Summary. Bronchopulmonary dysplasia (BPD) is the most common chronic lung disease of infancy. A ''New'' BPD has been characterized in preterm infants that may begin in utero, and then progress post-natally, resulting in arrested lung development and alveolar hypoplasia. Foundations for this ''New'' BPD may be derived from pro-inflammatory genes including tumor necrosis factor-a (TNFa). The hypothesis of the current study is that single nucleotide polymorphisms (SNPs) of the pro-inflammatory TNFa gene place preterm infants at increased risk for BPD. Preterm infants (105 in number) with birthweights 1 kg, who survived to at least 36 weeks postmenstrual age (PMA) or discharge were enrolled into this study. They were stratified for BPD according to their need for supplemental oxygen at 28 days and at 36 weeks PMA (non-, mild-, moderate-, or severe-BPD). DNA was extracted from these infants and subjected to analyses for the TNFa SNPs: À1,031, À863, À857, À308, and À238. The PHASE software (version 2.1) was used to reconstruct haplotypes and estimate their frequencies within the study population. Differences in birth weight (P < 0.001) and gestational age (P < 0.001), but not in racial distribution between the groups were found. Haplotype-specific analysis revealed no significant association between BPD severity and any of the 5-marker common haplotypes with 10 or more copies in this study population. Additionally, no significant association was observed in any three SNP haplotypes at À1,031, À863, and À857, and two SNP haplotypes at À308 and À238. We observed no association between BPD severity and the five TNFa SNPs investigated. Pediatr Pulmonol. 2007; 42:29-36. ß

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