This chapter focuses on the effects of various environmental toxicants such as environmental tobacco smoke, bioactivated environmental contaminants, oxidant gases, therapeutic glucocorticosteroids, and other miscellaneous compounds on the lung development of experimental models. Exclusive in utero exposure to ETS has been shown to accelerate the developmental pattern of Clara cell secretory protein expression in the rat, suggesting a potential acceleration of airway epithelial differentiation in the lung. Rats exposed to both in utero and postnatal ETS have decreased lung compliance, increased reactivity to methacholine and an increase in the number of neuroendocrine ceils per cm of basal lamina. In utero exposure to bioactivated compounds produces embryotoxic or teratogenic effects, including chromosomal aberrations. The herbicide dichlobenil specifically injures olfactory nasal mucosa in fetal and neonatal mice just as it does in adult mice. In mice, high levels of trichloroethylene exposure on gestational day 17 can cause a decrease in fetal lung weight and total lung phospholipid content, while not changing total DNA content. Benzo[a]pyrene causes lung tumors in offspring of mice treated at days 18 and 19 gestation and both males and females have increased incidence of tumors and increased numbers of tumors per animal. Although corticosteroids are beneficial in the short term, very little is known about their long-term effects on lung development and growth. Administration of betamethasone to pregnant animals has been shown to have mixed effects resulting in no changes in lung compliance or lung volume in postnatal term-born lambs, however, it increases lung function in preterm lambs by 50% over controls and also increases pulmonary antioxidant levels.