If the lower Apgar scores of the moderate-to-severe BPD group were due to neonatal asphyxia, reperfusion-induced oxidative stress following asphyxia may have caused lung injury and compensatory induction of HO-1, resulting in the deterioration of subsequent BPD and the elevation of CO-Hb levels in the moderate-to-severe BPD group during the early postnatal period, respectively [18]. This evidence concerns the gene HMOX1 and bronchopulmonary dysplasia.