Parakeets, canaries, finches, parrots and lung cancer: no association.

The relationship between pet bird keeping and lung cancer according to exposure to tobacco smoking was investigated in a case-control study in hospitals of New York City and Washington, DC, USA. Newly diagnosed lung cancer cases (n = 887) aged 40-79 years were compared with 1350 controls with diseases not related to smoking, of the same age, gender and date of admission as the cases. The prevalence of pet bird keeping was 12.5% in men and 19.1% in women. There was no association between ever keeping a pet bird and lung cancer in never smokers (men adjusted odds ratio (OR) = 0.70, 95% confidence interval (CI) 0.15-3.17; women, 1.32, 95% CI 0.65-2.70), or in smokers and non-smokers combined, after adjustment for ever smoking (men: 1.28, 95% CI 0.88-1.86; women: 1.17, 95% CI 0.83-1.64; all: 1.21, 95% CI 0.95-1.56). Risk did not increase in relation to duration of pet bird keeping. Cases and controls kept similar types of birds. There was a tenfold increase of lung cancer risk associated with smoking among non-bird keepers (adjusted OR = 9.15). There was no indication of a synergism, either additive or multiplicative, between smoking and pet bird keeping with respect to lung cancer risk. Either alone or in conjunction with smoking, keeping parakeets, canaries, finches or parrots is not a risk factor for lung cancer among hospital patients in New York and in Washington, DC.     

Tobacco smoking and lung cancer risk: an evaluation based on a systematic review of epidemiological evidence among the Japanese population

BACKGROUND: Although tobacco smoking is the best established risk factor for lung cancer, the association is not as strong among Japanese as among Western populations. It would be of value, therefore, to quantify that association in Japan based on a systematic review of epidemiological evidence for the primary prevention of lung cancer. METHODS: Original data were obtained from MEDLINE searches using PubMed, supplemented with manual searches. The evaluation of associations was based on the strength of evidence and the magnitude of the association, together with biological plausibility as previously evaluated by the International Agency for Research on Cancer. A meta-analysis was also conducted to estimate the summary measure of those associations. RESULTS: A total of 8 cohort studies and 14 case-control studies were identified, almost all of which consistently showed a strong association of current smoking with the risk of lung cancer. The summary relative risk for current smokers versus never smokers was estimated as 4.39 (95% confidence interval 3.92-4.92) for men and 2.79 (95% confidence interval 2.44-3.20) for women. Cohort studies and case-control studies gave reasonably consistent summary measures. The summary relative risks were 11.7 and 2.30 for squamous cell carcinoma and adenocarcinoma, respectively, in men, and were 11.3 and 1.37 correspondingly in women. CONCLUSION: There is convincing evidence that tobacco smoking strongly increases the risk of lung cancer in the Japanese population, with the relative risk for current smokers compared with never smokers measuring around 4.4 for men and 2.8 for women.     

Association between Cigarette Smoking and RASSF1A Gene Promoter Hypermethylation in Lung Cancer Patients: a Metaanalysis

Objectives: Epidemiological studies have shown that molecular mechanisms underlying the development oflung cancers differ between smokers and unsmokers. Aberrant promoter methylation in some tumor suppressorgenes is frequent in lung tumors from smokers but rare in those from non-smokers. Recently, many studies haveinvestigated the association between cigarette smoking and RASSF1A gene promoter hypermethylation in lungcancer patients, but a unanimous conclusion could not be reached. We therefore performed this meta-analysisto derive a more precise estimation of any association. Study Design: An electronic search of PubMed andChinese Biomedicine databases was conducted to select studies. A total of 19 case-control studies were chosen,and odds ratios (ORs) with confidence intervals (CIs) were used to assess the strength of associations. Results:The case-control studies covered 2, 287 lung cancer patients: 63.4%(1449) of the patients were smokers, 36.6%(838) were unsmokers. The overall results suggested that smokers with lung cancer had a 1.297-fold (95% CI:1.066~1.580, p=0.010, p=0.087) higher risk for RASSF1A gene hypermethylation than the non-smokers. In thestratified analysis, an increased risk of RASSF1A gene hypermethylation in smokers than in non-smokers wasfound in Asian (OR=1.481, 95%CI: 1.179~1.861, p=0.001, p=0.186). Conclusions: This meta-analysis supportsthe idea that RASSF1A gene hypermethylation is associated with cigarette smoking-induced lung cancer.     

