Prospective cohort studies have provided a useful tool for the study of the natural history of asthma and lung function and for the development of concepts of asthma phenotypes during childhood. However, although observational epidemiology has indicated a large number of credible associations between environmental variables and asthma onset in childhood, it can be argued that it has yet to fulfill the promise of identifying modifiable, causal risk factors that are amenable to intervention for the primary or secondary prevention of disease. The development of efficient, high-throughput genotyping that can be applied to large, longitudinal cohorts with detailed data on exposures and phenotypic outcomes, opens the way for studies of genetic effects and gene-environment interactions that may come closer to identifying causal pathways between exposure and disease. Therefore, there continues to be an important role for large-scale, observational studies with careful attention to definition and evaluation of outcomes and plausible risk factors.