Background The pathogenic mechanism of grain dust (GD)-induced occupational
asthma (OA) remains unclear.
Objective To understand further the mechanism of GD-induced OA.
Methods Fifteen employees working in a same GD industry, complaining of wor
k-related respiratory symptoms, were enrolled and were divided into two gro
ups according to the GD-bronchoprovocation test (BPT) result: six positive
responders were grouped as group III, nine negative responders as group II
and five healthy controls as group I. Serum GD-specific immunoglobulin (Ig)
E (sIgE), specific IgG (sIgG) and specific IgG4 (sIgG4) antibodies were det
ected by enzyme-linked immunosorbent assay. Basophil histamine release was
measured by the autofluorometric method, and changes of serum neutrophil ch
emotactic activity were observed by the Boyden chamber method.
Results For clinical parameters such as degree of airway hyperresponsivenes
s to methacholine, duration of respiratory symptoms, exposure duration, and
prevalences of serum sIgE, sIgG and sIgG4 antibodies, there were no signif
icant differences between group II and III (P > 0.05, respectively). Serum
neutrophil chemotactic activity increased significantly at 30min and decrea
sed at 240min after the GD-BPT in group In subjects (P<0.05, respectively),
while no significant changes were noted in group II subjects (P>0.05). Bas
ophil histamine release induced by GD was significantly higher in group III
than those of group I or group II (P<0.05, respectively), while minimal re
lease of anti-IgG4 antibodies was noted in all three groups.
Conclusions These results suggest that enhanced basophil histamine release
and serum neutrophil chemotactic activity might contribute to the developme
nt of GD-induced occupational asthma.