Passive and active smoking and breast cancer risk in Canada, 1994–97

Background: Studies comparing ever smokers with never smokers have found little increase in breast cancer risk. However, the five published studies examining passive smoking and breast cancer have all suggested associations with both passive and active smoking, particularly premenopausal risk. Methods: We analyzed data collected through the Canadian National Enhanced Cancer Surveillance System, from 805 premenopausal and 1512 postmenopausal women with newly diagnosed (incident), histologically confirmed, primary breast cancer and 2438 population controls. The mailed questionnaire included questions on breast cancer risk factors and a lifetime residential and occupational history of exposure to passive smoking. Results: Among premenopausal women who were never active smokers, regular exposure to passive smoke was associated with an adjusted breast cancer odds ratio (OR) of 2.3 (95% confidence interval [CI] 1.2–4.6). Passive exposure showed a strong dose–response trend (test for trend p=0.0007) with an OR of 2.9 (95% CI 1.3–6.6) for more than 35 years of passive residential and/or occupational exposure. When premenopausal women who had ever actively smoked were compared with women never regularly exposed to passive or active smoke, the adjusted OR for breast cancer was also 2.3 (95% CI 1.2–4.5). Among postmenopausal women who were never-active smokers, regular exposure to passive smoke was associated with an adjusted breast cancer OR of 1.2 (95% CI 0.8–1.8) and an OR of 1.4 (95% CI 0.9–2.3) for the most highly exposed quartile of women. The adjusted OR for postmenopausal breast cancer risk for ever-active smokers compared with women never regularly exposed to passive or active smoke was 1.5 (95% CI 1.0–2.3). Statistically significant dose–response relationships were observed with increasing years of smoking, increasing pack-years and decreasing years since quitting. Women with 35 or more years of smoking had an adjusted OR of 1.7 (95% CI 1.1–2.7). Conclusions: Active and passive smoking may be associated with increased breast cancer risk, particularly premenopausal risk.     

A null association between active or passive cigarette smoking and breast cancer risk

The effect of smoking on breast cancer risk has been null in large, well-conducted cohort studies. In a previous study, we stratified the population into active smokers, passive smokers, and never-active never-passive smokers and modeled early life cigarette smoke exposures as causal and later life cigarette smoke exposure as preventive. We observed a complex association between cigarette smoke and breast cancer risk. Using a similar design and population, this study did not confirm the earlier result. Neither ever-active smoking (adjusted odds ratio (OR) = 0.72, 95% confidence intervals (CI) 0.55–0.95) nor ever-passive smoking (adjusted OR = 0.85, 95% CI 0.63–1.1) were strongly associated with breast cancer risk compared with never-active never-passive smoking. No patterns of effects were observed in subgroup analyses.     

Active and passive smoking and the risk of breast cancer in women aged 36-45 years: a population based case-control study in the UK

Active smoking has little or no effect on breast cancer risk but some investigators have suggested that passive smoking and its interaction with active smoking may be associated with an increased risk. In a population based case-control study of breast cancer in women aged 36-45 years at diagnosis, information on active smoking, passive smoking in the home, and other factors, was collected at interview from 639 cases and 640 controls. Women were categorised jointly by their active and passive smoking exposure. Among never smoking controls, women who also reported no passive smoking exposure were significantly more likely to be nulliparous and to be recent users of oral contraceptives. Among those never exposed to passive smoking, there was no significant association between active smoking and breast cancer, relative risk (RR) of 1.12 (95% confidence interval (CI) 0.72-1.73) for past smokers and RR of 1.19 (95% CI 0.72-1.95) for current smokers, nor was there an association with age started, duration or intensity of active smoking. Compared with women who were never active nor passive smokers, there was no significant association between passive smoking in the home and breast cancer risk in never smokers, RR of 0.89 (95% CI 0.64-1.25), in past smokers, RR of 1.09 (95% CI 0.75-1.56), or in current smokers, RR of 0.93 (95% CI 0.67-1.30). There was no trend with increasing duration of passive smoking and there was no heterogeneity among any of the subgroups examined. In this study, there was no evidence of an association between either active smoking or passive smoking in the home and risk of breast cancer.     

