The early origins of asthma: who is really at risk?

Abstract

Asthma is largely a developmental disease in which the normal development of the respiratory and immune systems is altered by the impacts of environmental exposures acting on underlying genetic predispositions. This review will comment on the latest evidence in this field. There is increasing evidence that several potentially overlapping genetic predispositions may contribute to the development of asthma, including predisposition to abnormal lung growth, resulting in lower lung function; delayed immune maturation; predisposition to lower respiratory viral infections; early allergic sensitization; and predisposition to bronchial hyper-responsiveness. Networks of genes and environmental modification of gene expression via epigenetic mechanisms are also likely to be important. Antenatal exposures that increase the risk of asthma include tobacco smoke, ambient and indoor air pollution. Impacts of maternal nutrition and maternal diseases, such as asthma and diabetes, are also important. Early life environmental exposures may also increase the risk of asthma via impacts on lung growth and immune maturation. Synergistic interactions between viral lower respiratory infections and allergic sensitization in early life appear to be especially important in increasing the risk of subsequent asthma. The major risk factors for childhood asthma are a family history of asthma and allergies, early and persistent allergic sensitization to environmental allergens and viral lower respiratory illnesses in early life.