Predictors of tanning dependence in white non-Hispanic females and males.

BACKGROUND: Growing evidence suggests that some individuals may exhibit symptoms of dependence on ultraviolet (UV) light, a known carcinogen, in the context of tanning; however, few studies have investigated predictors of tanning dependence (TD). OBJECTIVE: To identify predictors of TD. METHODS: Non-Hispanics of European ancestry who had previously participated in a case-control study of early-onset basal cell carcinoma completed an online survey to ascertain TD and other behaviours (alcohol dependence, nicotine dependence, seasonal affective disorder (SAD), exercise 'addiction' and depression). Information on host factors, such as skin and eye colour and history of sunbathing and indoor tanning, was obtained from a study in which the participants were previously enrolled. Lifetime TD was assessed using the modified Cut down, Annoyed, Guilty, Eye-opener (mCAGE) and the modified Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (mDSM-IV-TR) questionnaires. Participants were classified as 'TD' if positive on both questionnaires and not TD if negative on both questionnaires. RESULTS: In total, 499 individuals completed the online survey (81.9% participation rate), and 24.4% were classified as 'TD'. In the multivariate model, women were more likely to be TD [odds ratio (OR) 6.93; 95% confidence intervals (95% CI) (3.36-14.27)] than men. Alcohol dependence (OR 6.55: 95% CI 3.19-13.42), SAD (OR 2.77; 95% CI 1.26-6.09) and exercise 'addiction' (OR 5.47; 95% CI 1.15-26.06) were all significant predictors for TD. CONCLUSION: Increased knowledge of those at risk for TD will allow appropriate interventions to be designed.

Dietary intake of flavonoids and oesophageal and gastric cancer: incidence and survival in the United States of America (USA).

BACKGROUND: Flavonoids, polyphenolic compounds concentrated in fruits and vegetables, have experimentally demonstrated chemopreventive effects against oesophageal and gastric cancer. Few epidemiologic studies have examined flavonoid intake and incidence of these cancers, and none have considered survival. METHODS: In this USA multicentre population-based study, case participants (diagnosed during 1993-1995 with oesophageal adenocarcinoma (OEA, n=274), gastric cardia adenocarcinoma (GCA, n=248), oesophageal squamous cell carcinoma (OES, n=191), and other gastric adenocarcinoma (OGA, n=341)) and frequency-matched controls (n=662) were interviewed. Food frequency questionnaire responses were linked with USDA Flavonoid Databases and available literature for six flavonoid classes and lignans. Case participants were followed until 2000 for vital status. Multivariable-adjusted odds ratios (ORs) and hazard ratios (HRs) (95% confidence intervals (CIs)) were estimated, comparing highest with lowest intake quartiles, using polytomous logistic and proportional hazards regressions, respectively. RESULTS: Little or no consistent association was found for total flavonoid intake (main population sources: black tea, orange/grapefruit juice, and wine) and incidence or survival for any tumour type. Intake of anthocyanidins, common in wine and fruit juice, was associated with a 57% reduction in the risk of incident OEA (OR=0.43, 95% CI=0.29-0.66) and OES (OR=0.43, 95% CI=0.26-0.70). The ORs for isoflavones, for which coffee was the main source, were increased for all tumours, except OES. Anthocyanidins were associated with decreased risk of mortality for GCA (HR=0.63, 95% CI=0.42-0.95) and modestly for OEA (HR=0.87, 95% CI=0.60-1.26), but CIs were wide. CONCLUSIONS: Our findings, if confirmed, suggest that increased dietary anthocyanidin intake may reduce incidence and improve survival for these cancers.

Alcohol intake and early-onset basal cell carcinoma in a case-control study.

