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REAL-TIME MEASUREMENT OF AIRWAY RESPONSES TO SULOFUR DIOXIDE (SO2) IN AN INTACT, AWAKE GUINEA PIG MODEL
Costa, D L., J Stanek, Q T. Krantz, J. P. Nolan, D Winsett, AND W P. Watkinson. REAL-TIME MEASUREMENT OF AIRWAY RESPONSES TO SULOFUR DIOXIDE (SO2) IN AN INTACT, AWAKE GUINEA PIG MODEL. Presented at SOT, San Francisco, CA, March 25-29, 2001.
Real-time measurment of airway responses to Sulfur Dioxide (SO2) in an intact, awake guinea pig model. J Stanek1,2, Q Krantz2, J Nolan2, D Winsett2, W Watkinson2, and D Costa2. 1College of Veterinary Medicine, NCSU, Raleigh, NC, USA; 2Pulmonary Toxicology Branch, ETD, NHEERL, US EPA, RTP, NC, USA.
Sulfur Dioxide (SO2) is a common component of polluted urban air and a major air pollutant produced during coal combustion. Exposure to SO2 has been shown to significantly alter airway compliance and resistance. Recently, high concentrations of SO2 during air pollution episodes have been associated with heart rate elevation. To determine the effects of SO2 during a real-time exposure, our laboratory has begun measuring the airway responses to SO2 using non-invasive methodology in an intact, awake guinea pig. To this end, animals were exposed to SO2 at concentrations of 0, 20, 50 and 100 ppm in the head-space of a double-chamber plethysmograph (nasal-thoracic). Changes in airway resistance and breathing frequency were monitored continuously for a 10-minute baseline period and the 60-minute exposure period. Exposure to SO2 produced a concentration dependent increase in airway resistance. Airway resistance was significantly increased at 50 and 100 ppm SO2 (p < 0.05), but not at 20 ppm (p > 0.05). This increase in airway resistance was evident by 30 minutes after the onset of exposure. Specifically, average airway resistance was increased over baseline by approximately 35 and 80%, respectively, at 50 and 100 ppm. In addition, a significant decrease in breathing frequency was detected in the animals exposed to 100 ppm SO2 (p < 0.05). Breathing frequency was approximately 15% lower in animals exposed to 100 ppm when compared to controls (0 ppm). In summary, exposure to SO2 produced significant changes in both airway resistance (50 and 100 ppm) and breathing frequency (100 ppm). Utilization of this model will allow study, in greater detail, of the neural mechanisms controlling the airway responses, as well as the possible cardiac responses to SO2. (Funded by the NCSU/EPA Cooperative Training Program CT826512010.) (This abstract does not reflect EPA policy.)