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Airway inflammation in aluminium potroom asthma
  1. T Sjåheim1,
  2. T S Halstensen2,
  3. M B Lund1,
  4. Ø Bjørtuft1,
  5. P A Drabløs3,
  6. D Malterud4,
  7. J Kongerud1
  1. 1Department of Respiratory Medicine, National Hospital, University of Oslo, Norway
  2. 2Department of Oral Biology, University of Oslo, Norway
  3. 3Health Department, Hydro Aluminium Karmøy, Norway
  4. 4Health Department, Elkem Aluminium Lista, Norway
  1. Correspondence to:
 Dr T Sjåheim
 Department of Respiratory Medicine, National Hospital, 0027 Oslo, Norway; tonebsodont.uio.no

Abstract

Aims: To examine whether asthma induced by exposure to aluminium potroom emissions (potroom asthma) is associated with inflammatory changes in the airways.

Methods: Bronchial biopsy specimens from 20 asthmatic workers (8 non-smokers and 12 smokers), 15 healthy workers (8 non-smokers and 7 smokers), and 10 non-exposed controls (all non-smokers) were analysed. Immunohistofluorescent staining was performed to identify mucosal total leucocytes (CD45+ leucocytes), neutrophils, and mast cells.

Results: Median RBM thickness was significantly increased in both asthmatic workers (8.2 μm) and healthy workers (7.4 μm) compared to non-exposed controls (6.7 μm). Non-smoking asthmatic workers had significantly increased median density of lamina propria CD45+ leucocytes (1519 cells/mm2v 660 and 887 cells/mm2) and eosinophils (27 cells/mm2v 10 and 3 cells/mm2) and significantly increased concentrations of exhaled NO (18.1 ppb v 6.5 and 5.1 ppb) compared to non-smoking healthy workers and non-exposed controls. Leucocyte counts and exhaled NO concentrations varied with smoking habits and fewer leucocytes were observed in asthmatic smokers than in non-smokers Asthmatic smokers had significantly increased numbers of eosinophils in lamina propria compared to non-exposed controls (10 v 3 cells/mm2). Both eosinophilic and non-eosinophilic phenotypes of asthma were recognised in the potroom workers and signs of airway inflammation were also observed in healthy workers.

Conclusions: Airway inflammation is a central feature of potroom asthma and exposure to potroom emissions induces pathological alterations similar to those described in other types of asthma. Cigarette smoking seems to affect the underlying mechanisms involved in asthma, as the cellular composition of airway mucosa appears different in asthmatic smokers and non-smokers.

  • DIC, differential interference contrast
  • FEV1, forced expiratory volume in one second
  • FVC, forced vital capacity
  • NO, nitric oxide
  • RBM, reticular basement membrane
  • PEF, peak expiratory flow
  • occupational asthma
  • airway inflammation
  • aluminium smelter

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Footnotes

  • Funding: This study was supported by grants from the Norwegian Research Council, University of Oslo, and Nordic Aluminium Industry’s Secretariat for Health, Environment and Safety (AMS)