Association between Smoking and p53 Mutation in Lung Cancer: A Meta-analysis

AimsTo carry out a meta-analysis on the relationship between smoking and p53 gene mutation in lung cancer patients.Materials and methodsPubMed, Web of Science, ProQest and Medline were searched by using the key words: ‘lung cancer or lung neoplasm or lung carcinoma’, ‘p53 mutation’ and ‘smoking’. According to the selection criteria, 15 articles were identified and methodologically analysed by stata 12.0 software package. Crude odds ratios with 95% confidence intervals calculated using the fixed-effects model were used to assess the strength of association between smoking and p53 mutation in lung cancer.ResultsIn total, 15 articles with 1770 lung cancer patients were identified; 69.6% of the patients were smokers, 30.4% were non-smokers. Overall, smokers with lung cancer had a 2.70-fold (95% confidence interval 2.04–3.59) higher risk for mutation than the non-smokers with lung cancer. In subgroup analyses, the increased risk of p53 mutation in smokers than in non-smokers was found in the non-small cell lung cancer (NSCLC) group (odds ratio = 2.38, 95% confidence interval = 1.71–3.32) and in the NSCLC and SCLC group (odds ratio = 3.82, 95% confidence interval = 2.19–6.69).ConclusionsThis meta-analysis strongly suggests that p53 mutation is associated with smoking-induced lung cancer. Smokers with lung cancer had a higher risk for p53 mutation than non-smokers.     

Association of Chlamydia pneumoniae immunoglobulin A seropositivity and risk of lung cancer.

Chlamydia pneumoniae is a common respiratory pathogen that has also been associated with risk for chronic diseases, including atherosclerotic cardiovascular disease. Two recent studies have reported an association between serological evidence of past infection with the organism and lung cancer. To further evaluate this association, we conducted a case-control study among a subgroup of white male smokers identified for a population-based case-control study of lung cancer in western Washington between 1993 and 1995. Serum specimens obtained at study enrollment from 143 cases and 147 controls were tested for C. pneumoniae IgG, IgM, and IgA antibodies. In multivariate analysis controlling for smoking variables and educational status, IgA antibody titer 216 was independently associated with risk of lung cancer among subjects <60 years of age [odds ratio (OR), 2.67; 95% confidence interval (CI), 1.21-5.89] but not among older subjects (OR, 0.69; 95% CI, 0.34-1.43). Among subjects <60 years of age, there was suggestive evidence of a stronger association among current smokers (OR 4.31; 95% CI, 1.36-13.68) than former smokers (OR 1.50; 95% CI, 0.48-4.75; P for interaction term, 0.26). Additional studies, including prospective serological evaluations, are needed to further assess the possible significance of this association.     

Smoking and lung cancer in Harbin, northeast China.

BACKGROUND: We studied the relationship between smoking and lung cancer risk in Harbin, Heilongjiang province, northeast China, an area with a very high baseline risk of lung cancer in both sexes, using data from a case-control study of lung cancer conducted between 1987 and 1990. PATIENTS AND METHODS: Cases were 218 patients with incident, histologically confirmed lung cancer and controls were 436 patients admitted to the same hospital with non-neoplastic and non-lung diseases. RESULTS: Compared with never-smokers, the multivariate odds ratio (OR) for current smokers was 3.47 [95% confidence interval (CI) 2.31--5.20], and for ex-smokers 1.53 (95% CI 0.81--2.87). Lung cancer risk increased by 20% (95% CI 14% to 28%) for an increment of 5 years in smoking duration, and by 29% (95% CI 15% to 45%) for an increment of five cigarettes per day. The OR for smokers reporting occupational exposure to selected known or likely lung carcinogens was 7.22, compared with non-smokers without occupational exposure. CONCLUSIONS: This study further confirms that cigarette smoking is a strong determinant of lung cancer also in this high-risk area of northeast China.     

NAT2 slow acetylator genotype is associated with increased risk of lung cancer among non-smoking Chinese women in Singapore.

