Project 2: Adolescent Exposure to BPA/Phthalates: Cognitive & Behavioral

项目 2：青少年接触 BPA/邻苯二甲酸盐：认知

基本信息

批准号：
7846647
负责人：
SUSAN A KORRICK
金额：
$ 4.36万
依托单位：
UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN
依托单位国家：
美国
项目类别：
财政年份：
2010
资助国家：
美国
起止时间：
2010-02-15 至 2012-11-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/7846647
关键词：
Achievement Address Adolescence Adolescent Affect Age Animal Model Animals Anxiety Area Attention Attention deficit hyperactivity disorder Behavior Behavior assessment Behavioral Birth Brain Brain Diseases Brain region California Child Childhood Chlorinated Hydrocarbons Cognitive Data Data Collection Development Exposure to Gonadal Hormones Gonadal Steroid Hormones Growth Growth and Development function Human Learning Life Lifestyle-related condition Longitudinal Studies Measurement Measures Memory Mental Depression Metal exposure Metals Outcome Parents Performance Pilot Projects Population Psychometrics Puberty Public Health Research Infrastructure Risk Factors Rodent Rodent Model Role Sampling Schizophrenia Short-Term Memory Source Symptoms System Testing Toxic effect Urine Verbal Learning Work age effect base bisphenol A boys developmental disease disability executive function girls high risk human data insight neurobehavior neurobehavioral neurodevelopment organochlorine exposure phthalates reproductive research study sex sexual dimorphism urinary visual motor

项目摘要

Despite prevalent population exposure to phthalates and bisphenol A (BPA), and evidence that human neurodevelopment is likely to be altered by their potential disruption of gonadal hormones, there are few, if any, human studies of these exposures and neurodevelopment. Adolescence is a key period of vulnerability to gonadal hormones which profoundly affect not only transition to reproductive maturity, but also adolescent transition to cognitive and behavioral maturity. Underlying this adolescent transition is substantial brain organizational development and growth, including growth in brain regions demonstrating sexual dimorphisms likely related to gonadal steroid effects. In fact, brain disorders that typically start in adolescence, e.g. schizophrenia, may, in part, reflect deficient development in these areas. The primary aim of this pilot project is to assess the relation of adolescent exposure to phthalates and BPA with adolescent neurobehavior. The proposal builds on an ongoing longitudinal study of 788 children who have been followed since birth to assess the relation of early life contaminant exposures (organochlorines and metals) with subsequent neurodevelopment. The study will use this parent study's established infrastructure (including adolescent neurobehavioral exams) and wealth of existing data to address 2 new themes: (1) the potential developmental toxicities of adolescent phthalate and BPA exposures, and (2) the identification of adolescent neurobehavioral outcomes likely to be sensitive to these exposures based on: (a) experimental studies of gonadal steroids and brain function, (b) animal or human evidence of sexual dimorphism in performance, or (c) analogy with Project 4's rodent model. New data collection will be urine samples (at adolescent, 13-15 yrs neurobehavior testing) for measurement of phthalate and BPA metabolites. The relation of these exposures with psychometric measures of: visual motor abilities, verbal abilities, working memory, behaviors related to Attention Deficit Hyperactivity Disorder (ADHD), and psychiatric symptoms (e.g., depression and anxiety) will be assessed. Secondary aims will be assessment of the potential for associations of phthalates or BPA with neurobehavior to differ by sex or by pubertal status. Comparing this work with Project 4's parallel animal model will, where there is convergence, increase confidence that observed effects are, in fact, exposure related. This will be among the first studies to provide insight into the role of these compounds as risk factors for adverse neurodevelopment in adolescence, an age at high risk for exposure effects, and an age when maladaptive neurobehavioral development can be a source of substantial disability

尽管人们普遍接触邻苯二甲酸盐和双酚 A (BPA)，并且有证据表明人类神经发育可能会因性腺激素的潜在破坏而改变，如果对这些暴露和神经发育的任何人类研究。青春期是脆弱的关键时期性腺激素不仅深刻影响到生殖成熟的过渡，而且影响青少年向认知和行为成熟过渡。青少年转变的基础是大量的大脑组织发展和成长，包括表现出性别二态性的大脑区域的增长可能与性腺类固醇作用有关。事实上，大脑疾病通常始于青春期，例如精神分裂症可能部分反映了这些领域的发育不足。该试点项目的主要目标旨在评估青少年接触邻苯二甲酸盐和 BPA 与青少年神经行为的关系。这该提案建立在对 788 名儿童进行的一项持续纵向研究的基础上，这些儿童自出生以来一直受到跟踪。评估生命早期污染物暴露（有机氯和金属）与随后的关系神经发育。该研究将使用本家长研究的既定基础设施（包括青少年神经行为检查）和丰富的现有数据来解决两个新主题：（1）潜力青少年接触邻苯二甲酸盐和 BPA 的发育毒性，以及 (2) 青少年邻苯二甲酸盐和 BPA 暴露的发育毒性的识别神经行为结果可能对这些暴露敏感，基于：（a）实验研究性腺类固醇和脑功能，（b）动物或人类表现上性别二态性的证据，或 (c) 与项目 4 的啮齿动物模型的类比。新的数据收集将是尿液样本（青少年，13-15 岁）神经行为测试）用于测量邻苯二甲酸盐和 BPA 代谢物。这些暴露的关系心理测量包括：视觉运动能力、语言能力、工作记忆、相关行为注意力缺陷多动障碍（ADHD）和精神症状（例如抑郁和焦虑）会进行评估。次要目标是评估邻苯二甲酸盐或 BPA 与神经行为因性别或青春期状态而异。将此作品与 Project 4 的平行动物进行比较在存在收敛的情况下，模型将增加人们对观察到的效果实际上是暴露的信心有关的。这将是首批深入了解这些化合物作为风险因素的作用的研究之一青春期神经发育不良、暴露影响高风险年龄以及适应不良的神经行为发育可能是严重残疾的根源