Cigarette smoking and colorectal cancer mortality in the cancer prevention study II

BACKGROUND: Recent studies suggest that long-term cigarette smoking is associated with an increased risk of colorectal cancer. Whether the association is causal or due to confounding remains unclear. METHODS: We examined cigarette smoking in relation to colorectal cancer mortality, evaluating smoking duration and recency and controlling for potential confounders in the Cancer Prevention Study II. This prospective nationwide mortality study of 1 184 657 adults (age > or =30 years) was begun by the American Cancer Society in 1982. After exclusions, our analytic cohort included 312 332 men and 469 019 women, among whom 4432 colon or rectal cancer deaths occurred between 1982 and 1996 among individuals who were cancer free in 1982. Rate ratios (RRs) and 95% confidence intervals (CIs) were estimated by fitting Cox proportional hazards models. All statistical tests were two-sided. RESULTS: Multivariate-adjusted colorectal cancer mortality rates were highest among current smokers, were intermediate among former smokers, and were lowest in lifelong nonsmokers. The multivariate-adjusted RR (95% CI) for current compared with never smokers was 1.32 (1.16-1.49) among men and 1.41 (1.26-1.58) among women. Increased risk was evident after 20 or more years of smoking for men and women combined as compared with never smokers. Risk among current and former smokers increased with duration of smoking and average number of cigarettes smoked per day; risk in former smokers decreased significantly with years since quitting. If the multivariate-adjusted RR estimates in this study do, in fact, reflect causality, then approximately 12% of colorectal cancer deaths among both men and women in the general U.S. population in 1997 were attributable to smoking. CONCLUSIONS: Long-term cigarette smoking is associated with increased risk of colorectal cancer mortality in both men and women. Clear reduction in risk is observed with early smoking cessation.     

Smoking-attributable cancer mortality in 1991: is lung cancer now the leading cause of death among smokers in the United States?

Findings from the new American Cancer Society prospective study of 1.2 million men and women indicate that mortality risks among smokers have increased substantially for most of the eight major cancer sites causally associated with cigarette smoking. Lung cancer risk for male smokers doubled, while the risk for females increased more than fourfold. On the basis of the new American Cancer Society relative risks, we project that cigarette smoking alone will contribute to slightly more than 157,000 of the 514,000 total cancer deaths expected to occur in the United States in 1991. Overall, smoking directly contributes to 21.5% of all cancer deaths in women but 45% of all cancer deaths in men. It would also appear that lung cancer has now displaced coronary heart disease as the single leading cause of excess mortality among smokers in the United States.     

Ecologic study of lung cancer risk factors in the U.S. and Japan, with special reference to smoking and diet.

Lung cancer mortality rates among United States and Japanese males were compared and related to smoking and dietary data. Mortality rates increased from 1950 to 1985 in both countries, but the absolute values are consistently lower in Japan (38.2 deaths/100,000 in 1985) than in the U.S. (72.2/100,000). The proportion of smokers is higher in Japan than in the U.S. since 1955. Japanese males start smoking considerably later than U.S. males, but smoke a higher quantity of cigarettes per day. Available information on inhalation practices and yield and type of cigarettes smoked showed no differences among the two countries large enough to account for the differences in mortality rates. Further data in this regard should be obtained. Dietary data show that fat consumption (as percentage of calories) is consistently higher in the U.S. than in Japan from 1950 (40% vs. 7.9%) through 1985 (43.5% vs. 24.5%). A linear relationship is observed between lung cancer mortality and fat intake. Our data support the hypothesis that dietary habits may modulate the carcinogenic effects of tobacco smoking.     

Ecologic Study of Lung Cancer Risk Factors in the U.S. and Japan, with Special Reference to Smoking and Diet

Lung cancer mortality rates among United States and Japanese males were compared and related to smoking and dietary data. Mortality rates increased from 1950 to 1985 in both countries, but the absolute values are consistently lower in Japan (38.2 deaths/100,000 in 1985) than in the U.S. (72.2/100,000). The proportion of smokers is higher in Japan than in the U.S. since 1955. Japanese males start smoking considerably later than U.S. males, but smoke a higher quantity of cigarettes per day. Available information on inhalation practices and yield and type of cigarettes smoked showed no differences among the two countries large enough to account for the differences in mortality rates. Further data in this regard should he obtained. Dietary data show that fat consumption (as percentage of calories) is consistently higher in the U.S. than in Japan from 1950 (40% vs. 7.9%) through 1985 (43.5% vs. 24.5%). A linear relationship is observed between lung cancer mortality and fat intake. Our data support the hypothesis that dietary habits may modulate the carcinogenic effects of tobacco smoking.     

