Genetic variation in myeloperoxidase modifies the association of serum α-tocopherol with aggressive prostate cancer among current smokers

We investigated associations of serum α- and γ-tocopherols and their effect modification by polymorphisms in oxidative stress regulatory enzymes in relation to prostate cancer risk. In a nested case-control study in the Carotene and Retinol Efficacy Trial, prerandomized serum α- and γ-tocopherol were assayed among 684 men with incident prostate cancer [375 nonaggressive and 284 aggressive cancer (stage III/IV or Gleason score ≥7)] and 1441 controls. Manganese superoxide dismutase Ala-16Val (rs4880), glutathione peroxidase 1 Pro200Leu (rs1050450), catalase -262 C > T (rs1001179), and myeloperoxidase (MPO) G-463A (rs2333227) were genotyped. A multivariate-adjusted inverse association of serum α-tocopherol with total prostate cancer risk was observed in current smokers (OR = 0.62, 95% CI = 0.40-0.96, 4th vs. 1st quartiles). High (≥median) compared to low serum concentrations of α- and γ-tocopherol were inversely associated with aggressive prostate cancer in current smokers (OR = 0.50, 95% CI = 0.32-0.78 and OR = 0.64, 95% CI = 0.43-0.95, respectively). The association was stronger among those with MPO G/A+A/A genotypes. Among current smokers with low serum α-tocopherol concentrations, MPO G/A+A/A, the genotypes downregulating oxidative stress, were associated with an increased risk for aggressive prostate cancer (OR = 2.06, 95% CI = 1.22-3.46). Conversely, current smokers with these genotypes who had high α-tocopherol concentrations had a reduced risk for aggressive prostate cancer (OR = 0.34, 95% CI = 0.15-0.80; P-interaction = 0.001). In conclusion, among current smokers, both high serum α- and γ-tocopherol concentrations were associated with reduced risks of aggressive prostate cancer. The α-tocopherol-associated risks are modified by polymorphism in MPO G-463A.     

中国六城市女性生理生育因素与乳腺癌关系的病例对照研究

目的研究城市女性乳腺癌的危险因素,探讨城市女性生理生育因素的变化与城市女性乳腺癌发病的关联强度,促进乳腺癌的预防和控制。方法采用病例对照的研究方法,新发病例通过北京、天津、上海、重庆、武汉、广州六城市的乳腺癌监测点确定,对照从当地正常人群数据库中随机抽样,对收集到3332对1：1年龄配对的病例和对照进行问卷调查。通过条件Logistic模型进行相对危险度及剂量-反应效应估计。结果在调整年龄、职业、饮食等因素后,城市女性中乳腺癌发病的危险因素为初潮年龄的提前（≤14岁,OR=1.37,95％CI=1.12－1.66）、月经持续天数长（〉7天,OR=1.18,95％ CI=1.00－1.38）、有痛经（OR=1.21,95％ CI=1.03－1.42）、结婚晚（≥28岁,OR：2.13,95％ CI=1.63－2.79）、首次怀孕晚（≥30岁,OR=2.13,95％CI=1.63－2.79）等,而保护性因素有月经间隔天数长（ 〉28天,OR=0.81,95％ CI=0.68－0.95）、绝经年龄早（≤45岁,OR=0.58,95％ CI=0.47－0.72）、怀孕次数多（≥2次,OR=0.67,95％ CI=0.45－0.99）,哺乳（≥4个月,OR=0.70,95％CI：0.60－0.83）。结论女性生理生育因素是影响城市女性乳腺癌发病的主要危险因素,可部分解释中国城市女性乳腺癌呈逐年上升趋势的原因。     

Insulation,asbestos, smoking habits,and lung cancer cell types

The association between occupational exposure to asbestos and histological type of lung cancer was analyzed in a multicenter hospital-based case-control study (2,871 male cases and 5,240 male controls) conducted from 1981-1991. Twenty-two percent of cases and 18% of controls were employed in asbestos-related occupations for at least 1 year. Most of these asbestos jobs were in the construction field. The odds ratio (OR) among current smokers was 1.0 [95% confidence intervals (CI) 0.9 to 1.3]; for ex-smokers, the OR was 1.4 (95% CI 1.1 to 1.6). In contrast, 10% of cases and 5% of controls self-reported that they were chronically exposed to asbestos for at least 1 year. Self-reported asbestos exposure was significantly related to all lung cancer cell types among smokers and ex-smokers, although a trend in the ORs with duration of self-reported exposure was not found for current smokers. Among 48 cases and 52 controls reporting distinct exposure to building insulation, the OR was 2.2 (95% CI 1.2 to 4.3) for current smokers, and 1.8 (95% CI 0.9 to 3.6) for ex-smokers, compared to subjects who were not exposed to building insulation and asbestos. A nonsignificant association with self-reported exposure to asbestos was observed for a small number of never smokers (eight of 83 nonsmoking cases, OR = 2.0, 95% CI 0.9 to 4.6). When examining these results and their causal implications, possible misclassification and reporting biases need to be considered.     

