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Purpose: To investigate the association of reproductive factors and hormone therapy, including type of hormone therapy, with risk of thyroid cancer in postmenopausal women., Methods: We assessed these associations with risk of incident thyroid cancer in a cohort of 145,007 postmenopausal women enrolled in the Women's Health Initiative. Over 12.7 years of follow-up, 296 cases of thyroid cancer were identified, including 243 with papillary thyroid cancer. Cox proportional hazards models were used to estimate hazard ratios and 95 % confidence intervals for exposures of interest., Results: In both age-adjusted and multivariable-adjusted analyses, menstrual and reproductive factors including age at menarche, age at menopause, age at first birth, age at last live birth, parity, duration of breastfeeding, miscarriages, stillbirths, hysterectomy, bilateral oophorectomy, and use of oral contraceptives were not associated with risk of all thyroid cancer or papillary thyroid cancer. In addition, ever use of menopausal hormone therapy, current or former use, duration of use, and type were not associated with risk., Conclusion: We found little support for associations of reproductive or hormonal factors with risk of developing thyroid cancer. Importantly, our study showed no association of type of hormone therapy used with thyroid cancer risk.

Background: Few cohort studies have examined smoking and alcohol consumption in relation to risk of thyroid cancer, and their findings are conflicting., Methods: We therefore assessed the association of smoking and alcohol intake with risk of thyroid cancer in a cohort of 159,340 women enrolled in the Women's Health Initiative. Over 12.7 years of follow-up 331 cases of thyroid cancer, of which 276 were papillary thyroid cancer, were identified. Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI)., Results: Compared to never smokers, ever smokers did not have altered risk. Current smokers had reduced risk for all thyroid cancer (HR 0.54, 95% CI 0.29-1.00) and for papillary thyroid cancer (HR 0.34, 95% CI 0.15-0.78); however, the number of current smokers among cases was small. No associations or trends were seen for amount smoked, age of starting smoking, or age at quitting. Smokers of ≥40 pack-years had a significantly reduced risk of papillary thyroid cancer (HR 0.44, 95% CI 0.21-0.89). In contrast, women who had smoked for < 20 years had increased risk of thyroid cancer (HR 1.35, 95% CI 1.05-1.74) and papillary cancer (HR 1.43, 95% CI 1.09-1.89). Alcohol intake was not associated with risk., Conclusion: Our findings suggest that current smoking and having higher pack-years of exposure are associated with a modestly reduced risk of thyroid cancer, whereas alcohol consumption does not appear to affect risk., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

The metabolic syndrome is associated with increased risk of diabetes and coronary heart disease. Although higher BMI and other related factors have been frequently associated with colorectal cancer, whether the metabolic syndrome is associated with the risk of colorectal cancer is unclear. We therefore assessed the association of the metabolic syndrome with the risk of colorectal cancer in a subsample of participants of the Women's Health Initiative who had repeated measurements of the components of the syndrome at baseline and during follow-up. Women with diabetes at baseline enrollment were excluded. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (95% CI) at baseline and in time-dependent analyses. Among 4862 eligible women, 81 incident cases of colorectal cancer were identified over a median follow-up of 12 years. Presence of the metabolic syndrome at baseline was associated with increased risk of colorectal cancer (HR 2.15, 95% CI 1.30-3.53) and colon cancer (HR 2.28, 95% CI 1.31-3.98). These associations were largely explained by positive associations of serum glucose and systolic blood pressure with both outcomes. Time-dependent covariate analyses supported the baseline findings. Our results suggest that the positive association of the metabolic syndrome with risk of colorectal cancer is largely accounted for by serum glucose levels and systolic blood pressure. The biological mechanism underlying these associations remains to be clarified.

