Tobacco smoking and chewing, alcohol drinking and lung cancer risk among men in southern India

In India, lung cancer is one of the most common and lethal cancers, and tobacco smoking remains its most important etiologic factors. The objective of our study is to examine the effects of different tobacco consumption forms, including smoking and chewing, on lung cancer risk of men in southern India, especially to compare the effects of bidi smoking to cigarette smoking on lung carcinogenesis. We also evaluated the possible role of Indian alcohol beverages and non-Indian alcohol beverages on lung carcinogenesis. We conducted a case-control study in Chennai and Trivandrum. In total, 778 lung cancer cases and 3,430 controls, including 1,503 cancer controls and 1,927 healthy controls, were recruited. The effects of cigarette, bidi smoking, chewing and alcohol drinking on the risk of lung cancer were estimated from unconditional multivariate logistic regression. We also applied the generalized additive model (GAM) with locally-weighted running-line smoothers (loess) to find the most plausible curve for the dose-response relationship. The results from GAM suggest a plateau after 35 years of smoking or 10 cigarette-equivalent pack-years for both cigarette and bidi. The OR is 4.54 (95%CI=2.96-6.95) and 6.45 (95%CI=4.38-9.50) for more than 30 years of cigarette-only and bidi-only smoking, respectively, and 6.87 (95%CI=4.62-10.2) and 10.7 (95%CI=5.82-19.6) for more than 12 weighted cumulative cigarette-only and bidi-only consumption, respectively. The lung cancer risk of former cigarette smokers drops down more quickly after quitting smoking compared to former bidi smokers. There is no evidence for the effect of chewing and lung cancer risk nor clear evidence of an effect of overall alcohol drinking among never-smokers, although Indian alcohol drinking seemed to remain associated with lung cancer risk under limited power (OR=2.67, 95%CI=1.02-7.02). Bidi smoking seems to have a stronger carcinogenic effect than cigarette smoking: this difference holds no matter which aspect of smoking was considered.     

Cigarette Smoking and Breast Cancer: a Case-control Study in Serbia

Background: Despite the fact that breast cancer is the most common female cancer worldwide, more than halfof the breast cancer risk factors remained unexplained. The aim of this study was to investigate the associationof cigarette smoking with risk of breast cancer. Materials and Methods: A case-control study was conductedin the Clinical Centre of Kragujevac, Serbia, covering 382 participants (191 cases and 191 controls). In theanalysis of data logistic regression was used. Results: Breast cancer risk was significantly increased in thosewho quit smoking at ≤50 years of age (OR=2.72; 95% confidence interval - 95%CI=1.02-7.27) and in those whoquit smoking less than 5 years before diagnosis of the disease (OR=4.36; 95%CI=1.12-16.88). When smokerswere compared with nonsmokers without passive exposure to smoking, former smoking significantly increasedbreast cancer risk (OR=2.37; 95%CI=1.07-5.24). Risk for breast cancer was significantly increased in those whoquit smoking at ≤50 years of age (OR=3.29; 95%CI=1.17-9.27) and in those who quit smoking less than 5 yearsbefore diagnosis of the disease (OR=5.46; 95%CI=1.34-22.28). Conclusions: These data suggest that cigarettesmoking is associated with an elevated risk of breast cancer among former smokers in Serbia.     

Association between Smokeless Tobacco Use and Waterpipe Smoking and the Risk of Lung Cancer: A Systematic Review and Meta-Analysis of Current Epidemiological Evidence