BACKGROUND: Previous epidemiological studies of overall alcohol intake and basal cell carcinoma (BCC) are inconsistent, with some evidence for differences by type of alcoholic beverage. While alcohol may enhance the carcinogenicity of ultraviolet (UV) radiation, this has not been evaluated in existing epidemiological studies. OBJECTIVES: To evaluate alcohol intake in relation to early-onset BCC, and explore potential interactions with UV exposure. METHODS: Basal cell carcinoma cases (n = 380) and controls with benign skin conditions (n = 390) under 40 years of age were identified through Yale Dermatopathology. Participants provided information on lifetime alcohol intake, including type of beverage, during an in-person interview. Self-reported data on indoor tanning and outdoor sunbathing were used to categorize UV exposure. We calculated odds ratios (OR) and 95% confidence intervals (CIs) using unconditional multivariate logistic regression in the full sample and in women only. RESULTS: There was no statistically significant association between lifetime alcohol intake and early-onset BCC overall [above median intake vs. no regular alcohol intake (OR 1·10, 95% CI 0·69-1·73)] or in women only (OR 1·21, 95% CI 0·73-2·01). Similarly, intake of red wine, white wine, beer or spirits and mixed drinks was not associated with early-onset BCC. In exploratory analyses, we saw limited evidence for an interaction (P(interaction) = 0·003), with highest risk for high alcohol and high UV exposures, especially in women, but subgroup risk estimates had wide and overlapping CIs. CONCLUSIONS: Overall, we did not observe any clear association between lifetime alcohol intake and early-onset BCC.

Flavonoid intake and risk of pancreatic cancer in the National Institutes of Health-AARP Diet and Health Study Cohort.

BACKGROUND: Limited epidemiological studies show inverse associations between dietary flavonoid intake and pancreatic cancer risk, but results are inconsistent and are based on few cases. We examined the association between intake of flavonoids and pancreatic cancer risk in the large, prospective National Institutes of Health-AARP Diet and Health Study Cohort. METHODS: During follow-up through 2006 (median follow-up 10.6 years), 2379 pancreatic cancer cases were identified. We used Cox proportional hazards modelling to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). RESULTS: We found no association between total flavonoid intake (Q5 vs Q1 HR=1.09, 95% CI: 0.96-1.24) or any flavonoid subtypes and pancreatic cancer risk. Significant interactions were not observed by age, sex, smoking status, BMI or diabetes. CONCLUSION: Our results do not support the hypothesis that flavonoids have a protective role in pancreatic cancer carcinogenesis.

Skin carotenoid status measured by resonance Raman spectroscopy as a biomarker of fruit and vegetable intake in preschool children.

BACKGROUND/OBJECTIVE: Dietary assessment in children is difficult, suggesting a need to develop more objective biomarkers of intake. Resonance Raman spectroscopy (RRS) is a non-invasive, validated method of measuring carotenoid status in skin as a biomarker of fruit/vegetable intake. The purpose of this study was to examine the feasibility of using RRS in preschool children, to describe inter-individual variability in skin carotenoid status and to identify factors associated with the biomarker in this population. SUBJECTS/METHODS: We conducted a cross-sectional study of 381 economically disadvantaged preschoolers in urban centers in Connecticut (USA). In all, 85.5% were black non-Hispanic or Hispanic/Latino, and 14.1% were obese and 16.9% were overweight by age- and sex-specific body mass index (BMI) percentiles. Children had their skin carotenoid status assessed by RRS in the palm of the hand. Fruit/vegetable consumption was assessed by a brief parent/guardian-completed food frequency screener and a liking survey. RESULTS: We observed inter-individual variation in RRS values that was nearly normally distributed. In multiple regression analysis, higher carotenoid status, measured by RRS, was positively associated with fruit/vegetable consumption (P=0.02) and fruit/vegetable preference (P<0.01). Lower carotenoid status was observed among younger children, those participating in the US Supplemental Nutrition Assistance Program, and those with greater adiposity (P<0.05 for all). CONCLUSIONS: We observed wide variability in skin carotenoid status in a population of young children, as assessed by RRS. Parent-reported fruit/vegetable intake and several demographic factors were significantly associated with RRS-measured skin carotenoid status. We recommend further development of this biomarker in children, including evaluating response to controlled interventions.

Intake of meat, meat mutagens, and iron and the risk of breast cancer in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial.

