Air pollutant exposure and progression of subclinical atherosclerosis during the critical transition from childhood to adulthood

从童年到成年的关键过渡期间空气污染物暴露和亚临床动脉粥样硬化的进展

• 批准号: 10319610
• 负责人: Shohreh F Farzan
• 金额: $ 57.36万
• 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: 2020-12-16 至 2025-10-31
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10319610
• 关键词: Accounting; Address; Adult; Affect; Age; Air Pollutants; Air Pollution; Atherosclerosis; Biological Markers; Body mass index; California; Cardiovascular Diseases; Cardiovascular Manifestation; Cardiovascular system; Carotid Arteries; Carotid Atherosclerotic Disease; Cessation of life; Child; Child Health; Childhood; Chronic; Clinical; Cross-Sectional Studies; Deposition; Development; Disease; Disease Progression; Elderly; Environmental Risk Factor; Ethnic Origin; Exposure to; Functional disorder; Glucose; Glycosylated hemoglobin A; Health; Homeostasis; Image; Intervention; Investigation; Knowledge; Life; Link; Lipids; Long-Term Effects; Longitudinal Studies; Measures; Morbidity - disease rate; Participant; Particulate Matter; Pathogenesis; Pathogenicity; Pattern; Phase; Phenotype; Population; Prevention strategy; Process; Race; Risk Factors; Role; Testing; Time; Ultrasonography; United States National Institutes of Health; ambient air pollution; arterial stiffness; atherogenesis; blood glucose regulation; blood lipid; blood pressure elevation; cardiometabolism; cardiovascular disorder prevention; cardiovascular disorder risk; cardiovascular health; carotid intima-media thickness; critical developmental period; critical period; early life exposure; emerging adult; follow-up; insight; intimal medial thickening; mortality; novel; prenatal; sex; tool; traffic-related air pollution; ultrasound; university student; young adult

Project Summary Cardiovascular disease (CVD) accounts for the largest proportion of mortality and morbidity worldwide. While a strong body of evidence supports a role for long-term air pollution exposure in CVD among adults, relatively little is known about how air pollution exposures may affect the development of subclinical atherogenesis in younger populations. Early markers of these pathogenic processes, including carotid artery intima-media thickness (CIMT), arterial stiffening (CAS), and arterial wall composition as measured by echogenicity, may provide insight into different facets of the beginnings of disease. The lack of longitudinal studies with repeated characterization of measures of subclinical atherosclerosis in younger populations is a major gap in the field and it is unclear whether early life exposures to air pollutants may impact the progression of carotid atherosclerosis from childhood into adulthood. We hypothesize that ambient and traffic-related air pollutant exposures may influence the development of adverse subclinical cardiovascular phenotypes, indicated by carotid atherosclerosis progression, as children grow into early adulthood. We will test this hypothesis within the Southern California Children's Health Study (CHS), one of the largest and most comprehensive investigations of the long-term effects of air pollution on children's health. Carotid artery ultrasounds were performed on a subset of CHS children at age 10, providing an early measure of subclinical atherosclerosis. As these participants now approach early adulthood (~21-23 years), we are uniquely poised to address the question of whether lifetime air pollution exposures are associated with changes in atherosclerosis markers from childhood into early adulthood. Using childhood carotid artery ultrasound images as a baseline measure, we propose to leverage ongoing follow-up of CHS participants to obtain a repeat assessment of subclinical atherosclerosis measures (CIMT and CAS), and calculate carotid echogenicity (GSM), a novel metric of arterial wall composition, from baseline and follow-up ultrasound images. We will evaluate the effects of residential ambient and traffic-related air pollutants on changes in these measures of subclinical atherosclerosis over time, as well as attained level of atherosclerosis in early adulthood. We will also evaluate the relation between air pollution exposure and biomarkers of cardiometabolic dysfunction (glucose, lipids, HbA1c), to begin to investigate potential mechanisms underlying early atherosclerosis. This novel study will fill a critical gap in our knowledge of subclinical atherosclerosis in children over time and investigate the impact of lifetime air pollution exposure on early phases of disease progression.

项目摘要 心血管疾病（CVD）占全球死亡率和发病率的最大比例。而 强有力的证据支持长期空气污染暴露在成年人CVD中的作用， 关于空气污染暴露如何影响亚临床动脉粥样硬化的发展， 年轻的人口。这些致病过程的早期标志物，包括颈动脉内膜中层 厚度（CIMT）、动脉硬化（CAS）和通过回声反射性测量的动脉壁成分，可以 提供了对疾病开始的不同方面的深入了解。缺乏重复的纵向研究 在年轻人群中亚临床动脉粥样硬化的测量特征是该领域的主要空白 目前还不清楚早期暴露于空气污染物是否会影响颈动脉粥样硬化的进展。 从童年到成年的动脉粥样硬化。我们假设环境和交通相关的空气污染物 暴露可能影响不良亚临床心血管表型的发展， 颈动脉粥样硬化进展，随着儿童成长到成年早期。我们将测试这个假设， 南加州儿童健康研究（CHS）是美国最大和最全面的儿童健康研究之一。 调查空气污染对儿童健康的长期影响。颈动脉超声检查 对10岁的CHS儿童亚组进行，提供亚临床动脉粥样硬化的早期测量。作为 这些参与者现在接近成年早期（约21-23岁），我们独特地准备解决 终生空气污染暴露是否与动脉粥样硬化标志物的变化相关的问题 从童年到成年早期。使用儿童颈动脉超声图像作为基线测量， 我们建议对CHS参与者进行持续随访，以获得亚临床的重复评估， 动脉粥样硬化测量（CIMT和CAS），并计算颈动脉回声（GSM），一种新的动脉指标， 壁组成，从基线和随访超声图像。我们将评估住宅的影响， 环境和交通相关的空气污染物对亚临床动脉粥样硬化这些指标的变化的影响 时间，以及在成年早期达到的动脉粥样硬化水平。我们还将评估 空气污染暴露和心脏代谢功能障碍的生物标志物（葡萄糖、脂质、HbA 1c），开始 研究早期动脉粥样硬化潜在机制。这项新的研究将填补我们的一个关键空白， 随着时间的推移，儿童亚临床动脉粥样硬化的知识，并调查终身空气污染的影响 在疾病进展的早期阶段暴露。