Engel Lawrence S, Satagopan Jaya, Sima Camelia S, Orlow Irene, Mujumdar Urvi, Coble Joseph, Roy Pampa, Yoo Sarah, Sandler Dale P, Alavanja Michael C
Department of Epidemiology, University of North Carolina Gillings School of Global Public Health, Chapel Hill, North Carolina, USA.
Environ Health Perspect. 2014 Feb;122(2):165-71. doi: 10.1289/ehp.1206274. Epub 2013 Nov 19.
Epidemiologic evidence suggests a negative relation between sunlight exposure and breast cancer risk. The hypothesized mechanism is sunlight-induced cutaneous synthesis of vitamin D.
Our goal was to examine sun exposure and its interaction with vitamin D receptor (VDR) gene variants on breast cancer risk.
We examined sun exposure and breast cancer incidence among 31,021 private pesticide applicators' wives, including 578 cases, enrolled in the prospective Agricultural Health Study cohort and followed 8.6 years on average. We estimated interactions between sun exposure, VDR variants, and breast cancer in a nested case-control study comprising 293 cases and 586 matched controls. Information on sun exposure was obtained by questionnaire at cohort enrollment. Relative risks were estimated using Cox proportional hazards regression for the cohort data and conditional logistic regression for the nested case-control data.
We observed a small decrease in breast cancer risk in association with usual sun exposure of ≥ 1 hr/day (versus < 1 hr/day) 10 years before the start of follow-up among all participants [hazard ratio (HR) = 0.8; 95% CI: 0.6, 1.0]. The association appeared to be slightly stronger in relation to estrogen receptor-positive tumors (HR = 0.7; 95% CI: 0.5, 0.9) than estrogen receptor-negative tumors (HR = 1.1; 95% CI: 0.6, 2.1). The HR for joint exposure ≥ 1 hr/day of sunlight and one VDR haplotype was less than expected given negative HRs for each individual exposure (interaction p-value = 0.07).
Our results suggest that sun exposure may be associated with reduced risk of breast cancer, but we did not find clear evidence of modification by VDR variants. Larger studies are warranted, particularly among populations in whom low levels of usual sun exposure can be more precisely characterized.
流行病学证据表明，阳光照射与乳腺癌风险之间存在负相关关系。推测的机制是阳光诱导皮肤合成维生素D。
我们的目标是研究阳光照射及其与维生素D受体（VDR）基因变异对乳腺癌风险的相互作用。
我们在31,021名私人农药施用者的妻子中研究了阳光照射与乳腺癌发病率，其中包括578例病例，这些人参与了前瞻性农业健康研究队列，平均随访8.6年。我们在一项包含293例病例和586例匹配对照的巢式病例对照研究中估计了阳光照射、VDR变异与乳腺癌之间的相互作用。阳光照射信息通过队列入组时的问卷调查获得。使用Cox比例风险回归对队列数据进行相对风险估计，并使用条件逻辑回归对巢式病例对照数据进行相对风险估计。
在所有参与者中，我们观察到随访开始前10年每天通常阳光照射≥1小时（相对于<1小时）与乳腺癌风险略有降低相关[风险比（HR）=0.8；95%置信区间：0.6,1.0]。与雌激素受体阴性肿瘤（HR = 1.1；95%置信区间：0.6,2.1）相比，这种关联在雌激素受体阳性肿瘤中似乎略强（HR = 0.7；95%置信区间：0.5,0.9）。对于阳光照射≥1小时/天和一种VDR单倍型的联合暴露，其HR低于根据每种个体暴露的阴性HR所预期的值（相互作用p值 = 0.07）。
我们的结果表明阳光照射可能与降低乳腺癌风险有关，但我们没有发现VDR变异修饰作用的明确证据。需要开展更大规模的研究，尤其是在那些能够更精确地描述通常阳光照射水平较低人群的研究。