Body mass index and waist circumference in relation to lung cancer risk in the Women's Health Initiative

Investigators in several epidemiologic studies have observed an inverse association between body mass index (BMI) and lung cancer risk, while others have not. The authors used data from the Women's Health Initiative to study the association of anthropometric factors with lung cancer risk. Over 8 years of follow-up (1998-2006), 1,365 incident lung cancer cases were ascertained among 161,809 women. Cox proportional hazards models were used to estimate hazard ratios adjusted for covariates. Baseline BMI was inversely associated with lung cancer in current smokers (highest quintile vs. lowest: hazard ratio (HR) = 0.62, 95% confidence interval (CI): 0.42, 0.92). When BMI and waist circumference were mutually adjusted, BMI was inversely associated with lung cancer risk in both current smokers and former smokers (HR = 0.40 (95% CI: 0.22, 0.72) and HR = 0.61 (95% CI: 0.40, 0.94), respectively), and waist circumference was positively associated with risk (HR = 1.56 (95% CI: 0.91, 2.69) and HR = 1.50 (95% CI: 0.98, 2.31), respectively). In never smokers, height showed a borderline positive association with lung cancer. These findings suggest that in smokers, BMI is inversely associated with lung cancer risk and that waist circumference is positively associated with risk.     

Tetrachloroethylene-contaminated drinking water in Massachusetts and the risk of colon-rectum, lung, and other cancers

We conducted a population-based case-control study to evaluate the relationship between cancer of the colon-rectum (n = 326), lung (n = 252), brain (n = 37), and pancreas (n = 37), and exposure to tetrachloroethylene (PCE) from public drinking water. Subjects were exposed to PCE when it leached from the vinyl lining of drinking-water distribution pipes. Relative delivered dose of PCE was estimated using a model that took into account residential location, years of residence, water flow, and pipe characteristics. Adjusted odds ratios (ORs) for lung cancer were moderately elevated among subjects whose exposure level was above the 90th percentile whether or not a latent period was assumed [ORs and 95% confidence intervals (CIs), 3.7 (1.0-11.7), 3.3 (0.6-13.4), 6.2 (1.1-31.6), and 19.3 (2.5-141.7) for 0, 5, 7, and 9 years of latency, respectively]. The adjusted ORs for colon-rectum cancer were modestly elevated among ever-exposed subjects as more years of latency were assumed [OR and CI, 1.7 (0.8-3.8) and 2.0 (0.6-5.8) for 11 and 13 years of latency, respectively]. These elevated ORs stemmed mainly from associations with rectal cancer. Adjusted ORs for rectal cancer among ever-exposed subjects were more elevated [OR and CI, 2.6 (0. 8-6.7) and 3.1 (0.7-10.9) for 11 and 13 years of latency, respectively] than were corresponding estimates for colon cancer [OR and CI, 1.3 (0.5-3.5) and 1.5 (0.3-5.8) for 11 and 13 years of latency, respectively]. These results provide evidence for an association between PCE-contaminated public drinking water and cancer of the lung and, possibly, cancer of the colon-rectum.     

