The role of air pollution in emotional neurodevelopment and risk for psychiatric disorders

空气污染在情绪神经发育和精神疾病风险中的作用

• 批准号: 10445289
• 负责人: Megan Marie Herting
• 金额: $ 52.41万
• 依托单位: UNIVERSITY OF SOUTHERN CALIFORNIA
• 依托单位国家: 美国
• 财政年份: 2020
• 资助国家: 美国
• 起止时间: 2020-09-21 至 2025-06-30
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10445289
• 关键词: 10 year old; Address; Adolescence; Adolescent; Adult; Affect; Affective; Age; Age of Onset; Aggressive behavior; Air Pollution; Amygdaloid structure; Anterior; Anxiety; Attention deficit hyperactivity disorder; Axon; Behavior; Behavioral; Biological; Blood; Brain; Brain region; Child; Childhood; Chronic; Cities; Clinical Markers; Data; Dendrites; Development; Diagnosis; Diagnostic; Diagnostic and Statistical Manual of Mental Disorders; Dimensions; Disease; Early Intervention; Emotional; Emotions; Enrollment; Environmental Health; Environmental Impact; Epidemiology; Exposure to; Functional Magnetic Resonance Imaging; Geography; Health Policy; Human; Individual; Inhalation Toxicology; Intervention; Knowledge; Link; Literature; Long-Term Effects; Longitudinal Studies; Measures; Mediation; Mental Depression; Mental Health; Mental disorders; Methodology; Morphology; Neurites; Neurotoxins; Nitrogen Dioxide; Ozone; Particulate Matter; Patient Self-Report; Policies; Prevention; Prevention program; Problem behavior; Psychopathology; Quality of life; Regulation; Research; Risk; Risk Factors; Role; Sampling; Signal Transduction; Structure; Testing; Time; Toxicology; Visit; ambient air pollution; anxiety symptoms; base; behavioral impairment; brain dysfunction; cognitive development; cohort; density; depressive symptoms; design; diagnostic criteria; early adolescence; emotional stimulus; fine particles; follow-up; gray matter; health data; improved; interest; modifiable risk; multi-ethnic; multimodal neuroimaging; neural circuit; neurodevelopment; neuroimaging; neuroimaging marker; neurophysiology; neurotoxic; novel; pollutant; postnatal; pre-clinical; prenatal; relating to nervous system; societal costs; sociodemographics; treatment program; urban area; white matter; 10 year old; Address; Adolescence; Adolescent; Adult; Affect; Affective; Age; Age of Onset; Aggressive behavior; Air Pollution; Amygdaloid structure; Anterior; Anxiety; Attention deficit hyperactivity disorder; Axon; Behavior; Behavioral; Biological; Blood; Brain; Brain region; Child; Childhood; Chronic; Cities; Clinical Markers; Data; Dendrites; Development; Diagnosis; Diagnostic; Diagnostic and Statistical Manual of Mental Disorders; Dimensions; Disease; Early Intervention; Emotional; Emotions; Enrollment; Environmental Health; Environmental Impact; Epidemiology; Exposure to; Functional Magnetic Resonance Imaging; Geography; Health Policy; Human; Individual; Inhalation Toxicology; Intervention; Knowledge; Link; Literature; Long-Term Effects; Longitudinal Studies; Measures; Mediation; Mental Depression; Mental Health; Mental disorders; Methodology; Morphology; Neurites; Neurotoxins; Nitrogen Dioxide; Ozone; Particulate Matter; Patient Self-Report; Policies; Prevention; Prevention program; Problem behavior; Psychopathology; Quality of life; Regulation; Research; Risk; Risk Factors; Role; Sampling; Signal Transduction; Structure; Testing; Time; Toxicology; Visit; ambient air pollution; anxiety symptoms; base; behavioral impairment; brain dysfunction; cognitive development; cohort; density; depressive symptoms; design; diagnostic criteria; early adolescence; emotional stimulus; fine particles; follow-up; gray matter; health data; improved; interest; modifiable risk; multi-ethnic; multimodal neuroimaging; neural circuit; neurodevelopment; neuroimaging; neuroimaging marker; neurophysiology; neurotoxic; novel; pollutant; postnatal; pre-clinical; prenatal; relating to nervous system; societal costs; sociodemographics; treatment program; urban area; white matter

