Active and passive smoking and risk of breast cancer by age 50 years among German women

Recent studies suggest that both active and passive smokers have an increased risk of breast cancer compared with women who have never been either actively or passively exposed. Data on lifetime active and passive smoking were collected in 1999-2000 from 468 predominantly premenopausal breast cancer patients diagnosed by age 50 years and 1,093 controls who had previously participated in a German case-control study conducted in 1992-1995. Compared with never active/passive smokers, former smokers and current smokers had odds ratios of 1.2 (95% confidence interval (CI): 0.8, 1.7) and 1.5 (95% CI: 1.0, 2.2), respectively, and ever active smokers had an odds ratio of 1.3 (95% CI: 0.9, 1.9). The risk increased with duration of smoking and decreased after cessation of smoking. Among never active smokers, ever passive smoking was associated with an odds ratio of 1.6 (95% CI: 1.1, 2.4). Exposure to environmental tobacco smoke during childhood or before the first pregnancy did not appear to increase breast cancer risk. At greatest risk were women who had a high level of exposure to both passive and active smoking (odds ratio = 1.8, 95% CI: 1.2, 2.7). This study strengthens the hypothesis of a causal relation between active and passive smoke exposures and breast cancer risk.     

A prospective study of job strain and risk of breast cancer

BACKGROUND: There is conflicting evidence on whether stress is a risk factor for breast cancer. The present study examined prospectively the relationship between stress at work and risk of breast cancer. METHODS: Participants comprised 26 936 postmenopausal women in the Nurses' Health Study ages 46-72 who were in paid employment, and who had no previous history of cancer. Multivariate-adjusted regression analysis was used to examine the relationship between job strain (measured by the Karasek Job Content Questionnaire in 1992) and risk of incident invasive and in situ breast cancer. RESULTS: From 1992 through 1994, 219 women were diagnosed with breast cancer. No evidence was found for a relationship between job stress and risk of breast cancer. Compared with women in low strain jobs, the multivariate-adjusted relative risks of breast cancer were RR = 0.78 (95% CI : 0.52-1.16) for high-strain jobs; RR = 0.76 (95% CI : 0.49-1.17) for active jobs; and RR = 0.94 (95% CI : 0.67-1.34) for passive jobs. Although job strain was related to less breast cancer screening among women in highly demanding jobs, it was not associated with tumour size. CONCLUSIONS: Job stress was not related to an increase in the incidence of breast cancer in the present cohort of nurses.     

Physical activity and risk of cancer in the NHANES I population.

We studied the relation between self-reported physical activity and cancer in the first National Health and Nutrition Examination Survey (NHANES I) cohort, originally examined between 1971-75, and followed prospectively through the Epidemiologic Follow-up Study (NHEFS), conducted between 1982-84. Among 5,138 men and 7,407 women 25-74 years old, for nonrecreational activity we observed increased risk of cancer among inactive individuals compared to very active persons (for men, relative risk [RR] 1.8, 95% confidence interval [CI] = 1.4, 2.4; for women RR 1.3, 95% CI = 1.0, 1.8). These findings were unchanged after adjustment for cigarette smoking, body mass index (BMI), and other potential confounders. Sites which demonstrated stronger inactivity-cancer associations included colorectum (RR 1.6, 95% CI = 0.7, 3.5) and lung (RR 1.6; 95% CI = 1.2, 3.5) among men, and breast (post-menopausal) (RR 1.7; 95% CI = 0.8, 2.9) and cervix (RR 5.2; 95% CI = 1.4, 14.5) among women, although these findings for women were based on relatively few cases. The association between inactivity and cancer was greater among persons of moderate (or lower) BMI, those cases occurring three or more years after baseline, and, in women, those more than 60 years old. In contrast, recreational exercise showed little relation to cancer, with the exception of prostate cancer. The results suggest that inactive individuals are at increased risk of cancer.     

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.     

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.     

