A prospective study on active and environmental tobacco smoking and bladder cancer risk (The Netherlands)

Objective: In a prospective cohort study among 120,852 adult subjects the authors investigated the associations between cigarette, cigar, pipe, environmental tobacco smoking (ETS), and bladder cancer. Methods: In 1986 all subjects completed a questionnaire on cancer risk factors. Follow-up for incident bladder cancer was established by linkage to cancer registries until 1992. The case–cohort analysis was based on 619 cases and 3346 subcohort members. Results: Compared with lifelong non-smokers the age- and sex-adjusted incidence rate ratios (RR) for ex- and current cigarette smokers were 2.1 (95% CI 1.5–3.0) and 3.3 (95% CI 2.4–4.6), respectively. The RR for smoking duration was 1.03 (95% CI: 1.02–1.04) per 1-year increment. The RR per 10 cigarettes/day was 1.3 (95% CI 1.2–1.4). Tar and nicotine exposure increased bladder cancer risk only weakly. It appeared that associations of cigarette smoking characteristics with bladder cancer risk were largely attributable to cigarette smoking duration only. Smoking cessation, age at first exposure, filter-tip usage, cigar and pipe smoking, and ETS were no longer associated with bladder cancer risk after adjustment for frequency and duration of smoking. Conclusions: The authors conclude that current cigarette smokers have a three-fold higher bladder cancer risk than non-smokers. Ex-smokers experience a two-fold increased risk. About half of male bladder cancer and one-fifth of female bladder cancer was attributable to cigarette smoking. Other smoking types (cigar, pipe, or ETS) were not associated with increased risks.     

Hormonal risk factors for endometrial cancer: modification by cigarette smoking (United States)

Objectives: To evaluate whether smoking modifies the risk of endometrial cancer associated with body mass index (BMI), postmenopausal hormone use, and other hormonal factors. Methods: Using multivariate adjusted models we examined interview data from a population-based case–control study of Wisconsin women (n = 740 cases, n = 2372 controls). Results: The relative risk for endometrial cancer associated with current smoking was 0.8 (95% CI: 0.6–1.0) compared to never smokers. No clear dose–response relationship was evident for pack-years smoked. When examined according to smoking status the risk associated with the highest quartile of BMI seemed to be greater among non-smokers (OR = 3.6, 95% CI: 2.4–5.3) than among current smokers (OR = 2.8, 95% CI: 1.4–5.6). Among postmenopausal women the risk associated with current use of postmenopausal hormones appeared to be greater among non-smokers (OR = 3.3, 95% CI: 2.3–4.9) than among current smokers (OR = 2.7, 95% CI: 1.3–5.5). Risk for long-term use (10 or more years) compared with never users was 8.3 (95% CI: 4.6–15.1) among never smokers and 2.5 (95% CI: 0.8–7.9) among current smokers. The risk associated with non-insulin-dependent diabetes was greater among non-smokers (OR = 2.5, 95% CI: 1.7–3.6) than current smokers (OR = 1.1, 95% CI: 0.4–3.1). There was no modifying effect of smoking on the risk associated with parity. Conclusion: These results suggest that smoking moderates the risk associated with endometrial cancer among women at greatest risk, specifically women who are obese or who use postmenopausal hormones.     

Rapid N-acetyltransferase 2 imputed phenotype and smoking may increase risk of colorectal cancer in women (Netherlands)

Objective: The relationship between smoking and colorectal cancer risk and whether such effect is modified by variations in the NAT2 genotype is investigated. Methods: In the prospective DOM (Diagnostisch Onderzoek Mammacarcinoom; 27,722 women) cohort follow-up from 1976 until 1987 revealed 54 deaths due to colon or rectal cancer, and follow-up from 1987 to 01-01-1996 revealed 204 incident colorectal cancer cases. A random sample (n = 857) from the baseline cohort was used as controls. Four NAT2 restriction fragment length polymorphisms (RFLPs) were analysed using DNA extracted from urine samples. Rapid or slow acetylator phenotype status was attributed to individuals. Results: Smoking may increase the risk for colon cancer (RR = 1.36, 95% CI 0.97–1.92) as well as for rectal cancer (RR = 1.31, 95% CI 0.76–2.25), although not statistically significant. Rapid NAT2 acetylation did not increase colorectal cancer risk, but in combination with smoking the risk was statistically significant increased, compared to women who had a slow NAT2 imputed phenotype and never smoked (RR = 1.56, 95% CI 1.03–2.37). For colon cancer, but not for rectal cancer the increased risk was statistically significant (RR = 1.67, 95% CI, 1.05–2.67 versus RR = 1.30 95% CI 0.63–2.68). Conclusions: Our study points to smoking as a risk factor for colon and rectal cancer and, in addition, especially in women with rapid NAT2 imputed phenotype.     

