Date of Award

31-8-2024

Document Type

Thesis

School

School of Chemical & Biotechnology

Programme

Ph.D.-Doctoral of Philosophy

First Advisor

Prof.Gino A Kurian

Keywords

Particulate Matter Air Pollution, Cardiovascular Disease, Mitochondria, Pharmacology, Toxicology

Abstract

Air pollution, characterized by the presence of harmful substances in the atmosphere, represents a significant environmental and public health challenge impacting millions worldwide. The World Health Organization (WHO) reports that approximately 90% of the global population resides in regions where air pollution surpasses the recommended thresholds for healthy air quality. Within the realm of air pollution, the composition of particulate matter emerges as a pivotal consideration, particularly regarding PM2.5, comprising minute particles originating from diverse sources such as combustion processes, industrial operations, and natural phenomena like wildfires and dust storms. PM2.5 exhibit a range of chemical and physical attributes contingent upon their origins, thereby influencing their toxicity and potential health implications.

While extensive research has scrutinized the association between PM2.5 exposure and respiratory ailments such as chronic obstructive pulmonary disease and cancer, the cardiotoxicity of PM2.5 have frequently been overlooked, even with evidences linking exposure to elevated risks of cardiovascular diseases like atherosclerosis and myocardial infarction (MI). In addition to its cardiotoxic effects, PM2.5 has been implicated in vascular toxicity as well. Residents in regions with high PM2.5 levels, such as those proximate to major roadways or industrial hubs, face amplified risks of atherosclerosis or exacerbation of pre- existing calcification conditions.

Nonetheless, the precise role of PM2.5 in promoting and inducing calcification remains unresolved. PM2.5 induced alterations in myocardial basal levels may compromise its resilience against stress, impede adaptive mechanisms, and hinder reparative processes, culminating in severe cardiac complications. The perturbed blood circulation stemming from PM2.5 exposure precipitates ischemia, prompting the body's efforts to alleviate blockages. Surgical interventions like Coronary Artery Bypass Grafting (CABG), angioplasty, or primary percutaneous coronary intervention (PPCI) may become necessary, leading to the risk of ischemia reperfusion injury (IR).

Furthermore, PM2.5 exposure increases the likelihood of MI occurrences and reducing the cardiac recovery post-MI. Even though there is an association between PM2.5 exposure and cardiac events such as IR and MI, the precise underlying mechanisms remain incompletely elucidated. Mitigating PM2.5-induced cardiotoxicity and enhancing myocardial resilience against stress necessitates the exploration of personalized protective measures and environmental pollution abatement strategies. Identifying suitable therapeutic agents to alleviate PM-induced cardiotoxicity and thereby increase the myocardial endurance against subsequent stress, including revascularization procedures, emerges as a critical imperative.

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