BACKGROUND: Epidemiological evidence on meat intake and breast cancer is inconsistent, with little research on potentially carcinogenic meat-related exposures. We investigated meat subtypes, cooking practices, meat mutagens, iron, and subsequent breast cancer risk. METHODS: Among 52 158 women (aged 55-74 years) in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, who completed a food frequency questionnaire, 1205 invasive breast cancer cases were identified. We estimated meat mutagen and haem iron intake with databases accounting for cooking practices. Using Cox proportional hazards regression, we calculated hazard ratios (HRs) and 95% confidence intervals (CIs) within quintiles of intake. RESULTS: Comparing the fifth to the first quintile, red meat (HR=1.23; 95% CI=1.00-1.51, P trend=0.22), the heterocyclic amine (HCA), 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx), (HR=1.26; 95% CI=1.03-1.55; P trend=0.12), and dietary iron (HR=1.25; 95% CI=1.02-1.52; P trend=0.03) were positively associated with breast cancer. We observed elevated, though not statistically significant, risks with processed meat, the HCA 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (DiMeIQx), mutagenic activity, iron from meat, and haem iron from meat. CONCLUSION: In this prospective study, red meat, MeIQx, and dietary iron elevated the risk of invasive breast cancer, but there was no linear trend in the association except for dietary iron.

Past body mass index and risk of mortality among women.

BACKGROUND: Epidemiologic studies of body mass index (BMI) in relation to mortality commonly exclude persons with health conditions and/or a history of smoking to prevent bias resulting from illness-related weight loss ('reverse causation'). Analysis of BMI from an earlier time period may minimize reverse causation without requiring exclusion of participants based on disease or smoking history. METHODS: We prospectively examined BMI based on technician measurements of weight and height from 10 years prior to start of follow-up in relation to subsequent mortality in a cohort of 50 186 women who were 40-93 years old at baseline in 1987-1989. Deaths were ascertained through the US National Death Index. Proportional hazards regression was used to estimate hazard ratios (HRs) of mortality, adjusted for age, education, race/ethnicity, income, menopausal hormone use, smoking and physical activity. RESULTS: During 10 years of follow-up through 1997, 5201 women died. Overall, we observed a J-shaped association between BMI and mortality, with increased risk for women who were underweight, overweight or obese. The HRs and 95% confidence intervals of mortality for BMI categories of <18.5, 18.5-20.9, 21.0-23.4 (reference), 23.5-24.9, 25.0-27.4, 27.5-29.9, 30.0-34.9 and 35.0+ kg m(-2) were 1.43 (1.19, 1.72), 1.07 (0.98, 1.17), 1.00 (reference), 1.10 (1.00, 1.20), 1.20 (1.11, 1.31), 1.23 (1.11, 1.37), 1.60 (1.44, 1.77) and 1.92 (1.64, 2.24). There was little evidence that pre-existing conditions (heart disease, diabetes and/or cancer) or smoking history modified the past BMI and mortality relation (P=0.54 and 0.76). CONCLUSIONS: In this large cohort of women, BMI based on technician measurements of weight and height from 10 years prior to baseline showed increased risk for mortality across the range of overweight and obesity, regardless of disease and smoking history. Observed associations between overweight, obesity and mortality in healthy individuals may also apply to persons with a history of disease or smoking.

Use of hair colouring products and breast cancer risk: a case-control study in Connecticut.

This case-control study was designed to test the hypothesis that the risk of breast cancer varies by type and colour of the hair colouring products used. A total of 608 cases and 609 controls were included in the study. We found no increased risk associated with the overall use of hair dye products or exclusive use of permanent or temporary types of hair dye products. Among those who reported to have exclusively used semi-permanent types of hair colouring products, some of the ORs were elevated. However, none of the ORs related to age at first use, duration of use, total number of applications, and years since first use, was statistically significant. There was also no increased risk of breast cancer associated with exclusive use of dark or light hair colouring products, or use of mixed types or colours of hair dye products. We also found no increased risk of breast cancer associated with hair dye use based on an individual's reason for using a hair colouring product, such as to cover grey or to change natural hair colour. These data suggest that the use of hair colouring products does not have a major impact on the risk of breast cancer.

Radiation exposure from diagnostic and therapeutic treatments and risk of breast cancer.