Cancer incidence among marine engineers,a population-based study (Iceland)

Objectives: Marine engineers are in their occupation exposed to different chemicals, organic solvents, exhaust gases, oils, and petroleum products, and were formerly exposed to asbestos. The aim was to study the cancer pattern, with particular attention to lung and bladder cancer, in an Icelandic cohort of marine engineers, indirectly controlling for their smoking habits. Methods: A cohort of 6603 male marine engineers was followed up from 1955 to 1998, a total of 167,715 person-years. The cohort was record linked by the engineers' personal identification numbers to population-based registers containing the vital and emigration status and cancer diagnosis. Standardized incidence ratios (SIRs) were calculated for all cancers and different cancer sites in relation to different lag time and year of graduation. Information on smoking habits was obtained by administering a questionnaire to a sample of the cohort (n = 1501). Results: In the total cohort 810 cancers were observed, whereas 794 were expected (SIR 1.0, 95% CI 1.0–1.1), and significantly increased risk of stomach cancer (SIR 1.3, 95% CI 1.0–1.5) and lung cancer (SIR 1.2, 95% CI 1.0–1.5) was found. Increased risk of all cancers (SIR 1.2, 95% CI 1.1–1.3), stomach cancer (SIR 1.5, 95% CI 1.1–1.9), lung cancer (SIR 1.4, 95% CI 1.2–1.8), pleural mesothelioma (SIR 4.8, 95% CI 1.3–12.3), and urinary bladder cancer (SIR 1.3, 95% CI 1.0–1.8) were observed when a 40-year lag time was applied. The engineers' smoking habits were similar to those in a sample of the general population. The predictive value for lung cancer was 1.03. Conclusions: The increased risk for mesothelioma is possibly attributable to the previous asbestos exposure. The excess of lung cancer could also be related to asbestos exposure. The high incidence of stomach cancer, lung cancer, and bladder cancer may be related to exposure to chemical risk factors, such as oils and petroleum products, as confounding due to smoking seems to be ruled out. In the light of the limited exposure information in the present study the importance of the different occupational exposures needs to be evaluated in further studies.     

A prospective study of lifestyle factors and the risk of pancreatic cancer in Nord-Trøndelag, Norway

Objectives: Cancer of the pancreas is highly fatal and, despite extensive scrutiny, only cigarette smoking stands out as a likely causal agent in epidemiological studies. To explore to what extent different lifestyle factors are associated with the risk of pancreatic cancer, data from a large health screening survey in a county in Norway were analyzed. Methods: Our study included 31,000 men and 32,374 women initially free from any diagnosed cancer, and during 12 years of follow-up, 166 incident cases of pancreatic cancer were diagnosed at the Cancer Registry. Results: Compared with never smokers, we found a two-fold increased risk among current smokers, and a dose–response association with number of cigarettes (p for trend = 0.02 for both men and women) and with number of pack-years (p for trend = 0.02 for men and 0.01 for women). The risk among former smokers quitting more than 5 years before study entry was close to the risk of never smokers. Compared with persons who reported never or infrequently to be physically worn out after a day's work, the relative risk (RR) among those who nearly always became worn out was 2.9 (95% confidence interval (CI) = 1.4–5.8) for men and 3.8 (95% CI = 1.6–9.2) for women. Divorced or separated men had a risk of 3.1 (95% CI = 1.3–7.2) compared with married men. We observed a higher risk among women in occupations of high socioeconomic status (RR = 2.5; 95% CI = 1.2–5.2), and among men occupied in farming, agriculture or forestry (RR = 2.1; 95% CI = 1.1–4.0), compared with persons in occupations of low socioeconomic status. Conclusions: Our results confirm the findings of previous studies that indicate a causal role of cigarette smoking in pancreatic cancer. Moreover, we found that the risk of former smokers may approach the risk of never smokers within a few years subsequent to quitting.     