The US Food and Drug Administration is assessing whether menthol should be banned as an additive to cigarettes. An important part of this determination concerns the health effects of mentholated relative to non-mentholated cigarettes. We examined the ecologic association between sales of mentholated cigarettes for the period 1950-2007, menthol preference by race and sex, and incidence rates of four tobacco-related cancers during 1973-2007. Total sales of mentholated cigarettes (market share) increased from about 3% in 1950 to slightly less than 30% in 1980 and remained fairly stable thereafter. Additional data show consistently that, compared to White smokers, Black smokers favor mentholated cigarettes by roughly a 3-fold margin. Differences in the incidence of lung cancer, squamous cell cancer of the esophagus, oropharyngeal cancer, and laryngeal cancer by race and sex and trends over a 35-year period, during which menthol sales were relatively stable and during which Black smokers were much more likely to smoke mentholated cigarettes compared to Whites, are not consistent with a large contribution of menthol, over and above the effect of smoking per se., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Purpose: To investigate the associations of anthropometric factors and physical activity with risk of thyroid cancer in a large prospective study., Methods: We examined these associations with risk of incident thyroid cancer in a cohort of 144,319 postmenopausal women enrolled in the Women's Health Initiative. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (95% CI) for factors of interest with risk of all thyroid cancer (n = 294) and of the two major subtypes: papillary (n = 245) and follicular thyroid cancer (n = 32)., Results: After adjustment for covariates, measured height at baseline was positively associated with thyroid cancer overall (HR for highest vs. lowest quartile 1.48, 95% CI 1.04-2.13, p for trend 0.02) and with papillary carcinoma (HR 1.49, 95% CI 1.01-2.21, p for trend 0.03, respectively). For each 5 cm-increase in height, the HR for all thyroid cancer was 1.15, 95% CI 1.04-1.27 and for papillary thyroid cancer was 1.14, 95% CI 1.03-1.27. In addition, self-reported weight at age 18 was positively associated with risk of papillary thyroid cancer. In contrast, baseline weight, body mass index, waist circumference, hip circumference, waist-hip ratio, weight change from age 18 to baseline, and level of self-reported recreational physical activity were not associated with risk., Conclusions: Our results suggest that attained stature is a risk factor for thyroid cancer in postmenopausal women. This association may reflect the influence of either genetic or environmental factors in early life on risk of thyroid cancer.

Background: Incidence rates of non-Hodgkin's lymphoma (NHL) increased substantially in the United States and worldwide during the latter part of the 20th century, but little is known about its etiology. Obesity is associated with impaired immune function through which it may influence the risk of NHL; other factors reflecting energy homeostasis (height, abdominal adiposity, and physical activity) may also be involved., Methods: We examined the association of anthropometric factors and physical activity with risk of NHL and its major subtypes in a large cohort of women aged 50-79 years old who were enrolled at 40 clinical centers in the United States between 1993 and 1998. Over a mean follow-up period of 11 years, 1123 cases of NHL were identified among 158,975 women. Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI)., Results: Height at baseline was positively associated with risk of all NHL and with that of diffuse large B-cell lymphoma (HRs(q4vs.q1) 1.19, 95% CI 1.00-1.43 and 1.43, 95% CI 1.01-2.03, respectively). Measures of obesity and abdominal adiposity at baseline were not associated with risk. Hazard ratios for NHL were increased for women in the highest quartile of weight and body mass index at age 18 (HRs(q4vs.q1) 1.29, 95% CI 1.01-1.65 and 1.27, 95% CI 1.01-1.59, respectively). Some measures of recreational physical activity were modestly associated with increased risk of NHL overall, but there were no clear associations with specific subtypes., Conclusion: Our findings regarding anthropometric measures are consistent with those of several previous reports, suggesting that early life influences on growth and immune function may influence the risk of NHL later in life., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Purpose: The contribution of menstrual and reproductive factors to risk of ductal carcinoma (DCIS) of the breast is poorly understood., Methods: The association between menstrual and reproductive factors and subsequent DCIS risk was examined in Women's Health Initiative (WHI) clinical trial participants, in which mammography was protocol mandated. The cohort consisted of 64,060 women, among whom 664 cases of DCIS were ascertained over a median follow-up of 12.0 years. Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (95% CI)., Results: After adjustment for covariates, only older age at menopause (HR ≥ 55 vs. 45-54 : 1.39, 95% CI 1.08-1.79) was significantly associated with risk; however, greater parity (HR ≥ 5 live births vs. 0: 0.70, 95% CI 0.47-1.03), among parous women, and age at first live birth (HR ≥ 30 years relative to <20 years: 1.32, 95% CI 0.92-1.90) were of borderline significance. Age at menarche and months of breast-feeding were not associated with risk. Associations did not differ between high- and low-/moderate-grade DCIS, or by level of body mass index or family history of breast cancer; however, there was a suggestion that the associations of age at menopause, parity, and age at first live birth were limited to women who had ever used hormone therapy., Conclusions: Findings from this large cohort of postmenopausal women suggest that age at menopause, and possibly, age at first live birth, and parity are associated with risk of DCIS, whereas age at menarche and duration of breast-feeding are not.

