Purpose: Although improvement in neonatal care techniques has increased survival of preterm infants, bronchopulmonary dysplasia (BPD) remains important factor of neonatal mortality and morbidity. BPD is a multifactorial disease associated with genetic and clinical risk factors related to lung development and perinatal inflammation. Interleukin-1 (IL-1) is a crucial cytokine at an early stage of inflammatory reaction. We attempted to determine the association between the IL-1 polymorphisms, clinical risk factors, and BPD in preterm infants born below 34 week’s gestation. Methods: The study was performed who consented infants born below 34 week’s gestation (n=104). The alleles of the 3 sites of the IL-1 gene (IL-1α-889, IL-1β-31, and IL-1β-511) were determined using Tagman®-based allelic discrimination assays. Clinical data were reviewed from the medical records. Results: A total of 31 infants with BPD and 73 control infants were enrolled in the study. Gestational age, birth weight were lower in the BPD group compared to the control group (28+4 week ± 2+3 vs. 30+6 week ± 2+3, P 0.001; 1,230g ± 420 vs 1,560g ± 410, P 0.001). The incidence of respiratory distress syndrome ( P = 0.002), patent ductus arteriosus ( P = 0.01), and retinopathy of prematurity ( P 0.001) was higher in the BPD group than in the control group. The frequency of the IL-1α-889 TT was higher in the BPD group than the control group (6.5% vs. 0.0%, P = 0.028). The frequencies of the IL-1α-889T, IL-1β-31T, IL-1β-511T were not different between the BPD and control groups. In logistic regression analysis, gestational age and RDS were associated with BPD. Conclusion: The group of patients with the IL-1α-889 T homozygote had a higher incidence of BPD compared to the other haplotypes. IL-1α-889 can be the possible candidate gene of the risk of BPD for larger population study, although our result could not confirm the association in multivariate analysis.