Breast cancer and cigarette smoking: a hypothesis

In many studies, cigarette smoking has been associated with a small increase in breast cancer risk. The authors evaluated the relation of smoking to breast cancer risk in two case-control studies carried out from 1982 through 1986. In Canada, 607 women with breast cancer and 1,214 controls matched on decade of age and neighborhood were interviewed at home. In the United States, 1,955 cases of breast cancer and 805 controls with other cancers were interviewed in the hospital. In both studies, breast cancer risk was associated weakly with cigarette smoking overall. The odds ratio for women who had smoked 25 or more cigarettes per day as compared with never smokers was 1.2 (95% confidence interval (CI) 0.9-1.6) in the Canadian study and 1.2 (95% Cl 0.9-1.6) in the US study. In both studies, breast cancer risk was more strongly related to commencement of smoking at a young age. Among women who smoked at least 25 cigarettes per day in the most recent year of smoking, the odds ratios for commencement before age 16 years were 1.7 (95% Cl 1.0-2.9) in the Canadian data and 1.8 (95% Cl 1.0-3.4) in the US data, and the odds ratios for commencement at even younger ages were higher. The associations were not explained by duration of smoking, by the time elapsed since commencement, or by factors associated with cigarette smoking such as alcohol consumption or oral contraceptive use. Our findings raise the hypothesis that exposure to cigarette smoke during adolescence may increase a woman's risk of breast cancer. The hypothesis has biologic plausibility: cigarette smoke contains known carcinogens, and the developing breast is especially susceptible to cancer initiation.     

Active cigarette smoking, household passive smoke exposure, and the risk of developing pancreatic cancer

OBJECTIVE: The objective of this study was to examine the association between active cigarette smoking, household passive smoke exposure, and pancreatic cancer risk using a prospective cohort design. METHODS: Two cohorts were established in Washington County, Maryland in 1963 (n = 45,749) and 1975 (n = 48,172). The Washington County Cancer Registry was used to ascertain the occurrence of pancreatic cancer in the 1963 cohort from 1963-1978 and in the 1975 cohort from 1975-1994. Poisson regression was used to analyze the associations between active smoking and household passive smoke exposure and pancreatic cancer risk. RESULTS: Current active smoking was associated with a two-fold increased risk of pancreatic cancer in both cohorts. Among never-smokers in each cohort, exposure to household passive smoke was not associated with an increased risk of pancreatic cancer, although the confidence limits were wide due to a small number of cases. CONCLUSIONS: This study further documents the approximate doubling of pancreatic cancer risk in current active smokers. Our results also indicate that household passive smoke exposure is not associated with pancreatic cancer risk, although our risk estimates lacked precision.     

Women, smoking, cigarette advertising and cancer

Cigarette smoking is a major cause of cancer in women, accounting for about one-fourth of their estimated 219,000 cancer deaths per year. Cigarette smoking specifically increases a woman's risk of developing cancer of the lung, larynx, esophagus, oral cavity, pancreas, kidney, bladder, and possibly uterine cervix. During the past twenty years, concerted efforts have been made by the tobacco industry to increase sales to women. Strategies have included development of "feminine" brands such as Virginia Slims, slick media campaigns portraying smoking as elegant and glamorous, and sponsorship of fashion, women's sports events, and even medical programs. Reversal of these alarming trends requires that women as well as men recognize the role of cigarette smoking in cancer causation, and support programs which promote non-smoking as well as combat the influence of the tobacco industry on women's smoking behavior.     

Menthol cigarette smoking and oesophageal cancer

Oesophageal cancer incidence and mortality among American blacks is over three times the rate for whites. Between 1950 and 1977 the age-adjusted oesophageal cancer mortality rate approximately doubled in non-whites while remaining virtually unchanged in whites. Between World War II and the 1970s menthol cigarette sales dramatically increased, roughly paralleling the increase in oesophageal cancer among blacks. The present study uses existing data from a large hospital-based case-control study to test whether menthol cigarette smoking is related to oesophageal cancer. Oesophageal cancer cases were current smokers. Controls were matched to the cases on age (+/- 5 years) and sex, had conditions thought not to be related to tobacco use, and were also current smokers. Tabular analyses showed no change in risk for males ever-smoking menthol versus those never smoking menthol cigarettes. For women, however, there was an increased risk. Results of logistic regression analyses performed to account for potential confounding factors showed a marginally significant (P = 0.08) decrease in risk among male short term (less than 10 years) menthol smokers versus male never-menthol smokers (OR = 0.50, 95% Cl: 0.23-1.07) but no increased risk for menthol smoking of longer duration. Duration of menthol smoking fitted as a continuous variable showed no increased risk (P = 0.9) after accounting for non-menthol cigarette smoking duration (about 2% per year increase, P = 0.02). For females, the logistic analysis produced a marginally significant (P = 0.07) increased risk for longer menthol use (OR = 2.30, 95% Cl: 0.93-5.72).(ABSTRACT TRUNCATED AT 250 WORDS)     