Project Abstract Outdoor air pollution, including fine particulate matter (PM2.5; and its constituents) and nitrogen dioxide (NO2), is ubiquitous in urban areas and is a neurotoxicant. Emerging toxicological and epidemiological evidence suggests that air pollution may contribute to increases in emotional behavioral problems and is linked to various mental health disorders in children, adolescents, and adults. These recent findings have elucidated the need to: 1) examine long-term effects of prenatal and childhood exposure; 2) identify pre-clinical neuroimaging biomarkers of neurotoxicological effects in neural circuitry implicated in mental health risk; and 3) investigate these effects in late-childhood and adolescence, as it is an opportune time to identify and intervene for those at risk for psychiatric disorders. We propose the first longitudinal study to examine how prenatal and childhood air pollution exposure impacts corticolimbic circuitry involved in emotion processing and regulation, and the onset of internalizing and externalizing psychopathology during the transition from late-childhood to early adolescence. Our hypothesis is that prenatal and childhood air pollution exposure contribute to increased risk for mental health disorders during adolescence through alterations in corticolimbic neural circuitry and emotional development. To test our hypothesis, the proposed project will create lifetime residential air pollution exposure estimates and leverage comprehensive neuroimaging of corticolimbic neural circuitry, emotion, and mental health data, from a multi-ethnic and geographically diverse cohort of 9- to 10-year-old children (N=11,873) enrolled in the nationwide longitudinal Adolescent Brain Cognitive Development (ABCD) study. Using multi-modal neuroimaging, we will elucidate the effects of prenatal and childhood air pollution exposure on changes in the structure (Aim 1) and function (Aim 2) of corticolimbic circuitry underlying emotional processing and regulation from late-childhood to early adolescence. In Aim 3, we will examine how prenatal and childhood air pollution exposure influences the development of emotional problems and subsequent risk for mental health disorders by using both: a) dimensional scales and b) mental health diagnostic criteria (based on Diagnostic and Statistical Manual of Mental Disorders). As an exploratory sub-aim, we will also examine a potential mediation of corticolimbic alterations at 9-10 yrs in the link between air pollution exposure during development and subsequent risk for internalizing and externalizing psychopathology at ages 11-12 yrs. This study is primarily focused on long-term prenatal and childhoodPM2.5 and NO2 exposure; however, we also plan to explore differential timing effects of these exposures as well as the potential neurotoxic effects of other ambient pollutants (i.e. ozone, PM components). The large, sociodemographic and geographic diverse sample of children from ABCD are at an opportune age to evaluate pre-clinical markers of psychopathology. This provides great promise for more robust and generalizable findings that have the potential to impact policy as well as identify early neuroimaging biomarkers as targets for early intervention.

项目摘要 室外空气污染，包括细颗粒物（PM2.5；及其成分）和二氧化氮（NO2）是 在城市地区无处不在，是一种神经毒性。新兴的毒理学和流行病学证据表明 空气污染可能导致情绪行为问题的增加，并与各种心理有关 儿童，青少年和成人的健康障碍。这些最近的发现阐明了：1） 检查产前和儿童暴露的长期影响； 2）确定临床前神经影像学生物标志物 与心理健康风险有关的神经回路中神经毒理学作用； 3）研究这些效果 在后期和青春期中，因为现在是时候确定和干预有风险的人 精神疾病。我们提出了第一项纵向研究，以研究产前和儿童空气污染 暴露会影响与情感处理和调节有关的皮质降虫电路，以及 从年龄晚期到青春期早期的过渡期间的内在化和外在化精神病理学。 我们的假设是产前和儿童空气污染暴露有助于增加心理健康的风险 通过改变皮质胶神经回路和情绪发展，青春期期间的疾病。到 检验我们的假设，拟议的项目将创建终生的住宅空气污染估计和 从A的综合神经影像学中，从A 在全国范围内注册的9至10岁儿童（n = 11,873）的多种族和地理上多样的队列 纵向青少年脑认知发展（ABCD）研究。使用多模式神经影像学，我们将 阐明产前和儿童空气污染对结构变化的影响（AIM 1）和 情感处理和调节的函数（目标2） 青春期早期。在AIM 3中，我们将研究产前和儿童空气污染的暴露如何影响 通过使用两者，出现情绪问题和随后患心理健康障碍的风险：a） 维度量表和b）心理健康诊断标准（基于精神的诊断和统计手册 疾病）。作为探索性子AIM，我们还将研究皮质唇改变的潜在介导 在开发过程中空气污染暴露与随后的内在化风险和 在11 - 12岁时外部化心理病理学。这项研究主要集中于长期产前和 Childhohehonepm2.5和No2暴露；但是，我们还计划探索这些暴露的差分定时效应 以及其他环境污染物（即臭氧，PM成分）的潜在神经毒性作用。大， 来自ABCD的儿童的社会人口统计学和地理不同样本正在适合评估 精神病理学前临床标记。这为更健壮和可推广的发现提供了巨大的希望 有可能影响政策的潜力，并确定早期神经影像标记物作为早期的目标 干涉。