A prospective study of tobacco use and multiple myeloma: evidence against an association

The relationship between the use of cigarettes and other tobacco products and the risk of multiple myeloma was examined in a cohort of nearly 250,000 American veterans followed prospectively for 26 years. Compared with men who had never used tobacco, the risk of death from myeloma was not increased among current (relative risk [RR]=0.9, 95 percent confidence interval [CI]=0.8–1.2) or former (RR=1.0, CI=0.8–1.3) cigarette smokers, nor among users of chewing tobacco or snuff (RR=1.0, CI=0.4–2.3). Risk was only slightly and nonsignificantly increased among pipe or cigar smokers (RR=1.2, CI=0.9–1.5). There was no indication of increasing risk with amount of tobacco used or earlier age at first use. With over 90 percent power to detect a 30 percent increased risk of this tumor occuring among current cigarette smokers, this study provides the strongest evidence to date against an association of cigarette smoking with multiple myeloma.Epidemiology and Biometry Program, Division of Cancer Etiology, National Cancer Institute. Westat, Inc. Rockville, MD. National Cancer Institute, 6130 Executive Blvd, Room 418, Rockville, MD 20892, USA.     

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.     

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.     

Soft tissue sarcoma and tobacco use: data from a prospective cohort study of United States veterans

A report of an increased risk of soft tissue sarcoma (STS) among users of smokeless tobacco led us to evaluate this association and the role of other types of tobacco in a prospective cohort mortality-study of United States veterans. A total of 248,046 veterans provided tobacco-use histories on a mail questionnaire in 1954 or 1957. Data on subsequent tobacco use were not collected. By 1980, 119 deaths from STS had occurred among the cohort members. Veterans who had ever chewed tobacco or used snuff had a nonsignificant 40 percent excess of STS (95 percent confidence interval [CI]=0.8–2.6; 21 deaths) in comparison with veterans who had never used any tobacco products. Risk was limited to former users (relative risk [RR]=1.5) with no excess seen among current users (RR=0.9). Frequent former users had higher risk (RR=1.9) than infrequent users (RR=1.3). Risk was slightly higher in persons who started using smokeless tobacco at younger ages, but did not increase with duration of use or with late age at cessation of use. Most veterans who used chewing tobacco or snuff also used some other form of tobacco. No STS deaths occurred among the 2,308 veterans who used smokeless tobacco only. An unexpected finding of the study was the significant excess of STS deaths among cigarette smokers (RR=1.8, CI=1.1–2.9). Risk was higher among ex-smokers (RR=2.2) than among current smokers (RR=1.5) and was not related to number of cigarettes per day, age started smoking, duration, or pack-years. Pipe and cigar smokers also experienced a nonsignificant excess risk (RR=1.6). The study findings may have been affected by limitations in the histories of tobacco use, the quality of death certificate data on STS, and the small number of STS deaths, particularly among users of smokeless tobacco.Drs Zahm and heineman are with the Occupational Studies Section, Environmental Epidemiology Branch, Epidemiology and Biostatistics Program, National Cancer Institute, Rockville, MD, USA. Dr Vaught is with Westat, Inc., Rockville, MD. USA. Address correspondence to Dr Zahm, Occupational Studies Section, National Cancer Institute, Executive Plaza North, Room 418, Rockville, MD 20892, USA.     

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.     

Cigarette smoking,glutathione-s-transferase M1 and t1 genetic polymorphisms,and breast cancer risk (United States)

Objective: It has been suggested that functional polymorphisms in genes encoding tobacco carcinogen-metabolizing enzymes may modify the relationship between tobacco smoking and breast cancer risk. We sought to determine if there is a gene–environment interaction between GSTM1 (GSTM1A and GSTM1B), and GSTT1 genotypes and cigarette smoking in the risk of breast cancer. Methods: Cases and controls were recruited in a case–control study conducted in Connecticut from 1994 to 1998. Cases were histologically confirmed, incident breast cancer patients, and controls were randomly selected from women histologically confirmed to be without breast cancer. A total of 338 cases and 345 controls were genotyped for GSTM1 and GSTT1. Results: None of the GSTM1 genotypes, either alone or in combination with cigarette smoking, was associated with breast cancer risk. There was, however, a significantly increased risk of breast cancer among postmenopausal women with a GSTT1 null genotype (OR = 1.9, 95% CI 1.2–2.9). There were also indications of increased risk of breast cancer associated with cigarette smoking for postmenopausal women with GSTT1-null genotype, especially for those who commenced smoking before age 18 (OR = 2.9, 95% CI 1.0–8.8). Conclusion: Women with a GSTT1-null genotype may have an increased breast cancer risk, especially postmenopausal women who started smoking at younger ages.     

