Student Research: David E. McBride
The objectives of this study were to determine whether or not exposure to ambient levels of ozone caused a differential inflammatory or functional response in asthmatic and nonasthmatic individuals. Ten asthmatic and eight nonasthmatic subjects were exposed to clean air, 120 ppb, or 240 ppb ozone for 90 minutes during intermittent moderate exercise. The pulmonary function measurements assessed were FEV1, total respiratory resistance (RT), forced vital capacity (FVC), and maximal flow at 50 and 75% (Vmax50 and Vmax75 of expired VC. Nasal lavage fluid (NALF) was analyzed for various mediators of inflammation. The cellular component consisted of white blood cell and epithelial cell counts and a white blood cell differential. Biochemical mediators included histamine, leukotriene B4 (LTB4), interleukin-8 (IL-8), platelet activating factor (PAF), and lactate dehydrogenase (LDH). Baseline measurements were conducted before the exposure followed by three post exposure measurements, immediately after (PE1), 4-6 hours (PE2), and 24 hours (PE3) after the exposure.
Results of this study showed no sginificant changes in pulmonary function in either the asthmatics or nonasthmatic subjects. WBC and epithelial cells recovered from the NALF indicate a dose response relationship with increasing ozone levels in the asthmatic subjects. Significant increases in WBC were detected immediately after and then again 24 hours after the exposure (P>0.05), and immediately after the exposure for epithelial cells (P>0.05), indicating a possible biphasic inflammatory response to ambient levels of ozone inhalation. No significant changes were seen in the nonasthmatic subjects. Individual changes in IL-8 concentrations were correlated with corresponding changes in WBC for air (r=0.61) and 240 ppb ozone (r=0.76) in the asthmatic subjects. We conclude that asthmatic individuals are more sensitive to the acute inflammatory effects producced by low levels of ozone than nonasthmatic individuals.