Smoking and invasive cervical cancer risk. Results from a case-control study

The association between cigarette smoking and risk of invasive cervical cancer was investigated in a case-control study conducted in four hospitals in Leipzig, German Democratic Republic in 1983-1985. Analyses were based on 225 women aged 64 years or younger with newly diagnosed invasive cervical cancer and 435 age-matched controls with orthopedic or skin diseases. The crude relative risk of invasive cervical cancer was significantly elevated for women who had ever smoked (relative risk (RR) = 1.5, 95% confidence interval (CI) = 1.1-2.1). Adjustment for number of sexual partners reduced the risk to RR = 1.2 (95% CI = 0.8-1.6). Furthermore, the risk for smokers depended significantly on number of sexual partners (p less than 0.05) and was increased only among women with no partner or one partner (RR = 2.7, 95% CI = 1.2-6.1).     

A prospective cohort study of bladder cancer risk in relation to active cigarette smoking and household exposure to secondhand cigarette smoke

Active cigarette smoking is a major risk factor for bladder cancer. Secondhand exposure to cigarette smoke may also contribute to bladder carcinogenesis. The authors conducted a prospective cohort study to examine the influence of both active smoking and household exposure to secondhand smoke (SHS) on subsequent bladder cancer risk. The study population included persons from two cohorts established from private censuses conducted in Washington County, Maryland, in 1963 (n = 45,749; 93 cases) and 1975 (n = 48,172; 172 cases). Poisson regression models were fitted to estimate the relative risk of bladder cancer associated with active and passive smoke exposure in the two cohorts (referent category: never smokers who did not live with any smokers). Current smokers had an elevated risk of bladder cancer in both the 1963 cohort (relative risk (RR) = 2.7, 95% confidence limits (CL): 1.6, 4.7) and the 1975 cohort (RR = 2.6, 95% CL: 1.7, 3.9) after adjustment for age, education, and marital status. Among nonsmoking women, current household SHS exposure was associated with bladder cancer risk in the 1963 cohort (RR = 2.3, 95% CL: 1.0, 5.4) but not in the 1975 cohort (RR = 0.9, 95% CL: 0.4, 2.3). This study further solidifies the evidence that active smoking is causally associated with bladder cancer. Additional studies are needed to determine whether passive smoking is a risk factor for bladder cancer.     

Diesel exhaust exposure and lung cancer: adjustment for the effect of smoking in a retrospective cohort study

BACKGROUND: The extent that cigarette smoking may confound the relationship between diesel exhaust exposure and lung cancer was assessed in a retrospective cohort study of 55,395 U.S. railroad workers followed from 1959 to 1976. METHODS: The relative risk (RR) of lung cancer due to diesel exhaust was indirectly adjusted using job-specific smoking data from a case-control study of railroad workers who died between 1981-1982 and from a survey of 514 living workers from an active railroad in 1982. Adjustment factors were developed based on the distribution of job-specific smoking rates. RESULTS: The unadjusted RR for lung cancer was 1.58 (95% CI = 1.14-2. 20) for workers aged 40-44 in 1959, who experienced the longest possible duration of exposure, and the smoking adjusted RR was 1.44 (1.01-2.05). CONCLUSIONS: After considering differences in smoking rates between workers exposed and unexposed to diesel exhaust in a relatively large blue-collar cohort, there were still elevated risks of lung cancer in workers in jobs with diesel exhaust exposure.     

Operating room nursing and lung cancer risk in a cohort of female registered nurses

