Appreciation of the early damage that occurs to the respiratory epithelium has been limited by the use of autopsy specimens from fatally stricken asthmatics as a source of representative specimens. The use of bronchoscopy to obtain specimens from patients early in the course of their asthma has allowed a new understanding of the evolution of pathological changes that occur in asthma. Newly diagnosed, mild asthmatics have been shown to have bronchial goblet cell hyperplasia in addition to increased numbers of mast cells and eosinophils in the respiratory epithelium, and increased eosinophil granule protein deposition within the lamina propria. Endothelial gaps in postcapillary venules are greater in asthmatic airways, suggesting that increased plasma transudation may contribute to the known epithelial cell shedding characteristic of asthma attacks. Asthmatic inflammation, even early in the course of the disease, includes vascular permeability changes, inflammatory cell infiltration, epithelial cell shedding, and goblet cell hyperplasia, replacing the normal ciliated epithelium. Current investigation evaluating the effects of asthmatic inflammation on epithelial cell attachment to each other and to the extracellular matrix molecules regulated by adhesion glycoproteins will likely enhance further the understanding of the pathological changes that occur within the asthmatic airway.