Higher eating frequency,but not skipping breakfast,is associated with higher odds of abdominal obesity in adults living in Puerto Rico

Puerto Ricans have a high prevalence of obesity, yet little information is available regarding its association with eating patterns in this population. We hypothesized that higher eating frequency and skipping breakfast would be associated with increased odds of abdominal obesity among adults living in Puerto Rico (PR). In a cross-sectional study of adults living in PR aged 30-75 years (N = 310), participants reported their frequency of eating meals per day including snacks and breakfast. Trained interviewers measured waist (WC) and hip circumferences. We calculated the waist-to-hip ratio (WHR) dividing the waist by the hip measurement. Abdominal obesity was defined as either high WC (men ≥94 cm; women ≥80 cm) or high WHR (men ≥0.90; women ≥0.85). We used logistic regression models to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs) to assess the association of eating frequency (≤1.5; 1.5-3; ≥3 times/day) and breakfast consumption (vs none) with abdominal obesity. Models were adjusted for age, sex, income, smoking, physical activity, TV watching, energy intake, diet quality, and eating frequency (only for breakfast consumption). Most participants consumed breakfast (70%), ate 1.5-3 times/d (47%), and had high WC (75%) and WHR (77%). Participants who ate 1.5-3 (OR: 2.75, 95% CI: 1.23-6.15) and ≥3 times/day (OR: 2.88; 95% CI: 1.14-7.31) were more likely to have high WC compared with participants who ate ≤1.5 times/d (P trend = .04). Breakfast consumption was not associated with abdominal obesity. In conclusion, higher eating frequency, but not skipping breakfast, is associated with abdominal obesity among adults in PR. Consuming less frequent meals may help prevent abdominal obesity in this population.     

Lung cancer and occupation: results of a multicentre case-control study.

The objective of the current study was to estimate the risk of lung cancer attributable to occupational factors and not due to tobacco. At 24 hospitals in nine metropolitan areas in the United States, 1793 male lung cancer cases were matched for race, age, hospital, year of interview, and cigarette smoking (never smoker, ex-smoker, smoker (1-19 and > or = 20 cigarettes per day)) to two types of controls (cancer and non-cancer hospital patients). Information on usual occupation, exposure to specific potential carcinogens, and cigarette smoking was obtained by interview. Risk of lung cancer was increased significantly for electricians; sheetmetal workers and tinsmiths; bookbinders and related printing trade workers; cranemen, derrickmen, and hoistmen; moulders, heat treaters, annealers and other heated metal workers; and construction labourers. All of these occupations are potentially exposed to known carcinogens. Odds ratios (ORs) were increased for exposure to coal dust (adjusted OR = 1.5; 95% confidence interval (95% CI) 1.1-2.1). After stratification, this association was statistically significant only after 10 or more years of exposure. Lung cancer was also related to exposure to asbestos (adjusted OR = 1.8; 95% CI 1.5-2.2). The ORs increased with increasing duration of exposure to asbestos for all smoking categories except for current smokers of 1-19 cigarettes per day. The statistical power to detect ORs among occupations that were previously reported to be at increased risk of lung cancer but that failed to show an OR of at least 1.5 in the current study was small. The cumulative population attributable risk (PAR) of lung cancer due to occupation was 9.2%. It is concluded that occupational factors play an important part in the development of lung cancer independently of cigarette smoking. Because occupations at high risk of lung cancer were under-represented, the cumulative PAR of the present study is likely to be an underestimate of the true contribution of occupation to risk of lung cancer.     

Serum carotenoids are associated with increased lung cancer risk among alcohol drinkers, but not among non-drinkers in a cohort of tin miners

To examine the association between pre-diagnostic serum carotenoid levels and lung cancer risk and the effects of alcohol intake on the carotenoid-lung cancer relationship, we conducted a case-control study in an occupational cohort from the Yunnan Tin Corporation in China. During 6 years of follow-up, 339 cases of confirmed lung cancer were diagnosed. Among these cases, those who donated pre-diagnostic blood (n = 108) were eligible for this study. For each case, two individuals alive and free of cancer at the time of case diagnosis, matched on age, sex, and date of blood collection, were selected as controls. Serum beta-carotene (odds ratios (ORs) for tertiles: 1, 1.3, 2.0) and beta-cryptoxanthin (ORs for tertiles: 1, 1.8, 2.9) levels were positively associated with lung cancer risk after adjustment for tobacco use and radon exposure. Among alcohol drinkers, higher serum carotenoid levels were significantly associated with increased lung cancer risk (alpha-carotene OR 2.2, 95% confidence interval (CI) 1.1-4.4, beta-carotene OR 7.6, 95% CI 3.1-18.6, lutein/zeaxanthin OR 2.3, 95% CI 1.2-6.6 and beta-cryptoxanthin OR 7.6, 95% CI 2.7-21.5). Conversely, risk estimates among non-drinkers suggest a possible protective association for higher carotenoid levels.     

Dietary antioxidants and lung cancer risk: a case-control study in Uruguay.