Among non-smokers, the factors resulting in lung carcinogenesis are poorly understood. We conducted a hospital-based case-control analysis of 294 Chinese women, of whom 217 were non-smokers, to evaluate the role of polymorphic N-acetyltransferase (NAT2) as a susceptibility factor for the disease. The proportion of slow acetylator genotypes among non-smoking cases (n = 92) and controls (n = 125) was 38.0 and 24.0%, respectively [odds ratio (OR) 2.0, 95% confidence interval (CI) 1.1-3.7]. No effect of NAT2 genotype was seen among smokers. Among non-smokers, the effect was marked for adenocarcinomas (OR 2.1, 95% CI 1.1-4.0). As NAT2 activity is known to modify risk of arylamine-induced carcinogenesis, our results suggest that exposure to arylamines in the environment may play a role in risk of lung cancer among non-smokers.     

CYP1A1 and GSTM1 polymorphisms in relation to lung cancer risk in Chinese women

We examined CYP1A1 (I462V) and GSTM1 null polymorphisms in 200 female cases and 144 female controls selected from a population-based case-control study of lung cancer conducted in northeast China, where the rates of lung cancer among Chinese women are especially high. The CYP1A1 codon 462 point mutation in exon 7 (I462V) causes an Ile-Val substitution near the heme binding site. This mutation correlates with inducibility of aryl hydrocarbon hydrolase (AHH) activity, which activates polycyclic aromatic hydrocarbons (PAHs) in tobacco smoke and in indoor air pollution from coal-burning stoves, a risk factor for lung cancer in this study population. We found that the CYP1A1 I462V genotype (combined ile/val and val/val) was significantly associated with lung cancer risk. The odds ratio (OR) was 2.5 (95% confidence interval [CI], 1.55-4.03) after adjustment for significant risk factors such as age, ever smoking status, family history of cancer, and eye irritation when cooking. The association was more pronounced among non-smokers (OR=3.67; 95% CI, 1.85-7.28) than among smokers (OR=1.74, 95% CI, 0.85-3.54). In contrast, we did not find a significant association with the GSTM1 null genotype. In summary, our case-control study of lung cancer among women in northeast China revealed an elevated risk associated with the CYP1A1 I462V genotype, but no interaction with smoking or indoor air pollution was found.     

Passive smoking and lung cancer in Chandigarh, India.

The aim of this study is to assess the relationship between exposure to environmental tobacco smoke (ETS) and lung cancer in non-smokers, a case-control study among lifetime non-smokers was conducted in Chandigarh, India. Cases consisted of 58 non-smoking histologically confirmed lung cancer patients; two controls for each case were selected, one among other patients admitted to the wards and one among the visitors to hospital patients. Subjects were asked about ETS exposure from different tobacco products in childhood and in adulthood at home, at the work place and in vehicles. Multivariate logistic regression analysis was used to assess the effects of the ETS exposure variables on lung cancer. Exposure to ETS during childhood was strongly associated with lung cancer (odds ratio (OR) = 3.9; 95% confidence interval (CI) = 1.9-8.2), the effect mostly arising from exposure to cigarettes smoke. The excess risk was observed with either a smoking father or mother. An increasing risk was found with increasing number of smokers and duration of exposure. Restricting the analysis to women produced higher estimates of the risk. No increased risk was found with exposure to a smoking spouse, except for those exposed only to cigarette smoke (OR = 5.1; 95% CI = 1.5-17). A weak association was seen between lung cancer and ETS exposure at the workplace, which increased with the number of years of exposure. Exposure in vehicles also was detected as a risk factor for lung cancer in non-smokers. This study suggests that ETS exposure may be a strong risk factor for lung cancer also in India, a country with low prevalence of smoking and, therefore, low rates of lung cancer. Other studies need to be conducted in similar settings to confirm the role played by ETS exposure early in life in the causation of lung cancer.     