Passive smoking and the use of noncigarette tobacco products in association with risk for pancreatic cancer: a case-control study

BACKGROUND: The associations between passive smoking and the use of noncigarette tobacco products with pancreatic cancer are not clear. METHODS: In this case-control study, the authors collected information on passive smoking and the use of noncigarette tobacco products in 808 patients with pancreatic adenocarcinoma and 808 healthy controls by personal interview. Multivariable logistic regression was performed to estimate the adjusted odds ratio (AOR) and 95% confidence interval (95% CI). RESULTS: The results confirmed the previously reported association between active smoking and increased risk for pancreatic cancer. The AOR was 1.7 (95% CI, 1.4-2.2) for regular smokers, 1.8 (95% CI, 1.4-2.4) for long-term smokers, and 3.1 (95% CI, 2.2-4.3) for former smokers. Although passive smoking showed a nonsignificantly elevated risk for pancreatic cancer in the entire study population (AOR, 1.3; 95% CI, 0.9-1.7), the association was present among ever smokers (AOR, 1.7; 95% CI, 1.03-2.6) but was absent among never smokers (AOR, 1.1; 95% CI, 0.8-1.6). Neither intensity nor duration of passive smoking modified the risk of pancreatic cancer among never smokers. The use of chewing tobacco, snuff, and pipes showed no significant risk elevation for pancreatic cancer after controlling for the confounding effects of demographics and other known risk factors. The use of cigars in never smokers showed a borderline significant increase of risk for pancreatic cancer (AOR, 2.2; 95% CI, 1.0-4.7; P = .05). CONCLUSIONS: The current observations did not support a role for passive smoking or the use of noncigarette tobacco products in the etiology of pancreatic cancer. The association between cigar use and the risk of pancreatic cancer needs to be confirmed in other study populations.     

Risk of endometrial cancer in relationship to cigarette smoking: results from the EPIC study

Current epidemiologic evidence indicates that cigarette smoking reduces the risk of endometrial cancer. We examined data from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort to analyze further aspects of the smoking-endometrial cancer relationship, such as possible modifying effects of menopausal status, HRT use, BMI and parity. In a total of 249,986 women with smoking exposure and menopausal status information, 619 incident endometrial cancer cases were identified during 1.56 million person-years of follow-up. Among postmenopausal women, the hazard ratio (HR) for current smokers versus never smokers was 0.70 (95% CI = 0.53-0.93), while it was 1.75 (95% CI = 1.13-2.70) among premenopausal women at recruitment. After adjustment for risk factors, the HR for postmenopausal women was slightly attenuated to 0.78 (95% CI = 0.59-1.03). No heterogeneity of effect was observed with HRT use or BMI. Among premenopausal women, current smokers of more than 15 cigarettes per day or who smoked for 30 years or more at the time of recruitment had a more than 2-fold increased risk of endometrial cancer compared to never smokers (HR = 2.54; 95% CI = 1.47-4.38 and HR = 2.23; 95% CI = 1.04-4.77, respectively). Past smoking was not associated with endometrial cancer risk, either among pre- or postmenopausal women. In this prospective study, we observed an increased risk of endometrial cancer with cigarette smoking in premenopausal women. The reduction of endometrial cancer risk observed among postmenopausal women does not have direct public health relevance since cigarette smoking is the main known risk factor for cancer.     

Circulating levels of insulin-like growth factors, their binding proteins, and breast cancer risk.

