Cardiovascular effects of air pollution

Abstract

Air pollution is composed of particulate matter (PM) and gaseous pollutants, such as nitrogen dioxide and ozone. PM is classified according to size into coarse particles (PM₁₀), fine particles (PM_2.5) and ultrafine particles. We aim to provide an original review of the scientific evidence from epidemiological and experimental studies examining the cardiovascular effects of outdoor air pollution. Pooled epidemiological studies reported that a 10μg/m³ increase in long-term exposure to PM_2.5 was associated with an 11% increase in cardiovascular mortality. Increased cardiovascular mortality was also related to long-term and short-term exposure to nitrogen dioxide. Exposure to air pollution and road traffic was associated with an increased risk of arteriosclerosis, as shown by premature aortic and coronary calcification. Short-term increases in air pollution were associated with an increased risk of myocardial infarction, stroke and acute heart failure. The risk was increased even when pollutant concentrations were below European standards. Reinforcing the evidence from epidemiological studies, numerous experimental studies demonstrated that air pollution promotes a systemic vascular oxidative stress reaction. Radical oxygen species induce endothelial dysfunction, monocyte activation and some proatherogenic changes in lipoproteins, which initiate plaque formation. Furthermore, air pollution favours thrombus formation, because of an increase in coagulation factors and platelet activation. Experimental studies also indicate that some pollutants have more harmful cardiovascular effects, such as combustion-derived PM_2.5 and ultrafine particles. Air pollution is a major contributor to cardiovascular diseases. Promotion of safer air quality appears to be a new challenge in cardiovascular disease prevention.

Keywords: Air pollution; Cardiovascular mortality; Infarctus myocardique; Mortalité cardiovasculaire; Myocardial infarction; Oxidative stress; Particulate matter; Particules fines; Pollution de l’air; Stress oxydatif.

Figure 1

Translational physiopathological mechanism between air pollution exposure and cardiovascular events. ACS: acute coronary syndrome; AHF: acute heart failure; BF: blood flow; BP: blood pressure; CO: carbon monoxide; E: epinephrine; PAH: polycyclic aromatic hydrocarbons; HDL: high-density lipoprotein; HRV: heart rate variability; LDL: low-density lipoprotein; NE: norepinephrine; NO: nitric oxide; NO₂: nitrogen dioxide; NSTEMI: non-ST-segment elevation myocardial infarction; O₃: ozone; PM: particulate matter; Sens. Rec.: sensitivity receptor; STEMI: ST-segment elevation myocardial infarction; UFP: ultrafine particle.