Background: Smokeless tobacco and waterpipes are used by hundreds of millions of people worldwide and consumption rates exceed that of cigarette smoking in much of South East Asia and parts of the Middle East. However, the cancer risks of these methods of tobacco consumption are less well-characterized than those of cigarette smoking. The objective of this study was to systematically review the epidemiological evidence on the association between smokeless tobacco use and waterpipe smoking and lung cancer risk. Methods: The MEDLINE, EMBASE, Web of Science and OpenSIGLE databases were searched to identify eligible case-control and cohort studies (published before 1st December 2020 in any language) that adjusted for cigarette smoking or included non-cigarette smokers only. Summary odds ratio/relative risk estimates and confidence intervals were extracted, and pooled risk ratios (RRs) for lung cancer were calculated using random effects meta-analysis. Results: The literature search identified 2,465 publications: of these, 26 studies including 6,903 lung cancer patients were included in the synthesis (20 studies of smokeless tobacco use, five of waterpipe smoking, one of both). Our results suggest that smokeless tobacco use is associated with an increased risk of lung cancer among non-cigarette smokers, and that betel quid tobacco may be particularly hazardous. The random effects meta-analysis showed that exclusive use of any type of smokeless tobacco (pooled RR = 1.53, 95%CI 1.09 – 2.14), betel quid chewing (pooled RR = 1.77, 95%CI 1.06 – 2.95), and waterpipe smoking (pooled RR = 3.25, 95%CI 2.01 – 5.25) were significantly associated with an increased risk of lung cancer. Conclusions: This meta-analysis of case-control/cohort studies supports the hypothesis that use of smokeless tobacco and waterpipe smoking is associated with increased risk of developing lung cancer. Considering the widespread and increasing use of smokeless tobacco in developing countries, and increasing prevalence of waterpipe smoking in almost all societies, these findings inform formulation of public health policy, legislation and tobacco control measures at national and international level to increase awareness and decrease the prevalence of smokeless tobacco use and waterpipe smoking.     

Smoking and bladder cancer in Spain: effects of tobacco type, timing, environmental tobacco smoke, and gender.

We examined the effects of dose, type of tobacco, cessation, inhalation, and environmental tobacco smoke exposure on bladder cancer risk among 1,219 patients with newly diagnosed bladder cancer and 1,271 controls recruited from 18 hospitals in Spain. We used unconditional logistic regression to estimate odds ratios (OR) and 95% confidence intervals (95% CI) for the association between bladder cancer risk and various characteristics of cigarette smoking. Current smokers (men: OR, 7.4; 95% CI, 5.3-10.4; women: OR, 5.1; 95% CI, 1.6-16.4) and former smokers (men: OR, 3.8; 95% CI, 2.8-5.3; women: OR, 1.8; 95% CI, 0.5-7.2) had significantly increased risks of bladder cancer compared with nonsmokers. We observed a significant positive trend in risk with increasing duration and amount smoked. After adjustment for duration, risk was only 40% higher in smokers of black tobacco than that in smokers of blond tobacco (OR, 1.4; 95% CI, 0.98-2.0). Compared with risk in current smokers, a significant inverse trend in risk with increasing time since quitting smoking blond tobacco was observed (> or =20 years cessation: OR, 0.2; 95% CI, 0.1-0.9). No trend in risk with cessation of smoking black tobacco was apparent. Compared with men who inhaled into the mouth, risk increased for men who inhaled into the throat (OR, 1.7; 95% CI, 1.1-2.6) and chest (OR, 1.5; 95% CI, 1.1-2.1). Cumulative occupational exposure to environmental tobacco smoke seemed to confer increased risk among female nonsmokers but not among male nonsmokers. After eliminating the effect of cigarette smoking on bladder cancer risk in our study population, the male-to-female incidence ratio decreased from 8.2 to 1.7, suggesting that nearly the entire male excess of bladder cancer observed in Spain is explained by cigarette smoking rather than occupational/environmental exposures to other bladder carcinogens.     

吸烟和环境烟草烟雾暴露与膀胱癌关系的病例对照研究

目的研究分析吸烟及环境烟草烟雾暴露与膀胱癌的关系。方法自1996年1月~1999年6月,上海市区开展了一项大规模的基于全人群的膀胱癌病例对照研究,共访问到608例膀胱癌病例和607例健康人群对照。使用非条件logistic回归分析,调整可能的混杂因素,估计吸烟及环境烟草烟雾暴露对膀胱癌发生的比数比和95%可信区间。结果男性吸烟者患膀胱癌的危险性是不吸烟者的1.67倍(95%CI1.23~2.27),且随着每天吸烟量、累积吸烟量、吸烟年限和吸烟深度的增加而增加,吸烟开始年龄越小危险性越大;戒烟后膀胱癌危险性有所降低。吸烟也显著增加女性膀胱癌的危险性,调整OR为4.19(95%CI1.65~10.65)。吸烟者的调整人群归因危险度男性、女性分别为32.04%和15.61%。未发现环境烟草暴露增加非吸烟者膀胱癌的危险性。结论进一步证实吸烟是膀胱癌发生的重要危险因素。环境烟草烟雾暴露是否增加膀胱癌危险性尚难定论。     