BACKGROUND: Earlier data support the hypothesis that the relation between circulating insulin-like growth factor-I (IGF-I) levels and breast cancer risk differs by menopausal status. The strong association of IGF-I with height in childhood and weak or no association between adult levels and adult height also suggest that IGF levels in young women may better reflect an exposure time period of importance to breast cancer. Few studies have assessed IGF binding protein-1 (IGFBP-1) or free IGF and breast cancer risk. MATERIALS AND METHODS: We conducted a large case-control study nested within the prospective Nurses' Health Study. Plasma concentrations of IGF-I, free IGF, IGFBP-3, and IGFBP-1 were measured in blood samples collected in 1989 to 1990. Eight hundred women were identified who had a diagnosis of invasive or in situ breast cancer after blood collection, up to 1998, 27% of whom were premenopausal at blood collection. To those 800 women, one to two controls were age-matched for a total of 1,129 controls. We used logistic regression models to estimate the relative risk (RR) of breast cancer associated with IGF levels.Findings: Among postmenopausal women, neither IGF-I, IGFBP-3, IGFBP-1, nor free IGF was associated with breast cancer risk [RRs, top versus bottom quintile: IGF-I, 1.0; 95% confidence interval (95% CI), 0.7-1.4; IGFBP-3, 0.8; 95% CI, 0.6-1.1; IGFBP-1, 0.9; 95% CI, 0.6-1.5; and free IGF, 1.0; 95% CI, 0.6-1.4]. Among premenopausal women, IGFBP-3, IGFBP-1, and free IGF similarly were not associated with breast cancer risk (RRs, top versus bottom quintile: IGFBP-3, 1.2; 95% CI, 0.8-2.3; IGFBP-1, 1.5; 95% CI, 0.8-3.0; and free IGF, 1.1; 95% CI, 0.7-2.1). Higher IGF-I plasma levels, however, were associated with a modestly elevated breast cancer risk (RR, 1.6; 95% CI, 1.0-2.6) among the premenopausal women, with a stronger association among premenopausal women ages < or =50 (RR, 2.5; 95% CI, 1.4-4.3); further adjustment for IGFBP-3 did not greatly change these estimates. INTERPRETATION: Circulating IGF-I levels seem to be modestly associated with breast cancer risk among premenopausal women, but not among postmenopausal women. IGFBP-3, IGFBP-1, and free IGF are not associated with breast cancer risk in either premenopausal or postmenopausal women in this cohort.     

The association of plasma DHEA and DHEA sulfate with breast cancer risk in predominantly premenopausal women.

Concentrations of adrenal androgens are positively associated with postmenopausal breast cancer risk; however, results in premenopausal women are conflicting. Therefore, we conducted a prospective nested case-control study within the Nurses' Health Study II cohort to examine the relationship of DHEA and DHEA sulfate (DHEAS) with breast cancer risk in predominantly premenopausal women. Blood samples were collected from 1996 to 1999. The analysis included 317 cases of breast cancer diagnosed after blood collection and before June 1, 2003; for each case, two controls were matched on age, fasting status, time of day and month of blood collection, race/ethnicity, and timing of blood draw within the menstrual cycle. No associations were observed between DHEA or DHEAS levels and breast cancer risk overall [in situ and invasive; DHEA relative risk (RR), top versus bottom quartile, 1.2; 95% confidence interval (95% CI), 0.8-1.8, P(trend) = 0.53; DHEAS RR, 1.3; 95% CI, 0.9-2.0; P(trend) = 0.07]. However, both DHEA and DHEAS were positively associated with estrogen receptor-positive/progesterone receptor-positive breast cancer (DHEA RR, 1.6; 95% CI, 0.9-2.8, P(trend) = 0.09; DHEAS RR, 1.9; 95% CI, 1.1-3.3, P(trend) = 0.02). We observed a significant interaction by age, with an RR for DHEAS of 0.8 (95% CI, 0.4-1.5, P(trend) = 0.62) for women <45 years old and 2.0 (95% CI, 1.2-3.5, P(trend) = 0.003) for women >/=45 years old; results were similar for DHEA. Our results suggest that adrenal androgens are positively associated with breast cancer among predominately premenopausal women, especially for estrogen receptor-positive/progesterone receptor-positive tumors and among women over age 45 years.     

The Copenhagen case-control study of renal pelvis and ureter cancer: role of smoking and occupational exposures