Glutathione S-transferase M1 polymorphism and lung cancer risk in African-Americans

Glutathione S:-transferase M1 (GSTM1) can detoxify many carcinogens, including polycyclic aromatic hydrocarbons such as those from cigarette smoke. Though a number of studies have been published about the association between GSTM1 polymorphism and lung cancer, this association has received limited attention in the African-American population. We conducted a case-control study to investigate the role of GSTM1 polymorphism in the development of lung cancer in African-Americans. Specimens of DNA from 117 lung cancer cases and 120 controls were assayed for detection of GSTM1 genotype by polymerase chain reaction (PCR). The odds ratios (ORs) and 95% confidence intervals (CIs) for lung cancer associated with homozygous deletion of the GSTM1 gene and other risk factors were estimated by logistic regression. Thirty-seven of the 117 cases (31. 6%) and 24 of the 120 controls (20.0%) had the GSTM1 null genotype; the OR was 2.10 (95% CI 1.07-4.11) after adjustment for age, gender and smoking. The association was higher for squamous cell carcinoma (OR 2.98, 95% CI 1.09-8.19) than for adenocarcinoma (OR 1.95, 95% CI 0.81-4.66). We observed a stronger association between GSTM1 null genotype and lung cancer among heavy smokers with > or =30 pack-years (OR 4.35, 95% CI 1.16-16.23). This association was also found in squamous cell carcinoma (OR 6.26, 95% CI 1.31-29.91). In the analysis combining GSTM1 polymorphism and smoking, smokers with the null genotype had high risk (OR 8.19, 95% CI 2.35-28.62) compared with non-smokers with the wild-type genotype, and the risk increased with smoking cigarette pack-years (P: = 0.0001 for trend). Our results suggest that GSTM1 polymorphism plays a role in the development of lung cancer and modifies the risk for smoking-related lung cancer in African-Americans.     

Dietary habits and lung cancer risk among non-smoking women.

A case-control study was conducted to investigate the relationship between diet and the risk of lung cancer among women non-smokers and to compare with women smokers in the same population. Data collected by personal interviews from 435 microscopically confirmed cases and 1710 controls were analysed using unconditional logistic regression. In addition to results for all study subjects, associations between diet and lung cancer risk were compared between two highly contrasting groups: smokers (odds ratio (OR) 7.03) and non-smokers (OR 1.00). A protective effect of frequent (daily or several times per week) black tea drinking appeared among non-smoking women (OR 0.65, 95% confidence interval (CI) 0.43-0.99). Among smoking women, protective effects were observed for frequent intake of milk/dairy products (OR 0.56, 95% CI 0.32-0.96), coffee (OR 0.47, 95% CI 0.25-0.88), and wine consumption (daily or weekly OR 0.60, 95% CI 0.37-0.98; monthly OR 0.60, 95% CI 0.39-0.94). Inverse associations with the risk appeared for physical exercise for smokers only, and for the body mass index both among non-smoking and smoking women. Some items of diet may contribute to variation in risk among women in the Czech Republic; their importance seems to vary in relation to their status in smoking, the dominant factor in the aetiology of lung cancer.     

Cigarette smoking and subsequent risk of lung cancer by histologic type in middle-aged Japanese men and women: the JPHC study

In order to update the findings of relative risk associated with cigarette smoking for lung cancer by histologic type in Japan, the data from a population-based cohort study of 91,738 men and women were analyzed. During 1990-1999, 422 lung cancer incident cases were identified. The relative risk for all incident cases associated with current smokers versus non-smokers was 4.5 [95% confidence interval (CI): 3.0-6.8] and 4.2 (95% CI: 2.4-7.2), for men and women, respectively. When divided by histologic type, relative risk for squamous cell carcinoma and small cell carcinoma was 12.7 (95% CI: 4.7-34.7) and 17.5 (95% CI: 4.9-62.1), while for adenocarcinoma it was 2.8 (95% CI: 1.6-4.9) and 2.0 (95% CI: 0.8-5.0) for men and women, respectively. We confirmed that the lung cancer risk in men rose with increasing cigarette smoking, especially the duration of smoking among current smokers and decreased after the cessation of smoking among former smokers. Unlike the US or European countries, the relative risk did not increase in this updated study, compared with previous studies in 1960s to 1990s in Japan either for all incident cases or for specific histologic types and the magnitude of relative risks was substantially lower than that observed in the US or European countries, especially for adenocarcinoma.     

