Carbon monoxide (CO) is an endogenously produced gas mediator produced by heme oxygenase (HO). Like nitric oxide (NO), CO is produced in the nasal mucosa. Given that induced NO synthase (iNOS) expression in nasal mucosa has been found to be up-regulated in allergic rhinitis, the current study investigated the expression of HO isoforms in allergic human nasal mucosa. Immunohistochemical staining for type 1 and 2 HO isoforms were carried out in nasal inferior turbinate mucosa from six patients with persistent allergic rhinitis, and compared with six control patients without nasal allergy. Focal and weak expression of HO-1 was observed in seromucous glands, with no difference between allergic and control specimens. Vascular endothelium, erythrocytes, smooth muscle and inflammatory cells (except macrophages) in the allergic group exhibited stronger HO-1 immunoreactivity compared to the control. Minimal expression was found in the respiratory epithelium in either group. Intravascular HO-1 expression was found in the allergic mucosa only. Intense HO-2 immunoreactivity was observed in the respiratory epithelium, vascular endothelium and seromucous glands in both allergic and control groups with no differences in intensity. In conclusion, unlike iNOS, HO-1 is minimally expressed in the nasal respiratory epithelium of either group. However, our findings suggest that it may be involved in the inflammatory process of allergic rhinitis at the submucosal level.