Household exposure to passive cigarette smoking and serum micronutrient concentrations

BACKGROUND: The associations observed between passive smoking and adverse health outcomes have generated controversy. In part, this could be because the diets of passive smokers, like those of active smokers, differ from those of persons who are not exposed to cigarette smoke, especially with regard to antioxidants. OBJECTIVE: Our objective was to assess the relation between household exposure to passive smoking and serum concentrations of retinol, tocopherols, and carotenoids. DESIGN: A cross-sectional study was conducted in Washington County, MD, to compare exposure to passive smoking at home, recorded in a private census of county residents in 1975, with micronutrient concentrations assayed in serum collected in 1974. This comparison was possible for 1590 control subjects in nested case-control studies conducted between 1986 and 1998. RESULTS: Among persons who were not current smokers, those who lived with smokers tended to have lower serum total carotenoid, alpha-carotene, ss-carotene, and cryptoxanthin concentrations than did those who lived in households with no smokers. There was little evidence that exposure to passive smoking was associated with reduced serum concentrations of lutein and zeaxanthin, lycopene, retinol, alpha-tocopherol, or gamma-tocopherol. CONCLUSIONS: Among nonsmokers, exposure to passive smoking tended to be associated with lower serum concentrations of the carotenoids most strongly associated with active smoking (total carotenoids, alpha-carotene, ss-carotene, and cryptoxanthin). The associations were weaker for passive smoking than for active smoking. The consistency of the associations observed for active and passive smoking indicates that exposure to passive smoking may result in decreased circulating concentrations of selected micronutrients.     

Bladder cancer and black tobacco cigarette smoking

A retrospective study was planned in the Hérault (Mediterranean) region of France where bladder cancer mortality and incidence rates are high. In the present paper, variations in bladder cancer risk according to various smoking-related variables, in particular time of exposure and type of tobacco, are examined. This case-control study with 219 male incident cases and 794 male population controls randomized from electoral rolls was carried out in 1987–89. Trained interviewers obtained information on demographics, dietary habits (coffee, alcohol, artificial sweeteners, vegetables, spices, etc.), occupational exposures and detailed history of tobacco smoking (average number of cigarettes per day, number of years of smoking, age at which they began and/or quitted smoking, use of filter-tip and type of tobacco). The odds ratio (OR) for cigarette smokers versus non-smokers was greater than 5. Results for number of cigarettes daily, duration of smoking and lifetime smoking showed a highly significant dose-response relationship, which was confirmed when these variables were treated as continuous in a logistic regression model. Eighty-eight percent of the smokers used black tobacco. Quitting smoking did not result in a significant reduction in bladder cancer risk. Higher risks were associated with starting to smoke at an early age (OR before age 13 versus after age 21=3.42; 95% CI 1.07–10.9) and with black tobacco smoking (OR black versus blond =1.63; 95% CI 0.73–3.64). Results suggest that black tobacco may be more harmful than blond tobacco and may have an early non-reversible role in bladder carcinogenesis.     

Breast cancer and active and passive smoking: the role of the N-acetyltransferase 2 genotype

The association of breast cancer with passive and active smoking was investigated in slow and fast acetylators of aromatic amines in a Geneva, Switzerland, study in 1996-1997. A slow acetylator was homozygous for one, or heterozygous for two, of three N-acetyltransferase 2 (NAT2) polymorphisms determined on buccal cell DNA from 177 breast cancer cases and 170 age-matched, population controls. The reference group consisted of women never regularly exposed to active or passive smoke. Among premenopausal women, the odds ratios were homogeneous in slow and fast acetylators: 3.2 (95% confidence interval (CI): 1.2, 8.7) for passive smoking and 2.9 (95% CI: 1.1, 7.5) for active smoking. Among postmenopausal women, the odds ratios for fast acetylators were 11.6 (95% CI: 2.2, 62.2) for passive and 8.2 (95% CI: 1.4, 46.0) for active smoking; the corresponding effects were also apparent but less strong in slow acetylators. After the nonexposed and the passive smokers were grouped in a single reference category, active smoking was associated with postmenopausal breast cancer in slow acetylators (odds ratio (OR) = 2.5, 95% CI: 1.0, 6.2) but not in fast acetylators (OR = 1.3, 95% CI: 0.5, 3.3). Thus, the associations of both passive and active smoking with breast cancer appear stronger in fast than in slow NAT2 genotypes. Separating passive smokers from the nonexposed impacts on the inference about a possible NAT2-smoking interaction.     