The association of clinically determined periodontal disease and edentulism with total cancer mortality: The National Health and Nutrition Examination Survey III

Increasing evidence supports a positive association between periodontal disease and total cancer risk. We evaluated the association of clinically assessed periodontal disease and a consequence, edentulism with total cancer mortality in participants without a prior cancer diagnosis in a U.S. nationally representative population. Included were 6,034 participants aged ≥40 years without a prior cancer diagnosis who participated in the National Health and Nutrition Examination Survey III. Periodontal health was measured by trained dentists. Cancer deaths (n = 702) were ascertained during a median of 21.3 years of follow-up. Cox proportional hazards regression was used to estimate the association of periodontal disease and edentulism with total cancer mortality using no periodontal disease/dentate as the reference and adjusting for potential demographic, lifestyle including smoking and social factor confounders. Fifteen percent had periodontitis and 17% were edentulous. Periodontitis was not statistically significantly associated with risk of total cancer death after multivariable adjustment. Edentulism was associated with an increased risk of cancer mortality (hazard ratio = 1.50, 95% confidence interval = 1.12–2.00) after multivariable adjustment, including in men and women and in each racial/ethnic group studied. The positive association was observed in overweight/obese participants but not participants with normal body mass index, more strongly in prediabetic/diabetic participants than in participants without diabetes and in ever cigarette smokers but not in never cigarette smokers. In this U.S. nationally representative population, those with edentulism, but not periodontal disease, had a higher risk of total cancer death, especially in those with shared risk factors for periodontal disease and cancer.     

Attributable and absolute risk of lung cancer death by smoking status: findings from the Japan Collaborative Cohort Study

Estimating the proportion of lung cancer deaths that can be avoided is important in assessing the potential impact of antismoking efforts on the reduction of lung cancer deaths. We calculated the population attributable risk (PAR) and absolute risk of lung cancer death according to smoking status based on the Japan Collaborative Cohort (JACC) Study. The analytic cohort included 45,010 males and 55,724 females aged 40-79 years. Cox proportional hazards model was used to determine age-adjusted relative risks and PAR according to smoking status. We also computed lung cancer mortality according to age and smoking status. In males, 52.2% and 14.8% of lung cancer deaths were attributable to current and former cigarette smoking, respectively. In females, the corresponding figures were 11.8% and 2.8%. Among current male smokers, the relative risk was strongly correlated with the intensity and duration of cigarette smoking. In contrast, the PAR was associated with an intermediate level of smoking except for the years of smoking: the largest PARs were observed in those with 20-29 cigarettes per day, 40-59 pack-years and 20-22 years old at starting smoking. Absolute risks were estimated to increase with age and duration of smoking and not to decrease even after cessation. These findings suggest that avoidable lung cancer deaths are primarily among light to moderate smokers who are considered amenable to population-based antismoking strategies. For all current smokers, immediate cessation is encouraged because it offers the only realistic way to avoid a substantial increase in lung cancer mortality brought about by further continuation of smoking.     

Differences in smoking prevalence and eligibility for low-dose computed tomography (LDCT) lung cancer screening among older U.S. adults: role of sexual orientation