Association of NAT2 and smoking in relation to breast cancer incidence in a population-based case-control study (United States)

Objective: To evaluate the potential interaction between N-acetyltransferase 2 (NAT2) and smoking in breast cancer incidence. Methods: The data are derived from a population-based case–control study of women aged 20–69 years who were residents of Massachusetts or Wisconsin during 1997–1998. Incident cases of invasive breast cancer were identified through state tumor registries and age-similar controls were selected at random from population lists. Telephone interviews were conducted to obtain information on known and suspected risk factors including smoking history. Women provided oral mucosal DNA through the mail for genetic studies. Results: A total of 791 cases and 797 controls were included in the analysis. Overall, smoking was modestly associated with breast cancer risk (multivariate odds ratio (OR) for ever smoking: 1.37; 95% confidence interval (CI): 1.12–1.69), and there was a trend in risk for greater pack-years of smoking among postmenopausal women (p for trend = 0.02). Overall, NAT2 was not related to invasive breast cancer (multivariate OR: 1.11; 95% CI: 0.90–1.36). Associations of smoking with breast cancer tended to be somewhat stronger among the women with the slow acetylator genotype for NAT2: when compared to those who never smoked and were rapid acetylators, the OR for ever smoking was 1.50 (95% CI: 1.11–2.02) in slow acetylators, and OR: 1.24 (95% CI: 0.91–1.70) in rapid acetylators. However, tests for multiplicative interaction were not significant in case–control comparisons, or in case-only analyses. Conclusion: Results of the study are compatible with the majority of previous studies that indicate little or no association of NAT2, smoking, or their interaction with the occurrence of breast cancer.     

Cigarette smoking and risk of epithelial ovarian cancer (Australia)

Objectives: We studied the association between cigarette smoking and ovarian cancer in a population-based case–control study. Methods: A total of 794 women with histologically confirmed epithelial ovarian cancer who were aged 18–79 years and resident in one of three Australian states were interviewed, together with 855 controls aged 18–79 years selected at random from the electoral roll from the same states. Information was obtained about cigarette smoking and other factors including age, parity, oral contraceptive use, and reproductive factors. We estimated the relative risk of ovarian cancer associated with cigarette smoking, accounting for histologic type, using multivariable logistic regression to adjust for confounding factors. Results: Women who had ever smoked cigarettes were more likely to develop ovarian cancer than women who had never smoked (adjusted odds ratio (OR) = 1.5; 95% confidence interval (CI) = 1.2–1.9). Risk was greater for ovarian cancers of borderline malignancy (OR = 2.4; 95% CI = 1.4–4.1) than for invasive tumors (OR = 1.7; 95% CI = 1.2–2.4) and the histologic subtype most strongly associated overall was the mucinous subtype among both current smokers (OR = 3.2; 95% CI = 1.8–5.7) and past smokers (OR = 2.3; 95% CI = 1.3–3.9). Conclusions: These data extend recent findings and suggest that cigarette smoking is a risk factor for ovarian cancer, especially mucinous and borderline mucinous types. From a public health viewpoint, this is one of the few reports of a potentially avoidable risk factor for ovarian cancer.     

Second primary tumors in patients with upper aerodigestive tract cancers: joint effects of smoking and alcohol (United States)

Objective: This study evaluated the joint effects of tobacco smoking and alcohol consumption on the risk of second primary tumors (SPT) in patients with early-stage head and neck squamous cell carcinoma (HNSCC). Methods: Data are presented for 1181 patients enrolled in a placebo-controlled chemoprevention trial of 13-cis-retinoic acid. Nearly 17% of patients presented with a SPT. The log rank test and Cox proportional hazards model were used to examine risk factors for SPT development. Results: After adjusting for the time from the index diagnosis to randomization, age at diagnosis, stage, and site of the primary cancer, the factors that emerged as simultaneous predictors of SPT development were continued smoking and alcohol intake after the index diagnosis. Increased SPT risk was associated with older age (RR = 2.1; 95% CI 1.5–2.8); stage II diagnosis (RR = 1.5; 95% CI 1.1–2.1); index diagnosis of pharyngeal cancer (RR = 1.6; 95% CI 1.1–2.5); current smoking at registration (RR = 2.1; 95% CI 1.3–3.6) and continued alcohol consumption post-diagnosis (RR = 1.3; 95% CI 1.0–1.7). Conclusion: Important associations exist between SPT development and continued smoking and alcohol consumption after treatment for HNSCC.     