Tobacco use and prostate cancer in Blacks and Whites in the United States

Prostate cancer occurs more frequently in Blacks than Whites in the United States. A population-based case-control study which investigated the association between tobacco use and prostate cancer risk was carried out among 981 pathologically confirmed cases (479 Blacks, 502 Whites) of prostate cancer, diagnosed between 1 August 1986 and 30 April 1989, and 1,315 controls (594 Blacks, 721 Whites). Study subjects, aged 40 to 79 years, resided in Atlanta (GA), Detroit (MI), and 10 counties in New Jersey, geographic areas covered by three, population-based, cancer registries. No excesses in risk for prostate cancer were seen for former cigarette smokers, in Blacks (odds ratio [OR]=1.1, 95 percent confidence interval [CI]=0.7–1.5) and in Whites (OR=1.2, CI=0.9–1.6), or for current cigarette smokers, in Blacks (OR=1.0, CI=0.7–1.4) and in Whites (OR=1.2, CI=0.8–1.7). Increases in risk were noted for smokers of 40 or more cigarettes per day, among former (OR=1.4, CI=1.0–1.5) and current (OR=1.5, CI=1.0–2.4) smokers. Duration of cigarette use and cumulative amount of cigarette use (pack-years) were not associated with prostate cancer risk for Blacks or Whites. By age, only the youngest subjects, aged 40 to 59 years, showed excess risk associated with current (OR=1.5, CI=1.0–2.3) and former (OR=1.7, CI=1.1–2.6) use of cigarettes, but there were no consistent patterns in this group according to amount or duration of smoking. Risks also were not elevated for former or current users of pipes, cigars, or chewing tobacco, but the risk associated with current snuff use was OR=5.5 (CI=1.2–26.2). This subgroup finding may have been due to chance. The results of the present study may be consistent with a small excess risk for prostate cancer associated with tobacco use, but the lack of consistent findings in population subgroups and the lack of a clear dose-response relationship argue more strongly that no causal association exists. The data do not indicate that the Black-White difference in prostate cancer risk is related to tobacco use.This research was performed under contracts: NO1-CP-51090, NO1-CN-0522, NO1-CP-51089, NO1-CN-31022, NO1-CP-51092, and NO1-CN-5227.     

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.     

The impact of smoking habits on lung cancer risk: 28 years' observation of 26,000 Norwegian men and women

While factory-made cigarettes dominate the market in most countries, the use of handrolled cigarettes accounts for a substantial proportion of the tobacco consumption in Norway. In the present study, we examined the impact of tobacco smoking on lung cancer in general, and the effect of handrolled cigarettes in particular. The data used was from a self-administered mailed questionnaire which included questions about smoking habits and which was completed by about 26,000 men and women in 1964–65. During the follow-up from 1966 to 1993, 333 lung cancers in men and 102 in women were registered. The analysis was performed by use of the Cox proportional hazards regression models. A clear dose-response relationship was found both for cigarette smoking, and for pipe smoking (in men). The dose-response relationship of cigarette smoking was seen in all the three histologic groups considered-squamous cell carcinoma, adenocarcinoma, and small cell carcinoma. The highest relative risks were noted in squamous cell and small cell carcinoma. A higher risk of lung cancer was found for cigarette-smoking women who started cigarette smoking before the age of 30 compared with similar groups of men. In a combined analysis of men and women, and elevated relative risk of 1.9 (95 percent confidence interval=1.2–3.3) was found for those smoking only handrolled cigarettes compared with those smoking factory-made filter cigarettes only.Authors are with the Cancer Registry of Norway, Oslo, Norway. Address correspondence to Mr Engeland, the Cancer Registry of Norway, Institute for Epidemiological Cancer Research, Montebello, N-0310 Oslo, Norway. This work was supported by grant no. 95080/001 from the Norwegian Cancer Society and Contract PH-64-499 from the US National Cancer Institute.     

