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Previous results regarding the associations between esophageal squamous-cell carcinoma (ESCC) risk and smoking/alcohol drinking in high-risk areas are inconsistent. We performed a large population-based case-control study from 2010 to 2013 in a high-incidence area of China, and enrolled 1353 ESCC cases and 1961 controls. Data regarding smoking and alcohol drinking were collected via face-to-face interviews using a structured questionnaire. Odd ratios (ORs) with 95% confidence intervals (CIs) were estimated using unconditional logistic regression models. After adjusting for alcohol drinking and other potential confounders, male heavy smokers (i.e., those who started smoked more than 20 cigarettes per day or 40 pack-years, or started smoking early), showed a moderately increased risk for ESCC; however, current smoking was not associated with an increased risk. Alcohol drinking among males significantly increased the risk for ESCC (OR = 2.20, 95%CI:1.79~2.70). We observed increasing excess ESCC risks with decreasing age at behavior initiation as well as with increasing duration and intensity of alcohol intake, which were particularly evident among current smokers. In contrast, neither smoking nor alcohol drinking was not associated with ESCC risk among females. In conclusion, alcohol drinking shows a monotonic dose-response relationship with ESCC risk among men, and this relationship is particularly evident among smokers.

This study aimed to examine whether dopamine (DA) pathway gene variation were associated with smoking cessation, and compare the relative importance of infulence factors on smoking cessation. Participants were recruited from 17 villages of Shandong Province, China. Twenty-five single nucleotide polymorphisms in 8 DA pathway genes were genotyped. Weighted gene score of each gene was used to analyze the whole gene effect. Logistic regression was used to calculate odds ratios (OR) of the total gene score for smoking cessation. Dominance analysis was employed to compare the relative importance of individual, heaviness of smoking, psychological and genetic factors on smoking cessation. 415 successful spontaneous smoking quitters served as the cases, and 404 unsuccessful quitters served as the controls. A significant negative association of total DA pathway gene score and smoking cessation was observed (p < 0.001, OR: 0.25, 95% CI 0.16-0.38). Dominance analysis showed that the most important predictor for smoking cessation was heaviness of smoking score (42%), following by individual (40%), genetic (10%) and psychological score (8%). In conclusion, although the DA pathway gene variation was significantly associated with successful smoking cessation, heaviness of smoking and individual factors had bigger effect than genetic factors on smoking cessation.

Background and Objectives: Nicotine dependence is influenced by genetic, individual, and psychological factors. We aimed to examine whether nicotinic acetylcholine receptor genes (CHRN) were associated with smoking cessation (SC) using genetic risk score and compare the relative contribution of genetic, individual and self-efficacy factors to SC., Methods: Eight hundred and nineteen male smokers (mean age: 59.62) were recruited from 17 villages of three counties in Shandong province, China. Thirty-two single nucleotide polymorphisms (SNPs) in seven CHRN genes were genotyped. Logistic regression was used to explore the relationship between genetic risk score and SC. Dominance analysis was performed to compare the relative contribution of genetic, individual, and self-efficacy factors on SC., Results: CHRNA3 genetic risk score was associated with SC. Dominance analysis showed that individual factor was the most important predictor for SC, followed by genetic and self-efficacy factors., Conclusions: CHRNA3 was associated with successful SC. Individual factor had more contribution than genetic factor to SC., Scientific Significance: Our findings provide support to the role of CHRN genes in the etiology of smoking cessation using genetic risk score. Individual factor should be particularly valued in smoking control intervention. (Am J Addict 2017;26:161-166)., (© 2017 American Academy of Addiction Psychiatry.)

Background and Objectives: Smoking and smoking cessation are both psychological and physiological traits. We aimed to investigate the interaction between dopamine pathway gene scores and nicotine dependence on smoking cessation in a rural Chinese male population., Methods: Participants were recruited from 17 villages in Shandong, China. DNA was extracted from blood sample of 819 participants. 25 single nucleotide polymorphisms (SNPs) in 8 dopamine (DA) pathway genes were genotyped. Weighted gene score of each gene is used to analyze the whole gene effect. Logistic regression was used to calculate odds ratios (OR) and multivariate-adjusted OR of each gene score for smoking cessation. Multiplicative model interaction was assessed through a cross-product interaction term of gene score by nicotine dependence in a multivariate logistic regression model., Results: After adjusting for age, occupation, education, marital status, self-rating anxiety score, and disease status, we observed significant negative associations of catechol-O-methyltransferase (COMT), dopamine receptor D2 (DRD2) gene score and smoking cessation, as well as significant positive associations between ankyrin repeat and kinase domain containing 1 (ANKK1), dopamine transporter (SLC6A3), dopamine receptor D4 (DRD4) gene score and smoking cessation. A significant multiplicative model interaction between nicotine dependence and the SLC6A3 gene score on smoking cessation was also observed (p = .03)., Conclusions and Scientific Significance: There is a significant multiplicative model interaction of SLC6A3 gene score and nicotine dependence on smoking cessation. This finding could help to identify smokers who may be at high risk of relapse, and thus to develop more professional and personalized smoking cessation treatment. (Am J Addict 2016;25:493-498)., (© 2016 American Academy of Addiction Psychiatry.)

