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Background: Radon and its decay products, a source of ionizing radiation, are primarily inhaled and can deliver a radiation dose to breast tissue, where they may continue to decay and emit DNA damage-inducing particles. Few studies have examined the relationship between radon and breast cancer.Methods: The Nurses' Health Study II (NHSII) includes U.S. female registered nurses who completed biennial questionnaires since 1989. Self-reported breast cancer was confirmed from medical records. County-level radon exposures were linked with geocoded residential addresses updated throughout follow-up. Time-varying Cox regression models adjusted for established breast cancer risk factors were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs).Results: From 1989 to 2013, 3966 invasive breast cancer cases occurred among 112,639 participants. Increasing radon exposure was not associated with breast cancer risk overall (adjusted HR comparing highest to lowest quintile = 1.06, 95% CI: 0.94, 1.21, p for trend = 0.30). However, women in the highest quintile of exposure (≥74.9 Bq/m3) had a suggested elevated risk of ER-/PR- breast cancer compared to women in the lowest quintile (<27.0 Bq/m3) (adjusted HR = 1.38, 95% CI: 0.97, 1.96, p for trend = 0.05). No association was observed for ER+/PR+ breast cancer.Conclusions: Although we did not find an association between radon exposure and risk of overall or ER+/PR+ breast cancer, we observed a suggestive association with risk of ER-/PR- breast cancer. [ABSTRACT FROM AUTHOR]

Background: Hepatocellular carcinoma (HCC), the most commonly occurring type of primary liver cancer, has been increasing in incidence worldwide. Vitamin D, acquired from sunlight exposure, diet, and dietary supplements, has been hypothesized to impact hepatocarcinogenesis. However, previous epidemiologic studies examining the associations between dietary and serum vitamin D reported mixed results. The purpose of this study was to examine the association between ambient ultraviolet (UV) radiation exposure and HCC risk in the U.S.Methods: The Surveillance, Epidemiology, and End Results (SEER) database provided information on HCC cases diagnosed between 2000 and 2014 from 16 population-based cancer registries across the U.S. Ambient UV exposure was estimated by linking the SEER county with a spatiotemporal UV exposure model using a geographic information system. Poisson regression with robust variance estimation was used to calculate incidence rate ratios (IRRs) and 95% confidence intervals (CIs) for the association between ambient UV exposure per interquartile range (IQR) increase (32.4 mW/m2) and HCC risk adjusting for age at diagnosis, sex, race, year of diagnosis, SEER registry, and county-level information on prevalence of health conditions, lifestyle, socioeconomic, and environmental factors.Results: Higher levels of ambient UV exposure were associated with statistically significant lower HCC risk (n = 56,245 cases; adjusted IRR per IQR increase: 0.83, 95% CI 0.77, 0.90; p < 0.01). A statistically significant inverse association between ambient UV and HCC risk was observed among males (p for interaction = 0.01) and whites (p for interaction = 0.01).Conclusions: Higher ambient UV exposure was associated with a decreased risk of HCC in the U.S. UV exposure may be a potential modifiable risk factor for HCC that should be explored in future research. [ABSTRACT FROM AUTHOR]

BACKGROUND: Studies have suggested associations between elevated blood pressure and short-term air pollution exposures, but the evidence is mixed regarding long-term exposures on incidence of hypertension. OBJECTIVES: We examined the association of hypertension incidence with long-term residential exposures to ambient particulate matter (PM) and residential distance to roadway. METHODS: We estimated 24-month and cumulative average exposures to PM[sub 10], PM[sub 2.5], and PM[sub 2.5-10] and residential distance to road for women participating in the prospective nationwide Nurses' Health Study. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated for incident hypertension from 1988 to 2008 using Cox proportional hazards models adjusted for potential confounders. We considered effect modification by age, diet, diabetes, obesity, region, and latitude. RESULTS: Among 74,880 participants, 36,812 incident cases of hypertension were observed during 960,041 person-years. In multivariable models, 10-µg/m³ increases in 24-month average PM[sub 10], PM[sub 2.5], and PM[sub 2.5-10] were associated with small increases in the incidence of hypertension (HR: 1.02, 95% CI: 1.00, 1.04; HR: 1.04, 95% CI: 1.00, 1.07; and HR: 1.03, 95% CI: 1.00, 1.07, respectively). Associations were stronger among women < 65 years of age (HR: 1.04, 95% CI: 1.01, 1.06; HR: 1.07, 95% CI: 1.02, 1.12; and HR: 1.05, 95% CI: 1.01, 1.09, respectively) and the obese (HR: 1.07, 95% CI: 1.04, 1.12; HR: 1.15, 95% CI: 1.07, 1.23; and HR: 1.13, 95% CI: 1.07, 1.19, respectively), with p-values for interaction < 0.05 for all models except age and PM[sub 2.5-10]. There was no association with roadway proximity. CONCLUSIONS: Long-term exposure to particulate matter was associated with small increases in risk of incident hypertension, particularly among younger women and the obese. [ABSTRACT FROM AUTHOR]

Previous studies evaluating the association of prenatal exposure to diethylstilbestrol (DES), a potent endocrine disruptor, with incidence of uterine leiomyomata (UL) have had conflicting results. We evaluated the association between prenatal DES exposure and incident UL in women in the Nurses' Health Study II from 1989 to 2009. Women were aged 25–42 years at enrollment and had a prenatal exposure window corresponding to DES use. The analytical sample was larger than previous studies and included 102,164 premenopausal women with intact uteri, no prior history of UL or cancer, and prenatal DES exposure. Multivariable-adjusted Cox proportional hazard models were used to estimate the relationship between DES exposure and UL risk. During 1,273,342 person-years of follow-up, there were 11,831 incident cases of UL. Women with prenatal exposure to DES had a higher incidence of UL compared with unexposed women, with an adjusted hazard ratio of 1.12 (95% confidence interval: 0.98, 1.27). Risk was strongest for women exposed to DES in the first trimester, when exposure corresponds to early stages of fetal Müllerian development (adjusted hazard ratio = 1.21, 95% confidence interval: 1.02, 1.43). These results suggest that first-trimester DES exposure may be associated with an increased risk of UL, but they must be interpreted with concern for detection and recall biases. [ABSTRACT FROM AUTHOR]