吸烟、被动吸烟与肺癌发病风险的病例对照研究

目的 探讨吸烟、被动吸烟与肺癌的关联.方法 采用病例对照研究设计,面访肺癌新发病例1 303例和按性别、年龄(±2岁)频数匹配的健康对照1 303例.结果 吸烟是男性肺癌的重要危险因素(调整OR=4.974,95％ CI:3.933 ～6.291),随着开始吸烟年龄提前、吸烟年限延长、日吸烟量、吸烟包年以及吸烟深度的增加,患肺癌危险性增高,呈剂量反应关系(Ptrend＜0.001),戒烟≥10年患肺癌的危险性降低45.4％.男性吸烟患肺鳞癌的危险性比患肺腺癌大.被动吸烟是非吸烟者肺癌的危险因素(调整OR=1.912,95％CI:1.486～2.460),工作环境被动吸烟的男性非吸烟者患肺癌的调整OR为2.221(95％CI:1.361 ～3.625),家庭环境被动吸烟的女性非吸烟者患肺癌的调整OR为1.804(95％ CI:1.270～2.562).68.04％男性肺癌的发生可归因于吸烟,26.51％非吸烟者肺癌的发生可归因于被动吸烟.结论 吸烟是肺癌的重要危险因素,工作环境被动吸烟是男性非吸烟者肺癌的主要危险因素,家庭环境被动吸烟是女性肺癌的主要危险因素.戒烟具有重大的公共卫生学意义.     

Active and passive cigarette smoke and breast cancer survival

PURPOSE: The association between active and passive cigarette smoking before breast cancer diagnosis and survival was investigated among a cohort of invasive breast cancer cases (n = 1273) participating in a population-based case-control study. METHODS: Participants diagnosed with a first primary breast cancer between August 1, 1996, and July 31, 1997, were followed-up until December 31, 2002, for all-cause mortality (n = 188 deaths), including breast cancer-specific mortality (n = 111), as reported to the National Death Index. RESULTS: In Cox models, the adjusted hazards ratios (HRs) for all-cause mortality were slightly higher among current and former active smokers, compared with never smokers (HR, 1.23; 95% confidence interval [95% CI], 0.83-1.84) and 1.19 (95% CI, 0.85-1.66), respectively). No association was found between active or passive smoking and breast cancer-specific mortality. All-cause and breast cancer-specific mortality was higher among active smokers who were postmenopausal (HR, 1.64; 95% CI, 1.03-2.60 and HR, 1.45; 95% CI, 0.78-2.70, respectively) or obese at diagnosis (HR, 2.10; 95% CI, 1.03-4.27 and HR, 1.97; 95% CI, 0.89-4.36, respectively). Associations between smoking and all-cause and breast cancer-specific mortality did not differ by cancer treatment. CONCLUSIONS: These data do not provide strong evidence for an association between smoking and all-cause or breast cancer-specific mortality, although smokers who are postmenopausal or obese at diagnosis may be at higher risk.     

A prospective cohort study of rectal cancer risk in relation to active cigarette smoking and passive smoke exposure

PURPOSE: The present investigation prospectively examined active cigarette smoking and household passive smoke exposure and the risk of developing rectal cancer. METHODS: Cigarette smoking data were collected on all household members during two private censuses in Washington County, Maryland. These two cohorts were followed up, one cohort from 1963-1978 and the other from 1975-1994 for first-time diagnoses of rectal cancer. We identified 148 and 169 rectal cancer cases in the 1963 and 1975 cohorts, respectively. Relative risks were estimated by means of Poisson regression models. RESULTS: In men, the adjusted relative risks (aRR) and 95% confidence intervals (CI) for the association between current smoking and rectal cancer were 3.1 (1.2-7.8) in the 1963 cohort and 1.8 (0.9-3.7) in the 1975 cohort; the corresponding aRRs in women were 0.9 (0.5-1.8) and 1.6 (0.9-3.8) in the 1963 and 1975 cohorts, respectively. In nonsmokers, household passive smoke exposure was strongly associated with rectal cancer among men in the 1963 cohort (aRR = 5.8; 1.8-18.4) but not the 1975 cohort (aRR = 1.1; 0.2-5.0). In women, household passive exposure was not strongly associated with rectal cancer in either cohort. CONCLUSIONS: The results of our study suggest that active cigarette smoking may contribute to rectal cancer risk, but inconsistencies in the findings preclude drawing strong, clear-cut inferences.     