The purpose of this study was to determine the past-year prevalence estimates of cigarette smoking and eligibility for low-dose computed tomography (LDCT) lung cancer screening among older U.S. adults and examine potential variations in these estimates by sexual orientation. Data were from the 2012–2013 National Epidemiologic Survey on Alcohol and Related Conditions (NESARC-III) and included in-person interviews with a nationally representative sample of non-institutionalized adults aged 18 and older. Eligibility for LDCT was based on U.S. Centers for Medicare and Medicaid Services (CMS) guidelines. Analyses included participants aged 55–77 (n?=?9,635). Overall, 17.5% of older adult respondents reported past-year smoking. Overall rates of past-year cigarette smoking were influenced by sex and sexual orientation with males reporting higher rates compared to females. Among both males and females, smoking was most prevalent among bisexual individuals. Eligibility for LDCT was also higher among males compared to females and among bisexually identified adults relative to homosexual and heterosexual-identified adults. Overall, 11.2% of older U.S. adults met eligibility for LDCT lung cancer screening. Eligibility for LDCT lung screening is associated with sexual orientation; the highest rates of eligibility are among bisexual women and men (26.9 and 24.5%, respectively). The current study found variations in cigarette smoking and eligibility for LDCT lung cancer screening (a proxy for chronic high-risk smoking) among older U.S. adults based on sexual orientation. Efforts to increase screening should take into account these differences.     

Cigarette smoking and survival after ovarian cancer diagnosis.

We have examined the association between cigarette smoking and ovarian cancer survival in 676 women with invasive epithelial ovarian cancer, recruited into a case-control study in the early 1990s. Information about cigarette smoking and other personal and reproductive factors was obtained from a personal interview at the time of diagnosis. Cox proportional hazards models were used to evaluate the association between cigarette smoking and time to ovarian cancer death. Current smokers at diagnosis were more likely to die early than women who had never smoked [adjusted hazard ratio (HR), 1.36; 95% confidence interval (95% CI), 1.01-1.84]. Increased risks of dying were greater among those who had accumulated more pack-years of smoking (HR for 30+ pack-years compared with never smokers, 1.94; 95% CI, 1.41-2.66) and smoked more cigarettes per day (HR, 1.93; 95% CI, 1.37-2.73). All these associations were stronger among women with late-stage disease (HR for current versus never smokers, 1.58; 95% CI, 1.15-2.18). Time since quitting had little effect on survival after adjusting for lifetime smoking exposure. These results validate and extend recent findings and suggest that premorbid cigarette smoking is related to worse outcome in ovarian cancer patients.     

Increased risk of colorectal cancer among smokers: Results of a 26-year follow-up of us veterans and a review

To clarify the relationship between tobacco use and risk of colorectal cancer, we evaluated a cohort of 248,046 American veterans followed prospectively for 26 years. In comparison with veterans who had never used tobacco, the risk of death was significantly increased for colon cancer and rectal cancer among current and former cigarette smokers and among pipe or cigar smokers, controlling for social class and occupational physical activity. Rectal-cancer risk was also significantly elevated among users of chewing tobacco or snuff. For both sites, risk increased significantly with pack-years, earlier age at first use, and number of cigarettes. These results reinforce 2 recent reports of the association of cigarette smoking and colorectal cancer in men and women. Inconsistencies in the findings of earlier epidemiologic studies appear to be due in large part to differences in length of follow-up or in choice of controls. Studies with at least 20 years of follow-up or population-based controls have tended to find elevated risk with tobacco smoking, while those with shorter follow-up or hospital controls have not. This, plus the strength and consistency of the association of smoking and colon polyps, suggest that smoking may primarily affect an early stage in the development of colon cancer. If this association is causal, tobacco use may be responsible for 16% of colon-cancer and 22% of rectal-cancer deaths among these veterans.     

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.     

Tobacco‐specific N‐nitrosamines and polycyclic aromatic hydrocarbons in cigarettes smoked by the participants of the Shanghai Cohort Study

Our recent studies on tobacco smoke carcinogen and toxicant biomarkers and cancer risk among male smokers in the Shanghai Cohort Study showed that exposure to tobacco‐specific nitrosamines (TSNA) and polycyclic aromatic hydrocarbons (PAH) is prospectively associated with the risk of cancer. These findings support the hypothesis that the smokers' cancer risk is a function of the dose of select tobacco carcinogens and highlight the importance of understanding the factors that affect the intake of these carcinogens by smokers. Given that tobacco constituent exposures are driven, at least in part, by the levels of these constituents in cigarette smoke, we measured mainstream smoke TSNA and PAH levels in 43 Chinese cigarette brands that participants of the Shanghai Cohort Study reported to smoke. In all brands analyzed here, mainstream smoke levels of NNN and NNK, the two carcinogenic TSNA, were generally relatively low, averaging (±SD) 16.8(±25.1) and 14.2(±9.5) ng/cigarette, respectively. The levels of PAH were comparable to those found in U.S. cigarettes, averaging 15(±9) ng/cigarette for benzo[a]pyrene, 119(±66) ng/cigarette for phenanthrene and 37(±19) ng/cigarette for pyrene. Our findings indicate that the generally low levels of NNN and NNK are most likely responsible for the relatively low levels of the corresponding biomarkers in the urine of the Shanghai Cohort Study participants as compared to those found in the U.S. smokers, supporting the role of the levels of these constituents in cigarette smoke in smokers' exposures. Our findings also suggest that, in addition to smoking, other sources contribute to Chinese smokers' exposure to PAH.     

