Sublethal toxicity of zinc chloride (ZnCl2; 7.5 ppm: 10% of 96 it LC50 value) on the aerial (accessory respiratory organs or air sacs) and branchial (gills) respiratory organs of Heteropneustes fossilis has been analysed histopathologically. Zinc chloride exposure causes certain common but severe damage to both tissues. The prominent changes in the accessory respiratory organs include periodic deformation of lamellar elements, haemorrhages due to necrosis and sloughing off of the respiratory epithelium, and hyperplasia accompanied by fusion of secondary lamellae. Subsequently, regeneration of the lamellar system from the focal inflammatory tissues takes place. Deposition of glycogen in the muscular layer-indicates disturbed aerial respiration. The alterations in the gills include periodic lifting off of the respiratory epithelium, extensive intercellular vacuolization and occasional fusion of secondary lamellae, resulting in increased thickness of primary and secondary lamellae. Fusion of secondary lamellae reduces the surface area for gaseous exchange. The increased thickness of the respiratory epithelium due to uncontrolled hyperplasia of the epithelial cells, also increases the diffusion distance between the ambient and vascular components. Vasodilation in the secondary lamellae of the gills and periodic fluctuations in the mucous cell density are also observed at various stages of ZnCl2 exposure.