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: 10267189
• 负责人: Megan Marie Herting
• 金额: $ 52.48万
• 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/10267189
• 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; cognitive development; cohort; density; depressive symptoms; design; early adolescence; emotional stimulus; fine particles; follow-up; gray matter; health data; improved; interest; modifiable risk; multi-ethnic; multimodality; 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）， 在城市地区普遍存在，是一种神经毒物。新出现的毒理学和流行病学证据表明 空气污染可能会导致情绪行为问题增加，并与各种心理问题有关 儿童、青少年和成人的健康障碍。这些最近的发现阐明了需要：1) 检查产前和儿童时期接触的长期影响； 2) 识别临床前神经影像生物标志物 与心理健康风险有关的神经回路的神经毒理学效应； 3）研究这些影响 在儿童晚期和青春期，因为这是识别和干预那些有风险的人的最佳时机 精神疾病。我们提出第一项纵向研究来检验产前和儿童期空气污染如何影响 暴露会影响参与情绪处理和调节的皮质边缘回路，以及 从童年晚期到青春期早期的过渡期间内化和外化精神病理学。 我们的假设是，产前和儿童时期接触空气污染会增加心理健康风险 青春期期间皮质边缘神经回路和情绪发展的改变引起的疾病。到 检验我们的假设，拟议项目将创建终生住宅空气污染暴露估计值， 利用皮质边缘神经回路、情绪和心理健康数据的综合神经影像 多民族、多地域的 9 至 10 岁儿童队列（N=11,873）在全国范围内注册 纵向青少年大脑认知发展（ABCD）研究。使用多模态神经影像学，我们将 阐明产前和儿童期空气污染暴露对结构变化的影响（目标 1）和 皮质边缘回路的功能（目标 2）是从童年晚期到情绪处理和调节的基础 青春期早期。在目标 3 中，我们将研究产前和儿童时期的空气污染暴露如何影响 使用以下两者会导致情绪问题的发展以及随后出现精神健康障碍的风险：a) b) 心理健康诊断标准（基于《心理诊断与统计手册》） 障碍）。作为一个探索性的子目标，我们还将研究皮质边缘改变的潜在中介作用 开发过程中空气污染暴露与随后的内化和风险之间的联系需要 9-10 年 在11-12岁的时候将精神病理学外化。这项研究主要关注长期产前和 童年PM2.5和NO2暴露；然而，我们还计划探索这些暴露的不同时间效应 以及其他环境污染物（即臭氧、PM 成分）的潜在神经毒性作用。大的、 来自 ABCD 的儿童的社会人口和地理样本处于评估的合适年龄 精神病理学的临床前标志物。这为更可靠和更普遍的发现提供了巨大的希望 有可能影响政策并确定早期神经影像生物标志物作为早期治疗的目标 干涉。