OBJECTIVES: Smoke generated during laser surgery and electrocautery contains respiratory irritants and human carcinogens. Although laboratory and animal studies have demonstrated that this smoke has inflammatory and mutagenic potential, no population-based studies of the health effects of exposure to surgical smoke have been published. We examined the association between duration of employment as an operating room nurse, a proxy measure for surgical smoke exposure, and subsequent lung cancer risk. METHODS: This study was conducted among 86 747 women in the Nurses' Health Study. Information on the duration of prior operating room employment was collected in 1984, and the women were followed for incident, confirmed lung cancer. Cox proportional hazards regression was used to model the incidence rate ratio of lung cancer for each exposure category using women with no prior operating room employment for comparison. All of the models were adjusted for age, smoking history, passive smoke exposure, fruit and vegetable consumption, and alpha carotene and lycopene intake. RESULTS: A history of operating room employment was not associated with an increased rate of lung cancer in multivariable analyses [rate ratio (RR) 0.99, 95% confidence interval (95% CI) 0.86-1.15]. In fact, nurses in the highest exposure category, > or =15 years of operating room employment, had a significantly lower rate of lung cancer than nurses with no prior operating room employment (RR 0.58, 95% CI 0.37-0.91), possibly due to confounding by overall health status or residual confounding by smoking history. CONCLUSIONS: Long-term exposure to surgical smoke, as measured by the duration of operating room employment, does not appear to increase the risk of lung cancer.     

Active and passive smoking and risk of colds in women

PURPOSE: To evaluate the association between active and passive smoking and frequency of colds in women. METHODS: Data on cigarette smoking and frequency and duration of colds were analyzed in the Women's Health Study (WHS), a randomized, double-blind, placebo-controlled trial of low-dose aspirin and vitamin E in the primary prevention of cardiovascular disease and cancer among 39,876 female health professionals. RESULTS: After adjustment for age, body-mass index, prevalence of asthma and chronic lung diseases, alcohol intake, physical activity, and multivitamin use, current heavy smokers had no appreciable increase in the frequency of colds (relative risk (RR) for >or= 3 versus no colds in the past year, 1.05; 95% confidence interval (CI), 0.80-1.39), but a significantly increased risk of prolonged colds (RR for colds of > 7 vs. 1-3 days, 2.53; 95% CI, 1.95-3.29). There was no difference in the number of days confined to home. Nonsmoking women passively exposed to cigarette smoke had a slightly increased risk of both more frequent colds (RR, 1.33; 95% CI, 1.18-1.51) and more prolonged colds during the previous year (RR, 1.12; 95% CI, 0.99-1.27). CONCLUSIONS: Women who are currently heavy smokers are at increased risk of having colds with longer duration compared with nonsmokers. Nonsmoking women passively exposed to cigarette smoking are at slightly increased risk of having more frequent and longer colds than nonsmoking women not exposed to passive smoke.     

Risk factors predicting the incidence of second primary breast cancer among women diagnosed with a first primary breast cancer.

This study examined risk factors for development of a contralateral breast cancer among 4,660 US women diagnosed with a first primary breast cancer between 1980 and 1982. The authors believe it to be the first prospective cohort study on this topic that has employed direct patient interviews. All subjects were interviewed within 6 months of the diagnosis of their initial tumor as part of the multi-center, population-based, case-control Cancer and Steroid Hormone Study, and they were followed until the end of 1986 through the Surveillance, Epidemiology, and End Results program. Exclusive of those diagnosed during the initial 6 months after diagnosis of a first primary, 136 second primary breast cancers were identified. Proportional hazards models were used to assess the independent effects of multiple predictors. Specific risk factors evaluated included: age at diagnosis of first primary, exposure to exogenous hormones, menstrual and reproductive histories, tumor characteristics, demographic variables, and treatment modalities. The age-specific incidence rates of second primary breast cancer were higher in all age categories than are the incidence rates of breast cancer in the general population, yet the age at diagnosis of first primary breast cancer was not an important predictor of contralateral breast cancer. The risk of contralateral breast cancer was increased among cohort members who reported a personal history of benign breast biopsy (multivariable-adjusted rate ratio (RR) = 1.69, 95% confidence interval (CI) 1.13-2.53) and in those with an initial tumor that was classified as lobular carcinoma (multivariable-adjusted RR = 1.96, 95% CI 1.17-3.27). Treatment with chemotherapy for the first primary was associated with a lower risk of development of a second breast cancer (multivariable-adjusted RR = 0.56, 95% CI 0.33-0.96), while radiation therapy had little effect on the risk (multivariable-adjusted RR = 1.19, 95% CI 0.78-1.80).     

