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

具体目标是评估产前和生命早期暴露于内分泌干扰物， 双酚A（BPA）和多环芳烃（PAH），在怀孕期间和幼儿期， 与青春期早期儿童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的纵向出生队列中进行， 纽约市的市中心社区正在进行的哥伦比亚中心儿童的 环境卫生。BPA和PAH暴露在同龄母亲和儿童中很普遍。两 在实验和初步的人体试验中， 问题研究这项研究是及时的;儿童肥胖在美国迅速增加， 在少数民族中最高。到5岁时，我们队列中43%的儿童体重超过85%。 年龄。这一流行病可能对公共卫生产生重大影响，特别是在少数民族中 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 队列中的儿童年龄为8-10岁，并将在5岁时评估身高、体重和身体成分， 7岁和8-10岁，代谢综合征组分在8-10岁。暴露剂量计为PAH 母亲产前个人空气样本中的PAH和BPA代谢物浓度以及 从怀孕期间的母亲和3岁、5岁和7岁的孩子身上收集和储存尿样 年我们假设产前暴露于PAH和BPA（1）将与体重增加相关 获得5岁至8-10岁以及8-10岁时BMI z评分、脂肪量和代谢的轨迹 综合征组分和（2）将改变参与脂肪形成的关键基因的甲基化状态， 饥饿控制测量脐带血细胞，这将介导之间的关联 出生后暴露于内分泌干扰物和儿童肥胖的结果。该研究将提供 关于产前/早期生活暴露于内分泌干扰物是否预示着童年的重要数据 肥胖/代谢综合征，并将测试关于潜在的表观遗传机制的假设。

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.