Allyson M Gregoire1, Trang VoPham2, Francine Laden3, Rina Yarosh4, Katie M O'Brien1, Dale P Sandler1, Alexandra J White5. 1. Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. 2. Epidemiology Program, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N, Seattle, WA 98109, USA. 3. Department of Epidemiology, Harvard T. H. Chan School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115, USA; Department of Environmental Health, Harvard T. H. Chan School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA. 4. Department of Epidemiology, University of North Carolina Gillings School of Global Public Health, Chapel Hill, NC, USA. 5. Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. Electronic address: alexandra.white@nih.gov.
Abstract
BACKGROUND: Ambient ultraviolet (UV) radiation has been increasing due to climate change. While this may result in adverse health consequences such as an increased incidence of skin cancer, UV radiation is also a source of vitamin D, which has been hypothesized to be protective for breast cancer risk. METHODS: Using a spatiotemporal kriging model, we estimated residential UV exposure levels for the enrollment addresses (2003-2009) of breast cancer-free women aged 35-74 years participating in the Sister Study and living in the contiguous United States (N = 48,450). Cox proportional hazards models were used to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (95% CIs) for the risk associated with UV exposure levels (mW/m2) categorized in quintiles. We examined the association for breast cancer overall (invasive and ductal carcinoma in situ) and by estrogen receptor (ER) status of the tumor. We considered effect modification by regular (≥4 times/week) vitamin D supplement use. RESULTS: Over a median of 10.5 years of follow up, 3,510 incident breast cancer diagnoses were reported. We found no evidence of an association between living in areas with higher levels of UV radiation and overall breast cancer risk (HRQ5 vs. Q1 = 1.00, 95% CI: 0.90, 1.11). Higher UV levels were inversely associated with the risk of ER- breast cancer (HRQ5 vs. Q1 = 0.73, 95% CI: 0.55-0.99), but not ER+ (HR Q5 vs. Q1 = 1.04, 95% CI: 0.92-1.18). For ER- breast cancer, the inverse association was only evident in women who did not regularly take vitamin D supplements (HRQ5 vs. Q1 = 0.52, 95% CI: 0.33-0.81) compared with those who did regularly take vitamin D supplements (HRQ5 vs. Q1 = 1.02, 95% CI: 0.68-1.54; p-for-heterogeneity = 0.12). CONCLUSIONS: The findings from this study support a role for UV exposure and vitamin D in the etiology of ER- breast cancer.
BACKGROUND: Ambient ultraviolet (UV) radiation has been increasing due to climate change. While this may result in adverse health consequences such as an increased incidence of skin cancer, UV radiation is also a source of vitamin D, which has been hypothesized to be protective for breast cancer risk. METHODS: Using a spatiotemporal kriging model, we estimated residential UV exposure levels for the enrollment addresses (2003-2009) of breast cancer-free women aged 35-74 years participating in the Sister Study and living in the contiguous United States (N = 48,450). Cox proportional hazards models were used to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (95% CIs) for the risk associated with UV exposure levels (mW/m2) categorized in quintiles. We examined the association for breast cancer overall (invasive and ductal carcinoma in situ) and by estrogen receptor (ER) status of the tumor. We considered effect modification by regular (≥4 times/week) vitamin D supplement use. RESULTS: Over a median of 10.5 years of follow up, 3,510 incident breast cancer diagnoses were reported. We found no evidence of an association between living in areas with higher levels of UV radiation and overall breast cancer risk (HRQ5 vs. Q1 = 1.00, 95% CI: 0.90, 1.11). Higher UV levels were inversely associated with the risk of ER- breast cancer (HRQ5 vs. Q1 = 0.73, 95% CI: 0.55-0.99), but not ER+ (HR Q5 vs. Q1 = 1.04, 95% CI: 0.92-1.18). For ER- breast cancer, the inverse association was only evident in women who did not regularly take vitamin D supplements (HRQ5 vs. Q1 = 0.52, 95% CI: 0.33-0.81) compared with those who did regularly take vitamin D supplements (HRQ5 vs. Q1 = 1.02, 95% CI: 0.68-1.54; p-for-heterogeneity = 0.12). CONCLUSIONS: The findings from this study support a role for UV exposure and vitamin D in the etiology of ER- breast cancer.
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