Dietary and Environmental Exposure to Cadmium and the Risk of Endometrial Cancer

饮食和环境中镉的暴露与子宫内膜癌的风险

• 批准号: 8272594
• 负责人: PAMELA L HORN-ROSS
• 金额: $ 23.77万
• 依托单位: CANCER PREVENTION INSTIT OF CALIFORNIA
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-06-01 至 2014-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8272594
• 关键词: Accounting; Air; Body Burden; Breathing; Cadmium; California; Cancer Etiology; Carcinogens; Chronic; Cohort Studies; Data; Databases; Development; Diagnosis; Diet; Dietary Cadmium; Dietary intake; Disease; Endometrial Carcinoma; Enrollment; Environmental Exposure; Environmental Pollution; Epidemiology; Estrogens; Etiology; Exposure to; Fossil Fuels; Future; Human; Malignant Neoplasms; Measurement; Measures; Metal exposure; Nested Case-Control Study; Play; Population; Process; Progestins; Property; Relative (related person); Research; Residual state; Risk; Risk Factors; Role; Seafood; Seeds; Smoking History; Soil; Source; Specimen; Testing; Trace metal; Urine; Vegetables; Woman; cancer risk; case control; cigarette smoking; cigarette smoking; disorder risk; improved; modifiable risk; nutrition; prospective; public health relevance; residence; teacher; toxic metal

DESCRIPTION (provided by applicant): Exposure to high levels of circulating estrogens unopposed by progestins is the primary cause of endometrial cancer. However, little is known about whether environmental contaminants that mimic the effects of estrogen increase the risk of this disease. Cadmium is a trace metal released into air and soil as a byproduct of industrial processes and is perhaps the most potent of these estrogenic contaminants with respect to endometrial cancer etiology. Major sources of non-occupational exposure to Cd include cigarette smoke, diet, and inhalation of ambient air contaminated by industrial processes and combustion of fossil fuels. This proposed study will test the emerging hypothesis that greater levels of Cd exposure increase endometrial cancer risk by utilizing existing data on dietary intake, residence, smoking history, and other risk factors and urine specimens from 356 women diagnosed with endometrial cancer and 683 matched controls enrolled in the Nutrition, Estrogens and Endometrial Cancer in Teachers (NEET) study, a nested case-control study within the California Teachers Study (CTS) cohort. The availability of these data, urine specimens for the measurement of Cd concentration-a classic measure of chronic exposure, and existing databases of environmental and dietary sources of Cd, will allow us to conduct a comprehensive assessment of exposure that incorporates a myriad of sources and evaluates the relative contribution of each source. This will also allow us to assess whether any observed elevations in risk are heterogeneous across exposure sources. The specific aims of this study will be to: 1) characterize exposure to Cd from dietary and environmental sources for all cases and controls in the NEET study; 2) evaluate the contributions of dietary intake and exposure from environmental sources on Cd concentrations measured in urine; and 3) estimate the effects of dietary, environmental, and total Cd exposure on the risk of endometrial cancer. The emerging evidence that Cd is a potential risk factor for endometrial cancer suggests a future direction for minimizing dietary and environmental exposures to this toxic metal. This study offers a unique and timely opportunity to improve our understanding of whether Cd plays an etiologic role in the development of this cancer and identify important, and potentially modifiable, sources of exposure to this metal. PUBLIC HEALTH RELEVANCE: Cadmium is a toxic metal known that is classified as a human carcinogen and is suspected of having estrogenic properties. By evaluating whether the risk of endometrial cancer is increased by exposure to cadmium, this proposed study offers a unique and timely opportunity to improve our understanding of a potentially modifiable risk factor for this disease and identify specific sources of cadmium that could be targeted for minimizing exposure.

描述（由申请人提供）：暴露于高水平的循环雌激素而不受孕激素的抵抗是子宫内膜癌的主要原因。 然而，对于模仿雌激素作用的环境污染物是否会增加这种疾病的风险，人们知之甚少。 镉是工业过程中释放到空气和土壤中的一种微量金属，可能是子宫内膜癌病因学中最有效的雌激素污染物。 非职业接触镉的主要来源包括吸烟、饮食和吸入工业过程和化石燃料燃烧污染的环境空气。 这项拟议的研究将通过利用现有的饮食摄入量，居住，吸烟史和其他风险因素以及来自356名被诊断患有子宫内膜癌的妇女和683名参加营养，雌激素和子宫内膜癌教师研究（NEET）的匹配对照的尿液标本的数据来测试新出现的假设，即更高水平的镉暴露会增加子宫内膜癌的风险，一项在加州教师研究（CTS）队列中进行的巢式病例对照研究。 这些数据的可用性，尿标本的测量镉浓度的一个经典的措施，慢性暴露，现有的数据库的环境和饮食来源的镉，将使我们能够进行全面的评估，结合了无数的来源，并评估每个来源的相对贡献。 这也将使我们能够评估任何观察到的风险升高是否在暴露源之间具有异质性。 本研究的具体目的是：1）描述NEET研究中所有病例和对照组的膳食和环境来源的镉暴露特征：2）评估膳食摄入和环境来源的暴露对尿镉浓度的贡献;评估饮食、环境和总镉暴露对子宫内膜癌风险的影响。 新出现的证据表明，镉是子宫内膜癌的一个潜在的危险因素，建议未来的方向，尽量减少饮食和环境暴露于这种有毒金属。 这项研究提供了一个独特的和及时的机会，以提高我们的理解是否镉在这种癌症的发展中起着病因学的作用，并确定重要的，潜在的可修改的，暴露于这种金属的来源。 公共卫生相关性：镉是一种已知的有毒金属，被归类为人类致癌物质，并被怀疑具有雌激素特性。 通过评估暴露于镉是否会增加子宫内膜癌的风险，这项拟议的研究提供了一个独特而及时的机会，以提高我们对这种疾病的潜在可改变的风险因素的理解，并确定特定的镉来源，可以有针对性地减少暴露。