Ozone-induced alteration in β-adrenergic pharmacological modulation of pulmonary macrophages

Abstract

Ozone is a ubiquitous air pollutant which can affect numerous functions of the respiratory system. However, previous work has not provided any information concerning its ability to modulate pharmacological receptors of pulmonary macrophages. This study examined, using a chemiluminescence assay, the β-adrenergic modulation of pulmonary macrophages harvested from rabbits exposed for 3 hr/day for 5 days to 0.1, 0.3 or 0.6 ppm ozone (O3) or to 3 hr/day for 20 days to 0.1 or 0.3 ppm. Receptor activity was monitored using release of reactive oxygen species (ROS) following administration to the cells of the β2-receptor agonist, isoproterenol. An O3-exposure concentration-dependent response was observed for isoproterenol efficacy following 5-day exposures, in that 0.1 ppm 01 induced a significant enhancement of β-adrenergic inhibition of ROS production, 0.3 ppm ozone produced no significant change from control, and 0.6 ppm decreased inhibition. No significant effects on P-adrenergic modulation were noted following the 20-day exposures. The results of this study suggest that short-term repeated exposures to 0.3 are capable of inducing alterations in the pharmacological functioning of pulmonary macrophages, while longer term exposures may result in adaptation. Alterations in receptor function have implications in terms of pulmonary defense and disease.