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

• 批准号: 8375029
• 负责人: SUSAN A KORRICK
• 金额: $ 5.37万
• 依托单位: UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-12-01 至 2013-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8375029
• 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; Child Development; Childhood; Cognitive; Data; Data Collection; Development; Exposure to; Gonadal Hormones; Gonadal Steroid Hormones; Growth; Growth and Development function; Human; Learning; Life; Longitudinal Studies; Measurement; Measures; Memory; Mental Depression; Metal exposure; Metals; Methods; 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; novel; organochlorine exposure; phthalates; reproductive; research study; sex; sexual dimorphism; urinary; visual motor

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）， 神经发育可能会被性腺激素的潜在破坏所改变，如果 任何关于这些暴露和神经发育的人类研究。青春期是易受伤害的关键时期 性腺激素不仅深刻地影响到生殖成熟的过渡， 过渡到认知和行为成熟。在这种青春期转变的基础上， 组织发展和成长，包括表现出性二态性的大脑区域的成长 可能与性腺类固醇的作用有关事实上，通常在青春期开始的大脑疾病，例如， 精神分裂症可能部分反映了这些区域的发育不足。该试点项目的主要目的是 评估青少年接触邻苯二甲酸酯和BPA与青少年神经行为的关系。的 这项提案是基于一项正在进行的纵向研究，该研究对788名儿童进行了跟踪， 评估生命早期接触污染物（有机氯和金属）与随后 神经发育本研究将使用本母研究的已建立基础设施（包括青少年 神经行为检查）和丰富的现有数据，以解决2个新的主题：（1）潜在的 青少年邻苯二甲酸酯和BPA暴露的发育毒性，以及（2）识别青少年 神经行为结果可能对这些暴露敏感，其依据是：（a） 性腺类固醇和脑功能，（B）动物或人类表现中的性二型性证据，或 (c)与Project 4的啮齿动物模型相似。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酯和BPA代谢物。这些暴露的关系 心理测量：视觉运动能力，言语能力，工作记忆，与 注意缺陷多动障碍（ADHD）和精神症状（例如，抑郁和焦虑）将 被评估。次要目的是评估邻苯二甲酸酯或BPA与 神经行为因性别或青春期状态而异。将这项工作与Project 4的平行动物进行比较 在存在趋同的情况下，模型将增加观察到的效应实际上是暴露的信心。 相关.这将是第一批深入了解这些化合物作为风险因素的研究之一 对于青春期的不良神经发育，暴露影响的高风险年龄，以及 适应不良的神经行为发育可能是严重残疾的根源。