title: Immunologic studies of the mechanisms of occupational asthma caused by western red cedar.
abstract: BACKGROUND
  Occupational asthma caused by western red cedar (Thuja plicata) is a common problem in sawmill industries. The objective of this study was to examine the cellular and immunologic mechanisms of western red cedar asthma (WRCA) more closely.
  
  
  METHODS
  Bronchial biopsy specimens, bronchoalveolar lavage (BAL) mast cells and peripheral blood basophils from patients with WRCA, patients with atopic asthma, and nonatopic control subjects were challenged in vitro with plicatic acid (PA), PA-human serum albumin conjugate (PA-HSA), grass pollen, or calcium ionophore.
  
  
  RESULTS
  PA (100 micrograms/ml) released histamine from the basophils of 9 of 11 patients with WRCA, 1 of 7 patients with atopic asthma, and 2 of 7 normal subjects. PA triggered histamine release from 10 of 11 bronchial biopsy specimens and 8 of 8 BAL samples from patients with WRCA. Interestingly, PA released histamine from BAL cells and bronchial biopsy specimens from 3 of 7 normal subjects but in none of the patients with atopic asthma. PA-HSA-induced histamine release from basophils and biopsy specimens was confined to patients with WRCA. PA-specific IgE was not detectable in serum from most patients with WRCA, and their serum did not transfer PA sensitivity to human lung fragments or lactate-stripped basophils. After pretreatment with anti-IgE in the absence of calcium, basophils from 14 subjects with WRCA still responded to PA (mean 64% to 67% of pretreatment response), whereas responses to grass pollen or anti-IgE were abolished.
  
  
  CONCLUSIONS
  This study confirms that PA releases histamine from bronchial mast cells of most patients with WRCA but not from those of patients with atopic asthma. The PA response of some normal subjects suggests that PA may have both specific and nonspecific actions on mast cells and basophils, whereas the serologic studies indicate histamine release in WRCA cannot simply be attributed to PA-specific IgE.
authors.affiliation: Department of Medicine, Vancouver General Hospital, University of British Columbia, Canada.
authors.forename: A
authors.initials: A
authors.lastname: Frew
authors.forename: H
authors.initials: H
authors.lastname: Chan
authors.forename: P
authors.initials: P
authors.lastname: Dryden
authors.forename: H
authors.initials: H
authors.lastname: Salari
authors.forename: S
authors.initials: S
authors.lastname: Lam
authors.forename: M
authors.initials: M
authors.lastname: Chan-Yeung
mesh_terms: D000328:Adult; D000485:Allergens / Q000276:immunology; D000704:Analysis of Variance; D001249:Asthma / Q000276:immunology*; D001491:Basophils / Q000276:immunology; D001980:Bronchi / Q000276:immunology; D001985:Bronchial Provocation Tests; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D017705:Lignans; D008297:Male; D009284:Naphthols / Q000276:immunology; D009784:Occupational Diseases / Q000276:immunology*; D014934:Wood
chemical_list: D000485:Allergens; D017705:Lignans; D009284:Naphthols; D007073:Immunoglobulin E; C008938:plicatic acid