Cardiac arrhythmia induction after exposure to residual oil fly ash particles in a rodent model of pulmonary hypertension.
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Recent epidemiological studies have reported a positive association between exposure to ambient concentrations of particulate matter (PM) and the incidence of cardiopulmonary-related morbidity and mortality. The present study examined the effects of fugitive residual oil fly ash (ROFA) PM on cardiac arrhythmia induction in healthy and cardiopulmonary-compromised rodents. Male Sprague-Dawley rats were implanted with radiotelemetry transmitters capable of monitoring the electrocardiogram and were subjected to one of two treatment regimens. Rats in the first treatment regimen (n = 16) served as normal control animals whereas rats in the second treatment regimen (n = 16) were injected with monocrotaline (MCT, 60 mg/kg, ip) to induce pulmonary vascular inflammation and hypertension and served as a model of cardiopulmonary disease. Rats within each treatment regimen were equally divided into four dose groups (0.0, 0.25, 1.0, 2.5 mg ROFA), instilled intratracheally, and monitored for 96 h. In the animals in the first treatment regimen, ROFA instillation caused dose-related increases in the incidence and duration of serious arrhythmic events that appeared to be associated with impaired atrioventricular conduction and myocardial hypoxia. There were no lethalities in the normal animals following ROFA instillation. The frequency and severity of arrhythmias were greatly exacerbated in the MCT-treated animals in the second treatment regimen and were accompanied by one, three, and two deaths in the low-, medium-, and high-dose groups, respectively. The results of the present study demonstrate substantial cardiac effects in normal and compromised rats after exposure to ROFA PM and implicate both conductive and hypoxemic arrhythmogenic mechanisms in the observed cardiac-related lethalities. These results support previous epidemiological studies that suggest a link between preexisting cardiopulmonary disease and potentiation of adverse health effects following exposure to anthropogenic particulates.Copyright 1998 Academic Press.