Purpose: Little is known about the risk factors for triple-negative breast cancer (TNBC), which has a worse prognosis compared to hormone receptor-positive breast cancer. We examined the association of smoking and alcohol intake with TNBC and estrogen receptor-positive (ER+) breast cancer., Methods: Among 148,030 women enrolled in the Women's Health Initiative, 300 TNBC cases and 2,479 ER+ cases were identified over a median of 8.0 years of follow-up. Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (95% CI)., Results: Cigarette smoking was not associated with TNBC, whereas drinkers had reduced risk compared to never drinkers. In contrast, both exposures showed slight positive associations with ER+ breast cancer: for women with ≥ 40 pack-years of smoking, the HR was 1.24, 95% CI 1.06-1.44; for women consuming ≥ 7 servings of alcohol per week, the HR was 1.26, 95% CI 1.06-1.50. Intakes of wine and hard liquor were also significantly positively associated with ER+ breast cancer., Conclusions: These findings from a large cohort of postmenopausal women suggest that smoking and alcohol consumption are not associated with increased risk of TNBC, but may be modestly associated with increased risk of ER+ breast cancer.

Objective: To assess the association of recreational physical activity and anthropometric factors in relation to risk of ductal carcinoma in situ (DCIS) of the breast., Methods: The association was examined in a cohort of 58,055 postmenopausal women participating in the Women's Health Initiative (WHI) clinical trials, among whom 450 cases of DCIS were ascertained after a median follow-up of 8.0 years. Cox proportional hazard models were used to estimate hazard ratios (HR) and 95% confidence intervals (95% CI)., Results: After adjustment for covariates, the hazard ratio for DCIS among women with ≥ 20 metabolic equivalent task-hours per week (MET-h/week) of total recreational physical activity compared to women who did not engage in any recreational physical activity (0 MET-h/week) was 0.97 (95% CI 0.70-1.34). Neither body mass index nor waist circumference was associated with risk. In addition, physical activity and anthropometric factors were not associated with risk of either high-grade or low-/moderate-grade DCIS., Conclusions: Recreational physical activity and anthropometric factors showed no association with risk of DCIS in postmenopausal women in the WHI clinical trial.

Objective: We used a nested case-control design within a large, multi-center cohort of women who underwent a biopsy for benign breast disease (BBD) to assess the association of broad histologic groupings and specific histologic entities with risk of breast cancer., Methods: Cases were all women who had a biopsy for BBD and who subsequently developed breast cancer; controls were individually matched to cases and were women with a biopsy for BBD who did not develop breast cancer in the same follow-up interval as that for the cases. After exclusions, 1,239 records (615 cases and 624 controls) were available for analysis. We used conditional logistic regression to estimate odds ratios and 95% confidence intervals (CIs)., Results: Relative to non-proliferative BBD/normal pathology, the multivariable-adjusted odds ratio for proliferative lesions without atypia was 1.45 (95% CI 1.10-1.90), and that for atypical hyperplasia was 5.27 (95% CI 2.29-12.15). The presence of multiple foci of columnar cell hyperplasia and of complex fibroadenoma without atypia was associated with a non-significantly increased risk of breast cancer, whereas sclerosing adenosis, radial scar, and papilloma showed no association with risk., Conclusion: Our results indicate that, compared to women with normal pathology/non-proliferative disease, women with proliferative disease without atypia have a modestly increased risk of breast cancer, whereas women with atypical hyperplasia have a substantially increased risk.