Smoking habits and occupational exposures were investigated for 96 patients with cancer of the renal pelvis and ureter (including papilloma) and 294 hospital controls. In comparison with persons who never smoked, significantly increased relative risks were seen for smokers of cigarettes alone (RR = 2.6; 95% CI: 1.0-6.7) and in combination with other types of tobacco (RR = 3.8; 95% CI: 1.3-11.5). Non-significantly increased relative risks were observed for pipe smokers (RR = 2.2; 95% CI: 0.1-97) and for mixed pipe, cigar, and cigarillo smokers (RR = 6.5; 95% CI: 0.4-21.2). A strong dose-effect (p less than 0.001) relationship was seen between the lifetime total amount of tobacco smoked and the risk of pelvis-ureter tumors, with the heaviest smokers having an 8-fold risk. Comparison with the dose-effect relationship for a parallel study of bladder cancer indicated that the relationship with tobacco was stronger for pelvis-ureter tumors. Deep inhalation of cigarette smoke increased the risk (RR = 3.4; 95% CI: 1.9-6.1), while stopping smoking (RR = 0.6; 95% CI: 0.3-1.1) and use of filter cigarettes (RR = 0.5; 95% CI: 0.3-0.9) decreased the risk. Significantly increased risks emerged for employment in the chemical, petrochemical and plastics industries (RR = 4.0; 95% CI: 1.6-9.8), and for exposure to coal and coke (RR = 4.0; 95% CI: 1.2-13.6), asphalt and tar (RR = 5.5; 95% CI: 1.6-19.6). Cigarette smoking accounted for 56% of male and 40% of female pelvis and ureter tumors in eastern Denmark.     

Expression patterns of potential therapeutic targets in prostate cancer

The aim of the study was to examine the risk of breast cancer associated with passive and active smoking and to explore risk heterogeneity among studies. Nineteen of 20 located published studies of passive smoking and breast cancer risk among women met basic quality criteria. Pooled relative risk estimates for breast cancer were calculated for 1) life-long non-smokers with regular passive exposure to tobacco smoke and 2) women who smoked. They were compared to women categorized as never regularly exposed to tobacco smoke. The pooled risk estimate for breast cancer associated with passive smoking among life-long non-smokers was 1.27 (95% confidence interval (CI), 1.11-1.45). In the subset of 5 studies (all case-control studies) with more complete exposure assessment (quantitative long-term information on the 3 major sources of passive smoke exposure: childhood, adult residential and occupational), the pooled risk estimate for exposed non-smokers was 1.90 (95%CI, 1.53-2.37). For the 14 studies with less complete passive exposure measures the risk was 1.08 (95%CI, 0.99-1.19) overall, 1.16 for 7 case-control and 1.06 for 7 cohort studies, although dose-response results in 3 of 4 Asian cohort studies suggested increased risk. The overall premenopausal breast cancer risk associated with passive smoking among life-long non-smokers was 1.68 (95%CI 1.33-2.12), and 2.19 (95% CI 1.68-2.84) for the 5 of 14 studies with more complete exposure assessment. For women who had smoked the breast cancer risk estimate was 1.46 (95%CI 1.15-1.85) when compared to women with neither active nor regular passive smoke exposure; 2.08 (95% CI 1.44-3.01) for more complete and 1.15 (95% CI 0.92-1.43) for less complete passive exposure assessment. Studies with thorough passive smoking exposure assessment implicate passive and active smoking as risk factors for premenopausal breast cancer. Cohort studies with thorough passive smoking assessment would be helpful and studies exploring biological mechanisms are needed to explain the unexpected similarity of the passive and active risks.     

Environmental tobacco smoke and lung cancer mortality in the American Cancer Society's Cancer Prevention Study II

Environmental tobacco smoke (ETS) has been classified as a human lung carcinogen by the United States Environmental Protection Agency (EPA), based both on the chemical similarity of sidestream and mainstream smoke and on slightly higher lung cancer risk in never-smokers whose spouses smoke compared with those married to nonsmokers. We evaluated the relation between ETS and lung cancer prospectively in the US, among 114,286 female and 19,549 male never-smokers, married to smokers, compared with about 77,000 female and 77,000 male never-smokers whose spouses did not smoke. Multivariate analyses, based on 247 lung cancer deaths, controlled for age, race, diet, and occupation. Dose-response analyses were restricted to 92,222 women whose husbands provided complete information on cigarette smoking and date of marriage. Lung cancer death rates, adjusted for other factors, were 20 percent higher among women whose husbands ever smoked during the current marriage than among those married to never-smokers (relative risk [RR]=1.2, 95 percent confidence interval [CI]=0.8-1.6). For never-smoking men whose wives smoked, the RR was 1.1 (CI=0.6-1.8). Risk among women was similar or higher when the husband continued to smoke (RR=1.2, CI=0.8-1.8), or smoked 40 or more cigarettes per day (RR=1.9, CI=1.0-3.6), but did not increase with years of marriage to a smoker. Most CIs included the null. Although generally not statistically significant, these results agree with the EPA summary estimate that spousal smoking increases lung cancer risk by about 20 percent in never-smoking women. Even large prospective studies have limited statistical power to measure precisely the risk from ETS.     

