Bronchopulmonary dysplasia (BPD) is a complex disorder secondary to gene-environment interactions, and is the commonest chronic lung disease in infancy. There is no specific or effective treatment available to date for BPD. Since the aetiopathogenesis of BPD is multifactorial, involving diverse molecular signaling pathways, a variety of biomarkers detected in biological fluids have been proposed for early identification of infants predisposed to BPD. This review will be restricted to biomarker studies in human infants, conducted mostly in the last decade. The majority of the studies have been conducted using blood, urine or tracheal aspirate samples. Despite the multitude of biomarkers proposed, most studies have been conducted in small numbers of infants, with few being replicated by independent investigators. Confirmatory studies with adequate sample sizes and assessment of the role of putative biomarkers in the aetiology of BPD in developmentally appropriate animal models and human lungs with BPD will enhance the potential for therapeutic interventions. Genomic and proteomic approaches have the greatest potential to significantly advance the field of biomarkers in BPD.