Body size and ovarian cancer: case–control study and systematic review (Australia)

Objective: Although increased body mass is an established risk factor for a variety of cancers, its relation with cancer of the ovary is unclear. We therefore investigated the association between measures of body mass index (BMI) and ovarian cancer risk. Methods: Data from an Australian case–control study of 775 ovarian cancer cases and 846 controls were used to examine the association with BMI. We have also summarized the results from a number of other studies that have examined this association. Results: There was a significant increased risk of ovarian cancer with increasing BMI, with women in the top 15% of the BMI range having an odds ratio (OR) of 1.9 (95% confidence interval (CI), 1.3–2.6) compared with those in the middle 30%. Stratifying by physical activity showed a stronger effect among inactive women (OR = 3.0, 95% CI 1.3–6.9). The overall effect was consistent with the findings of most prior population-based case–control studies, while cohort studies reported positive effects closer to the null. Hospital-based studies gave variable results. Conclusions: Taken together, the evidence is in favor of a small to moderate positive relation between high BMI and occurrence of ovarian cancer.     

Cigarette Smoking, Alcohol Consumption, and Endometrial Cancer Risk: A Population-based Study in Sweden

Objective: To assess effects of cigarette smoking and alcohol consumption on the risk of endometrial cancer among postmenopausal women. Methods: We performed a nationwide population-based case–control study among postmenopausal women aged 50–74 years in Sweden, including 709 incident endometrial cancer cases and 3368 controls. Results: Compared to never smokers, recent/current smokers had a decreased risk of endometrial cancer (multivariate OR 0.61, 95% CI 0.47–0.80), but former smokers presented no substantial difference in risk (multivariate OR 0.90, 95% CI 0.72–1.14). We observed a decreased risk of endometrial cancer for postmenopausal smoking, but there was no clear impact on risk for premenopausal smoking. The inverse association of smoking with risk was not explained by differences in body mass index between smokers and nonsmokers. Alcohol consumption was not clearly associated with risk of endometrial cancer. The multivariate OR for women consuming up to 1.6 g of alcohol per day was 1.12 (95% CI 0.88–1.44), and 0.92 (95% CI 0.70–1.20) for women consuming more than 4 g per day (p for trend over categories=0.44). Conclusions: Current cigarette smoking reduces the risk of postmenopausal endometrial cancer, but the inverse association dissipates after smoking cessation. Premenopausal smoking might not affect risk of postmenopausal endometrial cancer. Alcohol consumption is not materially associated with risk.     

A pooled analysis of case–control studies of thyroid cancer: cigarette smoking and consumption of alcohol, coffee, and tea

Objective: To analyze the role of smoking, alcohol, coffee and tea in relation to thyroid cancer, we conducted a pooled analysis of 14 case–control studies conducted in the United States, Europe, and Asia. Methods: The sample consisted of 2725 thyroid cancer cases (2247 females, 478 males) and 4776 controls (3699 females, 1077 males). Conditional logistic regression with stratification on study, age at diagnosis, and gender was used to compute odds ratios and 95% confidence intervals. Results: Thyroid cancer risk was reduced in persons who had ever smoked. The relationship was more pronounced in current smokers (OR = 0.6, 95% CI = 0.6–0.7) than former smokers (OR = 0.9, 95% CI = 0.8–1.1). There were significant trends of reduced risk with greater duration and frequency of smoking. For consumption of wine and beer, there was a significant trend of decreasing thyroid cancer risk (p = 0.02) that was not maintained after adjustment for current smoking (p = 0.12). Thyroid cancer risk was not associated with consumption of coffee or tea. These findings were consistent in both gender-specific and histology-specific (papillary and follicular) analyses. Conclusions: Pooled analyses of these geographically diverse case–control data indicate a reduced thyroid cancer risk associated with current smoking. A reduced risk associated with alcohol was eliminated after adjustment for smoking, and caffeinated beverages did not alter thyroid cancer risk.     

