Chronic obstructive pulmonary disease (COPD) is conventionally thought of as a disease of adult smokers, related to airway inflammation and structural airway changes (remodeling). However, there is important epidemiological evidence, from a series of studies with overlapping age groups from birth to late middle age that early life events, including antenatal influences on lung growth, program the child to be at increased risk for future COPD. This paper reviews the evidence for potential gene: environment interactions in this process, in particular with respect to the maternal genotype of the COPD patient. It explores the hypothesis that genes important in early lung development are also important in determining adult risk for COPD. Although the major preventable factor adversely impacting on child lung health is maternal smoking, the effects of viral infection, nutrition, and indoor and outdoor pollution are reviewed. The survivors of preterm birth are another important cohort who may develop premature COPD in adult life. Early life events provide the substrate for COPD, with later cigarette smoking, and occasionally other exposures, pulling the trigger to produce COPD. Although a rigorous anti-smoking program is necessary to halt this spiral of lung destruction leading to COPD, a focus on early (including prenatal) lung health is also important. Any model of COPD which does not take into account early life influences is likely to be fatally flawed.