ABSTRACT

The pathogenesis of RADS is uncertain but most likely involves generation of a localized inflammatory response in the airways following epithelial and subepithelial mucosal in­ jury. The epithelial damage leads to increased epithelial permeability and exposes subepi­ thelial irritant receptors to inhaled and environmental influences, including cold air, smoke, pollutants, and nonspecific irritants. Stimulation of the subepithelial receptors can cause nonspecific bronchial hyperreactivity and bronchospasm.