The upper airway mucosa is a main site for deposition of potentially noxious environmental molecules. As one might expect this mucosa is also well equipped to protect both itself and the rest of the body from harmful influences of foreign material. The regulation of the permeability of nasal and tracheobronchial mucosa is such that blood plasma may enter the airway lumen without making it any easier for foreign surface molecules to penetrate into the airway tissue. Thus, circulating humoral defence systems would be allowed to neutralize offending stimuli on the surface of a mucosa that maintains its absorption barrier uncompromised. Mechanisms involved in the direction-selective paracellular flux of solutes across the intact airway mucosa are the basis for the first part of this overview. If the inhalational insult or disease process are severe enough for epithelial lining cells to be shed, even this may occur without a deleterious loss of barrier function. If basal cells remain they may promptly flatten out and establish cell to cell contacts. If both columnar and basal cells are removed a provisional plasma-derived gel immediately covers the denuded basement membrane. Furthermore, beneath the gel restitution of a new epithelium proceeds speedily. These novel aspects on barrier restitution after shedding are the basis for the second part of the present overview. Most of the data that will be discussed have been generated in the human nose and the guinea-pig trachea. The focus is primarily on in vivo observations. Explanatory or expanding ex vivo findings have thus been included when the functional in vivo aspects have been first assessed.