Several epidemiologic studies have reported a positive association between breast cancer risk and high intake of sweets, which may be due to an insulin-related mechanism. We investigated this association in a population-based case-control study of 1,434 cases and 1,440 controls from Long Island, NY. Shortly after diagnosis, subjects were interviewed in-person to assess potential breast cancer risk factors, and self-completed a modified Block food frequency questionnaire, which included 11 items pertaining to consumption of sweets (sweet beverages, added sugars, and various desserts) in the previous year. Using unconditional logistic regression models, we estimated the association between consumption of sweets and breast cancer. Consumption of a food grouping that included dessert foods, sweet beverages, and added sugars was positively associated with breast cancer risk [adjusted odds ratio (OR) comparing the highest to the lowest quartile: 1.27, 95% confidence interval (CI): 1.00-1.61]. The OR was slightly higher when only dessert foods were considered (OR: 1.55, 95% CI: 1.23-1.96). The association with desserts was stronger among pre-menopausal women (OR: 2.00, 95% CI: 1.32-3.04) than post-menopausal women (OR: 1.40, 95% CI: 1.07-1.83), although the interaction with menopause was not statistically significant. Our study indicates that frequent consumption of sweets, particularly desserts, may be associated with an increased risk of breast cancer. These results are consistent with other studies that implicate insulin-related factors in breast carcinogenesis.

Evidence implicating hyperinsulinemia and insulin resistance in the etiology of colorectal cancer suggests that a diet characterized by a high glycemic index and load may increase the risk of this disease, but previous studies have yielded inconsistent results. We assessed the association between intake of total carbohydrates, sugars, fiber, and the glycemic index (GI) and glycemic load (GL) of individual diets, and risk of developing colorectal cancer among 158,800 participants in the Women's Health Initiative (WHI). We used a GI/GL database developed specifically for the WHI food-frequency questionnaire. Over an average of 7.8 years of follow-up, 1,476 incident cases of colorectal cancer were identified. Cox proportional hazards models were used to estimate the association between dietary factors classified by quintiles and risk of colorectal cancer, with adjustment for covariates. Total carbohydrate intake, glycemic index, glycemic load, and intake of sugars and fiber showed no association with colorectal cancer. Analyses by cancer subsite also yielded null results, with the exception of a borderline positive association between glycemic load and rectal cancer (HR for the highest versus lowest quintile 1.84, 95% confidence interval 0.95-3.56, p for trend 0.05). Analyses stratified by tertiles of body mass index and physical activity showed no evidence of effect modification by these factors. Results of this large study do not support of a role of a diet characterized by high glycemic index or load in colorectal carcinogenesis in postmenopausal women.

Free iron is a pro-oxidant and can induce oxidative stress and DNA damage. The carcinogenicity of iron has been demonstrated in animal models, and epidemiologic studies have shown associations with several human cancers. However, a possible role of excess body iron stores or of elevated iron intake in breast carcinogenesis has received little attention epidemiologically. We propose that iron overload and the disruption of iron homeostasis with a resulting increase in free iron may contribute to the development of breast cancer, and we summarize the relevant evidence from mechanistic studies, animal experiments, and studies in humans. Over time a high intake of iron can lead to iron overload. Furthermore, body iron stores increase in women following menopause. Reactive oxygen species produced by normal aerobic cellular metabolism can lead to the release of free iron from ferritin. In the presence of superoxide radical and hydrogen peroxide, stored ferric iron (Fe(3+)) is reduced to ferrous iron (Fe(2+)), which catalyzes the formation of the hydroxyl radical (*OH). *OH in turn can promote lipid peroxidation, mutagenesis, DNA strand breaks, oncogene activation, and tumor suppressor inhibition, increasing the risk of breast cancer. In addition to its independent role as a proxidant, high levels of free iron may potentiate the effects of estradiol, ethanol, and ionizing radiation - three established risk factors for breast cancer. In order to identify the role of iron in breast carcinogenesis, improved biomarkers of body iron stores are needed, as are cohort studies which assess heme iron intake. Ultimately, it is important to determine whether iron levels in the breast and iron-induced pathology are higher in women who go on to develop breast cancer compared to women who do not.