The impact of characteristics of cigarette smoking on urinary tract cancer risk: a meta-analysis of epidemiologic studies

BACKGROUND: Although narrative reviews have concluded that there is strong support for an association between cigarette smoking and urinary tract cancer, the association has never been quantified systematically in reviews. The purpose of this systematic review was to summarize and quantify the impact of different smoking characteristics (status, amount, duration, cessation, and age at first exposure) both unadjusted and adjusted for age and gender. METHODS: The authors included 43 epidemiologic studies (8 cohort and 35 case-control) and calculated summary odds ratios (SORs) by meta-regression analyses for different smoking characteristics. They also evaluated changes in summary estimates according to differences in study methodology. RESULTS: Smoking status and increased amount and duration of smoking were associated with a strong increased risk of urinary tract cancer. Smoking cessation and age at first exposure were negatively associated with the risk of urinary tract cancer. The age- and gender-adjusted SORs for current and former cigarette smokers compared with those for nonsmokers were 3.33 (95% confidence interval [CI], 2.63-4.21) and 1.98 (CI, 1.72-2.29), respectively. Even though the component studies differed in methodology, the results were rather consistent. CONCLUSIONS: The results suggest a substantial increase in risk of cancer of the urinary tract for cigarette smokers. Based on the results of this study and previous literature, the authors conclude that current cigarette smokers have an approximately threefold higher risk of urinary tract cancer than nonsmokers. In Europe, approximately half of urinary tract cancer cases among males and one-third of cases among females might be attributable to cigarette smoking.     

SULT1A1 Arg213His polymorphism and lung cancer risk: a meta-analysis

Background: The SULT1A1 Arg213His polymorphism is reported to be associated with lung cancer risk. However, this relationship remains controversial. For better understanding a meta-analysis was therefore performed. Methods: An extensive search was performed to identify all case-control studies investigating association between SULT1A1 Arg213His polymorphism and lung cancer risk. The strength was assessed by odds ratio (OR) with the corresponding 95% confidence interval (95%CI). Results: A total of five publications covering 1,669 cases and 1,890 controls were included in this meta-analysis. No significant association between SULT1A1 Arg213His polymorphism and lung cancer risk was observed in overall comparisons in all genetic models (dominant model: OR=1.33, 95%CI=1.00-1.76, P=0.05; additive model: OR=1.30, 95%CI=0.93-1.81, P=0.12; recessive model: OR=1.21, 95%CI=0.89-1.66, P=0.23). However, on subgroup analysis, an elevated risk in mixed populations with variant His allele was revealed in the dominant model (OR=1.66, 95% CI=1.06-2.62, P=0.03). Furthermore, the SULT1A1 Arg213His polymorphism was associated with an increased risk of lung cancer in both females and males in the dominant model (females: OR=1.72, 95%CI=1.29-2.27, P=0.00; males: OR=1.46, 95%CI=1.19-1.78, P=0.00). No significant association between this polymorphism and different smoking status (smokers and non-smokers) and the other ethnicities (Asians and Caucasians) was shown. Conclusions: The results of this meta-analysis indicate that the SULT1A1 Arg213His polymorphism is not associated with lung cancer risk in Asians and Caucasians, but possible elevation for genotype (GA/AA) in mixed populations and males and females needs further investigation.     

Folate intake, methylenetetrahydrofolate reductase polymorphisms, and risk of esophageal cancer

Aim: Genetic and environmental factors may play roles in the pathogenesis of esophageal cancer and susceptibility may be modified by functional polymorphisms in folate metabolic genes, such as methylenetetrahydrofolate reductase (MTHFR). We here evaluated associations of the MTHFR C677T polymorphism and folate intake with esophageal cancer. Methods: A matched hospital-based case-control study with 155 esophageal cancer and 310 non-cancer controls was conducted in a Chinese population with gene-environment interactions evaluated between the MTHFR C667T polymorphism and drinking and smoking, as well as folate intake. Results: Individuals carrying MTHFR 667CT [adjusted odds ratio (OR), 1.95; 95% confidence interval (CI), 1.23-2.62] and TT [adjusted odds ratio (OR), 3.36; 95% confidence interval (CI), 1.46-8.74] had significantly increased esophageal cancer risk compared with those with MTHFR 667CC genotype. Folate intake was seen to have non-significant preventive effect. In former, moderate and heavy drinkers, a high esophageal cancer risk was observed for those with an MTHFR 677T allele genotype [ORs: 5.0(1.29-18.88), 3.70(1.83-7.66) and 5.77(2.11-15.72), respectively]. Significant interaction was found for moderate-heavy drinking and the MTHFR 677T allele genotype for esophageal cancer risk (p<0.05). Significant increased risk was also found in moderate and heavy smokers with the two genotypes [ORs: 3.58(1.64-7.80) and 4.51(1.15-17.78), respectively]. High folate intake and MTHFR 677TT was associated with a non-significant tendency for decreased esophageal cancer risk. Conclusion: Our finding supports the hypothesis that MTHFR C667T polymorphisms play a role in pathogenesis of esophageal cancer in the Chinese population.     

