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Original article
Inflammation in induced sputum after aluminium oxide exposure: an experimental chamber study
  1. LIB Sikkeland1,
  2. N E Alexis2,
  3. RC Fry3,4,
  4. E Martin3,4,
  5. TE Danielsen5,
  6. P Søstrand5,
  7. J Kongerud1,6
    1. 1Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway
    2. 2Center for Environmental Medicine, Asthma and Lung Biology, UNC Chapel Hill, Chapel Hill, North Carolina, USA
    3. 3Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, North Carolina, USA
    4. 4Curriculum in Toxicology, University of North Carolina, Chapel Hill, North Carolina, USA
    5. 5Section for Occupational and Environmental Medicine, Oslo University Hospital, Oslo, Norway
    6. 6Department of Respiratory Medicine, Rikshospitalet, Oslo University Hospital, Oslo, Norway
    1. Correspondence to LIB Sikkeland, Department of Respiratory Medicine, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Norway, P.O. Box 4950 Nydalen, Oslo 0424, Norway; l.i.b.sikkeland{at}medisin.uio.no

    Abstract

    Introduction Workers in aluminium production are exposed to a complex mixture of particles and gases potentially harmful to the airways, among them aluminium oxide (Al2O3). With the use of an exposure chamber, we aimed to examine the effects of short-term controlled exposure to Al2O3 on lung function and inflammatory markers in healthy volunteers.

    Methods 15 men (age 19–31) were exposed in random order to clean air or Al2O3 particles (3.8–4.0 mg/m3) for 2 h including 30 min exercise (stationary bike, 75 W). The permissible exposure level (PEL) for Al2O3 by Occupational Safety and Health Administration, USA, is 5 mg/m3 time weighted average (TWA). Sham and particle exposures were separated by at least 2 weeks. Spirometry was carried out, and induced sputum and blood samples were collected 48 h before and 4 and 24 h after exposure.

    Results Levels of sputum neutrophils (mean (±SEM)) was increased 24 h post-Al2O3 vs pre-Al2O3 exposure (43% (4) vs 31% (4), p=0.01) and the protein level of interleukin (IL)-8 had a 4.8 (0.9)-fold change increase 24 h after exposure (p<0.01). Following Al2O3 exposure, gene signatures in sputum were significantly increased related to several pathways.

    Conclusions The present study suggests that controlled exposure to Al2O3 particles at levels below PEL (TWA) induces airway inflammation in healthy humans marked by elevated neutrophils and elevated IL-8. In addition, increased expression of genes associated with several biological processes was observed in sputum. Interestingly, inhaled Al2O3-induced effects were localised to the airways and not systemic.

    • Induced sputum
    • Inhalation Chamber
    • Al2O3
    • Exposure
    • Inflammation

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