Conclusion
It is well established that both genetic and environmental factors contribute to risk of asthma and related traits (i.e. recurrent wheeze), however, few studies have evaluated polygenic effects as well as interaction effects of multiple genes and environmental factors. This lack of evidence is likely due to heterogeneity of asthma phenotypes as well as the lack of studies with both available exposure and genetic datasets. The CHILD Cohort Study successfully addressed these limitations with in-depth phenotyping, as well as the availability of environmental and genetics data to allow for assessment of interaction effects. In this study, we calculated the polygenic effects of multiple genetic risk factors, which account for greater heritability of asthma and recurrent wheeze compared to each individual variant. Moreover, we observed modulating effects of breastfeeding at one year of life and exposure to traffic air pollution (NO2) on risk of recurrent wheeze during childhood. Our study identifies a period during early infancy when genetic risk of developing asthma and respiratory diseases may be assessed, and when early life interventions might modify risk of developing life-long respiratory diseases.