Premature birth means that instead of being fluid-filled and non-functional for many weeks, the immature lungs are gas-filled and have to support respiration. Often they are exposed to iatrogenic positive not physiological negative pressure expansion, infections, fluid overload and potentially hazardous treatments such as systemic steroids. Hence the respiratory sequelae of a premature birth need to be a major focus as more and more immature infants survive. Novel treatments, in particular, ‘gentle’ ventilator strategies (low mean airway pressures, faster rates), antenatal corticosteroids and inhaled surfactant have transformed the nature of the respiratory impairment from the traditional bronchopulmonary dysplasia (BPD) which was primarily an airways disease to ‘new’ BPD, more related to arrested alveolar development. However, our focus has long been on short term morbidity and mortality. As a community we have been particularly bad at following these young people up and appreciating their ongoing problems and risks. Specifically, paediatricians have sighed with relief when these children are no longer oxygen dependent, and have failed to keep these children under review. Furthermore, as we recently documented adult chest physicians rarely make enquiries about early life events.1 So survivors of prematurity are apt to disappear into a modern-day black hole.

In part, the problem may have arisen because of lack of appreciation of normal lung growth and the consequences of disease. There are three key stages which need to be optimal for long term lung health. First, lung growth in utero, ensuring the child is delivered with normally developed lungs, and second, the rate of lung growth in childhood, both determine whether the child will reach the full potential plateau at age 20–25 years.2 The airway generations are laid down by 16 weeks and primitive gas exchanging units develop from around 24 weeks of …