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: 10516055
• 负责人: Shohreh F Farzan
• 金额: $ 58.34万
• 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/10516055
• 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; Early Diagnosis; Elderly; Environmental Risk Factor; Ethnic Origin; Exposure to; Functional disorder; Glucose; Glycosylated hemoglobin A; Health; Homeostasis; Image; Intervention; Investigation; Knowledge; Life; Life Cycle Stages; 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; 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.

项目总结