title: Nasal mucosa inflammation induced by oxygen administration in humans.
abstract: BACKGROUND
  The effect of oxygen toxicity in human airways is still poorly documented. We prospectively evaluated the inflammatory reaction induced by nasal oxygen exposure in an experimental setting.
  
  
  METHODS
  Healthy subjects without nasal symptoms were exposed to high FIO2 during 5 h. Oxygen was delivered from a tank at a flow of 4 l/min to one nostril of each subject and both nostrils were studied. Mucociliary clearance was measured as saccharine nasal transit time (SNTT). Nasal lavage was performed with 5 ml normal saline and the fluid recovered was processed for cytology and measurements of cytokines concentrations: TNF alpha, IL-6, IL-8 and soluble ICAM-1. Under local anaesthesia, biopsies were performed for immunochemistry and electron microscopy.
  
  
  RESULTS
  After oxygen exposure mucociliary clearance decreased and SNTT increased from 16 [9-21] to 20.5 [14-32] min (median and extremes; P < 0.1). In the lavage fluid, concentration of IL-6 was higher in the oxygen-exposed nostril (40.5 [11-128] pg/ml) than in the non-exposed one (7 [0-34] pg/ml; P < 0.05). There was also a trend for a higher IL-8 in the exposed than in the non-exposed nostril, (respectively 501 [214-587] pg/ml and 214 [122-616] pg/ml, P < 0.08), and for a higher number of polymorphonuclear cells in exposed nostril. In the mucosal biopsies substance P was not found, but ICAM-1 expression was higher in the mucosa and submucosa of the exposed nostrils where mast cells were also more abundant and showed piecemeal degranulation.
  
  
  CONCLUSIONS
  In summary, we found clinical, functional and biological evidence of ongoing nasal inflammation following high FIO2 inhalation for 5 h. Since the histology and behaviour of nasal and bronchi mucosa are very similar, the same inflammatory events are likely to be occurring in the bronchi upon high concentrations of inhaled oxygen.
authors.affiliation: Department of Critical Care, University Hospital, Besançon, France.
authors.forename: G
authors.initials: G
authors.lastname: Capellier
authors.forename: Z
authors.initials: Z
authors.lastname: Zhang
authors.forename: M F
authors.initials: MF
authors.lastname: Maheu
authors.forename: H
authors.initials: H
authors.lastname: Pointet
authors.forename: E
authors.initials: E
authors.lastname: Racadot
authors.forename: B
authors.initials: B
authors.lastname: Kantelip
authors.forename: J
authors.initials: J
authors.lastname: Regnard
authors.forename: F
authors.initials: F
authors.lastname: Barale
mesh_terms: D000280:Administration, Inhalation; D000328:Adult; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D007378:Interleukins / Q000032:analysis; D008297:Male; D009079:Mucociliary Clearance / Q000187:drug effects; D009297:Nasal Mucosa / Q000737:chemistry / Q000187:drug effects / Q000473:pathology*; D010100:Oxygen / Q000008:administration & dosage / Q000009:adverse effects*; D011446:Prospective Studies; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D007378:Interleukins; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D010100:Oxygen