Introduction

Epidemiological studies have provided strong evidence that a suboptimal intrauterine environment can have long-term effects on postnatal lung function and respiratory symptoms or illness. Prenatal factors that have been causally related to long-term changes in respiratory function and health include impaired fetal nutrition and growth (Harding et al. 2004), maternal tobacco smoking and nicotine exposure (Joad 2004, Maritz 2004) and preterm birth (Albertine and Pysher 2004). Evidence is accruing that a number of common respiratory illnesses of childhood and adulthood may have their origins in fetal life, or that predisposing conditions may be laid down at the time (Shaheen and Barker 1994). Similarly, it is now recognised that alterations to the early postnatal environment can lead to persistent alterations in lung structure and function later in life.

Lung development and maturation are characterised by several distinct phases, namely the embryonic phase followed by the pseudoglandular, canalicular, saccular and alveolar phases. These are followed by the phase of equilibrated lung growth, the final stage of lung maturation (Kauffman et al. 1974). During each phase, specific structural changes occur which eventually result in a lung that can effectively fulfil its role as a gas exchanger, with an ability to resist infection and damage by inhaled toxic agents. Interference with the developmental programme of the lung during any of these phases may render the lung less effective as a gas exchanger or may render it more susceptible to disease.