Is there an association between passive smoking and breast cancer?

Recent epidemiological studies have suggested passive smoking as possible risk factors in breast cancer etiology. However, the evidence is not conclusive. We conducted a meta-analysis of the risk of breast cancer associated with passive smoking. Eleven studies were identified through Medline, Cancer Abstracts and abstract presented at related scientific meetings. Combined estimates of relative risks (RR) were calculated using fixed and random effect models. Significant heterogeneity was detected among the studies (² = 34.6, p < 0.01). The combined estimate of RR for ever exposure to passive smoking was 1.41 (95% confidence interval (CI): 1.14–1.75). The combined estimate for published studies was 1.43 (95% CI: 1.10–1.85). Only two studies reported significant dose-response relation between level of passive smoking and premenopausal breast cancer. Our analysis suggests a possible weak association between passive smoking and breast cancer. More studies are needed to establish whether the observed association is causal.     

The genetic epidemiology of second primary breast cancer.

It is well established that women with a family history of breast cancer run a higher risk of breast cancer than do women without a family history. The evidence, however, is less clear regarding a possible association between a family history of breast cancer and risk of second primaries. The purpose of this prospective study was to estimate the risk for second primary breast cancer associated with having a family history of breast, endometrial, and ovarian cancers. A cohort of 4,660 women with a first primary breast cancer diagnosed between 1980 and 1982 were interviewed as part of the Cancer and Steroid Hormone Study, a multi-center population-based case-control study, and followed through eight Surveillance, Epidemiology, and End Results (SEER) program registries for 4 to 6 years. Of these women, 136 developed a second primary breast cancer in the contralateral breast at least 6 months after diagnosis of the first primary. Cox proportional hazards modeling techniques were used to model the time to onset of second primary breast cancer while adjusting for multiple predictors. The risk of contralateral breast cancer was elevated among cohort members who reported a history of breast cancer in a first-degree relative (multivariable-adjusted rate ratio (RR) = 1.91, 95% confidence interval (CI) = 1.22-2.99). Early age at onset (< 46 years) in the relative further increased the risk of developing contralateral breast cancer (sister: multivariable-adjusted RR = 3.36, 95% CI 1.62-6.98; mother: multivariable-adjusted RR = 2.35, 95% CI 1.02-5.43). Bilateral breast cancer in mothers was also associated with more than a two and a half-fold increase in risk (multivariable-adjusted RR = 2.55, 95% CI 1.02-6.35). The association between family history of breast cancer and risk of contralateral breast cancer did not vary substantially according to age at onset of the first primary breast cancer. The age-adjusted rate ratio for development of a second primary breast cancer among women with a first-degree relative with endometrial cancer was 2.13 (95% CI 1.04-4.35), while the corresponding rate ratio among women with a family history of ovarian cancer was 1.69 (95% CI 0.42-6.83). There was little evidence that age at onset among the relatives with endometrial or ovarian cancer affected the risk. Some of these findings have not been previously reported and need replication in future studies.     

Diabetes mellitus as a predictor of cancer mortality in a large cohort of US adults

Several studies have suggested that diabetes mellitus may alter the risk of developing a variety of cancers, and the associations are biologically plausible. To learn more about the relation between diabetes and cancer mortality, the authors examined associations with selected cancers in a large, prospective US cohort of 467,922 men and 588,321 women who had no reported history of cancer at enrollment in 1982. After 16 years of mortality follow-up, diabetes was significantly associated with fatal colon cancer in men (multivariate relative risk (RR) = 1.20, 95% confidence interval (CI): 1.06, 1.37) and women (RR = 1.24, 95% CI: 1.07, 1.43) and with pancreatic cancer in men (RR = 1.48, 95% CI: 1.27, 1.73) and women (RR = 1.44, 95% CI: 1.21, 1.72). For men, diabetes was significantly associated with liver cancer (RR = 2.19, 95% CI: 1.76, 2.72) and bladder cancer (RR = 1.43, 95% CI: 1.14, 1.80). In addition, diabetes was significantly associated with breast cancer in women (RR = 1.27, 95% CI: 1.11, 1.45). These associations were not explained by high body mass. Our findings suggest that diabetes is an independent predictor of mortality from cancer of the colon, pancreas, female breast, and, in men, of the liver and bladder.     

