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Increased Non-conducted P-wave Arrhythmias after a Single Oil Fly Ash Inhalation Exposure in Hypertensive Rats
Citation:
FARRAJ, A., N. HAYKAL-COATES, D. W. WINSETT, M. S. HAZARI, A. CARLL, W. ROWAN, A. D. LEDBETTER, W. CASCIO, AND D. L. COSTA. Increased Non-conducted P-wave Arrhythmias after a Single Oil Fly Ash Inhalation Exposure in Hypertensive Rats . ENVIRONMENTAL HEALTH PERSPECTIVES. National Institute of Environmental Health Sciences (NIEHS), Research Triangle Park, NC, 117(5):709-715, (2009).
Impact/Purpose:
Exposure to combustion-derived fine particulate air pollution is associated with increased cardiovascular morbidity and mortality especially in individuals with cardiovascular disease, including hypertension. PM inhalation causes several adverse changes to cardiac function that are reflected in the electrocardiogram (ECG) including altered cardiac rhythm, myocardial ischemia, and reduced heart rate variability. The sensitivity and reliability of ECG-derived parameters as indicators of the cardiovascular toxicity of particulates in rats is unclear. Recently, investigators in the CALFINE study demonstrated an association between the fine PM-associated metals, Ni and Fe, in ambient air and increased mortality (Ostro et al. 2007). Kodavanti et al (2000) demonstrated that hypertensive rats develop greater pulmonary injury than normal rats after repeated ROFA inhalation, with ST depression evident during the first exposure. Their sensitivity to ST depression suggests that they may also be susceptible to cardiac arrhythmias and changes in HRV. Here, we examined the effects of a single acute ROFA inhalation exposure on ECG morphology, HRV, and arrhythmia development in hypertensive and normal rats. These assessments may serve as sensitive, reliable, and quantifiable indicators of adverse cardiac effects of PM. When compared to HRV and ECG morphology in this rat model of hypertension, cardiac arrhythmias were the most sensitive indicators of the adverse cardiovascular effects of ROFA inhalation, suggesting that cardiac arrhythmias may have predictive value in the assessments of the effects of air pollution. This model may in turn be used to compare the effects of other PM samples in their capacity to elicit cardiac arrhythmias in the context of hypertension, potentially facilitating cross-regional comparisons of the cardiovascular toxicity of PM. This study also demonstrated that normal non-hypertensive animals have very minimal responses to very high acute PM exposure, with only a mild inflammatory response and no evidence of cardiac arrhythmia. Healthy individuals or animals are thus much more resistant to the effects of air pollution than their diseased counterparts suggesting that the effects of air pollution be studied in the context of pre-existing disease in order to correctly assess the impact of particulate air pollution exposure. Taken together, the data suggest that cardiac arrhythmia is an early sensitive indicator of the propensity for particulate inhalation to modify cardiovascular function.
Description:
Exposure to combustion-derived fine particulate matter (PM) is associated with increased cardiovascular morbidity and mortality especially in individuals with cardiovascular disease, including hypertension. PM inhalation causes several adverse changes in cardiac function that are reflected in the electrocardiogram ECG) including altered cardiac rhythm, myocardial ischemia, and reduced heart rate variability (HRV). The sensitivity and reliability of ECG-derived parameters as indicators of the cardiovascular toxicity of PM in rats is unclear. Objective: We hypothesized that Spontaneously Hypertensive (SH) rats are more susceptible to the development of PM-induced arrhythmia, altered ECG morphology, and reduced HRV than Wistar Kyoto (WKY) rats, a related strain with normal blood pressure. Rats were exposed once by nose-only inhalation for 4 hours to residual oil fly ash (ROFA), an emission source particle rich in transition metals, or air, and then sacrificed 1 or 48 h later. ROFA-exposed SH rats developed non-conducted P-wave arrhythmias, but no changes in ECG morphology or HRV. There were no ECG effects in 1 ROFA-exposed WKY rats. ROFA-exposed SH rats also had greater pulmonary injury, neutrophil infiltration, and serum C-reactive protein than ROFA-exposed WKY rats. These results suggest that cardiac arrhythmias may be an early sensitive indicator of the propensity for particulate inhalation to modify cardiovascular function.