An association between low-dose diagnostic X-ray exposure or therapeutic radiation treatment and breast cancer risk has not been established. To further investigate the issue, we analysed data from a case-control study of breast cancer in Connecticut in 1994-1997. A total of 1217 subjects (608 breast cancer cases and 609 controls), 30-80 years old, participated in the study. A standardized, structured questionnaire was used to collect information through in-person interviews on diagnostic or therapeutic radiation and other breast cancer risk factors. An odds ratio (OR) of 1.7 (95% confidence interval (CI) 0.8-3.6) was observed for postmenopausal women with therapeutic radiation treatment for skin problems such as ringworm and acne, and an OR of 2.5 (95% CI 1.0-6.8) for those who reported having been treated six or more times. Radiation treatment received at younger ages seems to carry a higher risk. In earlier studies therapeutic radiation for skin problems has been associated with an increased risk of breast cancer. Therefore, it is possible that scattered radiation from these treatments could increase the risk of breast cancer. Radiation exposure from diagnostic X-rays was not associated with a significantly increased risk of breast cancer in this study.

Serum lycopene, other serum carotenoids, and risk of prostate cancer in US Blacks and Whites.

Epidemiologic studies investigating the relation between individual carotenoids and risk of prostate cancer have produced inconsistent results. To further explore these associations and to search for reasons prostate cancer incidence is over 50% higher in US Blacks than Whites, the authors analyzed the serum levels of individual carotenoids in 209 cases and 228 controls in a US multicenter, population-based case-control study (1986-1989) that included comparable numbers of Black men and White men aged 40-79 years. Lycopene was inversely associated with prostate cancer risk (comparing highest with lowest quartiles, odds ratio (OR) = 0.65, 95% confidence interval (CI): 0.36, 1.15; test for trend, p = 0.09), particularly for aggressive disease (comparing extreme quartiles, OR = 0.37, 95% CI: 0.15, 0.94; test for trend, p = 0.04). Other carotenoids were positively associated with risk. For all carotenoids, patterns were similar for Blacks and Whites. However, in both the controls and the Third National Health and Nutrition Examination Survey, serum lycopene concentrations were significantly lower in Blacks than in Whites, raising the possibility that differences in lycopene exposure may contribute to the racial disparity in incidence. In conclusion, the results, though not statistically significant, suggest that serum lycopene is inversely related to prostate cancer risk in US Blacks and Whites.

Nutrient intake and risk of subtypes of esophageal and gastric cancer.

Incidence rates for adenocarcinoma of the esophagus and gastric cardia have been rising rapidly. We examined nutrient intake as a risk factor for esophageal and gastric cancers in a population-based case-control study in Connecticut, New Jersey, and western Washington state. Interviews were completed for cases with histologically confirmed esophageal adenocarcinoma (n = 282), adenocarcinoma of the gastric cardia (n = 255), esophageal squamous cell carcinoma (n = 206), and noncardia gastric adenocarcinoma (n = 352), along with population controls (n = 687). Associations between nutrient intake and risk of cancer were estimated by adjusted odds ratios (ORs), comparing the 75th versus the 25th percentile of intake. The following nutrients were significantly inversely associated with risk of all four tumor types: fiber, beta-carotene, folate, and vitamins C and B6. In contrast, dietary cholesterol, animal protein, and vitamin B12 were significantly positively associated with risk of all four tumor types. Dietary fat [OR, 2.18; 95% confidence interval (CI), 1.27-3.76] was significantly associated with risk of esophageal adenocarcinoma only. Dietary nitrite (OR, 1.65; 95% CI, 1.26-2.16) was associated with noncardia gastric cancer only. Vitamin C supplement use was associated with a significantly lower risk for noncardia gastric cancer (OR, 0.60; 95% CI, 0.41-0.88). Higher intake of nutrients found primarily in plant-based foods was associated with a reduced risk of adenocarcinomas of the esophagus and gastric cardia, whereas higher intake of nutrients found primarily in foods of animal origin was associated with an increased risk.

Family history of cancer and risk of esophageal and gastric cancers in the United States.