Smoking and the risk of gastric cancer in the European Prospective Investigation Into Cancer and Nutrition (EPIC)

Smoking has recently been recognised as causally associated with the development of gastric cancer (GC). However, evidence on the effect by sex, duration and intensity of smoking, anatomic subsite and cessation of smoking is limited. Our objective was to assess the relation between tobacco use and GC incidence in the European Prospective Investigation into Cancer and Nutrition (EPIC). We studied data from 521,468 individuals recruited from 10 European countries taking part in the EPIC study. Participants completed lifestyle questionnaires that included questions on lifetime consumption of tobacco and diet in 1991-1998. Participants were followed until September 2002, and during that period 305 cases of stomach cancer were identified. After exclusions, 274 were eligible for the analysis, using the Cox proportional hazard model. After adjustment for educational level, consumption of fresh fruit, vegetables and preserved meat, alcohol intake and body mass index (BMI), there was a significant association between cigarette smoking and gastric cancer risk: the hazard ratio (HR) for ever smokers was 1.45 (95% confidence interval [CI] = 1.08-1.94). The HR of current cigarette smoking was 1.73 (95% CI = 1.06-2.83) in males and 1.87 (95% CI = 1.12-3.12) in females. Hazard ratios increased with intensity and duration of cigarette smoked. A significant decrease of risk was observed after 10 years of quitting smoking. A preliminary analysis of 121 cases with identified anatomic site showed that current cigarette smokers had a higher HR of GC in the cardia (HR = 4.10) than in the distal part of the stomach (HR = 1.94). In this cohort, 17.6 % (95% CI = 10.5-29.5 %) of GC cases may be attributable to smoking. Findings from this large study support the causal relation between smoking and gastric cancer in this European population. Stomach cancer should be added to the burden of diseases caused by smoking.     

Tobacco use and stomach cancer in Mizoram, India.

The incidence of stomach cancer in India is lower than that of any other country around the world. However, in Mizoram, one of the north-eastern state of India, a very high age-adjusted incidence of stomach cancer is recorded. A hospital-based case-control study was carried out to identify the influence of tobacco use on the risk of developing stomach cancer in Mizoram. Among the cases, the risk of stomach cancer was significantly elevated among current smokers [odds ratio (OR), 2.3; 95% confidence interval (95% CI), 1.4-8.4] but not among ex-smokers. Higher risks were seen for meiziol (a local cigarette) smokers (OR, 2.2; 95% CI, 1.3-9.3). The increased risk was apparent among subjects who had smoked for >or=30 years. The increased risk was significant with 2-fold increase in risk among the subjects who smoked for >or=11 pack-years. The risk increased with increasing cumulative dose of tobacco smoked (mg). Tuibur (tobacco smoke-infused water), used mainly in Mizoram, was seemed to increased the risk of stomach cancer among current users in both univariate and multivariate models (OR, 2.1; 95% CI, 1.3-3.1). Tobacco chewer alone (OR, 2.6; 95% CI, 1.1-4.2) showed significant risk. Tobacco use in any form [smoking and smokeless (tuibur and chewing)] increased the risk of stomach cancer in Mizoram independently after adjusting for confounding variables.     

Cigarette smoking,use of other tobacco products and stomach cancer mortality in US adults: The Cancer Prevention Study II