To examine the protective role of dietary antioxidants (carotenoids, vitamin C, vitamin E, glutathione, and flavonoids) in lung cancer risk, a case-control study involving 541 cases of lung cancer and 540 hospitalized controls was carried out in Uruguay. The relevant variables were energy adjusted using the residuals method and then categorized in quartiles. Adjusted odds ratios (ORs) for antioxidants were calculated through unconditional logistic regression. With the exception of lycopene and vitamin C, the remaining antioxidants were associated with significant reductions in risk of lung cancer. Of particular interest was the inverse association between dietary glutathione and lung cancer [OR of quartile with highest intake compared with lowest quartile = 0.42, 95% confidence interval (CI) = 0.27-0.63]. Also, carotenoids and vitamin E were associated with significant reductions in risk of lung cancer (OR = 0.43, 95% CI = 0.29-0.64 for total carotenoids and OR = 0.50, 95% CI = 0.39-0.85 for vitamin E). A joint effect for high vs. low intakes of beta-carotene and glutathione was associated with a significant reduction in risk (OR = 0.32, 95% CI = 0.22-0.46). It could be concluded that dietary antioxidants are associated with a significant protective effect in lung carcinogenesis and that the inverse association for glutathione persisted after controlling for total vegetables and fruits.     

Lung cancer and occupation: results of a multicentre case-control study.

The objective of the current study was to estimate the risk of lung cancer attributable to occupational factors and not due to tobacco. At 24 hospitals in nine metropolitan areas in the United States, 1793 male lung cancer cases were matched for race, age, hospital, year of interview, and cigarette smoking (never smoker, ex-smoker, smoker (1-19 and > or = 20 cigarettes per day)) to two types of controls (cancer and non-cancer hospital patients). Information on usual occupation, exposure to specific potential carcinogens, and cigarette smoking was obtained by interview. Risk of lung cancer was increased significantly for electricians; sheetmetal workers and tinsmiths; bookbinders and related printing trade workers; cranemen, derrickmen, and hoistmen; moulders, heat treaters, annealers and other heated metal workers; and construction labourers. All of these occupations are potentially exposed to known carcinogens. Odds ratios (ORs) were increased for exposure to coal dust (adjusted OR = 1.5; 95% confidence interval (95% CI) 1.1-2.1). After stratification, this association was statistically significant only after 10 or more years of exposure. Lung cancer was also related to exposure to asbestos (adjusted OR = 1.8; 95% CI 1.5-2.2). The ORs increased with increasing duration of exposure to asbestos for all smoking categories except for current smokers of 1-19 cigarettes per day. The statistical power to detect ORs among occupations that were previously reported to be at increased risk of lung cancer but that failed to show an OR of at least 1.5 in the current study was small. The cumulative population attributable risk (PAR) of lung cancer due to occupation was 9.2%. It is concluded that occupational factors play an important part in the development of lung cancer independently of cigarette smoking. Because occupations at high risk of lung cancer were under-represented, the cumulative PAR of the present study is likely to be an underestimate of the true contribution of occupation to risk of lung cancer.     

Polymorphisms in CYP1A1, GSTM1, GSTT1 and lung cancer below the age of 45 years

BACKGROUND: A genetic component of early-onset lung cancer has been suggested. The role of metabolic gene polymorphisms has never been studied in young lung cancer cases. Phase 1 and Phase 2 gene polymorphisms are involved in tobacco carcinogens' metabolism and therefore in lung cancer risk. METHODS: The effect of metabolic gene polymorphisms on lung cancer at young ages was studied by pooling data from the Genetic Susceptibility to Environmental Carcinogens (GSEC) database. All primary lung cancer cases of both sexes who were Caucasian and 相似文献   

N-acetyltransferase 2 polymorphisms, tobacco smoking, and breast cancer risk in the breast and prostate cancer cohort consortium

