Abstract

Background. Atmospheric air pollution with fine particles (PM 2.5) is one of the global challenges having an impact on the disease rate, mortality, and disability of the earth’s population. The optimal content of PM2.5 in the air is < 10 micrograms/m3 (according to WHO), however, this concentration is not completely safe. Currently the impact of fine particles that pollute ambient air on the progression of atherosclerosis and cardiovascular diseases (CVD) is being actively studied. Pathogenetic mechanisms enabling fine particles to partake in atherogenesis are being studied. Understanding specific fundamental mechanisms which underpin PM 2.5-induced atherogenesis allows to improve prevention-care intervention aimed to mitigate the negative impact of PM 2.5 on pathogeny of atherosclerosis and CVD. Objective. Study of the impact of fine particles polluting ambient air on the development and progression of atherosclerosis and CVD, as well as discussion of the main pathogenetic mechanisms that underpin this phenomenon. Methods. PubMed/Medline and Embase databases have been used for searching and analyzing modernday literature. We looked at the terms «fine particles», and «PM 2.5» in combination «atmospheric air» with «atherosclerosis». The search for literary sources has been carried out over the past 15 years. Results. Many experimental and clinical studies prove the connection between fine particles (PM 2.5) polluting ambient air and the risk of atherosclerosis progression and further CVD progression, all the way through to the increased risk of unfavorable cardiovascular events (acute myocardial infarction, cerebral vascular accidents) in persons inhabiting polluted areas. PM 2.5-induced atherosclerosis is underpinned by the following pathogenetic mechanisms: Induction of oxidative stress and enhancement of inflammatory reactions, progression of endothelial dysfunction, as well as dysfunction of vegetative nervous system, and imbalance of coagulative blood system.

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