Cigarette smoking is associated with increased risk of stomach cancer in many studies but there are limited data on this relationship in women and on risk associated with use of tobacco products other than cigarettes. We examined stomach cancer death rates in relation to cigarette smoking in women and use of cigarette, cigar, pipe, or smokeless tobacco in men in a nationwide prospective mortality study in the United States (US). Cohort follow-up from 1982-96 identified 996 and 509 stomach cancer deaths among 467,788 men and 588,053 women, respectively. Cox proportional hazards models were fitted to estimate rate ratios (RR) and 95% confidence intervals (CI) using non-users of tobacco as the referent group. Multivariate-adjusted RRs were the highest for men who currently smoked cigars (RR = 2.29, 95% CI = 1.49-3.51) or cigarettes (RR = 2.16, 95% CI = 1.75-2.67) and both increased with smoking duration. Women who currently (RR = 1.49, 95% CI = 1.18-1.88) or formerly (RR = 1.36, 95% CI = 1.08-1.71) smoked cigarettes were at significantly increased risk, as were men who formerly smoked cigarettes (RR = 1.55, 95% CI = 1.28-1.88), or currently (RR = 1.81, 95% CI = 1.40-2.35) or formerly (RR: 1.57, 95% CI = 1.22-2.03) used more than one type of tobacco. Men who reported a history of chronic indigestion or gastroduodenal ulcer had substantially higher mortality rates associated with current cigarette (RR = 3.45, 95% CI = 2.05-5.80) or cigar (RR = 8.93, 95% CI = 4.02-19.90) smoking, as did men who were current aspirin users. If causal, the estimated proportion of stomach cancer deaths attributable to tobacco use would be 28% in US men and 14% in women. We conclude that prolonged use of tobacco products is associated with increased stomach cancer mortality in men and women. The accumulated evidence from this and other studies support reconsidering stomach cancer as a tobacco-related cancer.     

Fruit and Vegetable Intake and Stomach Cancer among Male Adults: A Case-Control Study in Northern Viet Nam

Objective: This study investigated the association between fruit and vegetable intake and stomach cancer, with considering the impacts of Helicobacter pylori (H. pylori) infection and tobacco smoking. Methods: A case-control study featuring 80 male incident stomach-cancer cases and 126 male controls was conducted in a general hospital in Viet Nam. A semi-quantitative food frequency and demographic lifestyle questionnaire were used; and venous blood samples were collected to determine H. pylori status by IgG ELISA. The respective associations between fruit and vegetable intake and stomach cancer were examined using unconditional logistic regression analysis with adjustments for possible cofactors. Results: Fruit intake and stomach cancer showed a weak inverse association when this became non-significant after adjusting for H. pylori infection (OR = 0.50, 95%CI: 0.22–1.12, p trend = 0.094). Stratifying by H. pylori status returned a negative trend for fruit intake and stomach cancer among H. pylori-negative participants (OR = 0.21, 95%CI: 0.06–0.69, p trend = 0.010), but no significant interaction for H. pylori-positive participants (OR = 0.76, 95%CI: 0.21–2.68, p trend = 0.670). Vegetable intake and stomach cancer showed no association, regardless of H. pylori status. Compared to ever-smokers with low intake, never-smokers with high vegetable (OR = 0.25, 95% CI: 0.06–0.95) and fruit intake (OR = 0.20, 95%CI: 0.06–0.65) showed the lowest odds of stomach cancer. Conclusions: Fruit, but not vegetable, intake showed a weak inverse association with stomach cancer. H. pylori infection and tobacco-smoking status may influence the protective effects of fruit and vegetable intake on stomach cancer.     

Association of cigarette smoking with the risk of ovarian cancer

Cigarette smoking may be associated with ovarian cancer risk. This association may differ by histological type. The authors conducted a population-based case-control study in Canada of 442 incident cases of ovarian cancer and 2,135 controls 20-76 years of age during 1994-1997 to examine this association, overall and by histological type. Compared to women who never smoked, those who smoked had higher odds (odds ratio [OR] = 1.22; 95% confidence interval [CI] = 0.98-1.53) of having ovarian cancer, and the OR was larger for ex-smokers (1.30; 95% CI = 1.01-1.67) than for current smokers (1.10; 95% CI = 0.81-1.49). The association with cigarette smoking was stronger for mucinous tumors (OR = 1.77; 95% CI = 1.06-2.96) than for nonmucinous tumors (OR = 1.13; 95% CI = 0.89-1.44). In addition, the odds of smokers having mucinous tumors increased with years of smoking (OR = 1.36, 1.88, 1.19, 4.89 for <20, 21-30, 31-40 and >40 years, respectively; p for trend = 0.002), number of cigarettes smoked per day (OR = 1.55, 1.89, 2.28 for <10, 11-20 and >20 cigarettes/day, respectively; p for trend = 0.014) and smoking pack-years (OR = 1.13, 2.65, 1.77 and 2.39 for <10, 11-20, 21-30 and >30 pack-years, respectively; p for trend = 0.004). Our data suggest that cigarette smoking is associated with an increased risk of ovarian cancer, especially for mucinous types.     

