Carbon monoxide (CO) is an endogenous gas product of heme degradation by the enzyme heme oxygenase (HO), In lower resiratory tract inflammation CO is thought to play a cytoprotective role and used as a marker of oxidative stress. Although reported to be elevated in inflamed nasal airways, its role in nasal pathophysiology is not fully understood. The first part of this project investigates whether the immunoreactivity of inducible HO-1 and constitutive HO-2 isozymes are increased in human allergic rhinitis nasal mucosa and nasal polyps. In the second part, the effect of heme substrate analogue hemin on human nasal cilia beat frequency (CBF) in vitro is studied. Finally, a prospective double-blinded randomised controlled study has been undertaken to examine the effects of hemin and exogenous CO on nasal mucociliary clearance (MCC) in vivo.