Methyl isocyanate (MIC), inhaled or administered subcutaneously (sc) at lethal concentration/dose caused essentially similar histopathological changes in all the viscera except for the lungs. The observed congestion of the viscera, foci of hepatocellular necrosis with widening of Disse's spaces in the liver and tubulo-rhexis with degeneration in the kidneys are attributable mostly to the initial shock. In addition, the lungs revealed more distinct route specific patterns of histopathological lesions. Inhaled MIC caused acute eosinophilic necrosis of the bronchial epithelium and frank alveolar edema, while MIC administered sc led to prominent vascular endothelial damage and severe interstitial pneumonitis with normal bronchial epithelium. The differential loci of damage in the lungs may be attributed to the immediate contact surface available for interaction with MIC.