The contribution of cigarette smoking to bladder cancer in women (pooled European data)

Background: Using a combined analysis of 11 case–control studies from Europe, we have investigated the relationship between cigarette smoking and bladder cancer in women. Methods: Available smoking information on 685 female bladder cancer cases and 2416 female controls included duration of smoking habit, number of cigarettes smoked per day, and time since cessation of smoking habit for ex-smokers. Results: There was an increasing risk of bladder cancer with increasing duration of smoking, ranging from approximately a two-fold increased risk for a duration of less than 10 years (odds ratio (OR) = 1.9, 95% confidence interval (CI) 1.1–3.1) to over a four-fold increased risk for a duration of greater than 40 years (OR = 4.1, 95% CI 3.0–5.5). A dose–response relationship was observed between number of cigarettes smoked per day and bladder cancer up to a threshold limit of 15–20 cigarettes per day, OR = 3.8 (95% CI 2.7–5.4), after which no increased risk was observed. An immediate decrease in risk of bladder cancer was observed for those who gave up smoking. This decrease was over 30% in the immediate 1–4 years after cessation, OR = 0.68 (95% CI 0.38–1.2). However, even after 25 years the decrease in risk did not reach the level of the never-smokers, OR = 0.27 (95% CI 0.21–0.35). Conclusion: The proportion of bladder cancer cases among women attributable to ever smoking was 0.30, (0.25–0.35) and to current smoking was 0.18 (0.14–0.22). These attributable proportions are less than those observed among men, although they are likely to increase in the future as the smoking-related disease epidemic among women matures.     

Association of sedentary behaviour with colon and rectal cancer: a meta-analysis of observational studies

Background:

Sedentary behaviour is ubiquitous in modern society. Emerging studies have focused on the health consequences of sedentary behaviour, including colorectal cancer, but whether sedentary behaviour is associated with the risks of colon and rectal cancer remains unclear. No systematic reviews have applied quantitative techniques to independently compute summary risk estimates. We aimed to conduct a meta-analysis to investigate this issue.

Methods:

We searched PubMed, Embase, and Google Scholar databases up to May 2013 to identify cohort and case–control studies that evaluated the association between sedentary behaviour and colon or rectal cancer. A random-effect model was used to pool the results of included studies. Publication bias was assessed by using Begg''s funnel plot.

Results:

Twenty-three studies with 63 reports were included in our meta-analysis. These groups included 4 324 462 participants (27 231 colon cancer cases and 13 813 rectal cancer cases). Sedentary behaviour was significantly associated with colon cancer (relative risk (RR): 1.30, 95% confidence interval (CI): 1.22–1.39) but did not have a statistically significant association with rectal cancer (RR 1.05, 95% CI, 0.98–1.13). Subgroup analyses suggested that the odds ratio (OR) of colon cancer was 1.46 (95% CI: 1.22–1.68) in the case–control studies, and the RR was 1.27 (95% CI: 1.18–1.36) in the cohort studies, the OR of rectal cancer was 1.06 (95% CI: 0.85–1.33) in the case–control studies, and the RR was 1.06 (95% CI, 1.01–1.12) in the cohort studies.

Conclusion:

Sedentary behaviour is associated with an increased risk of colon cancer. Subgroup analyses suggest a positive association between sedentary behaviour and risk of rectal cancer in cohort studies. Reducing sedentary behaviour is potentially important for the prevention of colorectal cancer.     

Employment as butcher and cancer risk in a record-linkage study from Sweden

Objective: To investigate the risk of cancer among butchers and other meat workers in a large record-linkage study from Sweden. Methods: The Swedish Cancer Environment Register III contains nationwide data on cancer incidence during 1971–1989 for all residents, by occupation and industry of employment as reported at the 1960 and 1970 censuses. We identified 25,049 men classified as butchers or meat workers at either census. We used as a comparison group the remaining part of the active male population, after exclusion of workers with direct contact with animals. Results: Butchers in the meat industry had a slight increase in the risk of cancer (relative risk [RR] 1.1, 95% confidence interval [CI] 1.0–1.3), which was due to an increased risk of cancers of the oral cavity and pharynx (RR 1.6, 95% CI 1.0–2.7), stomach (RR 1.6, 95% CI 1.1–2.7), larynx (RR 1.4, 95% CI 0.6–3.4), and lung (RR 1.4, 95% CI 1.1–1.9). The risk of stomach cancer was highest during the first 5 years of the study, and among butchers from urban areas. No temporal or geographic variations were seen for lung cancer risk, with elevations restricted to squamous cell carcinoma. An increased risk of stomach, laryngeal and lung cancers was present in butchers and meat workers outside the meat industry. There was no clear indication of an increased risk of other neoplasms. Conclusions: The increased risk of oral, laryngeal, lung and stomach cancers among Swedish butchers may be at least partly due to confounding by tobacco smoking, alcohol drinking, and other lifestyle factors. However, exposures in the meat industry (e.g., viruses, nitrosamines, polycyclic aromatic hydrocarbons) may contribute the elevated cancer risks.     

