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ST Depression, Arrhythmia, Vagal Dominance, and Reduced Cardiac MicroRNA in Particulate-exposed Rats
Citation:
FARRAJ, A., M. S. HAZARI, C. LAMB, D. W. WINSETT, Y. Ge, A. D. Letbetter, A. P. Carll, M. E. BRUNO, A. J. GHIO, AND D. L. COSTA. ST Depression, Arrhythmia, Vagal Dominance, and Reduced Cardiac MicroRNA in Particulate-exposed Rats. AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY. American Thoracic Society, New York, NY, 44(2):185-196, (2011).
Impact/Purpose:
This study provides insight into the mechanisms that mediate electrocardiographic and rhythm disturbances associated with fine particulate matter (PM) air pollution exposure. We demonstrate that PM concentration influences both the quality and magnitude of adverse cardiac responses and triggers associated autonomic, inflammatory, an cardiac microRNA responses. This is the first study to demonstrate an effect of PM exposure on cardiac miRNA e ression in vivo.
Description:
Recently, investigators demonstrated associations between fine particulate matter (PM)-associated metals and adverse health effects. Residual oil fly ash (ROFA), a waste product of fossil fuel combustion from boilers, is rich in the transition metals Fe, Ni, and V, and when released as a fugitive particle, is an important contributor to ambient fine particulate air pollution. We hypothesized that a single inhalation exposure to transition metal-rich PM will cause concentration-dependent cardiovascular toxicity in Spontaneously Hypertensive (SH) rats. Rats implanted with telemeters to monitor heart rate and the electrocardiogram were exposed once by nose-only inhalation for 4 h to 3.5 mg/nr', 1.0 mg/nr' or 0.45 mg/m' of a synthetic PM (dried salt solution), similar in composition to a well-studied ROFA sample, consisting of Fe, Ni and V. Exposure to the high concentration of PM decreased T-wave amplitude and area, caused ST depression, reduced HR, and increased non-conducted P-wave arrhythmias. These changes were accompanied by increased pulmonary inflammation, lung resistance, and vagal tone as indicated by changes in markers of heart rate variability (increased RMSSD, LF, and HF and decreased LF/HF), and attenuated myocardial microRNA expression. The low and intermediate concentrations of PM had lesser effects on inflammatory, HRV, and miRNA endpoints, but nonetheless caused significant reductions in HR. Additionally, the intermediate concentration caused ST depression and increased QRS area while the low concentration increased T-wave parameters. Thus, PM-induced cardiac dysfunction is mediated by multiple mechanisms that may be dependent on PM concentration and myocardial vulnerability (This abstract does not reflect EPA policy).