The association between psychological factors and smoking cessation is complicated and inconsistent in published researches, and the joint effect of psychological factors on smoking cessation is unclear. This study explored how psychological factors jointly affect the success of smoking cessation using a Bayesian network approach. A community-based case control study was designed with 642 adult male successful smoking quitters as the cases, and 700 adult male failed smoking quitters as the controls. General self-efficacy (GSE), trait coping style (positive-trait coping style (PTCS) and negative-trait coping style (NTCS)) and self-rating anxiety (SA) were evaluated by GSE Scale, Trait Coping Style Questionnaire and SA Scale, respectively. Bayesian network was applied to evaluate the relationship between psychological factors and successful smoking cessation. The local conditional probability table of smoking cessation indicated that different joint conditions of psychological factors led to different outcomes for smoking cessation. Among smokers with high PTCS, high NTCS and low SA, only 36.40% successfully quitted smoking. However, among smokers with low pack-years of smoking, high GSE, high PTCS and high SA, 63.64% successfully quitted smoking. Our study indicates psychological factors jointly influence smoking cessation outcome. According to different joint situations, different solutions should be developed to control tobacco in practical intervention.

Background and Objectives: Genetic studies have revealed a significant association between variants in nicotinic acetylcholine receptor (CHRN) genes and smoking cessation, but the results are inconsistent. In this study, we aimed to examine the relationship between single nucleotide polymorphisms (SNPs) in seven CHRN genes and smoking cessation in a Chinese rural population., Methods: Participants were recruited from 17 villages of 3 counties in Shandong, China. DNA was extracted from the blood samples. Thirty-two SNPs in seven CHRN genes were genotyped. Logistic regression was used to explore the relationship between single SNP and smoking cessation. Pearson's χ(2) test was performed to test the association between haplotype and smoking cessation., Results: Rs578776 (in CHRNA3), rs660652 (in CHRNA3), and rs588765 (in CHRNA5) were significantly related to smoking cessation. Two haplotypes were associated with smoking cessation., Conclusions: This study confirmed the association between CHRN genes and smoking cessation in the Chinese rural population., Scientific Significance: Our findings provide confirmatory support to the role of CHRN genes to the etiology of smoking cessation in the Chinese rural population. (Am J Addict 2016;25:297-300)., (© 2016 American Academy of Addiction Psychiatry.)

Published articles reported controversial results about the association of 5-HTTLPR polymorphism with the risk of smoking behaviors. A meta-analysis was performed to assess the association between 5-HTTLPR polymorphism and smoking behaviors. A comprehensive search was conducted to identify studies (from January, 1990 to December, 2014) of the aforementioned association. The Q test and the I(2) statistic were used to examine between-study heterogeneity. Fixed or random effect model was selected based on heterogeneity test among studies. Meta-regression was used to explore the potential sources of between-study heterogeneity. Publication bias was estimated using funnel plots and Harbord test. Twenty-one published articles were included. Overall, we didn't find any significant association of 5-HTTLPR polymorphism with smoking initiation and smoking cessation in any of allele, dominant and recessive models. In the subgroup analysis stratified by ethnicity (Caucasian and Asian) or by whether smokers accepted the treatment for smoking cessation or not (Yes/No), there were still no significant associations detected in all genetic models. In conclusion, this meta-analysis suggested that there might be no association of 5-HTTLPR polymorphism with the risk of smoking behaviors. Further studies are needed to confirm these conclusions., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Objective: To estimate the mediating effect of smoking abstinence self-efficacy (SASE) on the association between awareness of smoking hazard and successful smoking cessation., Methods: A community-based case-control study was conducted in 642 smokers who successfully stopped smoking, and 700 smokers who failed in smoking cessation were used as controls. The awareness of smoking hazard was evaluated by total score of 12 items. The SASE was assessed by using Smoking Abstinence Self-Efficacy (ASES-S). The total effect was classified as direct effect and indirect effect through logistic regression analysis based on the KHB method., Results: After adjusting the potential confounders, including age, age of smoking initiation, occupation, educational level and marital status, the mediating effect of SASE accounted for 6.03% among the total effect of awareness of smoking hazard in those who successfully stopped smoking while the direct effect accounted for 93.97% among the total effect. In the three specific situation of SASE, the mediating effect of SASE accounted for 6.80% (positive/social situations), 3.08% (negative/affective situations) and 2.32% (habit/addictive situations) among the total effect, respectively., Conclusion: SASE has part mediating effect to influence on the association between the awareness of smoking hazard and successful smoking cessation. Improving smokers' awareness of smoking hazard may not only promote successful smoking cessation directly, but also contribute to quit smoking through improving the score of SASE.

