Short-term Exposure to Fine Particulate Matter and Myocardial Injury among Patients Undergoing Cardiac Catheterization
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Background/Aim: Fine particles (PM2.5) are associated with a higher risk for coronary events. Cardiac troponin T (cTnT) is a myocardium-specific protein which is measured clinically for the diagnosis and prognosis of myocardial infarction (MI). An elevation in circulating cTnT also occurs in non-ischemic conditions and indicates myocardial damage. We aimed to investigate short-term PM2.5 effects on cTnT and other myocardial injury-related biomarkers among participants undergoing cardiac catheterizations.
Methods: This study included 7,497 plasma cTnT measurements conducted in 2,739 participants presenting to Duke University Hospital (2000 to 2012), partly alongside with measurements of C-reactive protein, fibrinogen, white blood cells, N-terminal-pro brain natriuretic peptide (NT-pro BNP), and partial oxygen pressure (PaO2). Daily PM2.5 was predicted by a neural network-based hybrid model at a 1km resolution and was assigned to participants’ residential addresses. We applied generalized estimating equations to assess associations of PM2.5 with biomarker levels and the risk of a positive cTnT test (cTnT>0.1ng/mL).
Results: Mean PM2.5 concentration was 11.8 μg/m3. Median plasma cTnT was 0.05 ng/mL and the prevalence of a positive cTnT test was 35.6% at presentation. For a 10µg/m3 increase in PM2.5 one day before cTnT measurement, plasma cTnT increased by 11.1% (95% CI: 5.3–17.4) and the odds ratio of a positive cTnT test was 1.12 (95% CI: 1.03–1.23). Participants under 60 years [20.9% (95% CI: 10.2–32.6)] or living in rural areas [17.6% (95% CI: 7.3–28.7)] had stronger associations. There was additionally evidence for positive associations of PM2.5 with fibrinogen and NT-pro BNP within one day after exposure, as well as negative associations with PaO2 at lag 3-4 days.
Conclusions: Our study suggests that acute PM2.5 exposure may elevate indicators of myocardial injury and exertion which substantiates the association of air pollution exposure with adverse cardiovascular events. This abstract does not necessarily represent EPA policy.