ANTENATAL INTERVENTIONS IN CHILDHOOD ASTHMA

The occurrence of asthma in most young children is likely to result fr om altered or disrupted immune maturation, The persistence of Th2-like lymphocyte responses to common allergens rather than the extinction o f immune response (immune tolerance) or the deflection of response to a Th1 pattern (immune deviation) may underlie the development of asthm a and the atopic phenotype, It is likely that this failure of normal i mmune maturation begins early in life, and that both genetic predispos ition and environmental factors operating at critical times act jointl y to cause it. There is clear evidence that the development of immune response capability begins in utero, and that maternal allergic and ot her exposures can affect this process before birth. While there is som e evidence that the onset of atopy or atopic symptoms can be ameliorat ed or delayed in early life by reducing maternal prenatal allergen exp osure (either food or inhaled allergens), there is currently no convin cing 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 un proven to have a protective role on airway reactivity and asthma incidence and severity in adults, have any protective role in utero, In contrast, maternal s moking during pregnancy has been shown in several studies to be associ ated 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 in creased wheezing and asthma risk in children, make maternal smoking ce ssation the prenatal intervention most likely to be effective in reduc ing asthma risk in children.