Incidence of breast cancer in a Norwegian cohort of women with potential workplace exposure to 50 Hz magnetic fields.

BACKGROUND: The risk of breast cancer was investigated in a large dynamic population-based cohort of all 1.1 million economically active women in Norway with potential exposure to 50 Hz magnetic fields at the censuses of 1960, 1970, and 1980. METHODS: The follow-up period for the cohort was 1961-1992. For each woman, date of birth and census information on occupation and socioeconomic status were ascertained. These data were linked to the breast cancer morbidity information in the Cancer Registry of Norway. Exposure to magnetic fields was assessed a priori using two different approaches. In the first approach, hours per week in a potential magnetic field above background level (0.1 microT) were classified by an expert panel. In the second approach, measured magnetic fields from a separate study of men at work were allocated to the women's census job titles. In both approaches, exposure was cumulated over the years of employment (work hours and microT-years, respectively). RESULTS: The Poisson regression analysis showed a risk ratio (RR) of 1.14 (95% confidence interval (CI) = 1.10-1.19) in the highest exposure category compared to the lowest when using the first approach, and the corresponding RR was 1.08 (95% CI = 1.01-1.16) when using the second approach. For women younger than 50 years, RR was 1.20 (95% CI = 1.11-1.29) and 1.12 (95% CI = 0.98-1.28), respectively. CONCLUSIONS: The results give some support to the hypothesis that exposure to 50 Hz magnetic fields may increase the risk of breast cancer. However, since no direct information on exposure was available, no firm conclusions can be drawn.     

Meta-analysis of studies of passive smoking and lung cancer: effects of study type and continent

BACKGROUND: To calculate a pooled estimate of relative risk (RR) of lung cancer associated with exposure to passive smoking in never smoking women exposed to smoking spouses. This study is an updated meta-analysis that also assesses the differences between estimated risks according to continent and study type using meta-regression. METHODS: From a total of 101 primary studies, 55 studies are included in this meta-analysis, of which, 7 are cohort studies, 25 population-based case-control and 23 non-population-based case-control studies. Twenty previously published meta-analyses are also reviewed. Fixed and random effect models and meta-regression are used to obtain pooled estimates of RR and P-value functions are used to demonstrate consistency of results. RESULTS: The pooled RR for never-smoking women exposed to passive smoking from spouses is 1.27 (95% CI 1.17-1.37). The RR for North America is 1.15 (95% CI 1.03-1.28), Asia, 1.31 (95% CI 1.16-1.48) and Europe, 1.31 (1.24-1.52). Sequential cumulative meta-analysis shows no trend. There is no strong evidence of publication bias. CONCLUSIONS: The abundance of evidence, consistency of finding across continent and study type, dose-response relationship and biological plausibility, overwhelmingly support the existence of a causal relationship between passive smoking and lung cancer.     

Interaction between smoking and obesity and the risk of developing breast cancer among postmenopausal women: the Women's Health Initiative Observational Study

