The commonly held belief that adult onset wheezing illness is primarily non
atopic in nature suggests that the role of atopy in the pathophysiology of
bronchial hyperresponsiveness (BHR) in adult onset wheeze may be minimal.
This study examined risk factors for BHR (BHR: provocative dose causing a 2
0% fall in forced expiratory volume in one second PD20 less than or equal t
o 16.38 mu mol methacholine) among 82 subjects with adult onset wheeze and
among 191 subjects who had never wheezed. Subjects were identified from a c
ohort of subjects aged 39-45 yrs who were known to have had no childhood wh
eeze and who were involved in a 30 yr follow-up survey Risk factors for BHR
were examined among all subjects with BHR and among subjects with BHR stra
tified according to whether or not they had ever wheezed.
The prevalence of BHR was 40% (33/82) among the subjects with adult onset w
heeze and 11% (21/191) among the subjects who had never wheezed, Lower base
line lung function (odds ratio (OR)= 0.94; 95% confidence interval (CT)= 0.
92-0.97 per unit forced expiratory volume (FEV1)% predicted) and atopy (OR
= 7.23; Cl = 2.53-20.64 for all three measures of atopic compared to nonato
pic) were associated with BHR, while smoking and family history showed no s
tatistically significant relation to BHR This pattern was also apparent in
analyses stratified by symptom status. A family history of atopy increased
the risk that BHR was accompanied by wheezing symptoms (OR = 4.75; CI = 1.5
3-14.72 for more than one affected relative compared to no affected relativ
es).
These findings suggest that atopy is associated with bronchial hyperrespons
iveness in adults known to have had no childhood wheeze. A familial factor
reflecting genetic influences and/or shared environmental factors may influ
ence whether bronchial hyperresponsiveness is associated with symptoms.