控烟是预防肺癌的主要措施——记太原市肺癌病例对照流行病学调查

背景与目的：山西省太原市空气污染常较为严重。了解各种类型肺癌的危险因素,以采取有效的预防措施。方法：2005年3月—2007年9月,山西省太原市396例肺癌新发病例和465名健康对照者纳入本研究。利用太原市肿瘤医院病理学检查确诊的肺癌病例,配以人群为基础、随机选择的对照,进行病例对照询问调查和环境监测。分析时注意排除病例对照危险因素以外的危险因素并加以平衡,同时进行趋势检验;采用多因素非条件logistic回归分析法,分析各种危险因素,包括比值比（odds ratio,OR）及95%可信区间（95% confidence interval,95% CI）。结果：吸烟与肺癌密切相关。吸烟者发生肺癌危险度比不吸烟者显著升高（OR=3.75,95% CI：2.39~5.89）,特别是肺鳞癌和小细胞肺癌（OR=5.01和5.06）。肺癌与吸烟量、吸烟年数、吸烟深度均有显著的剂量效应关系。被动吸烟或长期在厨房使用固体燃料烹饪、取暖等亦对肺癌的发生、发展起着重要作用。PM2.5的研究刚刚开始,尚未发现室内颗粒物的污染与肺癌的发生明显相关。结论：太原市居民吸烟仍是肺癌的主要危险因素。被动吸烟、固体燃料烹饪也不容忽视。     

GSTM1、GSTT1基因多态性和吸烟与膀胱癌关系的病例对照研究

目的:应用全人群为基础的病例对照研究探讨GSTM1、GSTT1基因多态性和吸烟与膀胱癌危险性的关系。方法:采用多重PCR方法对404例正常对照和414例膀胱癌病例的基因组DNA进行GSTM1和GSTT1基因分型,应用非条件logistic回归分析方法进行统计分析。结果:与携带GSTM1( )基因型者比,GSTM1(-)基因型的男、女性患膀胱癌危险性分别为1.66(95%CI:1.18～2.33)和1.08(95%CI:0.59～1.98)。同样携带GSTM1(-)基因型,吸烟者比不吸烟者患膀胱癌的危险性更加明显。与不吸烟且携带GSTM1( )基因型男性比,GSTM1(-)基因型的目前吸烟者的OR值为2.99(95%CI:1.56～5.74),而携带GSTM1(-)基因型同时吸烟年限≥40年者OR为4.33(95%CI:2.14～8.73)。尽管女性吸烟例数较少,但携带GSTM1(-)基因型的吸烟女性患膀胱癌危险性显著高于不吸烟的GSTM1( )基因型者,OR值为6.72(95%CI:1.69～26.80)。与不吸烟且携带GSTT1( )基因型男性相比,携带GSTT1(-)基因型的吸烟者患男性膀胱癌危险的OR值为1.38(95%CI:0.79～2.42)。携带GSTT1(-)基因型的吸烟女性患膀胱癌危险性是不吸烟的GSTT1( )基因型者的3.04倍(95%CI:0.77～12.01)。结论:GSTM1(-)基因型能显著增加男性患膀胱癌的风险,该基因型与吸烟可能有一定的联合作用。GSTT1基因型可能与上海市区男、女性膀胱癌无关。     

