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Alcohol consumption has been inconsistently associated with breast cancer risk. Recent studies suggest that genetic polymorphisms of glutathione S-transferases (GSTs) may modify this relation. To determine if breast cancer risk is associated with GSTM1 and GSTT1 genetic polymorphisms, and to evaluate the effect modification between GST genotypes and alcohol consumption in the risk of breast cancer, we conducted a case-control study in the state of Connecticut in the period 1998 and 2001. Cases were histologically confirmed, incident breast cancer patients in New Haven County, CT. Controls were randomly selected from women histologically confirmed to be without breast cancer. The study results show that, while GSTM1 genotypes were not associated with breast cancer risk, GSTT1-null genotype was associated with a significant 90% increased risk for postmenopausal women (OR=1.9, 95% CI 1.2-3.0). Analysis by GST genotypes and alcohol consumption shows that GSTM1A ever-drinking women had a 2.5-fold (OR=2.5, 95% CI 1.1-5.5) increased risk of breast cancer compared to the GSTM1A never-drinkers, and the risk increases with duration and daily amount of alcohol consumption. Postmenopausal women with GSTT1-null genotype, who consumed a lifetime of >250 kg of spirit-equivalents, had an almost seven-fold increased risk (OR=6.8, 95% CI 1.4-33.9), and drinking commencing at younger ages appears to carry a higher risk. An OR of 8.2 (95% CI 1.2-57.4) was observed for those with GSTM1A, and GSTT1-null genotypes who had consumed a lifetime of >250 kg of spirit-equivalents. In conclusion, alcohol consumption may increase breast cancer risk among those who carry susceptible GST genotypes. [ABSTRACT FROM AUTHOR]

BACKGROUND: Increasingly, risk of bias tools are used to evaluate epidemiologic studies as part of evidence synthesis (evidence integration), often involving meta-analyses. Some of these tools consider hypothetical randomized controlled trials (RCTs) as gold standards. METHODS: We review the strengths and limitations of risk of bias assessments, in particular, for reviews of observational studies of environmental exposures, and we also comment more generally on methods of evidence synthesis. RESULTS: Although RCTs may provide a useful starting point to think about bias, they do not provide a gold standard for environmental studies. Observational studies should not be considered inherently biased vs. a hypothetical RCT. Rather than a checklist approach when evaluating individual studies using risk of bias tools, we call for identifying and quantifying possible biases, their direction, and their impacts on parameter estimates. As is recognized in many guidelines, evidence synthesis requires a broader approach than simply evaluating risk of bias in individual studies followed by synthesis of studies judged unbiased, or with studies given more weight if judged less biased. It should include the use of classical considerations for judging causality in human studies, as well as triangulation and integration of animal and mechanistic data. CONCLUSIONS: Bias assessments are important in evidence synthesis, but we argue they can and should be improved to address the concerns we raise here. Simplistic, mechanical approaches to risk of bias assessments, which may particularly occur when these tools are used by nonexperts, can result in erroneous conclusions and sometimes may be used to dismiss important evidence. Evidence synthesis requires a broad approach that goes beyond assessing bias in individual human studies and then including a narrow range of human studies judged to be unbiased in evidence synthesis. https://doi.org/10.1289/EHP6980 [ABSTRACT FROM AUTHOR]

Background The etiology of Hodgkin lymphoma (HL) remains incompletely characterized. Studies of the association between smoking and HL have yielded ambiguous results, possibly due to differences between HL subtypes. Patients and methods Through the InterLymph Consortium, 12 case–control studies regarding cigarette smoking and HL were identified. Pooled analyses on the association between smoking and HL stratified by tumor histology and Epstein–Barr virus (EBV) status were conducted using random effects models adjusted for confounders. Analyses included 3335 HL cases and 14 278 controls. Results Overall, 54.5% of cases and 57.4% of controls were ever cigarette smokers. Compared with never smokers, ever smokers had an odds ratio (OR) of HL of 1.10 [95% confidence interval (CI) 1.01–1.21]. This increased risk reflected associations with mixed cellularity cHL (OR = 1.60, 95% CI 1.29–1.99) and EBV-positive cHL (OR = 1.81, 95% CI 1.27–2.56) among current smokers, whereas risk of nodular sclerosis (OR = 1.09, 95% CI 0.90–1.32) and EBV-negative HL (OR = 1.02, 95% CI 0.72–1.44) was not increased. Conclusion These results support the notion of etiologic heterogeneity between HL subtypes, highlighting the need for HL stratification in future studies. Even if not relevant to all subtypes, our study emphasizes that cigarette smoking should be added to the few modifiable HL risk factors identified. [ABSTRACT FROM PUBLISHER]

