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Air pollution and cardiovascular disease: Can the Australian bushfires and global

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INTRODUCTION

Air pollutants have measurable health impacts, with particularly profound effects on cardiovascular health. Ambient air pollution is the number one environmental risk factor for all-cause mortality, and ranks 5th overall, higher than tobacco smoking, HIV/AIDS, and all forms of violence including war.[1] An estimated 8.8 million excess deaths a year are attributable to poor air quality with an associated healthcare cost of US$1–3 trillion.[2, 3] We cannot choose the air that we breathe and while air quality has improved in many developed countries since the 1970s, 90% of the world’s population currently live in areas where air pollution exceeds World Health Organization’s (WHO) guidelines, with a disproportionate percentage of those in developing countries. Worryingly, recent epidemiological evidence suggests that even air pollution levels below WHO guidelines are still associated with damaging health effects.[4, 5]

Numerous epidemiological studies have correlated increased air pollution to a range of cardiovascular diseases (CVDs) including arrhythmias,[6, 7] atherosclerosis[8] and acute myocardial infarction (AMI).[9] Despite the lungs being the major entry point of airborne pollutants into the body, 60% of deaths attributed to pollution are due to CVD, outweighing mortality due to respiratory disease.[1] These findings demonstrate that airborne pollutants play a key role in mediating CVD progression. With 30% of global CVD deaths currently attributable to air pollution, combatting poor air quality to reduce CVD morbidity should now be a global priority.

Here, we discuss the ways in which air pollution elicits its detrimental effects on the cardiovascular system and how two major events in 2020 drastically altered air pollution levels and their knock-on effects on CVD mortality. Using the Australian bushfires of 2019–2020 and the COVID-19 pandemic lockdown as examples, we consider the importance of reducing air pollution as a mechanism to combat CVD.

COMPOSITION AND SOURCES OF AIRBORNE POLLUTANTS

Air pollution is a heterogeneous mix of gases, semi-volatile liquids, and particles, the exact composition of which is dependent on pollutant sources and environmental factors. In general, these pollutants are classified into primary and secondary pollutants, formed via physico-chemical transformation of primary pollutants. Primary pollutants encompass particulate matter (PM), hydrocarbons, and inorganic gasses (e.g., ozone, nitrogen dioxide [NO2], sulfur dioxide [SO2]). Although negative correlations have been reported between gaseous pollutants, studies performed using isolation chambers found that ambient levels of these gases alone do not induce acute cardiovascular dysfunction.[10] It is proposed that instead of acting directly to induce CVD, gaseous pollutants can act as co-pollutants, amplifying the detrimental effects of PM.[11] Consequently, PM is currently considered to be the primary mediator of air pollutant-induced cardiovascular events and will be focused upon throughout this review.

Airborne PM is a mixture of solid and liquid particles of a variety of sizes suspended in the air. Particles are composed of various materials including, but not limited to, elemental or organic carbon, mineral dust, organic compounds (e.g., polycyclic aromatic hydrocarbons [PAHs]), biological material (e.g., cell fragments), metals (e.g., lead), and sea salt. Primary particles can react with gases in the atmosphere resulting in secondary PM formed of a core surrounded by a variety of chemical compounds. The availability of chemicals on the surface of particles changes their ability to induce pathological responses, and the cardiovascular effects of PM are highly dependent on their source. Urban PM has been linked to multiple cardiac effects while rural PM increased blood pressure. However, maritime wind PM was observed to have no adverse cardiac effects.[12] PM can also absorb biological material, such as endotoxins or viruses, enhancing pathogenicity.[13]

Due to the complex nature of PM, it is typically classified by the size of the particles (Figure 1A). Coarse particles have a diameter of 2.5–10 µm (PM10), and 10 of these particles could comfortably sit across the width of a human hair, making them small enough to deposit in the tracheobronchial tree of the lung. They are produced by sources including bushfires, road dust, agriculture, and sea spray. These particles are commonly comprised of dust, pollen, metals (e.g., silicone, aluminium), and ground materials. PM10 has a half-life of hours to days and are distributed up to 100 km from their source. Current WHO guidelines recommend that average daily exposure to PM10 is kept below 50 µg per cubic meter of air (µg/m3). An elevation in PM10 of 10 µg/m3 is estimated to increase daily cardiopulmonary mortality by 0.68%.[14]

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Composition of particulate matter (PM) in air pollution. (A) Particles with a diameter of 2.5–10 µm are classified as coarse particles (PM10). Fine particles have a diameter of 0.1–2.5 µm (PM2.5) and ultrafine particles have a diameter less than 0.1 µm. (B) PM2.5 derived from combustion have a complex composition typically with an elemental carbon core coated with a range of…



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2021-06-10 02:33:26

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