Smoking and Cancer Risk in Korean Men and Women

OBJECTIVE: In Korea, male smoking prevalence is among the world's highest, and mortality rates from smoking-caused cancers, particularly lung cancer, are escalating. This cohort study examined the effects of cigarette smoking on the risk of cancer mortality and incidence, and characterized the relationship of cancer risk with the amount and duration of cigarette smoking. METHOD: A nine-year prospective cohort study was carried out on 1,212,906 Koreans, 30-95 years of age. The study population includes participants in a national insurance program, who completed a questionnaire on smoking and other risk factors. The main outcome measures were death from cancer and cancer incidence, obtained through record linkage. At baseline, 472,970 men (57.0%) and 20,548 (5.4%) women were current cigarette smokers. RESULTS: In multivariate Cox proportional hazards models, controlling for age, current smoking among men increased the risks of mortality for cancer of the lung (relative risk (RR), 4.6; 95% confidence interval (CI), 4.0-5.3) and other cancers, including larynx, bile duct, esophagus, liver, stomach, pancreas, bladder, and also leukemia. Current smoking among women increased the risk of lung cancer mortality (RR = 2.5, 95% CI = 2.0-3.1). Similar results were found for incidence among men and women. CONCLUSION: In Korea, smoking is an independent risk factor for a number of major cancers. The findings affirm the need for aggressive tobacco control in Korea in order to minimize the epidemic of smoking-caused disease.     

Interleukin-12 and Interleukin-6 Gene Polymorphisms and Risk of Bladder Cancer in the Iranian Population

Interleukin-12 (IL-12) as an antitumor and interleukin-6 (IL-6) as an inflammatory cytokine, areimmunomodulatory products that play important roles in responses in cancers and inflammation. We testedthe association between two polymorphisms of IL-12(1188A>C; rs3212227) and IL-6 (-174 C>G) and the riskof bladder cancer in 261 patients and 251 healthy individuals. We also investigated the possible association ofthese SNPs in patients with high-risk jobs and smoking habits with the incidence of bladder cancer. The genotypedistributions of IL-6 (-174 C/G) genotype were similar between the cases and the control groups; however, amongpatients with smoking habits, the association between IL-6 gene polymorphism and incidence of bladder cancerwas significant. After a control adjustment for age and sex, the following results were recorded: CC genotype(OR= 2.11, 95%CI=1.56-2.87, p=0.007), GC genotype (OR=2.18, 95%CI=1.16-4.12, p=0.014) and GC+ CC(OR=2.6, 95%CI=1.43-4.47, p=0.011). A significant risk of bladder cancer was observed for the heterozygousgenotype (AC) of IL-12 (OR=1.47, 95%CI=1.01-2.14, p=0.045) in all cases, and among smokers (AC) (OR=3.13,95%CI=1.82-5.37, p=0.00014), combined AC+CC (OR=3.05, 95%CI=1.8-5.18, p=0.000015). Moreover amonghigh risk job patients, there was more than a 3-fold increased risk of cancer in the carriers of IL-12 betaheterozygous (OR=3.7, 95%CI=2.04-6.57, p=0.000056) and combined AC+CC(OR=3.29, 95%CI=1.58-5.86,p=0.00002) genotypes as compared with the AA genotype with low-risk jobs. As a conclusion, this study suggeststhat IL-12(3’UTR A>C) and IL-6 (-174 C>G) genotypes are significantly associated with an increased risk ofbladder cancer in the Iranian population with smoking habits and/or performing high-risk jobs.     

APEX1 Asp148Glu Gene Polymorphism is a Risk Factor for Lung Cancer in Relation to Smoking in Japanese