Cigarette smoking, alcohol intake, and thyroid cancer risk: a pooled analysis of five prospective studies in the United States

Objective

We examined the associations between cigarette smoking, alcohol intake, and thyroid cancer risk in a pooled analysis of five prospective studies.

Methods

Data from five prospective U.S. studies were standardized and then combined into one aggregate dataset (384,433 men and 361,664 women). Pooled hazard ratios (HR) and 95?% confidence intervals (CI) for thyroid cancer were estimated from mutually adjusted models of cigarette smoking and alcohol intake, which were additionally adjusted for age, sex, education, race, marital status, body mass index, and cohort.

Results

Over follow-up, 1,003 incident thyroid cancer cases (335 men and 668 women) were identified. Compared to never smokers, current smoking was associated with reduced risk of thyroid cancer (HR?=?0.68, 95?% CI 0.55–0.85); this association was slightly stronger among non-drinkers (HR?=?0.46, 95?% CI 0.29–0.74). No reduction in risk was observed for former, compared to never, smokers. Greater smoking intensity, duration, and pack-years were associated with further reductions in risk among former and current smokers. Alcohol intake was also inversely associated with thyroid cancer risk (≥7 drinks/week versus 0, HR?=?0.72, 95?% CI 0.58–0.90, p trend?=?0.002). Inverse associations with smoking and alcohol were more pronounced for papillary versus follicular tumors.

Conclusion

The results of this pooled analysis suggest that both cigarette smoking and alcohol consumption are associated with reduced risks of papillary thyroid cancer and, possibly, follicular thyroid cancer.     

Cigarette smoking and liver cancer among US veterans

The relationship of tobacco use with risk of primary liver cancer was investigated using data from a 26-year mortality follow-up of nearly 250,000 US veterans, mostly from World War I. Significantly increased risks for liver cancer (289 deaths) were associated with most forms of tobacco use, including pipe and cigar smoking. Elevated relative tisks (RRs) were seen for current cigarette smokers (RR=2.4; 95 percent confidence interval [CI] 1.6–3.5) and former cigarette smokers (RR=1.9, 1.2–2.9). A strong dose-response relationship (P<0.001) was found for cigarette smoking, with smokers of 40 or more cigarettes per day having almost a fourfold risk (RR=3.8, 1.9–8.0). Risks were also found to increase significantly with years of cigarette use and with earlier age at the start of cigarette smoking. These results are consistent with those of other cohort and case-control studies, suggesting that cigarette smoking may be related to the risk of liver cancer.All authors are in the Epidemiology and Biostatistics Program, Division of Cancer Etiology, National Cancer Institute. Address correspondence to Dr Hsing at Executive Plaza North, Room 415, Bethesda, MD 20892, USA.     

Cohort analysis of fruit and vegetable consumption and lung cancer mortality in European men

