Sunday, June 1, 2025
6/1/2025
Air Pollution, Coronary Events and Atherosclerotic Progression in a Susceptible Population - Abstract Cardiovascular health is a global public health priority. Atherosclerosis is the most common form of coronary heart diseases (CHD) which constitutes 17.5 million deaths worldwide annually. Globally, both outdoor and indoor air pollutants are known as major contributors to the burdens of CHD. Despite population-based evidence suggesting that exposure to ambient air pollutants and use of solid fuel for cooking causes increased mortality from CHD, there is little known about the impact of air pollution on CHD morbidity and progression. For example, the extent to which exposure to air pollution accelerates atherosclerosis, initiate plaque instability to rupture and develop coronary events, and the mechanistic pathways underneath are largely unknown. A better understanding of air pollutants as potential factors to the development and progression of this pervasive disease will be valuable for public health protection strategies, especially for susceptible population such as patients with atherosclerosis. Here we propose a longitudinal cohort study and present an overarching hypothesis that long-term exposure to air pollutants alter coronary biological process, accelerate disease progression, and contribute to CHD morbidity and mortality. This study builds upon a well-selected 3500 patients with atherosclerosis in Beijing retrieved from an existing cohort and will add two waves of clinic visits in 1100 subpopulation to examine disease progression. The cohort includes extensive data of novel subclinical markers from computed tomography angiography (CTA) reflecting plaque morphology, plaque vulnerability, vascular stenosis, and coronary inflammation, and also collects biomarkers related to their mechanistic pathways. We also propose to add state-of-the art air pollution exposure assessment to determine individual level of outdoor and indoor air pollution exposure of the highest quality to address our study hypotheses. Firstly, we will determine the impact of outdoor and indoor air pollution exposures on coronary events and total cardiovascular mortality. Secondly, we will investigate the effects of exposure to air pollution on atherosclerosis progression and high-risk plaque formation characterized by CTA outcomes. Thirdly, we will examine the effects of air pollution on biological markers of inflammation pathways and explore whether these pathways mediate any response of disease progression to air pollution exposure. Lastly, we will take the unique opportunity of the most stringent regulation period on air pollution in Beijing and assess whether long-term decline in ambient air pollution change the worsening of the disease progression and biological responses as our secondary hypothesis. Apart from the main analysis, we will also explore the potential of joint effects of air pollutant mixtures and independent effects of air pollution exposure from traffic noise on CHD. Findings from this study will not only extend scientific knowledge on air pollution and CHD physiopathology, but will provide information to guide public policy and inform clinical management for individuals at-risk of CHD.
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