Background: A number of studies have researched the association between monoamine oxidase gene (MAO) polymorphisms and smoking behavior, but the conclusion is quite inconsistent. A meta-analysis was conducted to assess the association of MAO-A C1460T, MAO-A VNTR and MAO-B G644A polymorphisms with smoking behavior., Methods: A comprehensive search was performed to identify all eligible studies. Meta-analysis was applied to calculate the pooled effect values and their 95% confidence intervals. Meta-regression and the 'leave one out' sensitivity analysis were used to explore potential sources of heterogeneity. The risk of bias was assessed by the Egger regression asymmetry test., Results: 11 articles conformed to the inclusion criteria. The meta-analysis showed T allele in MAO-A C1460T reduced the risk of heavy smoking (OR=0.66, 95% CI: 0.52-0.84; I(2)=0.0%), especially in Caucasians; the active group in MAO-A VNTR increased the likelihood of failed smoking cessation in males (OR=1.49, 95% CI: 1.01-2.22; I(2)=0.0%); A allele in MAO-B G644A reduced the risk of heavy smoking in males (OR=0.20, 95% CI: 0.04-0.98)., Conclusion: Our findings indicate that the low activity of monoamine oxidase gene polymorphisms has a protective effect on smoking cessation and heaviness. Some associations and applications should be further confirmed., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Aims: A meta-analysis was performed to assess the association of hepatic cytochrome P450 2A6 (CYP2A6) gene polymorphisms with cigarette consumption., Methods: A comprehensive search was conducted to identify the studies of the above-mentioned association. The fixed effect model (FEM) or random effect model (REM) was selected based on the homogeneity test among studies. Heterogeneity among studies was evaluated using the I(2). Meta-regression and the "leave one out" sensitive analysis were utilized to explore potential sources of heterogeneity. Publication bias was estimated by Harbord test. The effect of CYP2A6 gene polymorphisms on cigarette consumption was presented as standardized mean difference (SMD) with 95% confidence intervals (CI)., Results: After excluding one article that was the key contributor to between-study heterogeneity, there was a significant difference of cigarettes per day in groups of normal vs. reduced metabolizers of CYP2A6 gene (FEM: SMD = 0.134, 95%CI: 0.049-0.219). There was also a significant difference of age of smoking initiation between normal and intermediate metabolizers of CYP2A6 gene (FEM: SMD = 0.216, 95%CI: 0.056-0.377). No significant difference of tobacco dependence between normal and reduced metabolizers of CYP2A6 gene was found (FEM: SMD = 0.185, 95%CI = -0.001 to 0.371)., Conclusion: This meta-analysis suggests that CYP2A6 gene polymorphism is associated with daily cigarette consumption. Individuals with intermediate nicotine metabolism might also initiate smoking later than normal metabolism., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Objective: A Meta-analysis was performed to assess the association of defective hepatic cytochrome P450 2A6 (CYP2A6) gene with smoking behaviors., Methods: All eligible studies published up to 2014 were searched out from PubMed, China National Knowledge Internet (CNKI), ISI Web of knowledge (ISI), vip citation databases (VIP), Chinese BioMedical Literature (CBM) and Elsevier Science Direct, searching words were "smok*","nicotine dependence","CYP2A6","cytochrome P450 2A6","polymorphism","mut*"and"varia*", while 436 articles were concluded. Meta-analysis was performed using Statal 3.1., Results: A total of ten studies were finally included. We didn't find a significant effect of defective CYP2A6 gene on smoking initiation (fixed effect model (FEM): OR = 0.90, 95%CI: 0.78-1.03, I(2) = 25.8%), smoking persistence (random effect model (REM): OR = 0.85, 95%CI: 0.59-1.23, I(2) = 66.3%) and smoking cessation (REM: OR = 0.89, 95%CI: 0.57-1.40, I(2) = 67.1%). But it showed a significant protective effect of CYP2A6*4 on smoking initiation (FEM: OR = 0.78, 95%CI: 0.61-0.99, I(2) = 28.2%), smoking persistence (FEM: OR = 0.53, 95%CI: 0.36-0.77, I(2) = 41.0%) and smoking cessation (REM: OR = 0.49, 95%CI: 0.31-0.80, I(2) = 0.0%)., Conclusions: This Meta-analysis suggested that there was not a protective effect of defective CYP2A6 gene against smoking behaviors. But smokers with whole CYP2A6 gene deletion would be less likely to start smoking, less smoking persistence and more likely to quit smoking successful than smokers with wild CYP2A6 gene.