Common polymorphisms in the N-acetyltransferase 2 gene (NAT2) modify the association between cigarette smoking and bladder cancer and have been hypothesized to determine whether active cigarette smoking increases breast cancer risk. The authors sought to replicate the latter hypothesis in a prospective analysis of 6,900 breast cancer cases and 9,903 matched controls drawn from 6 cohorts (1989-2006) in the National Cancer Institute's Breast and Prostate Cancer Cohort Consortium. Standardized methods were used to genotype the 3 most common polymorphisms that define NAT2 acetylation phenotype (rs1799930, rs1799931, and rs1801280). In unconditional logistic regression analyses, breast cancer risk was higher in women with more than 20 pack-years of active cigarette smoking than in never smokers (odds ratio (OR) = 1.28, 95% confidence interval (CI): 1.17, 1.39), after controlling for established risk factors other than alcohol consumption and physical inactivity. However, associations were similar for the slow (OR = 1.25, 95% CI: 1.11, 1.39) and rapid/intermediate (OR = 1.24, 95% CI: 1.08, 1.42) acetylation phenotypes, with no evidence of interaction (P = 0.87). These results provide some support for the hypothesis that long-term cigarette smoking may be causally associated with breast cancer risk but underscore the need for caution when interpreting sparse data on gene-environment interactions.     

Case-control analysis of dietary folate and risk of bladder cancer

Dietary folate, a water-soluble B vitamin found in a variety of fruits and vegetables, is of particular interest as a chemopreventive agent due to its role in DNA methylation and DNA synthesis and repair. We hypothesized that individuals with low folate intake would be at an increased risk for bladder cancer. Using an ongoing case-control study we assessed dietary folate in 409 incident bladder cancer patients and 451 healthy control subjects. A food-frequency questionnaire was used to estimate naturally occurring food folate (microg/kcal/day), dietary folate equivalents (DFE) from food sources (microg DFE/kcal/day), and DFE from all sources (microg DFE/kcal/day). Unconditional logistic regression analyses were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Bladder cancer patients reported a statistically significant lower intake of folate than control subjects for food folate and DFE from food sources (P < 0.001) but not for DFE from all sources (P = 0.061). In the highest quartile of food folate intake there was a 54% reduced risk for bladder cancer (OR = 0.46; 95% CI = 0.29-0.73) after adjusting for age, gender, ethnicity, smoking, and total energy intake. Similarly, the highest quartile of intake was associated with a 59% reduced risk for DFE from food sources (OR = 0.41; 95% CI = 0.26-0.65) and a 35% reduced risk for DFE from all sources (OR = 0.65; 95% CI = 0.42-1.00). In the joint-effects analyses using never smokers with high folate intake as the reference group (OR = 1.0), heavy smokers with low food folate intake had a 2.31-fold (95% CI = 1.11-4.82) increased risk, whereas heavy smokers with high folate intake had a reduced OR of 1.31 (95% CI = 0.53-3.26). Although the ORs were not statistically significant, light smokers and high folate intake exhibited a protective effect (OR = 0.62; 95% CI = 0.20-1.94), whereas an increased risk was observed for light smoking and low folate intake (OR = 1.41; 95% CI = 0.57-3.45). These patterns were consistent for the joint effects of smoking and DFE from food sources and DFE from all sources. In summary, high intake of dietary folate was associated with an overall decrease in bladder cancer risk. These data may have important implications for cancer prevention; however, large, hypothesis-driven, population-based clinical trials will be required to confirm these findings.     

Recreational physical activity and risk of head and neck cancer: a pooled analysis within the international head and neck cancer epidemiology (INHANCE) Consortium

Increasing evidence suggests that physical activity could prevent cancer, but scanty data is available on head and neck cancer (HNC). The aim of our study is to clarify the effect of recreational physical activity (rPA) on HNC. We analyzed data from four case-control studies, including 2,289 HNC cases and 5,580 controls. rPA was classified as: none/low (reference group), moderate and high. We calculated summary Odds Ratios (ORs) by pooling study-specific ORs. Overall, moderate rPA was associated with 22% lower risk of HNC compared to those with none or very low rPA levels [OR?=?0.78, 95% Confidence Interval (95% CI): 0.66, 0.91]. Moderate rPA is associated with reduced risk of oral (OR?=?0.74, 95% CI: 0.56, 0.97) and pharyngeal cancer (OR?=?0.67, 95% CI: 0.53, 0.85), as well as high rPA levels (OR?=?0.53, 95% CI: 0.32, 0.88 for oral cavity, OR?=?0.58, 95% CI: 0.38, 0.89 for pharynx). High rPA levels, however, is associated with higher risk of laryngeal cancer (OR?=?1.73, 95% CI: 1.04, 2.88). Stratified analyses showed that such inverse association between moderate rPA and HNC was more evident among males (OR?=?0.75, 95% CI: 0.62, 0.90), subjects ≥45?years (OR?=?0.78, 95% CI: 0.66, 0.93), and ever smokers and ever drinkers (OR?=?0.72, 95% CI: 0.59, 0.88). High rPA significantly reduces HNC risk among subject ≥45?years (OR?=?0.66, 95% CI: 0.48, 0.91). Promoting rPA might be inversely associated with HNC.     

