Fumar , Adulto , Humanos , Nicotina/efeitos adversos , Fumar/efeitos adversos , Fumar Tabaco , Dispositivos para o Abandono do Uso de Tabaco
18.
Trials ; 23(1): 663, 2022 Aug 17.
Artigo em Inglês | MEDLINE | ID: mdl-35978355

RESUMO

BACKGROUND: About 85% of patients receiving opioid agonist therapy (OAT) for opioid dependence are smoking tobacco. Although smoke-related pulmonary diseases are significant contributors to morbidity and mortality, few smoking cessation interventions are evaluated within this group, and few OAT patients are offered smoking cessation as an integrated part of their addiction treatment. This study protocol describes an integrated smoking cessation intervention aimed at patients receiving OAT and smoking tobacco. METHODS: This is a multicentre, randomised controlled clinical trial that will recruit 266 daily tobacco smoking patients receiving OAT in OAT outpatient clinics in Bergen and Stavanger, Norway. The patients randomised for the intervention arm will be offered smoking cessation therapy consisting of weekly brief behavioural interventions and prescription-free nicotine replacement products. In the control arm, patients will receive standard care without any added interventions related to smoking cessation. The smoking cessation intervention includes psychoeducational techniques with components from motivational interviewing, and nicotine replacement products such as nicotine lozenges, patches, and chewing gum. The duration of the intervention is 16 weeks, with the option of extending it by a further 8 weeks. The main outcomes are measured at 16 weeks after initiation of the intervention, and sustained effects are evaluated 1 year after intervention initiation. The primary outcome is smoking cessation verified by carbon monoxide (CO) levels or at least a 50% reduction in the number of cigarettes smoked. Secondary outcomes are changes in psychological well-being, biochemical inflammation markers, changes in physical health, quality of life, and fatigue. DISCUSSION: Integration of other treatments to standard OAT care improves adherence and completion rates providing another rationale for integrated smoking cessation treatment. Thus, if integrated smoking cessation treatment is superior to standard care, this trial provides important information on further scale-up. TRIAL REGISTRATION: ClinicalTrials.gov NCT05290025. Registered on 22 March 2022.


Assuntos
Abandono do Hábito de Fumar , Fumar , Analgésicos Opioides/efeitos adversos , Humanos , Estudos Multicêntricos como Assunto , Qualidade de Vida , Ensaios Clínicos Controlados Aleatórios como Assunto , Fumar/efeitos adversos , Fumar/terapia , Abandono do Hábito de Fumar/métodos , Dispositivos para o Abandono do Uso de Tabaco
19.
PLoS One ; 17(8): e0270486, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35980977

RESUMO

OBJECTIVE: Smoking and obesity are established risk factors of dyslipidemia, however, the interplay between them has not been well studied. This study aims to explore the joint effect of smoking and body mass index (BMI) on serum lipid profiles. METHODS: The study consisted of 9846 Chinese adults (mean age = 49.9 years, 47.6% males, 31.2% ever smokers), based on the China Health and Nutrition Survey. Serum lipid profiles included total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), apolipoprotein A (APO-A), and apolipoprotein B (Apo-B). The joint effect of smoking and BMI on serum lipids were examined by the four-way decomposition analysis and multivariate linear regression models. RESULTS: The four-way decomposition showed that the interplay between smoking and BMI was complicated. There was only indirect effect (the mediated effect) between smoking and BMI on TC, LDL-C and APO-B. The pure indirect effect was -0.023 for TC, -0.018 for LDL-C, and -0.009 for APO-B. For TG, HDL-C and APO-A, the interaction effect was dominant. The reference interaction (the interactive effect when the mediator is left to what it would be in the absence of exposure) was 0.474 (P < 0.001) for TG, -0.245 (P = 0.002) for HDL-C, and -0.222 (P < 0.001) for APO-A, respectively. The effect of BMI on TG, HDL-C and APO-A were significantly higher in smokers than in nonsmokers (TG: 0.151 in smokers versus 0.097 in nonsmokers, HDL-C: -0.037 versus -0.027, APO-A: -0.019 versus -0.009, P for difference < 0.001 for all). CONCLUSION: These findings illustrate the joint effects of smoking and BMI on serum lipid profiles. There were significant interaction effects of smoking and BMI on TG, HDL-C and APO-A, while BMI maybe a mediator for the association of smoking with TC, LDL-C and APO-B. The effects between them were rather complex. Smoking cessation is necessary, especially for those overweight.


Assuntos
Fumar Cigarros , Fumar , Apolipoproteínas A , Apolipoproteínas B , Índice de Massa Corporal , HDL-Colesterol , LDL-Colesterol , Feminino , Humanos , Lipídeos , Masculino , Pessoa de Meia-Idade , Fumar/efeitos adversos , Triglicerídeos
20.
Front Immunol ; 13: 967506, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35967334

RESUMO

Background: Patients with systemic lupus erythematosus (SLE) are at increased risk of cardiovascular disease (CVD) compared to the general population. However, little is known about the effects of tobacco smoking on CVD in patients with SLE. Objective: To systematically review and summarize the available literature regarding the effects of tobacco smoking on developing CVD in patients with SLE. Methods: We retrieved relevant studies from the following databases: PubMed, EMBASE, Web of Science and China National Knowledge Internet (CNKI) database. Two reviewers independently reviewed the eligible studies, assessed their validity, and extracted relevant data. Sensitivity and subgroup analyses were performed to distinguish sources of heterogeneity. Results: A total of 10 studies, which comprised 6984 participants, were included in the analysis. The overall quality of evidence was rated as moderate to low. The smoking prevalence among CVD patients was 39.28% (271/690), which was higher than 31.36% (1974/6294) among non-CVD patients. Compared with never-smokers, the risk of developing CVD in current smokers was 1.42 (95% CI: 1.21-1.66). No significant publication bias was found in our meta-analysis. Conclusions: In spite of the several negative results, this study found that current smokers with SLE have an increased risk of developing CVD, although most of the included studies were in low-to-moderate quality. Systematic Review Registration: https://www.crd.york.ac.uk/prospero/, identifier CRD42022338109.


Assuntos
Doenças Cardiovasculares , Lúpus Eritematoso Sistêmico , Doenças Cardiovasculares/complicações , Doenças Cardiovasculares/etiologia , Humanos , Lúpus Eritematoso Sistêmico/complicações , Lúpus Eritematoso Sistêmico/epidemiologia , Prevalência , Fumar/efeitos adversos , Fumar/epidemiologia , Fumar Tabaco/efeitos adversos , Fumar Tabaco/epidemiologia
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