Cardiovascular effects of air pollution

Abstract

Air pollution is a heterogeneous mixture of gases, liquids and PM (particulate matter). In the modern urban world, PM is principally derived from fossil fuel combustion with individual constituents varying in size from a few nanometres to 10 microm in diameter. In addition to the ambient concentration, the pollution source and chemical composition may play roles in determining the biological toxicity and subsequent health effects. Nevertheless, studies from across the world have consistently shown that both short- and long-term exposures to PM are associated with a host of cardiovascular diseases, including myocardial ischaemia and infarctions, heart failure, arrhythmias, strokes and increased cardiovascular mortality. Evidence from cellular/toxicological experiments, controlled animal and human exposures and human panel studies have demonstrated several mechanisms by which particle exposure may both trigger acute events as well as prompt the chronic development of cardiovascular diseases. PM inhaled into the pulmonary tree may instigate remote cardiovascular health effects via three general pathways: instigation of systemic inflammation and/or oxidative stress, alterations in autonomic balance, and potentially by direct actions upon the vasculature of particle constituents capable of reaching the systemic circulation. In turn, these responses have been shown to trigger acute arterial vasoconstriction, endothelial dysfunction, arrhythmias and pro-coagulant/thrombotic actions. Finally, long-term exposure has been shown to enhance the chronic genesis of atherosclerosis. Although the risk to one individual at any single time point is small, given the prodigious number of people continuously exposed, PM air pollution imparts a tremendous burden to the global public health, ranking it as the 13th leading cause of morality (approx. 800,000 annual deaths).

Estimating the global abundance of ground level presence of particulate matter (PM2.5)

“…In recent years, researchers are finding it worthy to investigate potential links between PM 2.5 exposure and adverse birth outcomes (Slama et al, 2008;Dadvand et al, 2013), epigenetic alteration (Baccarelli et al, 2008;Salam et al, 2012;Byun et al, 2013;Hou et al, 2013) infant mortality (Woodruff et al, 1997;Lipfert et al, 2000;Dales et al, 2004;Glinianaia et al, 2004) atherosclerosis (Araujo et al, 2008;Araujo, 2011;Kaufman, 2011), stroke (Brook, 2008;Brook andRajagopalan, 2009, 2012;Maheswaran et al, 2010Maheswaran et al, , 2012, rheumatic autoimmune disease (Zeft et Table 1. Particulate matter and health outcomes for PM 10 , PM 2.5 and ultrafine particles (UFPs).…”

Differential oxidative stress response in young children and the elderly following exposure to PM2.5

“…Soluble transition metals and organic molecules adsorbed on to the surface of particles are capable of generating reactive oxygen intermediates in lung cells and activating redox-sensitive transcription factors to enhance inflammatory reactions [27]. Moreover, soluble constituents of PM 2.5 that can cross the pulmonary epithelium into the circulation may directly affect the cardiovascular system via imbalance of the autonomic nervous system, systemic oxidative stress, and inflammatory response [28].…”

Ambient particulate matter exposure and cardiovascular diseases: a focus on progenitor and stem cells

“…The Harvard Six Cities study showed that the cardiopulmonary mortality was increased up to 37% in the population exposed to high levels of ambient PM 2.5 over a period of 14–16 years 22. The analysis from a population of 50 million living in the major U.S. cities (The National Morbidity, Mortality and Air Pollution Study) indicated that an increase of 10 μg/m 3 in PM 10 was related to an increase in 0.68% in cardiopulmonary mortality 23, 24, 25. Every 10 μg/m 3 increase in PM 2.5 exposure was also associated with an increase in 4.5% in coronary artery disease (CAD) 26.…”