Triggering of Transmural Infarctions, but Not Nontransmural Infarctions, by Ambient Fine Particles

Abstract

BackgroundPrevious studies have reported increased risk of myocardial infarction (MI) after increases in ambient particulate matter (PM) air pollution concentrations in the hours and days before MI onset.ObjectivesWe hypothesized that acute increases in fine PM with aerodynamic diameter ≤ 2.5 μm (PM2.5) may be associated with increased risk of MI and that chronic obstructive pulmonary disease (COPD) and diabetes may increase susceptibility to PM2.5. We also explored whether both transmural and nontransmural infarctions were acutely associated with ambient PM2.5 concentrations.MethodsWe studied all hospital admissions from 2004 through 2006 for first acute MI of adult residents of New Jersey who lived within 10 km of a PM2.5 monitoring site (n = 5,864), as well as ambient measurements of PM2.5, nitrogen dioxide, sulfur dioxide, carbon monoxide, and ozone.ResultsUsing a time-stratified case-crossover design and conditional logistic regression showed that each interquartile-range increase in PM2.5 concentration (10.8 μg/m3) in the 24 hr before arriving at the emergency department for MI was not associated with an increased risk of MI overall but was associated with an increased risk of a transmural infarction. We found no association between the same increase in PM2.5 and risk of a nontransmural infarction. Further, subjects with COPD appeared to be particularly susceptible, but those with diabetes were not.ConclusionsThis PM–transmural infarction association is consistent with earlier studies of PM and MI. The lack of association with nontransmural infarction suggests that future studies that investigate the triggering of MI by ambient PM2.5 concentrations should be stratified by infarction type.

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.…”

Short-term exposure to particulate air pollution and risk of myocardial infarction: a systematic review and meta-analysis

“…After obtaining and reading full texts of the remaining articles, 34 studies were excluded: 4 had not sufficient data, 4 were the same or overlapping dataset, 12 were long-term exposure analysis, 5 were reviews or meta-analysis, 7 did not explore the effect of PM2.5 or PM10, and 2 were reported in nonEnglish language. Then, reviewing of reference lists of all the identified articles, related published reviews, metaanalysis, and excluding studies with the same or overlapping dataset in the same region, finally, 31 studies were included (Medina et al 1997;Hoek et al 2000;Linn et al 2000;Mann et al 2002;Sharovsky et al 2004;Peters et al 2005;Sullivan et al 2005;Zanobetti and Schwartz 2005;Barnett et al 2006;Cendon et al 2006;Lanki et al 2006;Pope et al 2006;Zanobetti and Schwartz 2006;Cheng et al 2009;Stieb et al 2009;Ueda et al 2009;Zanobetti and Schwartz 2009;Belleudi et al 2010;Hsieh et al 2010;Mate et al 2010;Rich et al 2010;Nuvolone et al 2011;von Klot et al 2011;Chang et al 2013;Rosenthal et al 2013;Wichmann et al 2013;Bard et al 2014;Milojevic et al 2014;Talbott et al 2014;Wichmann et al 2014;Xie et al 2014). The study screening process is presented briefly in Fig.…”

Refined ambient PM2.5 exposure surrogates and the risk of myocardial infarction

“…2 Briefly, all unscheduled hospital admissions with a primary diagnosis of acute myocardial infarction (International Classification of Diseases 9th Revision [ICD-9] code 410.01, 410.11, 410.21, 410.31, 410.41, 410.51, 410.61, 410.71, 410.31, 410.91) were extracted from the Myocardial Infarction Data Acquisition System (MIDAS), a New-Jersey-wide database of hospital discharges and death certificate registrations. 22,23 We included only those patients who were admitted between January 2004 and December 2006, were ≥18 years of age, were residents of New Jersey at the time of their MI, and had no previous diagnosis of MI.…”

“…Because we only observed a significantly increased relative odds of transmural MI associated with average PM 2.5 concentrations in the 24 hours preceding emergency department admission in the in initial analysis, 2 here, hourly ambient PM 2.5 exposures were computed and averaged over that 24 hour period for each exposure metric. Detailed descriptions of each exposure surrogate and comparisons between them are available elsewhere.…”

“…1 In our previous work, which was included in this meta-analysis, we reported an increased risk of transmural (full wall) MI, but not non-transmural (subendocardial) MI, associated with increased PM 2.5 concentration in the 24 hours before emergency department admission for that infarction. 2 In all of these studies, PM 2.5 measured at one or more nearby (within 10 km) central-site monitors was used as a proxy for a subject’s exposure to PM 2.5 of outdoor origin (i.e., exposure to ambient PM 2.5 ). This likely resulted in exposure error due, in part, to proximity to local sources, human activity patterns (e.g., time spent in various locations) and temporal and spatial variability in the efficiency with which ambient PM 2.5 penetrates into and persists in the indoor environment.…”