Background: Studies have suggested that leanness in adulthood may be a risk factor for lung cancer; however, there is justifiable concern that the observed association may be due to residual confounding by smoking, preclinical weight loss, competing causes of death, or some combination of these., Methods: To examine this association we used data from the Canadian National Breast Screening Study, which included 89,835 women ages 40-59 years at recruitment between 1980 and 1985. During a mean of 16 years of follow-up, we observed 750 incident lung cancer cases. We used Cox proportional hazards models to estimate hazard ratios and 95% confidence intervals for the association between body mass index (BMI) and lung cancer., Results: After adjustment for pack-years of smoking and other covariates, there was some evidence for inverse associations in current smokers (hazard ratio for highest BMI quintile relative to the lowest = 0.63; 95% confidence interval = 0.48-0.83) and in former smokers (0.69; 0.39-1.23), whereas in never-smokers, BMI was positively associated with lung cancer (2.19; 1.00-4.80). The results for current and former smokers were not altered by exclusion of cases diagnosed within the first 5 years of follow-up; however, in never-smokers the strength of the association was reduced., Conclusions: The present study contributes to the aggregate evidence suggesting that there may be an inverse association between BMI and lung cancer among smokers. However, the contrasting pattern of associations between BMI and lung cancer seen in ever-smokers and never-smokers in this study requires explanation.

Since the 1950s, cigarettes sold in the United States have undergone a progressive modification, including the addition of filters and a reduction in the average machine-measured tar and nicotine yield per cigarette by over 60%. These, and other, temporal changes in manufactured cigarettes, coupled with the complexity of smoking behavior, make it difficult to assess the impact of the newer cigarettes on health. Recently, some researchers have suggested that the newer products, marketed as being less harmful, may in fact provide no benefit compared to the older, higher tar cigarettes. The primary purpose of this review is to critically evaluate the available epidemiologic evidence on the health effects of low-tar cigarettes. This body of data provides the only means of assessing the effects of long-term exposure to these products, as they are actually used. After identifying important methodological problems confronting research in this area, studies of lung cancer, coronary heart disease, chronic obstructive pulmonary disease, and total mortality are examined in terms of their strengths and weaknesses and their results. Thirty-five studies of lung cancer are suggestive that smokers of low tar cigarettes have a lower risk (by 20-30%) compared to smokers of higher tar cigarettes. Only a minority of studies of heart disease provide evidence of a reduction in risk, on the order of 10%. Studies concerning chronic obstructive pulmonary disease (COPD) are inconsistent, but the majority suggest decreased risk in smokers of lower tar cigarettes. Finally, studies that included total mortality indicate with a high degree of consistency that the total death rate is reduced in smokers of lower tar cigarettes, on the order of 10-20%. Because of the multiplicity of factors involved in smoking behavior, including compensation for reduced nicotine, and the modest magnitude of the apparent reduction in risk, the relative benefits of low tar cigarettes remain uncertain. Additional analyses of existing data sets could further clarify the impact of low-tar cigarettes.

Background: Exposure to electromagnetic fields (EMF) has been hypothesized to increase the risk of breast cancer by inhibiting the normal nocturnal rise in melatonin levels., Methods: Information on electric blanket use was collected in a large, 2-stage, population-based, case-control investigation of breast cancer, The Long Island Breast Cancer Study Project (LIBCSP) and the EMF and Breast Cancer on Long Island Study (EBCLIS). The LIBCSP used a comprehensive questionnaire, including questions about electric appliance use, with responses available on 1354 cases diagnosed between mid-1996 and mid-1997 and 1426 control subjects. EBCLIS enrolled 576 cases and 585 control subjects who had participated in the LIBCSP and who had lived in their current homes for at least 15 years. EBCLIS participants were interviewed to obtain additional information on EMF exposures, including detailed questions on electric blanket use., Results: Analyses of both the EBCLIS and the LIBCSP groups showed no association with breast cancer for ever-use of electric blankets, current or former use, use directly on the body, or use throughout the night in either pre- or postmenopausal women (range of adjusted odds ratios for ever vs. never use: 0.9-1.2). Furthermore, there was no trend in risk with increased duration of use, frequency of use, or other indicators of more intense exposure to EMF. Electric blanket use was not associated with hormone receptor status of the tumor., Conclusions: The results of this large investigation are consistent with those of most previous studies, and do not support the hypothesis that electric blanket use is associated with increased breast cancer risk.