The worldwide rates for histology- and subsite-specific types of esophageal and gastric cancer reveal strikingly divergent patterns. The contribution of environmental and genetic factors has been explored in several high-incidence areas, but data on genetic influences are scarce for Western countries. Using data from a multicenter, population-based, case-control study on 1,143 cases and 695 controls in the United States, we evaluated whether a family history of digestive or other cancers was associated with an increased risk of esophageal adenocarcinoma (n = 293), esophageal squamous cell carcinoma (n = 221), gastric cardia adenocarcinoma (n = 261) or non-cardia gastric adenocarcinoma (n = 368). After adjusting for other risk factors, individuals reporting a family history of digestive cancers experienced no increased risk of either type of esophageal cancer but they were prone to adenocarcinomas of the gastric cardia [odds ratio (OR) = 1.34, 95% confidence interval (CI) 0.91-1.97] and non-cardia segments (OR =1.46, 95% CI 1.03-2.08). This familial tendency, particularly for non-cardia gastric tumors, was largely explained by an association with family history of stomach cancer (OR = 2.52, 95% CI 1.50-4.23). In addition, family history of breast cancer was associated with increased risks of esophageal adenocarcinoma (OR = 1.74, 95% CI 1.07-2.83) and non-cardia gastric adenocarcinoma (OR = 1.76, 95% CI 1.09-2.82). Also seen were non-significant familial associations of esophageal squamous-cell cancer with prostate cancer as well as non-cardia gastric cancer with leukemia and brain tumors, though these relationships must be interpreted with caution. Our data point to the role of familial susceptibility to gastric cancer, but not to any form of esophageal cancer, in the United States.

Lactation and breast cancer risk: a case-control study in Connecticut.

In this report, we examined the relationship between lactation and breast cancer risk, in a case-control study of breast cancer, conducted in Connecticut between 1994 and 1998. Included were 608 incident breast cancer cases and 609 age frequency matched controls, aged 30-80 years old. Cases and controls were interviewed by trained study interviewers, using a standardized, structured questionnaire, to obtain information on lactation and other major risk factors. Parous women who reported ever lactation had a borderline significantly reduced risk of breast cancer (OR = 0.83, 95% CI, 0.63-1.09). An OR of 0.53 (95% CI, 0.27-1.04) was observed in those having breastfed more than 3 children compared to those who never lactated. Women having breastfed their first child for more than 13 months had an OR of 0.47 (95% CI, 0.23-0.94) compared to those who never breastfed. Lifetime duration of lactation also showed a risk reduction while none of the ORs were statistically significant. Further stratification by menopausal status showed a risk reduction related to lactation for both pre- and postmenopausal women, while the relationship is less consistent for the latter. These results support an inverse association between breastfeeding and breast cancer risk.

Randomized trial of supplemental beta-carotene to prevent second head and neck cancer.

Beta-carotene has established efficacy in animal models of oral carcinogenesis and has been shown to regress oral precancerous lesions in humans. The purpose of this study was to see whether these effects extended to the prevention of oral/pharyngeal/laryngeal (head and neck) cancer in humans. The subject population for this randomized, placebo-controlled, double-blinded clinical trial included 264 patients who had been curatively treated for a recent early-stage squamous cell carcinoma of the oral cavity, pharynx, or larynx. Patients were assigned randomly to receive 50 mg of beta-carotene per day or placebo and were followed for up to 90 months for the development of second primary tumors and local recurrences. After a median follow-up of 51 months, there was no difference between the two groups in the time to failure [second primary tumors plus local recurrences: relative risk (RR), 0.90; 95% confidence interval (CI), 0.56-1.45]. In site-specific analyses, supplemental beta-carotene had no significant effect on second head and neck cancer (RR, 0.69; 95% CI, 0.39-1.25) or lung cancer (RR, 1.44; 95% CI, 0.62-3.39). Total mortality was not significantly affected by this intervention (RR, 0.86; 95% CI, 0.52-1.42). Whereas none of the effects were statistically significant, the point estimates suggested a possible decrease in second head and neck cancer risk but a possible increase in lung cancer risk. These effects are consistent with the effects observed in trials using intermediate end point biological markers in humans, in which beta-carotene has established efficacy in oral precancerous lesions but has no effect or slightly worsens sputum cytology, and in animal carcinogenicity studies, in which beta-carotene has established efficacy in buccal pouch carcinogenesis in hamsters but not in animal models of respiratory tract/lung carcinogenesis, with some suggestions of tumor-promoting effects in respiratory tract/lung. If our results are replicated by other ongoing/completed trials, this suggests a critical need for mechanistic studies addressing differential responses in one epithelial site (head and neck) versus another (lung).

