The mechanisms of air pollution and particulate matter in cardiovascular diseases

Abstract

Clinical and epidemiological studies demonstrate that short- and long-term exposure to air pollution increases mortality due to respiratory and cardiovascular diseases. Given the increased industrialization and the increased sources of pollutants (i.e., cars exhaust emissions, cigarette smoke, industry emissions, burning of fossil fuels, incineration of garbage), air pollution has become a key public health issue to solve. Among pollutants, the particulate matter (PM) is a mixture of solid and liquid particles which differently affects human health depending on their size (i.e., PM with a diameter <10 μm reach the lung and PM with a diameter <2.5 μm penetrate deeper into the lung). In particular, the acute exposure to PM and PM increases the rate of cardiovascular deaths. Thus, appropriate interventions to reduce air pollution may promote great benefits to public health by reducing the risk of cardiovascular diseases. Several biological mechanisms have been identified to date which could be responsible for PM-dependent adverse cardiovascular outcomes. Indeed, the exposure to PM and PM induces sustained oxidative stress and inflammation. PM is also able to increase autonomic nervous system activation. Some potential therapeutic approaches have been tested both in pre-clinical and clinical studies, based on the intake of antioxidants from dietary or by pharmacological administration. Studies are still in progress to increase the knowledge of PM activation of intracellular pathways and propose new strategies of intervention.

A time‐to‐event analysis on air pollutants with the risk of cardiovascular disease and mortality: A systematic review and meta‐analysis of 84 cohort studies

“…Acute arterial vasoconstriction was also demonstrated in subjects exposed to diesel exhaust 53,54 . Particulate matter causes an increased concentration of cytosolic calcium and reduced sarcoplasmic reticulum ion stores causing reduced cardiac contractility and increased calcium‐activated nuclear signaling leading to hypertrophy 55 . Endothelial oxidative stress depletes the availability of nitric oxide which regulates vascular tone and progression cause atherosclerosis by promoting pro‐atherogenic factors and inhibiting anti‐atherogenic factors 56‐58 .…”

Smoking Influence on the Outcomes and Complications of Coronary Bypass Surgery

“…Табакокурение является одним из основных факто-ров риска развития сердечно-сосудистых заболеваний (ССЗ), в том числе ишемической болезни сердца (ИБС) [3][4][5]. Доказано, что под воздействием токсичных ком-понентов табачного дыма у курящего человека проис-ходит гиперактивация симпато-адреналовой системы, которая приводит к избытку катехоламинов и способ-ствует гиперкоагуляции, вазоконстрикции, развитию дислипидемии и инсулинорезистентности [6][7][8].…”

Mitochondrial toxicity of tobacco smoke and air pollution

“…Both short and long term exposure to air pollution (especially PM 2.5 , PM 10 , ground level ozone) increase the risk of cardiovascular events (hypertensive episodes, myocardial infarction, cardiac arrhythmia, stroke and heart failure) and cardiovascular attributed mortality, especially in individuals with pre-existent cardiovascular disease, the elderly, those that live in urban areas, impoverished communities where unrefined fuels are used indoors and certain occupations 234, 236–244 . In adults of more advanced age, increased exposure to ambient air pollution is positively associated with increased mtDNA to nuclear DNA ratio and blood pressure 245 .…”