Objective: To measure the relation between environmental tobacco smoke, as estimated by smoking in spouses, and long term mortality from tobacco related disease., Design: Prospective cohort study covering 39 years., Setting: Adult population of California, United States., Participants: 118 094 adults enrolled in late 1959 in the American Cancer Society cancer prevention study (CPS I), who were followed until 1998. Particular focus is on the 35 561 never smokers who had a spouse in the study with known smoking habits., Main Outcome Measures: Relative risks and 95% confidence intervals for deaths from coronary heart disease, lung cancer, and chronic obstructive pulmonary disease related to smoking in spouses and active cigarette smoking., Results: For participants followed from 1960 until 1998 the age adjusted relative risk (95% confidence interval) for never smokers married to ever smokers compared with never smokers married to never smokers was 0.94 (0.85 to 1.05) for coronary heart disease, 0.75 (0.42 to 1.35) for lung cancer, and 1.27 (0.78 to 2.08) for chronic obstructive pulmonary disease among 9619 men, and 1.01 (0.94 to 1.08), 0.99 (0.72 to 1.37), and 1.13 (0.80 to 1.58), respectively, among 25 942 women. No significant associations were found for current or former exposure to environmental tobacco smoke before or after adjusting for seven confounders and before or after excluding participants with pre-existing disease. No significant associations were found during the shorter follow up periods of 1960-5, 1966-72, 1973-85, and 1973-98., Conclusions: The results do not support a causal relation between environmental tobacco smoke and tobacco related mortality, although they do not rule out a small effect. The association between exposure to environmental tobacco smoke and coronary heart disease and lung cancer may be considerably weaker than generally believed.

Polycyclic aromatic hydrocarbons (PAH) are potent mammary carcinogens in rodents, but their effect on breast cancer development in women is not clear. To examine whether currently measurable PAH damage to DNA increases breast cancer risk, a population-based case-control study was undertaken on Long Island, NY. Cases were women newly diagnosed with in situ and invasive breast cancer; controls were randomly selected women frequency matched to the age distribution of cases. Blood samples were donated by 1102 (73.0%) and 1141 (73.3%) of case and control respondents, respectively. Samples from 576 cases and 427 controls were assayed for PAH-DNA adducts using an ELISA. The geometric mean (and geometric SD) of the log-transformed levels of PAH-DNA adducts on a natural scale was slightly, but nonsignificantly, higher among cases [7.36 (7.29)] than among controls [6.21 (4.17); P = 0.51]. The age-adjusted odds ratio (OR) for breast cancer in relation to the highest quintile of adduct levels compared with the lowest was 1.51 [95% confidence interval (CI), 1.04-2.20], with little or no evidence of substantial confounding (corresponding multivariate-adjusted OR, 1.49; 95% CI, 1.00-2.21). There was no consistent elevation in risk with increasing adduct levels, nor was there a consistent association between adduct levels and two of the main sources of PAH, active or passive cigarette smoking or consumption of grilled and smoked foods. These data indicate that PAH-DNA adduct formation may influence breast cancer development, although the association does not appear to be dose dependent and may have a threshold effect.

Whether environmental contaminants increase breast cancer risk among women on Long Island, NY, is unknown. The study objective is to determine whether breast cancer risk is increased in relation to organochlorines, compounds with known estrogenic characteristics that were extensively used on Long Island and other areas of the United States. Recent reports do not support a strong association, although there are concerns with high risks observed in subgroups of women. Blood samples from 646 case and 429 control women from a population-based case-control study conducted on Long Island were analyzed. No substantial elevation in breast cancer risk was observed in relation to the highest quintile of lipid-adjusted serum levels of p,p'-bis(4-chlorophenyl)-1,1-dichloroethene (DDE) [odds ratio (OR), 1.20 versus lowest quintile; 95% confidence interval (CI), 0.76-1.90], chlordane (OR, 0.98; 95% CI, 0.62-1.55), dieldrin (OR, 1.37; 95% CI, 0.69-2.72), the sum of the four most frequently occurring PCB congeners (nos. 118, 153, 138, and 180; OR, 0.83; 95% CI, 0.54-1.29), and other PCB congener groupings. No dose-response relations were apparent. Nor was risk increased in relation to organochlorines among women who had not breastfed or were overweight, postmenopausal, or long-term residents of Long Island; or with whether the case was diagnosed with invasive rather than in situ disease, or with a hormone receptor-positive tumor. These findings, based on the largest number of samples analyzed to date among primarily white women, do not support the hypothesis that organochlorines increase breast cancer risk among Long Island women.