Macular pigment in donor eyes with and without AMD: a case-control study.

PURPOSE: To determine whether there is an association between the density of macular pigment in the human retina and the risk of age-related macular degeneration (AMD). METHODS: Retinas from 56 donors with AMD and 56 controls were cut into three concentric regions centered on the fovea. The inner, medial, and outer regions covered the visual angles 0 degrees to 5 degrees, 5 degrees to 19 degrees, and 19 degrees to 38 degrees, respectively. The amounts of lutein (L) and zeaxanthin (Z) extracted from each tissue sample were determined by high-performance liquid chromatography. RESULTS: L and Z levels in all three concentric regions were less, on average, for the AMD donors than for the controls. The differences decreased in magnitude from the inner to medial to outer regions. The lower levels found in the inner and medial regions for AMD donors may be attributable, in part, to the disease. Comparisons between AMD donors and controls using the outer (peripheral) region were considered more reliable. For this region, logistic regression analysis indicated that those in the highest quartile of L and Z level had an 82% lower risk for AMD compared with those in the lowest quartile (age- and sex-adjusted odds ratio = 0.18, 95% confidence interval = 0.05-0.64). CONCLUSIONS: The results are consistent with a theoretical model that proposes an inverse association between risk of AMD and the amounts of L and Z in the retina. The results are inconsistent with a model that attributes a loss of L and Z in the retina to the destructive effects of AMD.

Joint effects of nine polychlorinated biphenyl (PCB) congeners on breast cancer risk.

BACKGROUND: Polychlorinated biphenyls (PCB) have been a major environmental health concern because of their wide distribution and persistence in the environment. Estimating joint effects of all congeners in a single analysis is complicated by correlation among exposure levels, and the resulting collinearity makes the results difficult to interpret. METHODS: Patients with breast-related surgery at Yale-New Haven Hospital were interviewed using a standardized questionnaire, and breast adipose tissue samples were analysed for nine PCB congeners (74, 118, 138, 153, 156, 170, 180, 183, 187). The study recruited 490 women (304 cases and 186 controls) between 1994 and 1997. Logistic ridge regression was used to analyse the instability caused by collinearity. RESULTS: Although total PCB did not appear to be associated with breast cancer risk, significant differences in effect were observed among the nine congeners. Logistic ridge regression demonstrated a protective effect on breast cancer risk for a potentially anti-oestrogenic and dioxin-like congener, 156, while two phenobarbital, CYP1A and CYP2B inducers had an adverse effect, 180 and 183. This analysis also suggested that a protective effect for another phenobarbital congener, 153, was largely explained by instability caused by collinearity. CONCLUSIONS: These results indicate that studies of PCB congeners and health require an in-depth statistical analysis in order to better understand the complex issues related to their collinearity.

Food group intake and the risk of oral epithelial dysplasia in a United States population.

OBJECTIVES: Oral epithelial dysplasia (OED) is a histopathologic diagnosis associated with an increased risk of oral cancer. The paper explores the relationship between OED risk and food group intake. METHODS: In this case-control study, incident cases of OED were identified through two oral pathology laboratories. Controls, pair-matched 1:1 to cases on age (+/- 5 years), gender, appointment date (+/- 1 year), and surgeon, were identified through the office in which the respective case was biopsied. Exposure data were obtained via a telephone interview and mailed food-frequency questionnaire. Conditional logistic regression was used to obtain odds ratio point estimates. RESULTS: Based upon 87 matched pairs and after controlling for smoking, drinking, and other potential covariates there was an apparent inverse relationship between OED risk and the consumption of fruits and vegetables, with the intake of these foods being associated with a strong attenuating effect among smokers. OED risk decreased with increased poultry consumption, but increased modestly with bread/cereal and dairy food intake. CONCLUSIONS: This investigation provides evidence that some aspects of diet may be associated with the risk of OED. It also suggests that in oral carcinogenesis the role of diet is not simply one of a late effect.

Oxychlordane and trans-nonachlor in breast adipose tissue and risk of female breast cancer.

