The alveolar damage produced by a variety of toxic agents, whether air-borne or blood-borne, progresses to a sequence of nonspecific changes histologically regarded as diffuse alveolar damage. Ultrastructurally, their alveolar damage can be divided into epithelial and endothelial type according to their target cells. The epithelial and endothelial type of alveolar damage was demonstrated in the experimental models of paraquat and monocrotaline toxicity, respectively. The two types of alveolar damage show different courses in the development of the sequent changes, which may influence the time courses and the patterns of final alveolar fibrosis. However, the endothelial type of alveolar damage may also induce secondary injury to the epithelial cells, so that the damage of this type finally becomes similar to that in the epithelial type. The mechanism of secondary epithelial damage was discussed on the basis of the antioxidation function of the lung. In many pneumotoxins, however, the detailed pathogenesis of alveolar changes remains to be clarified.