In this thesis, we examined the hypothesis that early growth and adverse environmental exposures in fetal life and infancy, in combination with genetic susceptibility, lead to structural and functional adaptations in early lung development, with subsequently lower lung function and higher risk of chronic obstructive respiratory diseases in later life. Furthermore, we explored epigenetic mechanisms as a potential pathway explaining environmental and genetic factors that influence the development of lower lung function and risk of respiratory diseases. By identification of early life growth and environmental exposures, genetic variants, and DNA-methylation as underlying mechanism, we improve the understanding of the origins of chronic obstructive respiratory diseases in childhood and adulthood. Furthermore, we might be able to develop new preventive strategies and therapeutic interventions for pregnant women and young children, aiming at reducing the burden of later life chronic obstructive respiratory diseases.