Risk of gastroesophageal cancer among smokers and users of Scandinavian moist snuff

Although Scandinavian moist snuff ("snus"), no doubt, is a safer alternative to smoking, there is limited evidence against an association with gastroesophageal cancers. In a retrospective cohort study, we investigated esophageal and stomach cancer incidence among 336,381 male Swedish construction workers who provided information on tobacco smoking and snus habits within a health surveillance program between 1971 and 1993. Essentially complete follow-up through 2004 was accomplished through linkage to several nationwide registers. Multivariable Cox proportional hazards regression models estimated relative risks (RR) and 95% confidence intervals (CIs). Compared to never-users of any tobacco, smokers had increased risks for adenocarcinoma (RR = 2.3, 95% CI 1.4-3.7) and squamous cell carcinoma (RR = 5.2, 95% CI 3.1-8.6) of the esophagus, as well as cardia (RR = 2.1, 95% CI 1.5-3.0) and noncardia stomach (RR = 1.3, 95% CI 1.2-1.6) cancers. We also observed excess risks for esophageal squamous cell carcinoma (RR = 3.5, 95% CI 1.6-7.6) and noncardia stomach cancer (RR = 1.4, 95% CI 1.1-1.9) among snus users who had never smoked. Although confounding by unmeasured exposures, and some differential misclassification of smoking, might have inflated the associations, our study provides suggestive evidence for an independent carcinogenic effect of snus.     

A cytochrome P4502E1 genetic polymorphism and tobacco smoking in breast cancer

Known breast-cancer risk factors account for only part of the variability in breast-cancer incidence. Tobacco smoke is not commonly considered a breast carcinogen, but many of its constituents, such as N-nitrosamines, are carcinogenic in laboratory animal studies. Herein, we assessed a cytochrome P4502E1 (CYP2E1) genetic polymorphism (a Dral restriction enzyme site in intron 6) as a risk factor for breast cancer in both premenopausal and postmenopausal women. Because N-nitrosamines are metabolically activated by CYP2E1, the risk among women smokers was investigated. Caucasian women were enrolled in a case-control study of breast cancer between 1986 and 1991. A subset of the women (219 premenopausal and 387 postmenopausal women) consented to phlebotomy. The allelic frequencies for the premenopausal women (D allele = 0.91 and C allele = 0.09) and postmenopausal women (D allele = 0.93 and C allele = 0.07) were similar to those previously reported. There was no statistically significant association between the CYP2E1 polymorphism and breast-cancer risk for premenopausal or postmenopausal women (adjusted odds ratio (OR) = 1.04, 95% confidence interval (CI) = 0.48, 2.24, and OR = 1.01, 95% CI = 0.55, 1.84, respectively). When the women were categorized as nonsmokers versus smokers (those who smoked more than one cigarette per week for more than 1 yr), premenopausal women with one or two C alleles who had a history of smoking were found to be at increased risk (unadjusted OR = 7.00, 95% CI = 0.75, 14.53, and adjusted OR = 11.09, 95% CI = 1.51, 81.41), although the number of study subjects with those genotypes was small. The small number of study subjects with a C allele precluded meaningful classification by level of smoking, but categorizing the smokers into two groups (above and below the median) also suggested an increased risk. Premenopausal women with the DD genotype and postmenopausal women with any genotype were not at increased risk. Breast-cancer risk was not related to the CYP2E1 genotype in either premenopausal nonsmokers or smokers (adjusted OR = 0.66, 95% CI = 0.20, 2.17, and OR = 2.13, 95% CI = 0.60, 7.59, respectively) or postmenopausal nonsmokers or smokers (OR = 0.90, 95% CI = 0.34, 2.35, and OR = 1.02, 95% CI = 0.46, 2.23, respectively), although the difference in the ORs for premenopausal nonsmokers and smokers suggests an increased risk for smokers. While there are limitations to this study, particularly related to the small number of subjects with the DC and CC genotypes, the study suggests that some women may be susceptible to tobacco smoke because of a CYP2E1 polymorphism. However, these results are preliminary and must be replicated. © 1996 Wiley-Liss, Inc.

