Most lung disease throughout life is programmed in utero or early post-natal life. Factors in the fetal environment such as maternal smoking and diet can lead to reduced lung function, immunological modification or symptoms from birth. There are clear genetic components documented for cystic fibrosis, alpha1 anti-trypsin deficiency and asthma. In early life, the outcomes for those predisposed to asthma or allergy appear to be dependent on the relative timing of exposure to infective agents, allergens or helminths. Abnormal airway structure is present in both transient and persistent wheezers. New drugs and environmental manipulations will need to be developed with an understanding of the mechanisms associated with this early programming.