Our aim was to examine the relationship between fruit and vegetable consumption and lung cancer mortality in a cohort of European males. Around 1970, dietary intake of Finnish, Italian and Dutch middle-aged men was assessed using a cross-check dietary history. Complete baseline information was available for 3,108 men, of whom 1,578 were baseline smokers. We used Cox proportional hazard analyses to calculate risk estimates for the consumption in country-specific tertiles on lung cancer in smokers. During 25 years of follow-up, 149 lung cancer deaths occurred in the smokers. Fruit consumption was inversely associated with lung cancer mortality among smokers; compared with the lowest, adjusted RRs for the intermediate and highest tertiles were 0.56 (0.37-0.84) and 0.69 (0.46-1.02), p-trend 0.05. Only in the Dutch cohort was this association statistically significant [adjusted relative risks (RRs) 1.00, 0.33 (0.16-0.70) and 0.35 (0.16-0.74), p-trend 0.004]. In Finland lung cancer risk was lower with higher fruit intake but not significantly, whereas in Italy no association was observed. Stratifying on cigarette smoking intensity (non, light and heavy) revealed an inverse association in the heavy smokers only [adjusted RRs (95% confidence intervals [CI]) 1; 0.47 (0.26-0.84); 0.40 (0.20-0.78)). Vegetable consumption was not related to lung cancer risk in smokers. However, analyses stratified on cigarette smoking intensity gave some indication for a lower lung cancer risk with higher intake. In conclusion, in this prospective analysis among European smoking men, fruit intake was inversely related to lung cancer mortality. This association was confined to heavy cigarette smokers.     

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.     

Epidemiology of bladder cancer in Alexandria,Egypt: Tobacco smoking

The relationship between smoking and bladder cancer risk was investigated using data from a case-control study conducted between January 1994 and July 1996 in Alexandria, Egypt. Cases were 151 males with incident, histologically confirmed invasive cancer of the bladder, and controls were 157 males admitted to hospital for acute, non-neoplastic, non-urinary tract, non-smoking-related conditions. With reference to never smokers, ex-smokers had a multivariate odds ratio (OR) of 4.4 [95% confidence interval (CI) 1.7–11.7] and current smokers of 6.6 (95% CI 3.1–13.9). The ORs were 5.4 for <20 and 7.6 for ≥20 cigarettes per day. After adjustment for cigarette smoking, the ORs were 0.8 for waterpipe and 0.4 for hashish smokers. The risk was significantly related to duration of smoking (OR of 16.5 for >40 years), and inversely related to age at starting (OR of 8.8 for starting <20 years), and inversely related to time since quitting smoking. Compared with never smokers who did not report a clinical history of schistosomiasis, the OR was 9.4 for smokers with a history of schistosomiasis, and 10.7 for smokers ever employed in high-risk occupations compared with non-smokers not reporting such a history. Thus, our results, while not giving indications of an increased bladder cancer risk with habits other than cigarette smoking, found a remarkably strong association with various measures of cigarette smoking that could explain 75% of bladder cancer cases among males from Alexandria. The prevalence of smoking was very low among women, and consequently tobacco was not a relevant risk factor for female bladder cancer. Int. J. Cancer 73:64–67, 1997. © 1997 Wiley-Liss, Inc.     

Cigar and pipe smoking and cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC)

The carcinogenicity of cigar and pipe smoking is established but the effect of detailed smoking characteristics is less well defined. We examined the effects on cancer incidence of exclusive cigar and pipe smoking, and in combination with cigarettes, among 102,395 men from Denmark, Germany, Spain, Sweden and the United Kingdom in the EPIC cohort. Hazard ratios (HR) and their 95% confidence intervals (CI) for cancer during a median 9‐year follow‐up from ages 35 to 70 years were estimated using proportional hazards models. Compared to never smokers, HR of cancers of lung, upper aerodigestive tract and bladder combined was 2.2 (95% CI: 1.3, 3.8) for exclusive cigar smokers (16 cases), 3.0 (2.1, 4.5) for exclusive pipe smokers (33 cases) and 5.3 (4.4, 6.4) for exclusive cigarette smokers (1,069 cases). For each smoking type, effects were stronger in current smokers than in ex‐smokers and in inhalers than in non‐inhalers. Ever smokers of both cigarettes and cigars [HR 5.7 (4.4, 7.3), 120 cases] and cigarettes and pipes [5.1 (4.1, 6.4), 247 cases] had as high a raised risk as had exclusive cigarette smokers. In these smokers, the magnitude of the raised risk was smaller if they had switched to cigars or pipes only (i.e., quit cigarettes) and had not compensated with greater smoking intensity. Cigar and pipe smoking is not a safe alternative to cigarette smoking. The lower cancer risk of cigar and pipe smokers as compared to cigarette smokers is explained by lesser degree of inhalation and lower smoking intensity.     

