Exposure to particulate air pollution also may be associated with acute heart attack. This may be due, in part to a sympathetic stress response, as detected by changes in heart rate variability, the production of cytokines, and an increased vulnerability to plaque rupture (Circulation. 2001;104:986, J Am Coll Cardiol. 2002;39:935, Circulation. 2004;109:2655).
In a study of 772 patients with an acute heart attack the risk of an heart attack was increased in the two hours after exposure to elevated levels of fine particles in the air (odds ratio 1.48 compared with low levels of fine particles); this effect lasted for up to 24 hours after exposure (Circulation. 2001;103:2810).
In a systematic review and meta-analysis of data from 34 studies, carbon monoxide, nitrogen dioxide, sulfur dioxide, and small particulate matter (less than 10 microns and less than 2.5 microns) were all associated with an increased risk of heart attack with the overall population attributable risk ranging from 1 to 5 percent (JAMA. 2012;307(7):713).
Short-term particulate exposures contributed to acute coronary events (heart attack) in patients with underlying coronary artery disease. Individuals with stable presentation and those with angiographically demonstrated clean coronaries are not as susceptible to short-term particulate exposure. (Circulation. 2006;114(23):2443).
PM1, PM2.5 and PM10 are risk factors of all-cause, cardiovascular, stroke, respiratory, and COPD mortality. PM1 accounts for the vast majority of short-term PM2.5- and PM10-induced mortality. Smaller size fractions of PM have a more toxic mortality impacts.