1 This article is a US Government work and, as such, is in the public domain in the United States of America.

     

Tobacco Smoke Exposure and Breast Cancer Risk in Thai Urban Females

The incidence of urban female breast cancer has been continuously increasing over the past decade with unknown etiology. One hypothesis for this increase is carcinogen exposure from tobacco. Therefore, the objective of this study was to investigate the risk of urban female breast cancer from tobacco smoke exposure.The matched case control study was conducted among Thai females, aged 17-76 years and living in Bangkok or its surrounding areas. A total of 444 pairs of cases and controls were recruited from the Thai National Cancer Institute. Cases were newly diagnosed and histologically confirmed as breast cancer while controls were selected from healthy women who visited a patient, matched by age ± 5 years. After obtaining informed consent, tobacco smoke exposure data and information on other potential risk factors were collected by interview. The analysis was performed by conditional logistic regression, and presented with odds ratio (ORs) and 95% confidence intervals(CI). From all subjects, 3.8% of cases and 3.4% of controls were active smokers while 11.0% of cases and 6.1% of controls were passive smokers. The highest to lowest sources of passive tobacco smoke were from spouses (40.8%), the workplace (36.8%) and public areas (26.3%), respectively. After adjusting for other potential risk factors or confounders, females with frequent low-dose passive smoke exposure (≤7 hours per week) from a spouse or workplace had adjusted odds ratio 3.77 (95%CI=1.11-12.82) and 4.02 (95%CI=1.04-15.50) higher risk of breast cancer compared with non-smokers, respectively. However, this study did not find any association ofbreast cancer risk in high dose passive tobacco smoke exposure, or a dose response relationship in cumulative passive tobacco smoke exposure per week, or in the active smoker group. In conclusion, passive smoke exposure may be one important risk factor of urban female breast cancer, particularly, from a spouse or workplace. This risk factor highlights the importance of avoiding tobacco smoke exposure as a key measure for breast cancer prevention and control.     

Differential effect of NAT2 on the association between active and passive smoke exposure and breast cancer risk.

BACKGROUND: Polymorphisms in the N-acetyltransferase 2 (NAT2) gene influence the rate of metabolism of aromatic and heterocyclic amines present in tobacco smoke. Because the physicochemical composition of mainstream and sidestream smoke differ, we conducted a case-control study to assess a possible differential effect of NAT2 genotype on the relationship between active/passive smoke exposure and breast cancer risk. METHODS: Breast cancer patients diagnosed by 50 years of age and population-sampled controls were interviewed to obtain detailed lifetime active and passive smoking history. NAT2 genotype was determined in 422 breast cancer patients and 887 controls. Multivariate logistic regression analysis was performed to estimate breast cancer risk in relation to smoking history by acetylator status and interaction effects. RESULTS: Compared with women never regularly exposed to tobacco smoke, odds ratios (ORs) for current smoking and ex-smoking were 1.7 [95% confidence interval (CI): 1.0-2.9] and 1.2 (95% CI, 0.7-2.0) in slow acetylators, and not increased in rapid acetylators. Active smoking variables, such as pack-years, duration of smoking, and time since cessation, showed significant dose-response relationships with breast cancer risk among slow acetylators but not rapid acetylators. In contrast, passive smoking was associated with higher risk in rapid than in slow acetylators, with ORs of 2.0 (95% CI, 1.0-4.1) and 1.2 (95% CI, 0.7-2.0), respectively. CONCLUSIONS: Our results suggest that the NAT2 status has a differential effect on the association of active and passive smoking with breast cancer and demonstrate the need to consider possible different mechanisms associated with exposure to main- and sidestream tobacco smoke.     

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

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

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.     