Smoking and non-Hodgkin's lymphoma: a case-control study in the Rhône-Alpes region of France

Objective: To study the relation between smoking and non-Hodgkin/s lymphoma (NHL), in the Rhône-Alpes region of France. Methods: We conducted a hospital-based case–control study that included 180 cases of NHL and 360 age-, gender-matched hospital controls. Matched univariable and multivariable logistic regression models were used for analysis. Results: For the whole study population as well as for men, smoking does not elevate the risk of NHL. However, the risk of NHL is higher for women who currently smoke compared to women who have never smoked (odds ratio [OR] = 2.40, 95% confidence interval [95% CI] = 1.19–4.84). Among ever smokers, the OR of NHL is 5.04 (95% CI = 1.40–18.12) for women who have smoked for more than 30 years compared with those who have never smoked. Similarly, women who started to smoke before the age of 20 years compared with women who have never smoked are at greater risk of developing NHL (OR = 2.40, 95% CI = 0.99–5.85). In the total population (women and men), smoking may be associated with one histologic subtype, follicular NHL with an adjusted OR for the current smokers compared to subjects having never smoked of 3.20, 95% CI = 0.79–12.97. Conclusions: In spite of the small number of subjects in the subgroups, a relation is observed between smoking and NHL among women, but not men, and in the total population a relation is suggested between smoking and follicular NHL.     

Are Coffee, Tea, and Total Fluid Consumption associated with Bladder Cancer Risk? Results from the Netherlands Cohort Study

Objectives: Coffee, tea, and fluid consumption have been thought to influence bladder cancer incidence. In a large prospective study, these associations were investigated. Methods: In 1986, cohort members (55–69 years) completed a questionnaire on cancer risk factors. Follow-up was established by linkage to cancer registries until 1992. The multivariable case–cohort analysis was based on 569 bladder cancer cases and 3123 subcohort members. Results: The incidence rate ratios (RR) for men consuming <2 cups of coffee/day was 0.89 (95% CI 0.51–1.5) using the median consumption category (4–<5 cups/day) as reference. This RR increased to 1.3 (95% CI 0.94–1.9) for men consuming 7 cups/day, although no clear dose–response association was found. The RRs decreased from 1.2 (95% CI 0.56–2.7) for women consuming <2 cups of coffee/day to 0.36 (95% CI 0.18–0.72) for women consuming 5 cups/day compared to the median consumption category (3–<4 cups/day). Men and women who abstained from drinking tea had a RR of 1.3 (95% CI 0.97–1.8) compared to those consuming 2–<3 cups of tea per day (median consumption category). The RR for men and women comparing highest to lowest quintile of total fluid consumption was 0.87 (95% CI 0.63–1.2). Conclusion: The data suggest a possible positive association between coffee consumption and bladder cancer risk in men and a probable inverse association in women. Tea consumption was inversely associated with bladder cancer. Total fluid consumption did not appear to be associated with bladder cancer.     

Cumulative genetic defects in carcinogen metabolism may increase breast cancer risk (The Netherlands)

Variants in the metabolic genes NAT1, NAT2, GSTM1 or GSTT1, may cause differences in individual detoxifying capacity of possible carcinogens. We examined the cumulative effect of putative at risk genotypes on breast cancer risk and we examined the extent to which these polymorphisms modify the association between smoking and breast cancer. A case cohort study was conducted in the DOM cohort with 676 breast cancer cases and a random sample of 669 individuals. No effect of the NAT1, NAT2 or GSTM1 genotypes on breast cancer risk was observed. However, women with GSTT1 null genotype had a 30% increased breast cancer risk compared to women with GSTT1 present (RR = 1.30 (95% confidence interval (CI) 1.04–1.64)). Smoking did not influence breast cancer risk nor did genetic variations in NAT1, NAT2 or GSTM1 in combination with smoking. Compared to women who never smoked with GSTT1 present, women with GSTT1 null genotype and who formerly smoked showed an increased breast cancer risk (RR = 2.55 (95% CI 1.10–5.90)), but current smokers who smoked 20 cigarettes or more per day did not (RR = 1.06 (95% CI 0.51–2.18)). Increasing numbers of putative at risk genotypes increased breast cancer risk in a dose dependent manner (p for trend 0.01). The risk was more than doubled in women with all four risk genotypes, RR = 2.45 (95% CI 1.24–4.86), compared to women with zero putative at risk genotypes. In conclusion, the results of this study suggest that presence of three or more putative at risk genotypes increases breast cancer risk.     