Risk factors for oral and pharyngeal cancer in never smokers

Information on the etiology of oral and pharyngeal cancer in never smokers should help us to understand and quantify risk factors for the disease in the absence of the residual confounding and interaction by smoking. Out of a total of 528 cases with histologically confirmed incident cancers of the oral cavity and pharynx, 42 (10 men and 32 women) who described themselves as lifelong non-smokers were considered. Controls were 864 lifelong non-smokers (442 men and 422 women) admitted to hospital for acute, non-neoplastic, non-alcohol-related conditions. The major risk factor for cancer of the oral cavity and pharynx in never smokers was alcohol consumption (mainly wine) with an odds ratio (OR) about three-fold higher in drinkers than non-drinkers. A direct relation was also found for the duration of the habit, with an OR of 3.6 (95% confidence intervals, CI, 1.2-11.2) for drinking for 35 years or longer. Among the few selected indicator foods considered, a direct association was found with butter (OR 2.7, 95% CI 1.4-5.1 for high intake compared to low), and a non-significant inverse association with carrots (OR 0.6, 95% CI 0.3-1.3) and fresh fruit (OR 0.7, 95% CI 0.3-1.6) for the highest tertile of intake compared to the lowest. Thus, even in the absence of smoking, reducing alcohol and saturated fat intake and increasing fruit and carrot consumption may have favorable effects on oral and pharyngeal cancer risk.     

Prognostic value of smoking status in operated non-small cell lung cancer

Despite the indisputable link between smoking and the increased risk for lung cancer, the inclusion of this factor in prognostic survival analysis has been scarce. Important clinical questions regarding the smoking status are the basis of this study and are as follow: what is the prognostic benefit of having been a non-smoker or having stopped smoking prior to developing lung cancer and what is the prognostic benefit of smoking cessation at the time of diagnosis of lung cancer? Cigarette smoking status of 311 patients operated for non-small cell lung cancer (NSCLC) by a single surgeon was determined based on two independent questionnaires taken prospectively prior to lung operation. Of all patients analysed, 169 (54.3%) were current smokers, 25 (8.0%) were non-smokers, 82 (26.4%) were former smokers and 35 (11.3%) were recent quitters. A Cox multiple regression model was used to test the prognostic value of smoking status on survival together with other relevant clinicopathological factors. For overall survival, older age (P = 0.011), presence of lymph node metastases (P < 0.001) and current smoking (P = 0.001) were independent predictors of poor prognosis, while non-smokers (relative risk = 0.447, 95% confidence interval = 0.206-0.970, P = 0.042), former smokers (relative risk = 0.543, 95% confidence interval = 0.350-0.843, P = 0.006) and recent quitters (relative risk = 0.340, 95% confidence interval = 0.164-0.705, P = 0.004) had a significant better prognosis compared to current smokers (referent group). Similar results were obtained for disease-free survival. These results indicate that smoking cessation is beneficial for lung cancer patients at any time point prior to lung operation and current smoking at the time of operation is associated with poor prognosis.     

The UDP-glucuronosyltransferase 2B17 gene deletion polymorphism: sex-specific association with urinary 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol glucuronidation phenotype and risk for lung cancer.

4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone is a potent and abundant procarcinogen found in tobacco smoke, and glucuronidation of its major metabolite, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), by UDP-glucuronosyltransferases (UGT) including UGT2B17 is an important mechanism for 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone detoxification. Both copies of the UGT2B17 gene are deleted in approximately 10% of Whites and the deletion is associated with a reduction in NNAL glucuronidation activity in vitro. In this study, we examined the effects of the UGT2B17 deletion (0/0) on NNAL glucuronidation rates in a sample of 82 healthy cigarette smokers and further examined its effects on lung cancer risk in a separate case-control study. In the healthy smokers study, a lower urinary ratio of NNAL-glucuronide to NNAL was observed in women with the UGT2B17 deletion (0/0) as compared with women with either the wild-type or heterozygous genotypes (P = 0.058). There were no significant differences in this ratio by genotype in men (P = 0.597). In the case-control study of 398 lung cancer patients and 697 community controls, the UGT2B17 deletion (0/0) was associated with a significant increase in risk of lung cancer in women (odds ratio, 2.0; 95% confidence interval, 1.01-4.0). The risk for the subset of women with lung adenocarcinoma was 2.8 (95% confidence interval, 1.2-6.3). The deletion was not associated with other lung histologic types in women and was not associated with the risk for any lung histologic types in men. The association of the UGT2B17 deletion with increased lung adenocarcinoma in women is consistent with its association with decreased NNAL glucuronidation rates in women and with studies showing that NNAL is a selective inducer of lung adenocarcinoma in experimental animals.