Clara cells are the principal epithelial cell phenotype present in the distal airway in many species1 and are the primary cellular site of xenobiotic metabolism by the cytochrome p-450 (CYP) monooxygenase system in the lung. 2, 3 These cells represent the predominant secretory cell within distal conducting airways of mammals and exhibit functional alterations with chronic pulmonary diseases in human. Moreover, 84% of adenocarcinomas of human lung are the nonciliated bronchiolar cell type4, and 85% of peripheral adenocarcinomas of human lungs has Clara cell granule. 5 The functional roles of Clara cell secretions that are induced by exposure to various environmental agents are poorly understood. One of the presumed functions of Clara cells6 and type II pneumocytes7 is to synthesize and secrete pulmonary surfactant, which is particularly important during birth when lung expansion is required. The intracellular mechanism involved in mediating the secretion of Clara cells by beta-adrenergic receptor (β-AR) agonist is via cyclic 3’, 5’adenosine monophosphate-dependent protein kinase A. Activation of these receptors mediates mucus secretion, surfactant secretion, and airway smooth muscle cell relaxation. 8