Cigarette smoking and alcohol consumption and the risk of pancreatic cancer: a case-control study in Shanghai,China

Cancer of the pancreas has been rising in incidence in Shanghai, China since the early 1970s. In 1987–89, this malignancy ranked eighth in cancer incidence among men and ninth among women in Shanghai. To examine risk factors for this tumor in urban Shanghai, a population-based case-control study was conducted. Cases (n=451) were permanent residents of Shanghai, 30 to 74 years of age, newly diagnosed with pancreatic cancer between 1 October 1990 and 30 June 1993. Deceased cases (19 percent) were excluded from the study. Controls (n=1,552) were selected among Shanghai residents, frequency-matched to cases by gender and age. Cases and controls were interviewed about their demographic background and potential risk factors, including tobacco, alcohol and beverage consumption, diet, and medical history. Adjusted odds ratios (OR) and 95 percent confidence intervals (CI) were estimated using logistic regression models. Current cigarette smoking was associated with excess risk of pancreatic cancer in both men (OR=1.6, CI=1.1–2.2) and women (OR=1.4, CI=0.9–2.4). ORs increased significantly with number of cigarettes smoked per day, and with duration and packyears of smoking. Risk increased three-to sixfold among those in the highest categories of cigarette consumption, while risk decreased with increasing years since smoking cessation. Former smokers who stopped smoking for 10 or more years had risks comparable to nonsmokers. No association was found between alcohol use and pancreatic cancer. After adjustment for potential confounding factors, it was estimated that during the study period, nearly 25 percent of pancreatic cancer cases among men and six percent of cases among women could be attributed to smoking. Our findings add to the accumulating evidence linking smoking and pancreatic cancer, and suggest that the rising incidence of this malignancy in Shanghai may be related at least partly to the increasing prevalence of smoking.Dr Ji, formerly with the Shanghai Cancer InstituteDr McLaughlin, formerly with the National Cancer InstituteDr Hatch, formerly with Columbia University     

A prospective study of cigarette tar yield and lung cancer

We examined the relationship of cigarette tar yield and other cigarette-usage characteristics in current smokers to the incidence of lung cancer in a study population of 79,946 Kaiser Permanente Medical Care Program members, aged 30–89 years, who completed a detailed, self-administered, smoking-habit questionnaire during the years 1979 through 1985. Mean length of follow-up was 5.6 years. There were 302 incident lung cancers, of which 89 percent occurred in current or former smokers. The tar yield of the current cigarette brand was unassociated with lung cancer incidence (relative risk [RR]=1.02 per 1 mg tar-yield in men, 95 percent confidence interval [CI]=0.98–1.05; RR=0.99, CI=0.96–1.03 in women). However, in long-term (>20 years) smokers, the risk of lung cancer was decreased in women who had smoked filtered cigarettes for 20 or more years relative to lifelong smokers of unfiltered cigarettes (RR=0.36, CI=0.18–0.75), but not in men who had smoked filtered cigarettes for 20 or more years (RR=1.04, CI=0.58–1.87).Authors are with the Division of Research, Kaiser Permanente Medical Care Program, 3451 Piedmont Avenue, Oakland, CA 94611, USA. Address correspondence to Dr Sidney. This study was funded by grants R01 CA 36074 and R35 CA 49761 from the US National Cancer Institute.     

Lung cancer and women: results of a French case-control study

Ninety-six women with histologically confirmed lung cancer and 192 matched controls were involved in an international case-control study conducted from 1976 to 1980. The aim of this study was an examination of the effects of different smoking habits, especially the type of cigarettes smoked (light or dark tobacco and filter or nonfilter use) on the occurrence of lung cancer in French females. All these patients were either nonsmokers or lifetime cigarette smokers. Matched relative risk (RR) of smokers compared to nonsmokers was found to be increased for both Kreyberg I (RR = 6.6) and Kreyberg II (RR = 2.1) categories; however, this increase was significant (P less than 0.0001) only for Kreyberg I lung cancer. A significant increase (P less than 0.0001) in matched RR was found with early age at first cigarette smoked, daily consumption, duration of smoking, frequency of inhalation, use of dark tobacco and use of nonfilter cigarettes. Matched RR associated with smokers not always using dark tobacco and those smoking only dark tobacco as compared to nonsmokers were significantly increased (trend test P less than 0.0001). On the contrary, the increase of RR was not significant when either daily consumption, or duration of smoking, or age at first cigarette was taken into account. Lung cancer appeared to be associated with daily consumption and use of nonfilter cigarettes in a matched logistic regression.     

