ABSTRACT
Although there appears to be a general consensus that developmental immaturity, mechanical ventilation, and often, infection are major contributors to the development of bronchopulmonary dysplasia (BPD), or chronic lung disease of early infancy (CLD), available evidence indicates that effects arising from exposure to elevated oxygen tensions are also important in the etiology of the disease (1-4). Although the hypothesis that hyperoxia contributes significantly to the development of CLD has not been proved with certainty, the support for a causal relation is sufficient to warrant the use of this working hypothesis.
