Agudo Antonio, Peluso Marco, Munnia Armelle, Luján-Barroso Leila, Barricarte Aurelio, Amiano Pilar, Navarro Carmen, Sánchez María-José, Quirós J Ramón, Ardanaz Eva, Larrañaga Nerea, Tormo María-José, Chirlaque María-Dolores, Rodríguez-Barranco Miguel, Sánchez-Cantalejo Emilio, Cellai Filippo, Bonet Catalina, Sala Núria, González Carlos A
Unit of Nutrition and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology-IDIBELL, L'Hospitalet de Llobregat, 08908 Barcelona, Spain.
ISPO-Cancer Prevention and Research Institute, 50139 Florence, Italy.
Carcinogenesis. 2017 Jul 1;38(7):691-698. doi: 10.1093/carcin/bgx047.
Epidemiologic evidence linking environmental exposure to polycyclic aromatic hydrocarbons (PAH) with breast cancer is limited. Measurement of DNA adducts formed by aromatic compounds, including PAH, has been carried in breast tissue samples and white blood cells from women with breast cancer and different kinds of controls. However, these studies provide inconsistent results and bias cannot be ruled out. During the 7-year follow-up period, 305 women were diagnosed with first primary breast cancer in the EPIC-Spain cohort, and were compared with a sample of 149 women without breast cancer at recruitment, using a case-cohort approach. Aromatic adducts to DNA from leukocytes collected at recruitment were measured by means of the 32P-post-labelling technique. The relative risk and 95% confidence interval (CI), adjusted by relevant confounders, were estimated by a modified version of Cox proportional hazards model. There was a significant increased risk for developing breast cancer when DNA adduct concentrations were doubled, with adjusted RR of 1.61 (95% CI 1.29-2.01). The increase in breast cancer risk was observed both for pre- and post-menopausal women. There was a significant interaction with tobacco smoking and body mass index, with higher effect of DNA adducts on breast cancer risk among smokers and women with normal weight. The results from our study support the hypothesis that factors leading to higher levels of aromatic DNA adducts in white blood cells may be involved in development of breast cancer.
将环境暴露于多环芳烃（PAH）与乳腺癌联系起来的流行病学证据有限。在乳腺癌患者及不同类型对照的乳腺组织样本和白细胞中，已对包括PAH在内的芳香族化合物形成的DNA加合物进行了测量。然而，这些研究结果并不一致，且无法排除偏差。在7年的随访期内，EPIC-西班牙队列中有305名女性被诊断为原发性乳腺癌，采用病例队列研究方法，将她们与招募时149名无乳腺癌的女性样本进行比较。采用³²P后标记技术测量招募时采集的白细胞中DNA的芳香族加合物。通过Cox比例风险模型的改良版本估计经相关混杂因素调整后的相对风险和95%置信区间（CI）。当DNA加合物浓度翻倍时，患乳腺癌的风险显著增加，调整后的RR为1.61（95%CI 1.29 - 2.01）。绝经前和绝经后女性均观察到乳腺癌风险增加。吸烟与体重指数之间存在显著交互作用，在吸烟者和体重正常的女性中，DNA加合物对乳腺癌风险的影响更大。我们的研究结果支持以下假设：导致白细胞中芳香族DNA加合物水平升高的因素可能与乳腺癌的发生有关。
