Analysis of toxic lung damage may focus on the offending agent and define patterns of bioactivation and interactions with the target tissues. It may also focus on a study of the biological response. While it was originally thought that cell proliferation, particularly Type II epithelial cell proliferation following lung injury, was a common event, it now has become obvious that on occasion proliferation occurs only late after the initial lung damage. Also Type II cell proliferation can occur in the absence of alveolar Type I cell damage. Delayed reepithelialization of the alveolar surface may lead to pulmonary fibrosis. Toxicological interactions often can be best recognized and defined by the extensive lesions that result from concomitant or sequential exposure to such toxic agents as ozone and acidic aerosols or anticancer drugs and oxygen. A correlation of cell proliferation and tumor development in mouse lung has shown that target cell hyperplasia is not a necessary prerequisite for enhanced tumor development. On the other hand, oxygen-induced proliferation of the neuroendocrine cell population results in the short-term development of neuroendocrine lung cell cancer in hamsters. While it is possible to draw some conclusions from an analysis of the lung response to toxic injury, predictions made from such knowledge are sometimes, but not necessarily always, correct.