Tubal sterilization and risk of breast cancer mortality in US women

Objective: To investigate the hypothesis that tubal sterilization is associated with a reduced risk of breast cancer. Methods: We examined this hypothesis in a large prospective study of US adults. After 14 years of mortality follow-up, 3837 deaths from breast cancer were observed in a cohort of 619,199 women who were cancer-free at study entry in 1982. Results: Cox proportional hazards models (adjusted for multiple breast cancer risk factors) showed a significant inverse association between tubal sterilization and breast cancer mortality (adjusted rate ratio (RR) = 0.82, 95% confidence interval (CI) 0.70–0.96). Women who were sterilized before age 35 had a lower risk (adjusted RR = 0.69, 95% CI 0.53–0.88) than women who were sterilized at 35 years of age or older (adjusted RR = 0.92, 95% CI 0.75–1.13). Also, sterilizations performed before 1975 resulted in a lower risk (RR = 0.75, 95% CI 0.62–0.91) than those performed during or after 1975 (RR = 0.98, 95% CI 0.74–1.29), possibly reflecting the likelihood of greater tissue damage with earlier procedures. Conclusions: These results suggest that tubal sterilization may lower subsequent risk of breast cancer, especially among women who are sterilized at a relatively young age. Additional studies are needed to confirm or refute these findings.     

The fraction of lung cancer attributable to smoking in the Norwegian Women and Cancer (NOWAC) Study

Background We examined the association between active and passive smoking and lung cancer risk and the population attributable fraction (PAF) of lung cancer due to active smoking, in the Norwegian Women and Cancer Study, a nationally representative prospective cohort study.Methods We followed 142,508 women, aged 31–70 years, who completed a baseline questionnaire between 1991 and 2007, through linkages to national registries through December 2015. We used Cox proportional hazards models, to estimate hazard ratios (HRs) with 95% confidence intervals (CIs). We calculated PAF to indicate what proportion of lung cancer cases could have been prevented in the absence of smoking.Results During the more than 2.3 million person-years of observation, we ascertained 1507 lung cancer cases. Compared with never smokers, current (HR 13.88, 95% CI 10.18–18.91) smokers had significantly increased risk of lung cancer. Female never smokers exposed to passive smoking had a 1.3-fold (HR 1.34, 95% CI 0.89–2.01) non- significantly increased risk of lung cancer, compared with never smokers. The PAF of lung cancer was 85.3% (95% CI 80.0–89.2).Conclusion More than 8 in 10 lung cancer cases could have been avoided in Norway, if the women did not smoke.Subject terms: Epidemiology, Oncology     

Effects of beta-carotene supplementation on cancer incidence by baseline characteristics in the Physicians' Health Study (United States)

Objectives: The Physicians' Health Study (PHS) was a randomized trial of beta-carotene (50 mg, alternate days) and aspirin in primary prevention of cancer and cardiovascular disease among 22,071 US male physicians. This report updates results for beta-carotene and examines effect modification by baseline characteristics. Methods: Beta-carotene's effect on cancer over nearly 13 years was examined overall and within subgroups defined by baseline characteristics using proportional-hazards models. Results: 2667 incident cancers were confirmed, with 1117 prostate, 267 colon, and 178 lung cancers. There were no significant differences with supplementation in total (relative risk (RR) = 1.0, 95% confidence interval (CI) = 0.9–1.0); prostate (RR = 1.0, 95% CI = 0.9–1.1); colon (RR = 0.9, 95% CI = 0.7–1.2); or lung (RR = 0.9, 95% CI = 0.7–1.2) cancer, and no differences over time. In subgroup analyses, total cancer was modestly reduced with supplementation among those aged 70+ years (RR = 0.8, 95% CI = 0.7–1.0), daily drinkers of alcohol (RR = 0.9, 95% CI = 0.8–1.0), and those in the highest BMI quartile (RR = 0.9, 95% CI = 0.7–1.0). Prostate cancer was reduced with supplementation among those in the highest BMI quartile (RR = 0.8, 95% CI = 0.6–1.0), and colon cancer was reduced among daily drinkers of alcohol (RR = 0.5, 95% CI = 0.3–0.8). Conclusions: The PHS found no overall effect of beta-carotene on total cancer, or the three most common site-specific cancers. The possibility of risk reduction within specific subgroups remains.