Obesity is a well-established risk factor for postmenopausal breast cancer. Recent studies suggest that smoking increases the risk of breast cancer. However, the effect of co-occurrence of smoking and obesity on breast cancer risk remains unclear. A total of 76,628 women aged 50-79 years enrolled in the Women's Health Initiative Observational Study were followed through August 14, 2009. Cox proportional hazards regression models were used to estimate hazard ratios and 95% confidence intervals. Over an average 10.3 years of follow-up, 3,378 incident cases of invasive breast cancer were identified. The effect of smoking on the risk of developing invasive breast cancer was modified significantly by obesity status among postmenopausal women, regardless of whether the obesity status was defined by body mass index (P(interaction) = 0.01) or waist circumference (P(interaction) = 0.02). A significant association between smoking and breast cancer risk was noted in nonobese women (hazard ratio = 1.25, 95% confidence interval: 1.05, 1.47) but not in obese women (hazard ratio = 0.96, 95% confidence interval: 0.69, 1.34). In conclusion, this study suggests that the effect of smoking exposure on breast cancer risk was modified by obesity among postmenopausal women. The modification effect did not differ by general versus abdominal obesity.     

Second primary cancers following anal and cervical carcinoma: evidence of shared etiologic factors.

The authors examined the incidence of second primary cancers occurring after cervical and anal cancer. Data from the Connecticut Tumor Registry for 1935-1988 and eight other US tumor registries for 1973-1988 were used. Women with primary invasive cervical cancer had a relative risk of 4.6 (95% confidence interval (CI) 2.4-8.1) for subsequent invasive anal cancer. Increased relative risks after cervical cancer were also found for cancers of the oral cavity (relative risk (RR) = 2.2), stomach (RR = 1.5), rectum (RR = 1.4), larynx (RR = 3.4), lung (RR = 3.0), vagina (RR = 5.6), bladder (RR = 2.7), for kidney (RR = 1.9); decreased relative risks were noted for melanoma (RR = 0.5) and breast cancer (RR = 0.8). Patients with a primary diagnosis of anal cancer had relative risks for subsequent invasive and in situ cervical cancer of 1.3 (95% CI 0.2-4.5) and 3.4 (95% CI 0.9-8.8), respectively. Anal cancer was also associated with increased relative risks of subsequent lung (RR = 2.5) and prostate (RR = 1.8) cancers, whereas the relative risk of uterine cancer was 0.2 (95% CI 0.0-0.9). These findings support other evidence for common factors, such as human papillomavirus infection and cigarette smoking, in the etiology of cervical and anal cancer.     

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.     

中国非吸烟女性肺癌危险因素的病例-对照研究

目的探讨中国非吸烟女性患肺癌的危险因素。方法应用1∶2配对的病例对照方法,收集2001年9月~2004年2月在北京、上海和成都指定医院经病理诊断确诊的非吸烟女性新发肺癌住院病例157例,按照性别、年龄(±2岁)、不吸烟等配对因素选取医院对照和人群对照。利用统一调查表对调查对象进行面对面问卷调查,收集病例和对照有关危险因素的暴露史等情况。通过单因素分析和多因素条件Logistic回归分析筛选肺癌的主要危险因素。结果单因素分析发现28个暴露因素与非吸烟女性肺癌发生有关。多因素分析发现,被动吸烟指数≥50人年(OR=1·77,95%CI为1·07~2·92)、经常吃动物内脏(OR=1·85,95%CI为1·06~3·22)、职业接触粉尘(OR=2·47,95%CI为1·21~5·03)和工作场所通风不良(OR=4·02,95%CI为1·74~9·29)为非吸烟女性肺癌发生的危险因素;常吃蔬菜(OR=0·26,95%CI为0·12~0·59)、经常服用维生素(OR=0·53,95%CI为0·30~0·93)、结婚后家庭人均月收入≥500元(OR=0·50,95%CI为0·28~0·91)和初次生育年龄在24~30岁之间(OR=0·53,95%CI为0·32~0·90)为非吸烟女性肺癌发生的保护因素。趋势性检验发现,被动吸烟与非吸烟女性发生肺癌的相对危险度之间存在一定剂量反应关系。结论被动吸烟、职业接触粉尘、经常吃动物内脏和工作场所通风不良会增加非吸烟女性患肺癌的危险性。常吃蔬菜和经常服用维生素等因素可以降低非吸烟女性发生肺癌的危险性。