Ischemic Heart Disease Events Triggered by Short-Term Exposure to Fine Particulate Air Pollution

Abstract

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. Methods and 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 Յ2.5 m; PM 2.5 ) elevated by 10 g/m 3 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 Exposure to Fine Particulate Matter Air Pollution Is Preferentially Associated With the Risk of ST‐Segment Elevation Acute Coronary Events

“…Significant PM 2.5 effects were observed only for patients with existing CAD. These results are largely consistent with previously reported results16, 17 and suggest that elevated PM 2.5 exposures can contribute to triggering of acute coronary events, acutely destabilizing and rupturing atherosclerotic plaque, in those with existing clinically significant CAD but not in those with clean coronary arteries.…”

“…Odds ratios using both the standard linear and threshold models were estimated for all ACS, STEMI, NSTEMI, UA, and NSTE‐ACS events for all patients and for patients with and without CAD. For comparison purposes, and consistent with reporting from various studies and reviews of the literature,1, 2, 3, 4, 5, 6, 7, 8, 11, 14, 15, 16 odds ratios associated with 10‐μg/m 3 incremental increases in PM 2.5 concentration are presented.…”

Air pollution and cardiac remodeling: a role for RhoA/Rho-kinase

“…Recent studies (21, 58) have shown that commonly encountered levels of airborne pollutants can result in a prohypertensive response in humans that may be exaggerated in predisposed individuals. This potentiating effect of inhaled particulates has been noted with other chronic conditions or risk factors such as atherosclerosis, diabetes, and postmenopausal status (31,40,49). Although the precise mechanisms remain elusive, there is increasing evidence that PM 2.5 exposure results in rapid changes in the vasculature (7, 32).…”

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

“…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. Conversely, it was estimated that each 10 μg/m 3 decrease in PM 2.5 was associated with an increase in 0.61 years in mean life expectancy in the United States 27.…”