DNA repair enzymes play an important role in the development of various kinds of cancer. We hereanalyzed associations of XPD Lys751Gln, APEX1 Asp148Glu, XRCC1 Arg399Gln, and XRCC3 Thr241Metgene polymorphisms in DNA repair pathways in relation to the risk of lung cancer using PCR-RFLP. The studyinvolved 104 lung cancer patients and 120 non-cancer controls divided into non-smokers and smokers. Wefound a statistically significant interaction between APEX1 Asp148Glu and the risk for lung cancer (adjustedOR 2.78, 95% CI 1.58-4.90, p=0.0004), of both adenocarcinoma (adjusted OR 2.24, 95%CI 1.18-4.25, p=0.014)and squamous cell carcinoma (adjusted OR 4.75, 95%CI 1.79-12.60, p=0.002) types. XRCC1 Arg399Gln showeda borderline significant association with adenocarcinoma (adjusted OR 1.89, 95%CI 1.00-3.57, p=0.051). Thecombined effect of smoking and presence of the APEX1 Asp148Glu demonstrated a significant association withrisk of lung cancer (adjusted OR 3.61, 95% CI 1.74-7.50, p = 0.001). The XPD Lys751Gln and XRCC3 Thr241Metgenotypes displayed no statistically significant risk. Our findings suggest that the APEX1 Asp148Glu is associatedwith increased risk for primary lung cancer in Japanese individuals partaking in smoking.     

Cannabis smoking and lung cancer risk: Pooled analysis in the International Lung Cancer Consortium

To investigate the association between cannabis smoking and lung cancer risk, data on 2,159 lung cancer cases and 2,985 controls were pooled from 6 case‐control studies in the US, Canada, UK, and New Zealand within the International Lung Cancer Consortium. Study‐specific associations between cannabis smoking and lung cancer were estimated using unconditional logistic regression adjusting for sociodemographic factors, tobacco smoking status and pack‐years; odds‐ratio estimates were pooled using random effects models. Subgroup analyses were done for sex, histology and tobacco smoking status. The shapes of dose‐response associations were examined using restricted cubic spline regression. The overall pooled OR for habitual versus nonhabitual or never users was 0.96 (95% CI: 0.66–1.38). Compared to nonhabitual or never users, the summary OR was 0.88 (95%CI: 0.63–1.24) for individuals who smoked 1 or more joint‐equivalents of cannabis per day and 0.94 (95%CI: 0.67–1.32) for those consumed at least 10 joint‐years. For adenocarcinoma cases the ORs were 1.73 (95%CI: 0.75–4.00) and 1.74 (95%CI: 0.85–3.55), respectively. However, no association was found for the squamous cell carcinoma based on small numbers. Weak associations between cannabis smoking and lung cancer were observed in never tobacco smokers. Spline modeling indicated a weak positive monotonic association between cumulative cannabis use and lung cancer, but precision was low at high exposure levels. Results from our pooled analyses provide little evidence for an increased risk of lung cancer among habitual or long‐term cannabis smokers, although the possibility of potential adverse effect for heavy consumption cannot be excluded.     

谷胱甘肽转硫酶T1、M1基因型和烟酒茶嗜好与食管癌、胃癌

目的 :研究谷胱甘肽转硫酶T1、M1(GSTT1、GSTM 1)基因多态性和烟酒茶嗜好及其相互作用与食管癌、胃癌易感性的关系。方法 :在上消化道癌高发区淮安市进行了病例 -对照研究 (食管癌 141例 ,胃癌 15 3例 ;人群对照 2 2 3例 ) ,调查研究对象的烟酒茶嗜好习惯 ,以多重PCR方法分析GSTT1、GSTM1基因型。结果 :食管癌组GSTM1-基因型频度 (75 .18% )显著高于对照组 (5 9.6 4 % ,P =0 .0 0 2 4 ;多因素调整OR =2 .33,95 %CI =1.39～ 3.92 )。吸烟或不饮茶与GSTM 1 基因型在增加食管癌发生的风险中有明显的协同作用。在GSTT1 基因型者中 ,吸烟习惯显著增加食管癌、胃癌的危险性 ;在GSTM1 基因型者中 ,经常饮酒显著增加食管癌、胃癌的危险性。结论 :食管癌、胃癌的发生与生活习惯、GSTM1和GSTT1基因型以及它们的相互作用有关。     

Modifying Effect of Smoking on GSTM1 and NAT2 in Relation to the Risk of Bladder Cancer in Mongolian Population: A Case-Control Study