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。     

Lung cancer and indoor air pollution in rural china

PURPOSE: Indoor air pollution has been linked with lung cancer in China. In contrast to previous studies conducted in urban areas with high levels of industrial pollution, we undertook a lung cancer case-control study in a rural area of China, where residents live in underground dwellings. We evaluated the effects of radon, wood and coal combustion, cooking oil fumes, and environmental tobacco smoke on lung cancer risk.METHODS: We enrolled 886 lung cancer cases (656 males, 230 females) diagnosed between 1994-98, aged 30-75 years and 1765 frequency matched population-based controls from two prefectures in Gansu Province in Northwestern China. We conducted interviews with subjects or next of kin on smoking, housing characteristics, fuel use and cooking practices. Year-long radon detectors were placed in current and former homes of subjects.RESULTS: Subjects primarily used coal (22%), wood (56%) or a combination of both (22%) for heating. Odds Ratios (OR) for lung cancer rose with increasing percent of time that coal was used to heat homes over the past 30 years (ORs = 1.00, 1.17, 1.35, 1.23 compared to wood only, adjusted to smoking, P for trend = 0.025). Among non-smoking females and males, the OR for ever exposed to environmental tobacco smoke was 1.19, 95% CI = 0.7-2.0 with a significant trend for increasing years of exposure. Fumes from cooking with rapeseed oil increased the risk of lung cancer (OR = 1.56, 95% CI = 1.0-2.5) among non-smoking women. Among these women, occasional and frequent eye and throat irritation during cooking appeared to be associated with increased risk of lung cancer (ORs = 1.00, 1.42, 2.28, p trend < 0.01), whereas, increasing level of smokiness during cooking did not appear to affect risk.CONCLUSIONS: There is a suggestion that coal used for heating, environmental tobacco smoke, and cooking oil fumes contribute to the risk of lung cancer in this rural area of China.     

Breast cancer risk and ovariectomy, hysterectomy, and tubal sterilization in the women's contraceptive and reproductive experiences study

Removal or impairment of ovaries before menopause may affect a woman's breast cancer risk by altering her cumulative exposure to ovarian hormones. The Women's Contraceptive and Reproductive Experiences Study, a population-based, multicenter case-control study of incident invasive breast cancer, recruited women aged 35-64 years (4,490 cases and 4,611 controls) who provided data on ovariectomy, hysterectomy, and tubal sterilization during in-person interviews. Controls were frequency-matched to cases by age, race, and study site. Unconditional logistic regression analysis was used. Women who had not undergone premenopausal reproductive surgery were the referent group. Bilateral ovariectomy was associated with reduced breast cancer risk overall (odds ratio (OR) = 0.59, 95% confidence interval (CI): 0.50, 0.69) and among women <45 years of age (ORs ranged from 0.31 to 0.52), but not among those who were older at surgery. It was also associated with a reduced risk for estrogen and progesterone receptor-positive tumors (OR = 0.63, 95% CI: 0.52, 0.75) but not receptor-negative tumors. Hysterectomy with ovarian conservation (OR = 0.83, 95% CI: 0.72, 0.96) and hysterectomy with partial ovary removal (OR = 0.73, 95% CI: 0.59, 0.91) were also associated with lower risk. No association with breast cancer risk was observed with tubal sterilization only or partial ovariectomy without hysterectomy. Reproductive organ surgeries may alter ovarian hormone levels, thereby affecting breast cancer risk.     

