Exposure of rats to 150 ppm NO2 for 2 hours causes death from pulmonary oedema. Continuous exposure to 25 ppm for 150 days causes gross enlargement with loss of elastic recoil and proliferative and metaplastic epithelial changes in the vicinity of the terminal bronchioles. Continuous exposure to 2 ppm results in an initial loss of cilia and focal hyperplasia of the terminal bronchiolar epithelium, but these changes, for the most part, quickly subside. Chronic daily exposure of rats to tobacco smoke results in proliferative and metaplastic epithelial changes in the vicinity of the terminal and respiratory bronchioles. Also, both at this site and elsewhere, aggregates of golden-brown pigment-laden macrophages accumulate in the lungs. The proliferative/metaplastic changes are similar to those seen in response to NO2, asbestos and other irritant gases and particles. The aggregates of golden-brown macrophages are seemingly a special feature of the response to tobacco smoke. Some rats exposed for over two years to tobacco smoke, develop foci of squamous metaplasia, firstly in the region of terminal bronchioles, but later at points scattered throughout the lung parenchyma. Comparable changes have not been reported in rats exposed to NO2. Although no strictly comparable data for NO2 and tobacco smoke exposure are available, it is reasonable to conclude that, whereas the NO2 in tobacco smoke may contribute to the production of cuboidal/columnar metaplasia in the vicinity of terminal bronchioles, it otherwise plays little part in the aetiology of lesions in the lungs of smoke-exposed rats.