Objectives: Tobacco smoking is the predominant risk factor for bladder cancer as it contains cancer-causing chemicals. However, genetic factors may play important role in response towards chemical carcinogens. In this study we aim to investigate genetic polymorphisms of glutathione S-transferase M1 (GSTM1) and N-acetyltransferase 2 (NAT2) as determinants of bladder cancer risk, independently and in combination with tobacco use in the Mongolian population. Materials and Methods: The current study was a hospital-based case-control study including 60 histologically confirmed bladder cancer patients and 60 cancer-free controls. PCR-RFLP assay was used to determine the presence of GSTM1 and NAT2 polymorphisms in bladder cancer patients and controls. GSTM1 and NAT2 were tested using binary logistical regression analysis with adjustment or stratification according to the smoking. Results: There were 46 men and 14 women diagnosed with bladder cancer, with mean age was 58±4. The controls included 37 men and 23 women with a mean age of 57±3. The frequency of GSTM1 null genotype was higher in controls (71.67%) than in bladder cancer patients (58.33%) without statistical significance (OR=0.5534; 95% CI=0.2586-1.1843), (p=0.128). The NAT2 low acetylator phenotype was more common in patients with bladder cancer (15%) than in controls (5%). Furthermore, individuals with NAT2 low acetylator phenotype had a nearly 3.35-fold increased risk to develop bladder cancer (OR=3.35; 95% CI=0.8604-13.0657), (p=0.081) while the risk was even higher when combined with null GSTM1 genotype (OR=4; 95% CI=0.4459-37.5308), (p=0.213) but there was no statistical significance. Prevalence of smoking in bladder cancer patients was higher than controls and increased significantly the risk of bladder cancer (OR=8.31; 95% CI=3.66-18.88). Smokers with GSTM1 null genotype were at 5-fold higher risk of bladder cancer (OR=5.0; 95% CI=1.55-16.16), (p=0.007) while NAT2 low acetylator phenotype increased bladder cancer risk by 20-fold (OR=20.5; 95% CI=2.33-80.86), (p=0.006). Conclusion: The current study shows that tobacco smokers with the NAT2 low acetylator phenotype and GSTM1 null genotype have the highest risk of bladder cancer in the Mongolian population.     

Cigarette smoking and colorectal cancer risk in Germany: a population-based case-control study

Studies have shown fairly consistent positive relationships between smoking and risk of colorectal adenomas, but have yielded inconsistent results for colorectal cancer. Issues relating to the duration, cumulative dose of smoking and the effect of smoking cessation on colorectal cancer risk still need clarification. In a population-based case-control study in Germany, we recruited 540 incident cases of colorectal cancer and 614 controls matched to cases by sex, 5-year age groups and county of residence from January 2003 to June 2004. Subjects were aged>or=30 years, and provided information on risk factors of colorectal cancer, including lifetime cigarette smoking habits, in personal interviews. Odds ratios (OR) and 95% confidence intervals (CI) were computed using conditional logistic regression models, adjusting for potential confounders. Compared with nonsmokers, there was an increased risk for smoking for >or=30 years (OR: 1.25, 95% CI: 0.90-1.75) and a significant risk increase for >or=40 pack-years of smoking (OR: 1.92, 95% CI: 1.13-3.28). Stratification by sex yielded higher risk estimates among females than that among males, with adjusted ORs of 3.5 (95% CI: 1.29-9.52) and 1.15 (0.69-1.91) for women and men, respectively, following >or=30 pack-years of smoking (pinteraction=0.18). Among smokers, risk reduction was observed after >or=20 years of quitting smoking and was significant for >or=40 years (OR: 0.46; 95% CI: 0.21-0.98), when compared to current smokers (p for linear trend=0.05). This study supports the hypothesis that smoking for a long duration at a high cumulative dose increases the risk for colorectal cancer, particularly among women, and suggests that there is risk reduction after longterm smoking cessation.     

Smoking addiction and the risk of upper‐aerodigestive‐tract cancer in a multicenter case–control study

