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最大的比例。而a 强有力的证据支持成人长期空气污染暴露的作用，相对较 关于空气污染暴露可能影响亚临床动脉粥样形成的发展知之甚少 年轻人。这些致病过程的早期标记，包括颈动脉内膜 厚度（CIMT），动脉僵硬（CAS）和动脉壁组成，以回声性测量，可能 提供有关疾病开端不同方面的见解。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度量的表征是该领域的主要差距 目前尚不清楚早期生命暴露于空气污染物是否会影响颈动脉的进展 从童年到成年的动脉粥样硬化。我们假设这种环境和交通相关的空气污染物 暴露可能会影响不良亚临床心血管表型的发展，由 随着儿童成年，颈动脉粥样硬化的进展。我们将在 南加州儿童健康研究（CHS）是最大，最全面的之一 对空气污染对儿童健康的长期影响的调查。颈动脉超声是 在10岁的CHS儿童子集上进行，提供了亚临床动脉粥样硬化的早期度量。作为 这些参与者现在接近成年早期（〜21-23岁），我们有独特的准备解决 终生空气污染暴露是否与动脉粥样硬化标记的变化有关 从童年到成年初。使用儿童颈动脉超声图像作为基线量度， 我们建议利用CHS参与者正在进行的随访，以获得亚临床的重复评估 动脉粥样硬化措施（CIMT和CAS），并计算颈动脉回声（GSM），这是一种新型动脉指标 壁组成，来自基线和后续超声图像。我们将评估住宅的影响 环境和交通相关的空气污染物对这些亚临床动脉粥样硬化的变化的变化 时间，以及成年初的动脉粥样硬化水平。我们还将评估 心脏代谢功能障碍（葡萄糖，脂质，HBA1C）的空气污染暴露和生物标志物开始开始 研究早期动脉粥样硬化的潜在机制。这项新的研究将填补我们的关键空白 随着时间的流逝，儿童亚临床动脉粥样硬化的了解并研究了终生空气污染的影响 在疾病进展的早期阶段暴露。