Objective: To study the association between reasons for smoking and results related to successful smoking cessation., Methods: A community-based case-control study was conducted with 642 male adults recognized as successful spontaneous smoking quitters being the subject cases while another 700 male adults who had failed to quit smoking were served as the controls. Russell Reason for Smoking Questionnaire (RRSQ) was used to investigate the reasons for smoking. Dominance logistic regression was performed to determine the relative importance of reasons for starting smoking and the endpoint of successful quit smoking., Results: After adjusting the potential confounders of age, age of smoking initiation, marital status, profession, and education, the adjusted means of sedative and stimulation of RRSQ in the successful quitters were significant lower than that in the failed quitters. Results from the dominance logistic regression showed that the first two important factors for smoking cessation were sedative and stimulation of RRSQ, followed by psychological image, automatic, hand-mouth activity, indulgence, and addiction., Conclusion: This study demonstrated that factors as dependence-addiction showed more important impacts than the social-psychological ones on the endpoint of successful smoking cessation.

Mitogen/extracellular signal-regulated kinase-5 (MEK5)/extracellular signal-regulated protein kinase-5 (ERK5) pathway plays a pro-oncogenic role in tumourigenesis by anticell apoptosis, promoting cell proliferation and differentiation in response to extracellular stimuli. As overexpressed MEK5/ERK5 is involved in the development of lung cancer, we hypothesised that the single nucleotide polymorphisms (SNPs) in MEK5 and ERK5 genes may influence gene expression and thus be associated with lung cancer risk. Five putative functional polymorphisms (rs3743353T>C, rs7172582C>T and rs2278076A>G of MEK5 and rs3866958G>T and rs2233083C>T of ERK5) were genotyped in two independent case-control studies with a total of 1559 lung cancer patients and 1679 controls in southern and eastern Chinese population. We found the rs3866958G>T of ERK5 was significantly associated with lung cancer risk, while other SNPs were not. Compared with the rs3866958TG/TT genotypes, the GG genotype conferred an increased risk of lung cancer (odds ratio = 1.30, 95% confidence interval = 1.12-1.51, P = 5.0×10(-4)), and this effect was more pronounced in smokers, accompanying with a significant interaction with smoking (P interaction = 0.013). The GG genotype also had significant higher mRNA levels of ERK5 in lung cancer tissues than TG/TT genotypes (P = 1.0×10(-4)); the luciferase reporter with the G allele showed significant higher transcription activities than the T allele, especially after the treatment with tobacco extract in vitro. Our data indicated that the functional polymorphism rs3866958G>T in ERK5 was associated with an increased lung cancer risk in smokers by virtue of the positive interaction with smoking on promoting the ERK5 expression, which might be a valuable indicator for predicting lung cancer risk in smokers.

• Trends in lung cancer mortality from smoking were estimated globally and regionally. • Globally, the ASMR of lung cancer from smoking decreased, but the death number rose. • Men's ASMR decreased more significantly than women's, especially in young people. • Most countries have achieved a significant reduction in ASMRs since 1990. • The estimated annual growth rate of ASMR in lung cancer in 20 countries exceeded 1 %. Understanding the global trend of lung cancer deaths attributable to smoking is crucial for prioritizing global lung cancer prevention, as well as tobacco control. We assessed patterns of smoking-induced lung cancer deaths at global, regional, and national levels from 1990 to 2017. We extracted detailed data on lung cancer deaths attributable to smoking from the Global Burden of Disease 2017 Study. The estimated annual percentage change (EAPC) was used to quantify temporal trends in the age-standardized mortality rate (ASMR) of smoking-induced lung cancer. In 2017, estimated 1.19 million lung cancer deaths were attributable to smoking, accounting for 63.17 % of all lung cancer deaths. The corresponding ASMR decreased by 13.36 % from 17.29/100,000 in 1990 to 14.98/100,000 in 2017, with an EAPC of −0.59 (95 % confidence interval: −0.66, −0.53). The ASMR of lung cancer in most geographic regions has significantly decreased since 1990; however, the EAPC of ASMR in 20 countries exceeded 1 during the same period. The reductions in the ASMR were pronounced in areas with high Socio-demographic Index and high disease burden, and kept pace with the decrease of smoking prevalence at least 10 years ago. Despite the decline in lung cancer ASMR attributable to smoking over the past 28 years, the corresponding number of lung cancer deaths increased steadily due to population aging and growth. Tobacco prevention needs to be strengthened, especially in countries with high smoking prevalence and countries where the ASMR of smoking-induced lung cancer is increasing. [ABSTRACT FROM AUTHOR]