Although previous studies on tobacco and alcohol and the risk of upper‐aerodigestive‐tract (UADT) cancers have clearly shown dose‐response relations with the frequency and duration of tobacco and alcohol, studies on addiction to tobacco smoking itself as a risk factor for UADT cancer have not been published, to our knowledge. The aim of this report is to assess whether smoking addiction is an independent risk factor or a refinement to smoking variables (intensity and duration) for UADT squamous cell carcinoma (SCC) risk in the multicenter case–control study (ARCAGE) in Western Europe. The analyses included 1,586 ever smoking UADT SCC cases and 1,260 ever smoking controls. Addiction was measured by a modified Fagerström score (first cigarette after waking up, difficulty refraining from smoking in places where it is forbidden and cigarettes per day). Adjusted odds ratios (ORs) and 95% confidence intervals (95% CIs) for UADT cancers with addiction variables were estimated with unconditional logistic regression. Among current smokers, the participants who smoked their first cigarette within 5 min of waking up were two times more likely to develop UADT SCC than those who smoked 60 min after waking up. Greater tobacco smoking addiction was associated with an increased risk of UADT SCC among current smokers (OR = 3.83, 95% CI: 2.56–5.73 for score of 3–7 vs. 0) but not among former smokers. These results may be consistent with a residual effect of smoking that was not captured by the questionnaire responses (smoking intensity and smoking duration) alone, suggesting addiction a refinement to smoking variables.     

Association between long‐term low‐intensity cigarette smoking and incidence of smoking‐related cancer in the national institutes of health‐AARP cohort

An increasing proportion of US smokers smoke ≤10 cigarettes per day (CPD) or do not smoke every day, yet the health effects of low‐intensity smoking are poorly understood. We identified lifelong smokers of <1 or 1‐10 CPD and evaluated risk of incident cancer among 238,525 cancer‐free adults, aged 59‐82, in the NIH‐AARP Diet and Health Study. A questionnaire administered in 2004‐2005 assessed CPD during nine age‐periods (<15 to ≥70). We estimated hazard ratios (HR) and 95% confidence intervals (CI) using multivariable‐adjusted Cox proportional hazards regression with age as the underlying time metric. Of the 18,233 current smokers, (7.6%), 137 and 1,243 reported consistently smoking <1 CPD and 1‐10 CPD, respectively. Relative to never smokers, current smokers who reported consistently smoking 1‐10 CPD over their lifetime were 2.34 (95% CI = 1.86‐2.93) times more likely to develop smoking‐related cancer. Current lifetime smokers of <1 CPD were 1.89 (95% CI = 0.90‐3.96) times more likely to develop tobacco‐related cancer, although the association did not reach statistical significance. Associations were observed for lifelong smoking of ≤10 CPD with lung cancer (HR = 9.65, 95% CI = 6.93‐13.43); bladder cancer (HR = 2.22, 95% CI = 1.22‐4.05); and pancreatic cancer (HR = 2.03, 95%CI: 1.05‐3.95). Among lifelong ≤10 CPD smokers, former smokers had lower risks of smoking‐related cancer with longer time since cessation and longer smoking duration. Lifelong <1 and 1‐10 CPD smokers are at increased risk of incident cancer relative to never smokers and would benefit from cessation, providing further evidence that even low‐levels of cigarette smoking cause cancer.     

The Relationship Between Tobacco Advertisements and Smoking Status of Youth in India

Objective: To examine the relationship between tobacco advertisements, counter-advertisements, and smokingstatus among Indian youth. Materials and Methods: Global Youth Tobacco Survey (GYTS) data was used; thedata encompassed a representative two-stage probability sample of 60,001 students aged 13–15 years in 24states in India. These students were interviewed with an anonymous, self-administered questionnaire. Binarylogistic regression analyses were performed with smoking status as the dependent variable, and exposure tocigarette advertisements or counter-advertisements as independent variables. Results: Students watching antismokingmedia messages were less likely to be current smokers, which was true for both boys [OR = 0.89, 95%CI (0.81–0.98)] and girls [OR = 0.79, 95% CI (0.69–0.90)]. This relationship was stronger among past smokersfor boys [OR = 0.56, 95%CI (0.52–0.60)] and girls [OR = 0.49, 95% CI (0.45–0.53)]. On the other hand, studentswho were exposed to cigarette brand names during sports events and other televised programs, newspapers ormagazines, and being offered free cigarette or cigarette-branded merchandise promotions were significantlymore likely to be smokers, with effects ranging from moderate (OR=1.19) to very strong (OR=3.83). Conclusions:This is the first attempt from India to investigate the relationship between smoking and advertising. When thedata were collected, cigarette advertising was legal and highly correlated with smoking behavior. Today, indirectsurrogate advertising still exists; future research should examine its effect, as it is likely to have the same impactas direct advertising on smoking behavior. Finally, counter-advertising has a protective effect on youth and mayfunction as a cessation aid.