CYP1A1, cigarette smoking, and colon and rectal cancer

Cytochrome P-450 (CYP) is involved in the activation and metabolism of polycyclic aromatic hydrocarbons in tobacco products. The authors evaluated the association of two polymorphisms in the CYP1A1 gene--the noncoding Msp I polymorphism in the 3'-untranslated region and the Ile462Val polymorphism in exon 7--with colon and rectal cancer. The authors used data from two incident case-control studies of colon cancer (1,026 cases and 1,185 controls) and rectal cancer (820 cases and 1,036 controls) conducted in California and Utah (1991-2002). CYP1A1 genotype was not associated with colon or rectal cancer. Having GSTM1 present, a CYP1A1 variant allele, and the rapid-acetylator NAT2 imputed phenotype was associated with increased risk of colon cancer (odds ratio = 1.7, 95% confidence interval: 1.2, 2.3). Among men, the greatest colon cancer risk was observed for having any CYP1A1 variant allele and currently smoking (odds ratio = 2.5, 95% confidence interval: 1.3, 4.8; Wald chi(2)test: p < 0.01). Assessment of GSTM1 and CYP1A1 and rectal cancer in men showed a twofold elevation in risk for more than 20 pack-years of smoking, except among those with GSTM1 present who had a variant CYP1A1 allele. These data support the association between smoking and colon and rectal cancer. Smoking may have a greater impact on colorectal cancer risk based on CYP1A1 genotype; this might further be modified by GSTM1 for rectal cancer risk.     

Quantitative aspects of passive smoking and lung cancer

The exposure of passive smokers to cigarette smoke is estimated to be equivalent to 0.1-1.0 cigarette/day actively smoked. According to the reported relationships of dose and time, lung cancer incidence and other relative risk figures relating to nonsmokers have been calculated for ages 40, 50, 60, 70, and 79. Risks for smokers with a daily consumption of 0.1-1.0 cigarette were found to be in the range of R = 1.03 to 1.36. As it applies to passive smokers, this range of exposure may be neglected because it has no major effect on lung cancer incidence. The results of four previous studies dealing with passive smoking and lung cancer are compared with the current calculated risks, and the differences are discussed.     

The influence of maternal cigarette smoking, snuff use and passive smoking on pregnancy outcomes: the Birth To Ten Study

This article describes the patterns and effects of maternal snuff use, cigarette smoking and exposure to environmental tobacco smoke during pregnancy on birthweight and gestational age, in women living in Johannesburg and Soweto in 1990. A cohort of 1593 women with singleton live births provided information about their own and household members' usage of tobacco products during pregnancy. The women completed a questionnaire while attending antenatal services. Data on gestational age and birthweight were obtained from birth records. Women who smoked cigarettes or used snuff during pregnancy accounted for 6.1% and 7.5% of the study population respectively. The mean birthweight of non-tobacco users was 3148 g [95% CI 3123, 3173] and that of the smokers 2982 g [95% CI 2875, 3090], resulting in a significantly lower mean birthweight of 165 g for babies of smoking mothers (P = 0.005). In contrast, women using snuff gave birth to infants with a mean birthweight of 3118 g [95% CI 3043, 3192], which is a non-significant (P = 0.52) decrease (29.4 g) in their infants' birthweights compared with those not using tobacco. A linear regression analysis identified short gestational age, female infant, a mother without hypertension during pregnancy, coloured (mixed racial ancestry), and Asian infants compared with black infants, lower parity, less than 12 years of education and smoking cigarettes as significant predictors of low birthweight, while the use of snuff during pregnancy was not associated with low birthweight. The snuff users, however, had a significant shorter gestational age than the other two groups of women. The birthweight reduction adjusted for possible confounders was 137 g [95% CI 26.6, 247.3 (P = 0.015)] for cigarette smokers and 17.1 g [95% CI -69.5, -102.7, P = 0.69] for snuff users respectively, compared with the birthweight of non-tobacco users. Among women who did not smoke cigarettes or use snuff, exposure to environmental tobacco smoke did not result in significant effects on the birthweight of their infants. In conclusion, infants of cigarette smokers had significantly lower birthweights than those of non-tobacco users or snuff users who are exposed to nicotine during pregnancy. Passive smoking did not affect birthweight significantly in this population.