Cigarette smoking and pancreatic cancer: an analysis from the International Pancreatic Cancer Case-Control Consortium (Panc4)

BackgroundTo evaluate the dose–response relationship between cigarette smoking and pancreatic cancer and to examine the effects of temporal variables.MethodsWe analyzed data from 12 case–control studies within the International Pancreatic Cancer Case–Control Consortium (PanC4), including 6507 pancreatic cases and 12 890 controls. We estimated summary odds ratios (ORs) by pooling study-specific ORs using random-effects models.ResultsCompared with never smokers, the OR was 1.2 (95% confidence interval [CI] 1.0–1.3) for former smokers and 2.2 (95% CI 1.7–2.8) for current cigarette smokers, with a significant increasing trend in risk with increasing number of cigarettes among current smokers (OR = 3.4 for ≥35 cigarettes per day, P for trend <0.0001). Risk increased in relation to duration of cigarette smoking up to 40 years of smoking (OR = 2.4). No trend in risk was observed for age at starting cigarette smoking, whereas risk decreased with increasing time since cigarette cessation, the OR being 0.98 after 20 years.ConclusionsThis uniquely large pooled analysis confirms that current cigarette smoking is associated with a twofold increased risk of pancreatic cancer and that the risk increases with the number of cigarettes smoked and duration of smoking. Risk of pancreatic cancer reaches the level of never smokers ∼20 years after quitting.     

Mortality risk in former smokers with breast cancer: Pack‐years vs. smoking status

It is unclear why successful quitting at time of breast cancer diagnosis should remove risk from a significant lifetime of smoking. Studies concluding this may be biased by how smoking is measured in many epidemiological cohorts. In the late 1990s, a randomized trial of diet and breast cancer outcomes enrolled early‐stage female breast cancer survivors diagnosed within the previous 4 years. Smoking history and key covariate measures were available at study entry for 2,953 participants. Participants were followed for an average of 7.3 years (96% response rate). There were 10.1% deaths (83% from breast cancer). At enrollment, 55.2% were never smokers, 41.2% former smokers and 4.6% current smokers. Using current smoking status in a Cox regression, there was no increased risk for former smokers for either all‐cause mortality [hazard ratio (HR) = 1.11; 95% confidence interval (CI) = 0.87–1.41; p‐value = 0.42) or breast cancer mortality. However, when we categorized on extensive lifetime exposure, former smokers with 20+ pack‐years of smoking (25.8%) had a significantly higher risk of both all‐cause (HR = 1.77; 95% CI = 1.17–2.48; p‐value = 0.0007) and breast cancer‐specific mortality (HR = 1.62; 95% CI = 1.11–2.37; p‐value = 0.01). Lifetime smoking exposure, not current status, should be used to assess mortality risk among former smokers.     

Cigarette smoking and risk of glioma: a prospective cohort study

The etiology of glioma, the most commonly diagnosed malignant brain tumor among adults in the United States, is poorly understood. N-nitroso compounds are known carcinogens, which are found in cigarette smoke and can induce gliomas in rats. On this basis, it has been hypothesized that cigarette smoking may be associated with an increased risk of glioma. We investigated the association between cigarette smoking and glioma risk in the National Breast Screening Study, which included 89,835 Canadian women aged 40-59 years at recruitment between 1980 and 1985. Linkages to national cancer and mortality databases yielded data on cancer incidence and deaths from all causes, respectively, with follow-up ending between 1998 and 2000. Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between cigarette smoking and risk of glioma. During a mean of 16.4 years of follow-up, we observed 120 incident glioma cases. Among ever smokers, women who reported having quit smoking had a 51% increase in risk of glioma compared with never smokers (HR = 1.51, 95% CI = 0.97-2.34), while current smokers did not appear to have an increase in risk. When the association with former smokers was further examined by years since quitting, women who had quit smoking >10 years before baseline were at a decreased risk of glioma compared with women who had quit within the 10 years prior to baseline (HR = 0.55, 95% CI = 0.29-1.07), indicating that the association between former smokers and glioma may be driven by women, who recently quit smoking. Compared with nonsmokers, duration of cigarette smoking, number of cigarettes smoked per day and pack-years of smoking were associated with increased glioma risk, although the increases in risk were relatively modest. The present study provides some support for a positive association between cigarette smoking and risk of glioma.