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. [ABSTRACT FROM AUTHOR]

Purpose: We used data from a population-based case–control study conducted among women in Connecticut to examine the impact of educational attainment, income, body mass index (BMI), cigarette smoking, and alcohol use on multiple myeloma risk. Methods: This population-based case–control study included 179 individuals with myeloma, aged 21 to 84 years, diagnosed between 1996 and 2002 and identified through the Yale Cancer Center''s Rapid Case Ascertainment Shared Resources. Population controls were recruited among Connecticut residents from two sources: random-digit dialing for controls less than 65 years of age and Centers for Medicare and Medicaid Services (CMS) for controls 65 years of age and older. Data were collected through in-person interviews. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using unconditional logistic regression. Results: Educational attainment was inversely associated with risk, adjusted for age and race (P=0.004). Risk was significantly elevated for subjects with less than a high school education compared with individuals with a graduate or professional degree (OR=2.1, 95% CI=1.1–4.3). Similarly, an increased risk was observed for those in the lowest annual income category (<$10,000) compared with those in the highest (>$75,000) (OR=1.93, 95% CI=0.9–4.4). There was a suggestion of increasing risk with increasing BMI; however, the dose–response relationship was not statistically significant. We found no evidence of increased risk of myeloma risk for smoking and alcohol use. Conclusion: Our findings support a previously observed association, that the risk of multiple myeloma increases with decreasing SES. The SES-related exposures that may contribute to multiple myeloma risk remain to be determined. [Copyright &y& Elsevier]

PURPOSE: In the Agricultural Health Study we evaluated the mortality experience of 52,395 farmers and 32,347 of their spouses in Iowa and North Carolina obtain information on cancer and other chronic disease risks from agricultural exposures and other factors associated with rural lifestyle.METHODS: Standardized mortality ratios (SMRs) adjusted for race, gender, age, and calendar time were computed for the prospective cohort, using the general population in each state as the referent.RESULTS: After an average follow-up of 3.7 years, the SMRs for most causes of death were significantly less than 1.0. Significant deficits were observed for all causes (SMR = 0.5), all cancers combined (SMR = 0.5), and for cancers of the lung (SMR = 0.3), female genital organs (SMR = 0.4), prostate (SMR = 0.6) and bladder (SMR = 0.6), as well as diabetes (SMR = 0.3), cardiovascular disease (SMR = 0.5), and chronic obstructive pulmonary disease (SMR = 0.2). Non-significant excesses involving at least 3 deaths occurred for liver cancer (SMR = 2.1), multiple myeloma (SMR = 1.6), leukemia (SMR = 1.4), and Parkinson''s disease among spouses (SMR = 2.7. Among farmers elevated SMRs were noted for Hodgkin''s disease (SMR = 2.9) and cancer of the thyroid gland (SMR = 2.9), and non-motor vehicle accidents (SMR = 1.1). Soft tissue sarcoma (SMR = 1.1 for spouses; SMR = 1.6 for applicators) was elevated in both groups. NHL had an SMR of 1.0 among applicators and spouses. Stratification by presence of livestock or corn on the farm, farm size, and duration of handling pesticides revealed no obvious mortality differences.CONCLUSION: Despite a very low initial mortality experience compared to the general population, Agricultural Health Study farmers and their spouses appear to have rates for some cancers and chronic diseases that deserve continued monitoring and further scrutiny. [Copyright &y& Elsevier]