Sensitivity of bronchoprovocation and tracheal mucous velocity in detecting airway responses to O3

Abstract

This study was undertaken to determine whether measurements of tracheal mucous velocity or airway reactivity to inhaled carbachol more sensitively detect airway effects of inhaled ozone (O3) in conscious sheep. Dose-response curves of mean pulmonary flow resistance (RL) to carbachol were obtained by measuring RL after five breaths of carbachol aerosol with stepwise increases in drug concentration. The animals then breathed 0.5 ppm O3 through an endotracheal tube for 2 h. The dose-response curves were repeated immediately after the 0.5 ppm O3 exposure and 24 h later. In the eight sheep studied, there were no significant alterations in base-line RL immediately after or 24 h after 0.5 ppm O3. Airway hyperreactivity was not apparent immediately after the sheep breathed 0.5 ppm O3, but it was evident 24 h later. In contrast, six sheep that breathed 0.5 ppm O3 in the same manner for 2 h did not show a significant depression in tracheal mucous velocity the same day or 24 h later. Exposure to 1 ppm O3 for 2 h resulted in airway hyperreactivity immediately after the exposure and elevated base-line RL 24 h later; 2 ppm O3 produced an increase in base-line RL immediately after exposure. We conclude that, in conscious sheep, airway hyperreactivity appears to be a more sensitive indicator of airway effects produced by short-term exposure to 0.5 ppm O3 than depression of tracheal mucous velocity.

Ozone Differentially Modulates Airway Responsiveness in Atopic Versus Nonatopic Guinea Pigs

“…Many species, including guinea pigs, have previously been shown to display a large range of sensitivity to bronchoprovocation agents, and to the extent of resultant measured airway responsiveness (Turner & Martin, 1997). This variability may reflect interindividual differences in airway receptor number or sensitivity (Abraham et al, 1980;Ahmed et al, 1980). Susceptibility to O 3 -induced alterations in airway responsiveness has also been shown to be variable within any particular exposure group (Douglas et al, 1977;Snapper et al, 1978;Habib et al, 1979;Abraham et al, 1980).…”

“…EPA, 1996;McDonnell et al, 1999;Thurston & Ito, 1999;Peden, 2000). A relationship between O 3 exposure and airway responsiveness is also supported by controlled studies; concentrations 0.3 ppm have produced transient AHR in normal laboratory animals (Abraham et al, 1980;Holtzman et al, 1983;Gordon et al, 1984;Gross & Sargent, 1992), and clinical studies noted AHR following exposure of normal humans to as low as 0.08 ppm (Seltzer et al, 1986;Horstmann et al, 1990;Ying et al, 1990;Linn et al, 1994).…”

Effect of oxidant air pollutants on the respiratory system: insights from experimental animal research

“…Ozone may also cause acute airflow limitation, as shown by increased airway resistance and reduced dynamic compliance. These acute obstructive effects quickly reverse after cessation of exposure [12,38,39]. Airflow limitation is also observed after chronic exposures, mainly caused by fibrotic lesions, and in these cases it persists after cessation of exposure [12].…”

“…A reversible increase in airway responsiveness to several contractile agents is observed in animals after acute exposure to a concentration of O 3 ranging 0.5-3 ppm [35,38,[43][44][45][46][47][48][49][50][51][52]. Increased airway responsiveness to histamine has also been reported following exposure to 4 ppm or higher concentrations of NO 2 in guinea-pigs [53][54].…”

Hyperoxia-Induced Airway Hyperreactivity in Neonatal Guinea Pigs Is Not Inflammation Dependent

“…Ozone exposure has long been recognized as producing airway hyperreactivity in humans and animals (Lee et al, 1977;Golden et al, 1978;Holtzman et al, 1979;Abraham et al, 1980). The role of inflammation in the etiology of the increased reactivity is controversial.…”