BACKGROUND: Organochlorine compounds, including organochlorine pesticides, have been suggested by some, but not all, studies to be associated with female breast-cancer risk. So far, studies relating organochlorine compounds and breast-cancer risk have mainly focused on polychlorinated biphenyls (PCBs) and dichlorodiphenyltrichloroethane (DDT) as risk factors for female breast cancer. This paper examines the hypothesis that environmental exposure to trans-nonachlor (TNC) and oxychlordane (OCD), a major metabolite of the insecticide chlordane, increases the METHODS: A total of 304 histologically confirmed, incident primary breast-cancer patients and 186 histologically confirmed incident benign breast-disease controls were included in the study between 1994 and 1997. Breast adipose tissue not needed for diagnostic purposes was collected and analysed for TNC, OCD and other organochlorine compounds. A standardised, structured questionnaire was used to obtain information on major known, or suspected, risk factors for breast cancer. RESULTS: The age and lipid-adjusted geometric mean adipose-tissue levels of OCD were similar between the cases [36.4 p.p.b., 95% confidence interval (CI) 34.7-38.2 p.p.b.] and controls (38.0 p.p.b., 95% Cl 35.7-40.6 p.p.b.). The age and lipid-adjusted geometric mean adipose-tissue levels of TNC between the cases (55.5 p.p.b., 95% CI 52.6-58.5 p.p.b.) and controls (58.1 p.p.b., 95% CI 54.2-62.3 p.p.b.) were also similar. There was no association between breast-cancer risk and mean adipose-tissue levels of OCD and TNC. The covariate-adjusted odds ratio (OR) was 0.7 (95% CI 0.4-1.3) for OCD and 1.1 (95% CI 0.6-1.9) for TNC, when the highest quartile was compared with the lowest. The risk also did not vary based on oestrogen or progesterone receptor status or menopausal status. DISCUSSION: We found no significantly increased risk of breast cancer associated with breast adipose-tissue levels of OCD or TNC; this is consistent with recent epidemiological studies, indicating that environmental exposure to organochlorine compounds does not have an overall significant impact on breast-cancer risk.

Relation between body mass index and lung cancer risk in men and women never and former smokers.

The authors assessed body mass index (BMI), measured as Quetelet's index (weight in kilograms divided by the square of height in meters), in relation to lung cancer risk in never and former smokers by using data from a population-based, individually matched, case-control study conducted in New York State from 1982 to 1985. To be included in the study, subjects must never have smoked more than 100 cigarettes in their lifetime (never smokers) or not have smoked more than 100 cigarettes during the last 10 years (former smokers). Data on height and weight were complete for 412 of 439 case-control pairs. A positive relation was found between BMI and lung cancer risk for both never smokers (188 case-control pairs) and former smokers (224 pairs). When subjects were combined, those in the eighth (highest) octile (BMI > 30.84) had more than twice the odds of being cases compared with those in the lowest octile (BMI < or =21.26, 95 percent confidence interval: 1.2, 4.4). These study results are consistent with those from studies of BMI and other cancer sites but differ from lung cancer results usually found in predominantly smoking populations.

Breast cancer risk associated with congeners of polychlorinated biphenyls.

Experimental studies show that hormonal and nonhormonal activities of polychlorinated biphenyls (PCBs) are structure dependent, suggesting that the breast cancer risk associated with PCBs may vary according to specific PCB congeners. In 1994-1997, the authors conducted a case-control study of Connecticut women to investigate whether breast cancer risk is associated with body burden of PCBs and varies by PCB congeners. A total of 304 breast cancer cases and 186 controls aged 40-79 years were recruited into the study. Fresh breast adipose tissue was analyzed for PCBs. The age- and lipid-adjusted geometric mean tissue levels of total PCBs were not significantly different (p = 0.46) for the cases (478.6 parts per billion) and controls (494.1 parts per billion). The covariate-adjusted odds ratio was 0.7 (95% confidence interval: 0.4, 1.1) for all study participants when the third tertile was compared with the lowest tertile. No individual congeners or groups of congeners were associated with a significantly increased risk of breast cancer. Further stratification by type of breast disease; menopausal, parity, and lactation status; and body size also showed no significant association with body levels of PCBs. These results suggest that environmental exposure to PCBs may not substantially affect breast cancer risk.