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.