Antenatal interventions in childhood asthma.

The occurrence of asthma in most young children is likely to result from altered or disrupted immune maturation. The persistence of Th2-like lymphocyte responses to common allergens rather than the extinction of immune response (immune tolerance) or the deflection of response to a Th1 pattern (immune deviation) may underlie the development of asthma and the atopic phenotype. It is likely that this failure of normal immune maturation begins early in life, and that both genetic predisposition and environmental factors operating at critical times act jointly to cause it. There is clear evidence that the development of immune response capability begins in utero, and that maternal allergic and other exposures can affect this process before birth. While there is some evidence that the onset of atopy or atopic symptoms can be ameliorated or delayed in early life by reducing maternal prenatal allergen exposure (either food or inhaled allergens), there is currently no convincing evidence that prenatal maternal allergen avoidance will diminish asthma incidence in children. There are similarly no data available to evaluate if dietary antioxidants, postulated but unproven to have a protective role on airway reactivity and asthma incidence and severity in adults, have any protective role in utero. In contrast, maternal smoking during pregnancy has been shown in several studies to be associated with reductions in pulmonary function measures (flows at low lung volumes) in both infants and older children that are consistent with abnormalities seen in asthmatics. This finding, coupled with the clear association of postnatal environmental tobacco smoke exposure with increased wheezing and asthma risk in children, make maternal smoking cessation the prenatal intervention most likely to be effective in reducing asthma risk in children.