Passive smoking exposure and female breast cancer mortality

BACKGROUND: Several studies have reported positive associations between environmental tobacco smoke (ETS) and increased risk of breast cancer. However, studies of active smoking and risk of breast cancer are equivocal and in general do not support a positive association. To try to resolve this paradox, we examined the association between breast cancer mortality and potential ETS exposure from spousal smoking in an American Cancer Society prospective study of U.S. adult women. METHODS: We assessed breast cancer death rates in a cohort of 146 488 never-smoking, single-marriage women who were cancer free at enrollment in 1982. Breast cancer death rates among women whose husbands smoked were compared with those among women married to men who had never smoked. Cox proportional hazards modeling was used to control for potential risk factors other than ETS exposure. RESULTS: After 12 years of follow-up, 669 cases of fatal breast cancer were observed in the cohort. Overall, we saw no association between exposure to ETS and death from breast cancer (rate ratio [RR] = 1.0; 95% confidence interval [CI] = 0.8-1.2). We did, however, find a small, not statistically significant increased risk of breast cancer mortality among women who were married before age 20 years to smokers (RR = 1. 2; 95% CI = 0.8-1.8). CONCLUSIONS: In contrast to the results of previous studies, this study found no association between exposure to ETS and female breast cancer mortality. The results of our study are particularly compelling because of its prospective design as compared with most earlier studies, the relatively large number of exposed women with breast cancer deaths, and the reporting of exposure by the spouse rather than by proxy.     

Active and passive smoking with breast cancer risk for Chinese females:a systematic review and meta-analysis

Previous studies suggested that smoking and passive smoking could increase the risk of breast cancer, but the results were inconsistent, especial y for Chinese females. Thus, we systematical y searched cohort and case-control studies investigating the associations of active and passive smoking with breast cancer risk among Chinese females in four English databases （PubMed, Embase, ScienceDirect, and Wiley） and three Chinese databases （CNKI, WanFang, and VIP）. Fifty-one articles （3 cohort studies and 48 case-control studies） covering 17 provinces of China were finally included in this systematic review. Among Chinese females, there was significant association between passive smoking and this risk of breast cancer [odds ratio （OR）： 1.62; 95% confidence interval （CI）： 1.39-1.85; I2 = 75.8%, P 〈 0.001; n = 26] but no significant association between active smoking and the risk of breast cancer （OR：1.04;95%CI：0.89-1.20;I2=13.9%, P=0.248;n=31）. The OR of exposure to husband’s smoking and to smoke in the workplace was 1.27 （95% CI： 1.07-1.50） and 1.66 （95% CI： 1.07-2.59）, respectively. The OR of light and heavy passive smoking was 1.11 and 1.41, respectively, for women exposed to their husband’s smoke （〈20 and≥20 cigarettes per day）, and 1.07 and 1.87, respectively, for those exposed to smoke in the workplace （〈300 and≥300 min of exposure per day）. These results imply that passive smoking is associated with an increased risk of breast cancer, and the risk seems to increase as the level of passive exposure to smoke increases among Chinese females. Women with passive exposure to smoke in the workplace have a higher risk of breast cancer than those exposed to their husband’s smoking.     

Passive smoking and lung cancer in Japanese non-smoking women: a prospective study

Although smoking is a major cause of lung cancer, the proportion of lung cancer cases among Japanese women who never smoked is high. As the prevalence of smoking in Japan is relatively high in men but low in women, the development of lung cancer in non-smoking Japanese women may be significantly impacted by passive smoking. We conducted a population-based prospective study established in 1990 for Cohort I and in 1993 for Cohort II. The study population was defined as all residents aged 40-69 years at the baseline survey. 28,414 lifelong non-smoking women provided baseline information on exposure to tobacco smoke from their husband, at the workplace and during childhood. Over 13 years of follow-up, 109 women were newly diagnosed with lung cancer, of whom 82 developed adenocarcinoma. Compared with women married to never smokers, hazard ratio (HR) [95% confidence interval (CI)] for all lung cancer incidence in women who lived with a smoking husband was 1.34 (95% CI 0.81-2.21). An association was clearly identified for adenocarcinoma (HR 2.03, 95% CI 1.07-3.86), for which dose-response relationships were seen for both the intensity (p for trend = 0.02) and amount (p for trend = 0.03) of the husband's smoking. Passive smoking at the workplace also increased the risk of lung cancer (HR 1.32, 95% CI 0.85-2.04). Moreover, a higher risk of adenocarcinoma was seen for combined husband and workplace exposure (HR 1.93, 95% CI 0.88-4.23). These findings confirm that passive smoking is a risk factor for lung cancer, especially for adenocarcinoma among Japanese women.     

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.