Nondaily smokers should be asked and advised to quit

BACKGROUND: Nondaily smokers are a growing subpopulation of smokers. Current cessation guidelines were developed for daily smokers, and how clinicians might help nondaily smokers is not clear. METHODS: Analyzing the 2000 National Health Interview Survey in 2004, we compared characteristics of nondaily smokers with never smokers and daily smokers. We used multivariate logistic regression to compare predictors of wanting to quit in 6 months between nondaily and daily smokers. RESULTS: About one in five current smokers was a nondaily smoker. Nondaily smokers reported better health than daily smokers, but had some health status indicators suggesting worse health than never smokers. Nondaily smokers were more likely to want to quit (odds ratio [OR]=1.31, 95% confidence interval [CI]=1.10-1.56) than daily smokers, but were less likely to report a physician having asked about tobacco use (41% vs 50%, p<0.0001) or advised quitting (31% vs 41%, p<0.0001). In both nondaily and daily smokers, physician advice (nondaily OR=1.50, 95% CI=1.03-2.2; daily OR=1.58, 95% CI=1.32-1.89), and the belief that secondhand smoke harms others (nondaily OR=1.48, 95% CI=1.04-2.1; daily OR=1.80, 95% CI=1.56-2.1), predicted wanting to quit. Higher-educated nondaily smokers were less likely to want to quit (OR=0.54, 95% CI=0.32-0.91), unlike in daily smokers (OR=1.48, 95% CI=1.15-1.89). Latino nondaily smokers were less likely (OR=0.43, 95% CI=0.30-0.64) than whites, and African-American daily smokers were more likely (OR=1.27, 95% CI=1.04-1.55) than whites, to want to quit. CONCLUSIONS: While daily smokers may seem a higher cessation priority, nondaily smokers may be more likely to quit with brief interventions. Cessation messages should address health risks of any smoking, ethnic differences, smoke-free messages, and situational triggers.     

Cigarette smoking and risk of bladder, pancreas, kidney, and colorectal cancers in Iowa

PURPOSE: Although there are numerous reports on the effects of cigarette smoking and cancer, they have infrequently compared risks at more than one cancer site after multivariate adjustment. We analyzed data from a population-based case-control study that included five anatomic sites to evaluate the association between cigarette smoking and each cancer site and to rank the associations by site. METHODS: Study respondents included 1452 bladder, 406 kidney, 376 pancreatic, 685 colon, and 655 rectal cancer cases, as well as 2434 population controls. A self-administered questionnaire was used to collect information on cigarette smoking and other potential confounders including occupation, drinking water source, and dietary practices. Logistic regression models were used to calculate odds ratios (ORs) and 95% confidence intervals (CIs), after adjustment for age, total energy intake, and other site- and sex-specific confounders. RESULTS: In both sexes, cigarette smoking (ever vs. never) was associated with risk of bladder cancer (OR = 2.5; 95% CI, 2.0-3.1 for males; OR = 2.7; 2.0-3.6 for females) and pancreatic cancer (OR = 1.8; 1.2-2.8 for males; OR = 2.1; 1.4-3.1 for females). Cigarette smoking also increased the risk of kidney cancer among males (OR = 1.8; 1.3-2.7), and to a lesser degree, among females (OR = 1.2; 0.8-1.8). No association was found for colon or rectal cancer in either sex. CONCLUSIONS: Cigarette smoking increased the risk of bladder, kidney, and pancreatic cancer in men and women. The rankings of multivariate-adjusted ORs from highest to lowest were bladder, pancreas, kidney, and colorectum, with little difference between men and women.     

Cigarette smoking and risk of breast carcinoma in situ

BACKGROUND: Although the associations with cigarette smoking have been explored extensively for invasive breast cancer, the relation to in situ cancer has not previously been examined in depth. METHODS: We analyzed data from a population-based case-control study of women living in Wisconsin, Massachusetts, and New Hampshire. Eligible cases of incident breast carcinoma in situ were reported to statewide registries in 1997-2001 (n = 1878); similarly aged controls (n = 8041) were randomly selected from population lists. Smoking history and other risk factor information were collected through structured telephone interviews. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated from logistic regression models adjusting for potential confounders. RESULTS: In multivariate models, the OR for breast carcinoma in situ among current smokers was 0.8, compared with never-smokers (95% CI = 0.7-1.0). Risk estimates increased towards the null with greater time since smoking cessation. Odds ratios were also less than 1.0 among women who initiated smoking in adolescence (OR = 0.8) or after a full-term birth (OR = 0.7), relative to women who never smoked. The reduced odds ratios associated with current smoking were strongest among women with annual screening mammograms (OR = 0.7; 95% CI = 0.6-0.9). Odds ratios were not less than 1.0 among current smokers without a recent screening mammogram (1.3; 0.9-2.0). CONCLUSIONS: Our findings suggest an inverse association between current smoking and risk of breast carcinoma in situ among women undergoing breast cancer screening.