Ischemic heart disease events triggered by short-term exposure to fine particulate air pollution.
BACKGROUND
Recent evidence suggests that long-term exposure to particulate air pollution contributes to pulmonary and systemic oxidative stress, inflammation, progression of atherosclerosis, and risk of ischemic heart disease and death. Short-term exposure may contribute to complications of atherosclerosis, such as plaque vulnerability, thrombosis, and acute ischemic events. These findings are inconclusive and controversial and require further study. This study evaluates the role of short-term particulate exposure in triggering acute ischemic heart disease events.


RESULTS
A case-crossover study design was used to analyze ischemic events in 12,865 patients who lived on the Wasatch Front in Utah. Patients were drawn from the cardiac catheterization registry of the Intermountain Heart Collaborative Study, a large, ongoing registry of patients who underwent coronary arteriography and were followed up longitudinally. Ambient fine particulate pollution (particles with an aerodynamic diameter < or = 2.5 microm; PM2.5) elevated by 10 microg/m3 was associated with increased risk of acute ischemic coronary events (unstable angina and myocardial infarction) equal to 4.5% (95% confidence interval, 1.1 to 8.0). Effects were larger for those with angiographically demonstrated coronary artery disease.


CONCLUSIONS
Short-term particulate exposures contributed to acute coronary events, especially among 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.
Pope
C Arden
CA
Brigham Young University, Provo, UT 84602-2363, USA. cap3@byu.edu
Muhlestein
Joseph B
JB
May
Heidi T
HT
Renlund
Dale G
DG
Anderson
Jeffrey L
JL
Horne
Benjamin D
BD
D000328:Adult; D000368:Aged; D006328:Cardiac Catheterization; D003324:Coronary Artery Disease / Q000150:complications / Q000209:etiology / Q000503:physiopathology; D003328:Coronary Thrombosis / Q000150:complications / Q000209:etiology / Q000503:physiopathology; D003331:Coronary Vessels / Q000473:pathology / Q000503:physiopathology; D018592:Cross-Over Studies; D018450:Disease Progression; D004781:Environmental Exposure; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000209:etiology*; D017202:Myocardial Ischemia / Q000209:etiology* / Q000503:physiopathology*; D018384:Oxidative Stress / Q000502:physiology; D010316:Particle Size; D052638:Particulate Matter / Q000009:adverse effects*; D013997:Time Factors; D014589:Utah
D052638:Particulate Matter