Project 1: Endocrine Disruptors & Obesity Among Inner-City Children

具体目的是评估产前和早期接触内分泌干扰物， 双酚A(BPA)和多环芳烃(PAH)，在怀孕和儿童早期是 与青春期早期儿童的肥胖和代谢综合征有关。这项研究将 在非洲裔美国人和多米尼加儿童正在进行的纵向出生队列中进行 纽约市的市中心社区由哥伦比亚儿童中心开展 环境卫生。双酚A和多环芳烃暴露在队列母亲和儿童中很普遍。两者都有 化合物与实验性和初步人类的肥胖和代谢综合征有关 学习。这项研究是及时的；在美国，儿童肥胖率正在迅速上升， 在少数族裔人群中最高。到5岁时，我们队列中43%的儿童超过85%的体重 对于年龄来说。这一流行病可能会对公共卫生产生重大影响，特别是在少数群体中。 肥胖与2型糖尿病和心血管疾病的风险有关。我们建议遵循以下原则 队列中的儿童年龄在8-10岁，并在5岁时评估身高、体重和身体成分， 7岁和8-10岁，以及8-10岁的代谢综合征成分。曝光剂量计为PAH 孕妇产前个人空气中的浓度和多环芳烃和双酚A代谢物的浓度 从怀孕期间的母亲和3、5和7岁的孩子那里收集和储存的尿样 好几年了。我们假设，产前暴露于多环芳烃和双酚A(1)将与较高的体重相关 从5岁到8-10岁，到8-10岁，通过BMI z-Score、脂肪质量和新陈代谢获得轨迹 综合征成分和(2)将改变参与脂肪形成的关键基因的甲基化状态和 饥饿控制测量在脐带和血细胞之间，这将调解之间的联系 出生后暴露于内分泌干扰物与儿童肥胖结局。这项研究将提供 关于产前/早产期对内分泌干扰物的过度依赖是否可以预测儿童的重要数据 肥胖/代谢综合征，并将测试关于潜在表观机制的假说。

The specific aims are to evaluate whether prenatal and early-life exposures to the endocrine disruptors, bisphenol A (BPA) and polycyclic aromatic hydrocarbons (PAH), during pregnancy and early-childhood are associated with obesity and metabolic syndrome among children during early adolescence. The research will be conducted within the ongoing longitudinal birth cohort of African American and Dominican children from inner-city communities in New York City being conducted by the Columbia Center for Children's Environmental Health. BPA and PAH exposures are widespread among cohort mothers and children. Both compounds have been linked to obesity and metabolic syndrome in experimental and preliminary human studies. The research is timely; childhood obesity is increasing rapidly within the United States, with rates highest among minority populations. By age 5 years, 43% of our cohort children exceed the 85% of weight for age. The epidemic is likely to have significant public health implications, particularly among minority populations, as obesity is linked to risk of type 2 diabetes and cardiovascular disease. We propose to follow the children in the cohort to age 8-10 years and will assess height, weight, and body composition at ages 5, 7 and 8-10 years and metabolic syndrome components at ages 8-10. Exposure dosimeters are PAH concentrations in maternal prenatal personal air samples and PAH and BPA metaboltites concentrations in urine samples collected and stored from the mother during pregnancy and from the child at ages 3,5, and 7 years. We hypothesize that prenatal exposure to PAH and BPA (1) will be associated with higher weight gain trajectories from age 5 to 8-10, and at age 8-10 years with BMI z-score, fat mass and metabolic syndrome components and (2) will alter the methylation status of key genes involved in adipogenesis and hunger control measured in umbilical cord while blood cells, which will mediate the association between postnatal exposures to the endocrine disruptors and childhood obesity outcomes. The research will provide important data on whether prenatal/early-life expsoures to endocrine disruptors predicts childhood obesity/metabolic syndrome and will test hypotheses regarding underlying epigenentic mechansisms.