Lung cancer and use of cigarettes: a French case-control study

A case-control study of 1,625 cases and 3,091 controls was conducted in France from 1976 to 1980 to compare the effects of different smoking habits, especially the use of filter cigarettes, tobacco types (light or dark), and the use of hand-rolled or manufactured cigarettes on the occurrence of lung cancer. All cases had histologically confirmed lung cancer; the controls were matched by sex, age, hospital of admission, and interviewer. The reported results concern only male nonsmokers and males who smoked (or had smoked) cigarettes exclusively, i.e., a total of 1,217 Kreyberg I and Kreyberg II cancer cases and 1,915 controls. Cigarette smoking was associated with both Kreyberg I and Kreyberg II cell categories although with different relative risks (RR) (17.2 and 3.6, resp.). Within the Kreyberg I category, RR were significantly increased (P less than .0001) with certain indices of duration and intensity of cigarette exposure, such as early age at first cigarette smoked, daily consumption, depth of inhalation, and duration of smoking. A significant difference in risk was found within the Kreyberg I category for nonfilter versus filter cigarette smokers (RR = 18.1 and 10.9, resp.) and dark versus light tobacco smokers (RR = 18.1 and 4.9, resp.) but not for hand-rolled versus manufactured cigarette smokers (RR = 19.8 and 16.0, resp.). When all the covariates were taken into account in a matched logistic regression, lung cancer risks for nonfilter versus filter cigarette smokers was RR = 1.23, for hand-rolled versus manufactured cigarette users RR = 1.22, and for dark versus light tobacco users RR = 1.94.     

A large-scale cohort study on risk factors for primary liver cancer, with special reference to the role of cigarette smoking

A large-scale cohort study in Japan (1966–1982) on life styles and primary liver cancer in men (123 out of 1709273 person-years) revealed a close association with cigarette smoking comparable to that for lung cancer, the relative risk (r.r.) for those smoking 1–29 and 30 or more cigarettes daily being 3.09 (1.78–5.35), 6.83 (3.56–13.10) for liver cancer, and 4.45 (3.77–5.25), 6.80 (5.51–8.41) for lung cancer, respectively. For liver cirrhosis, daily cigarette smoking was of less importance compared to daily alcohol drinking, r.r.=1.17 (1.00–1.36) and 1.82 (1.63–2.04). However, for liver cancer, the risk from daily cigarette smoking was much higher than from daily alcohol drinking, r.r=3.14 (1.82–5.42) and 1.89 (1.40–2.55). The risk of liver cancer among the liver cirrhosis cases was therefore calculated as 2.67 (1.49–4.79) for daily cigarette smokers and 1.00 (0.72–1.38) for daily alcohol drinkers. These results must be of special importance in interpreting the reason for the increasing, unique mortality trend of liver cancer in men in recent years in Japan.     

Risk of hepatocellular carcinoma and habits of alcohol drinking,betel quid chewing and cigarette smoking: a cohort of 2416 HBsAg-seropositive and 9421 HBsAg-seronegative male residents in Taiwan

Objectives: Hepatitis B virus (HBV) is a major cause of hepatocellular carcinoma (HCC) in the world. The specific aim of this study is to assess the associations between the risk of HCC and habits of alcohol drinking, betel quid chewing and cigarette smoking among subjects with and without chronic HBV infection. Methods: A total of 11,837 male residents in Taiwan were recruited in this community-based cohort study. Hepatitis B surface antigen (HBsAg) and antibody against hepatitis C virus (anti-HCV) in serum were determined by enzyme immunoassay, and the habits of alcohol drinking, betel quid chewing and cigarette smoking were collected through standardized personal interview according to a structured questionnaire. During the follow-up period of 91,885 person-years, 115 incident HCC cases were identified through data linkage with national cancer registry profile. The relative risk (RR) of developing HCC for habits of various substance use and chronic HBV infection were estimated by Cox's proportional hazards regression analyses. Results: Significantly increased HCC risk was observed for seropositives of HBsAg or anti-HCV, alcohol drinkers, betel quid chewers and cigarette smokers. There was a significant dose–response relationship between the risk of HCC and the number of habits of substance use. The highest multivariate-adjusted HCC risk was observed among HBsAg-seropositive substance users (RRs: 17.9–26.9), followed by HBsAg-seropositive non-users (RRs: 13.1–19.2), HBsAg-seronegative substance users (RRs: 1.6–2.7) and HBsAg-seronegative non-users (referent with RR = 1). The multivariate-adjusted relative HCC risks for habits of use of various substances were more profound among HBsAg-seronegatives than HBsAg-seropositive ones. Conclusion: Habitual alcohol drinking, betel quid chewing and cigarette smoking are associated with an increased risk of HCC. Abstinence from substance use is important for the prevention of HCC in areas where chronic HBV infection is endemic.     

