BRONCHIAL RESPONSIVENESS TO INHALED METABISULFITE IN ASTHMATIC-CHILDREN INCREASES WITH AGE

Inhaled bisulfite (HSO3) aerosol produces bronchoconstriction in asthm atics but not in normals. This effect is probably due to local formati on Of SO2 which stimulates vagal afferents in the airway mucosa, and g ives rise to bronchoconstriction that is partly due to a cholinergic r eflex. Metabisulfite (MBS) produces bronchoconstriction in most adult asthmatics, but its effect in children has received little attention. The present study was done to assess MBS-induced bronchoconstriction a s a function of age in asthmatic children, and to compare MBS responsi veness with the response to inhaled metacholine (MCH), which is common ly used for bronchoprovocation testing. In 36 children with moderate a sthma, selected to cover the age range between 3 and 20 years, we comp ared airway responsiveness to MBS and MCH, expressed as the provocativ e dose that causes a 20% fall in baseline forced expiratory volume in 1 sec (FEV1,PD20). We also measured the PD20 to MBS after pretreatment with the anticholinergic ipratropiumbromide, to estimate the noncholi nergic component of the response. After bronchial provocation with MCH , a PD20 was reached in 32 children, and no significant relation of PD 20 to age was found. A PD20[MBS] was seen in only 17 patients, and mor e frequently in older children. There was a significant negative corre lation between age and PD20[MBS]. Ipratropium pretreatment reduced the response to MBS in 14 of the 17 children who had a PD20[MBS]. The PD2 0[MBS] after ipratropium pretreatment was also significantly negativel y related with age. This suggested that the increased prevalence of MB S responsiveness was due to an increase of the noncholinergic componen t of the response. We conclude that, in this cross-sectional study, th e sensitivity of asthmatic children to MBS-induced bronchoconstriction increases with age, and that this is because of an increase of the no ncholinergic component of the response to MBS. We speculate that this reflects an abnormal development of the autonomic control of airway ca liber in children with asthma. (C) 1993 Wiley-Liss, Inc.