Air Pollution, Intima-media Thickness, and Lung Function in College Students

大学生空气污染、内膜中层厚度与肺功能

• 批准号: 7663140
• 负责人: Edward Avol
• 金额: $ 69.02万
• 依托单位: UNIVERSITY OF SOUTHERN CALIFORNIA
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-09-30 至 2011-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7663140
• 关键词: Acute; Address; Adult; Affect; Age; Air Pollutants; Air Pollution; American; American Heart Association; Anti-Inflammatory Agents; Anti-inflammatory; Area; Arterial Fatty Streak; Atherosclerosis; Birth; Blood; Bone Marrow; C-reactive protein; California; Cardiovascular Diseases; Cardiovascular system; Carotid Arteries; Cessation of life; Child health care; Childhood; Chronic; Chronic lung disease; Clinical; Code; Cohort Studies; Data; Deposition; Development; Diabetes Mellitus; Diet; Disease; Dose; Dyslipidemias; Environment; Epidemiology; Equation; Exposure to; Government; Growth; Individual; Inflammation; Inflammatory; Inflammatory Bowel Diseases; Inflammatory Response; Knowledge; Lead; Life; Life Expectancy; Link; Lipids; Low-Density Lipoproteins; Lung; Lung diseases; Measures; Mediating; Modeling; Modification; Monitor; Morbidity - disease rate; Nitrogen Dioxide; North America; Organ; Oryctolagus cuniculus; Oxidative Stress; Ozone; Particulate Matter; Passive Smoking; Pathology; Pathway interactions; Pattern; Pharmaceutical Preparations; Phenotype; Pneumonia; Pollution; Population; Predisposing Factor; Prevention; Process; Prospective Studies; Protein C; Proteins; Publishing; Reaction; Recording of previous events; Recruitment Activity; Reporting; Research; Research Personnel; Residencies; Respiratory System; Respiratory physiology; Respiratory tract structure; Rheumatoid Arthritis; Risk; Science; Smoking; Statistical Models; Students; Testing; Thick; Time; Tissues; Translating; Universities; Weight; atherogenesis; base; body system; chemokine; clinically relevant; cytokine; interest; intima media; monocyte; mortality; non-smoking; pollutant; population based; prenatal; programs; prospective; research study; residence; respiratory; response; university student; uptake; young adult

DESCRIPTION (provided by applicant): This project pursues the hypothesis that lifetime cumulative exposure to ambient air pollution is associated with sonographically measured carotid intima-media thickness (CIMT) at age 18-20. CIMT is an established marker of subclinical atherosclerosis - the primary pathogenic process of cardiovascular diseases (CVD). CIMT gradually increases from birth to death and is associated with subclinical inflammation at all ages, and is a strong determinant of CVD. Ambient air pollution is associated with cardiovascular mortality and morbidity and is a cause of pulmonary and systemic inflammation - a hallmark of atherosclerosis. Significant associations between air pollution and CIMT have been reported in adults. Long-term exposure to air pollution also adversely affects lung function (LF) which is a strong predictor of CVD mortality. Both pulmonary and systemic inflammation is an important correlate of poor LF. Poor LF also modifies the distribution and uptake of pollutants in the respiratory tract, leading to higher tissue dose. Given systemic inflammation affecting CIMT, LF and dyslipidemia, low LF, high C-reactive protein (CRP) and high lipids (LDL) these markers will be used to those most susceptible to atherogenic effects of air pollution. CIMT, lifetime residential history, cardio-respiratory covariates, LF, LDL and CRP will be assessed among 800 non-smoking USC College students with lifetime California residencies. Statewide air pollution monitoring information will be assembled to interpolate monthly fine particulate matter (PM2.5), nitrogen- dioxide (NO2) and ozone (O3) concentrations to each residence across lifetime. Concentrations will be weighted by activity levels and time spent indoors and outdoors to individually derive estimates of lifetime exposure. The association between exposure and CIMT and the interaction with LF, CRP and LDL will be investigated with multivariate regressions, tests for interactions, and structural equation modeling. The American Heart Association recommends focusing on prevention of atherosclerosis in early life. Air pollutants represent ubiquitous inflammatory exposures, and millions of young Americans live in areas that exceed current government standards. Small differences in CIMT and LF at a young age translate into clinically relevant diseases, including CVD - the leading cause of mortality in the U.S.

描述（由申请人提供）：该项目追求这样的假设：终生累积暴露于环境空气污染与 18-20 岁时超声测量的颈动脉内膜中层厚度 (CIMT) 相关。 CIMT 是亚临床动脉粥样硬化（心血管疾病 (CVD) 的主要致病过程）的既定标志物。 CIMT 从出生到死亡逐渐增加，与所有年龄段的亚临床炎症相关，是 CVD 的重要决定因素。环境空气污染与心血管死亡率和发病率相关，并且是肺部和全身炎症（动脉粥样硬化的一个标志）的原因。据报道，成人空气污染与 CIMT 之间存在显着关联。长期暴露于空气污染也会对肺功能（LF）产生不利影响，而肺功能是 CVD 死亡率的有力预测因素。肺部和全身炎症都是 LF 不良的重要相关因素。较差的低频还会改变呼吸道中污染物的分布和吸收，导致组织剂量更高。鉴于影响 CIMT、LF 和血脂异常、低 LF、高 C 反应蛋白 (CRP) 和高脂质 (LDL) 的全身炎症，这些标志物将用于那些最容易受到空气污染致动脉粥样硬化影响的人群。 CIMT、终生居住史、心肺协变量、LF、LDL 和 CRP 将对 800 名在加州终生居住的非吸烟南加州大学学生进行评估。将汇总全州范围内的空气污染监测信息，以插值每个住宅在整个生命周期内每月的细颗粒物 (PM2.5)、二氧化氮 (NO2) 和臭氧 (O3) 浓度。浓度将根据活动水平和室内外时间进行加权，以分别得出终生暴露的估计值。将通过多元回归、相互作用检验和结构方程模型来研究暴露与 CIMT 之间的关联以及与 LF、CRP 和 LDL 的相互作用。美国心脏协会建议在生命早期重点预防动脉粥样硬化。空气污染物代表着无处不在的炎症暴露，数百万美国年轻人生活在超出当前政府标准的地区。年轻时 CIMT 和 LF 的微小差异会转化为临床相关疾病，包括 CVD——美国的主要原因死亡。