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Cardiovascular Effects of Air Pollut...
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Leiser, Claire L.,
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Cardiovascular Effects of Air Pollution: Understanding Biological Risk, Progression of Heart Failure, and Exposure Measurement Error /
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Cardiovascular Effects of Air Pollution: Understanding Biological Risk, Progression of Heart Failure, and Exposure Measurement Error // Claire L Leiser.
作者:
Leiser, Claire L.,
面頁冊數:
1 electronic resource (88 pages)
附註:
Source: Dissertations Abstracts International, Volume: 86-07, Section: A.
Contained By:
Dissertations Abstracts International86-07A.
標題:
Environmental health. -
電子資源:
https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=31559650
ISBN:
9798302157874
Cardiovascular Effects of Air Pollution: Understanding Biological Risk, Progression of Heart Failure, and Exposure Measurement Error /
Leiser, Claire L.,
Cardiovascular Effects of Air Pollution: Understanding Biological Risk, Progression of Heart Failure, and Exposure Measurement Error /
Claire L Leiser. - 1 electronic resource (88 pages)
Source: Dissertations Abstracts International, Volume: 86-07, Section: A.
Research suggests causal associations between air pollution exposure and cardiovascular disease risk, however biologic pathways between these associations are largely unknown. Furthermore, it is possible that exposure measurement error results in biased estimates of health effects from analytic models, thus further evidence for a true causal effect is important to inform public health decision-making. We investigated associations of air pollution exposure between biologic pathways, progression of subclinical cardiovascular disease, and exposure measurement error in many large, epidemiological cohorts representing varying geographical regions. Our first analysis aimed to estimate the association between outdoor air pollution concentrations and the prevalence of a cardiovascular disease associated acquired somatic mutation (clonal hematopoiesis of indeterminate potential, or CHIP) in two cohorts, the Multi-Ethnic Study of Atherosclerosis and the Women's Health Initiative. We did not detect an association between air pollutants and CHIP. We then performed an analysis of the association of outdoor air pollution concentrations on longitudinal progression of subclinical echocardiographic findings suggesting pre-heart failure or heart failure in the Hispanic Latino Community Health Study/ Study of Latinos. We identified an association between air pollutants and subclinical changes consistent with development of early heart failure with reduced ejection fraction. Finally, we estimated differences in cardiovascular disease risk from varying geographic distances from the same predictive model in a pooled analysis of four harmonized epidemiological cohorts. We did not identify a strong impact of decreasing the resolution of the predictive model on inferences regarding air pollution - outcome relationships. Across our three studies, our results provide new insights into our understanding of the relationship between air pollution and cardiovascular disease. While we did not find that acquired somatic mutations related to CHIP were likely mediators of this relationship, nor that exposure misestimation due to reduced spatial precision of pollutant concentration predictions results in bias, we did confirm the relationship between air pollutants and cardiovascular mortality and the evolution of heart failure with reduced ejection fraction. Further research is needed to elucidate specific biological pathways of these exposure outcome relationships.
English
ISBN: 9798302157874Subjects--Topical Terms:
543032
Environmental health.
Subjects--Index Terms:
Air pollution
Cardiovascular Effects of Air Pollution: Understanding Biological Risk, Progression of Heart Failure, and Exposure Measurement Error /
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Research suggests causal associations between air pollution exposure and cardiovascular disease risk, however biologic pathways between these associations are largely unknown. Furthermore, it is possible that exposure measurement error results in biased estimates of health effects from analytic models, thus further evidence for a true causal effect is important to inform public health decision-making. We investigated associations of air pollution exposure between biologic pathways, progression of subclinical cardiovascular disease, and exposure measurement error in many large, epidemiological cohorts representing varying geographical regions. Our first analysis aimed to estimate the association between outdoor air pollution concentrations and the prevalence of a cardiovascular disease associated acquired somatic mutation (clonal hematopoiesis of indeterminate potential, or CHIP) in two cohorts, the Multi-Ethnic Study of Atherosclerosis and the Women's Health Initiative. We did not detect an association between air pollutants and CHIP. We then performed an analysis of the association of outdoor air pollution concentrations on longitudinal progression of subclinical echocardiographic findings suggesting pre-heart failure or heart failure in the Hispanic Latino Community Health Study/ Study of Latinos. We identified an association between air pollutants and subclinical changes consistent with development of early heart failure with reduced ejection fraction. Finally, we estimated differences in cardiovascular disease risk from varying geographic distances from the same predictive model in a pooled analysis of four harmonized epidemiological cohorts. We did not identify a strong impact of decreasing the resolution of the predictive model on inferences regarding air pollution - outcome relationships. Across our three studies, our results provide new insights into our understanding of the relationship between air pollution and cardiovascular disease. While we did not find that acquired somatic mutations related to CHIP were likely mediators of this relationship, nor that exposure misestimation due to reduced spatial precision of pollutant concentration predictions results in bias, we did confirm the relationship between air pollutants and cardiovascular mortality and the evolution of heart failure with reduced ejection fraction. Further research is needed to elucidate specific biological pathways of these exposure outcome relationships.
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https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=31559650
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