Abstract Lung development is orchestrated by highly integrated morphogenic programs of interrelated patterns of gene and protein expression. Both genetic and epigenetic influences may alter the developing lung in the canalicular and saccular phase of lung development that lead to the development of bronchopulmonary dysplasia (BPD). Maternal exposures to toxins, and especially tobacco smoke associated nicotine nitrosamine ketones, fetal and neonatal infections (with or without chorioamnionitis) and techniques of neonatal ventilator management including surfactant therapy in concert with innate genetic susceptibility have life-long consequences for the infant afflicted with BPD. Exposure to supplemental oxygen poses another threat to the prematurely newborn and increases the risk for BPD and retinopathy of prematurity, but other effects in later life have been note among infants given oxygen as newborns. Thus a greater focus on these epigenetic influences and novel strategies to care for the preterm infant will hopefully reduce the worldwide burden of BPD and increase awareness regarding epigenetic mechanisms that determine long term health and well-being