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.     

Smoking history and survival among lung cancer patients

Two population-based case-control studies of lung cancer were conducred on the Island of Oahu, Hawaii, between 1979 and 1985. Interview information concerning smoking habits and other characteristics was obtained from a total of 463 men and 212 women with histologically confirmed lung cancer. Records from the Hawaii Tumor Registry were revicwed for information on the stage, histology, and follow-up status of these patients. Cigarette smoking was found to be positively related to the age-adjusted risk of death among women (relative risk (RR) -1.6; 95 percent confidence interval (CI)=1.0–2.4), but not among men (RR=0.8; 95 percent CI=0.5–1.2). Among women, the age-adjusted median survival time for never smokers was 33 months (n=53) compared with a median survival of 18 months (n=159) for smokers. Both past and current female smokers were at greater risk of death than never-smokers, and there was a significant trend in the risk of death by the number of cigarettes smoked per day (P=0.04), and the age at which the subjects started smoking (P=0.01). The effects of tumor stage and histology upon the association between tobacco smoking and survival were also explored.Drs Goodman, Kolonel, Wilkins, and Le Marchand are with the Epidemiology Program, Cancer Research Center of Hawaii, University of Hawaii, 1236 Laubela Street, Sulte 407, Honolulu, HI 96813. Dr Yoshizawa was at the Cancer Research Center at the time of the research and now is with Triton Biosciences Inc., Alameda, CA. Address reprint requests to Dr Goodman. This study was supported in part by Public Health Service grants PO1-CA-33619 and RO1-CA-26515, and contract NO1-CN-55424 from the National Cancer Institute, National Institutes of Health, Department of Health and Human Services.     

Tobacco,alcohol, and diet in the etiology of laryngeal cancer: a population-based case-control study

Cancer of the larynx constitutes an increasingly important problem in Polish males during the last 25 years. A population-based case-control study of laryngeal cancer among people under 65 years of age was conducted in Lower Silesia, a province in Southwest Poland, from 1986 to 1987, with 249 newly-diagnosed cancer cases and 965 controls. The estimated relative risk (RR) for smoking and alcohol are both very high: for smoking more than 30 cigarettes, RR=59.7 (95 percent confidence interval [CI]: 13.0–274); for drinking vodka regularly for more than 30 years, RR=10.4 (95 percent CI: 4.0–27.2). Exposures to alcohol and tobacco show a clear multiplicative effect in all categories of exposure. The risk was shown to be reduced by quitting smoking (RR=0.3, 95 percent CI: 0.14–0.64, after 10 years) or by having a history of intermittent smoking. Poor nutrition was also identified as a strong independent risk factor. However, data quality regarding this factor is not as high as for tobacco and alcohol. Smoking alone accounts in this study for an estimated 95.2 percent of all the cases of laryngeal cancer.This work was conducted within the framework of the PR-6 Cancer Control in Poland-National Cancer Program and was supported by the Humboldt Foundation.     

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.     

Cigar, pipe, and cigarette smoking and bladder cancer risk in European men

Objective: Estimating the risk of bladder cancer from cigar and pipe smoking is complicated by a small number of non-cigarette smokers included in most relevant studies. Methods: We undertook a pooled analysis of the data on men from six published case–control studies from Denmark, France, Germany, and Spain, to assess the association between pipe and cigar smoking and bladder cancer, and to compare it with the risk from cigarette smoking. Complete history of tobacco smoking was ascertained separately for cigarettes, cigars, and pipe. Odds ratios (ORs) were estimated after adjusting for age, study, and employment in high-risk occupations. Results: The pooled data set comprised 2279 cases and 5268 controls, of whom 88 cases and 253 controls smoked only cigars or pipe. The OR for pure cigarette smoking was 3.5 (95% confidence interval [CI] 2.9–4.2), that for pure pipe smoking was 1.9 (95% CI 1.2–3.1) and that for pure cigar smoking was 2.3 (95% CI 1.6–3.5). The increase in the OR of bladder cancer that was observed with duration of smoking was non-significantly lower for cigars than for cigarettes. Conclusion: Our results suggest that smoking of cigars and pipe is carcinogenic to the urinary bladder, although the potency might be lower than for cigarettes.