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Proinflammatory doses of diesel exhaust in healthy subjects fail to elicit equivalent or augmented airway inflammation in subjects with asthma
  1. Annelie F Behndig1,2,
  2. Nirina Larsson1,2,
  3. Joanna L Brown3,4,
  4. Nikolai Stenfors1,
  5. Ragnberth Helleday1,2,
  6. Sean T Duggan5,
  7. Rosamund E Dove1,5,
  8. Susan J Wilson3,
  9. Thomas Sandstrom1,2,
  10. Frank J Kelly5,
  11. Ian S Mudway5,
  12. Anders Blomberg1,2
  1. 1Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden
  2. 2Department of Medicine, Division of Respiratory Medicine and Allergy, University Hospital, Umeå, Sweden
  3. 3Histochemistry Research Unit, Sir Henry Wellcome Laboratories, Southampton General Hospital, Southampton, UK
  4. 4Respiratory Department, Imperial College Healthcare NHS Trust, Hammersmith Hospital, London, UK
  5. 5MRC–HPA Centre for Environment and Health, School of Biomedical and Health Sciences, King's College London, UK
  1. Correspondence to Dr Ian S Mudway, King's College London, MRC–HPA Centre for Environment and Health, School of Biomedical and Health Sciences, 4th Floor Franklin-Wilkins Building, 150 Stamford Street, London SE1 9NH, UK; ian.mudway{at}


Background Exposure to traffic-derived air pollutants, particularly diesel emissions, has been associated with adverse health effects, predominantly in individuals with pre-existing respiratory disease. Here the hypothesis that this heightened sensitivity reflects an augmentation of the transient inflammatory response previously reported in healthy adults exposed to diesel exhaust is examined.

Methods 32 subjects with asthma (mild to moderate severity) and 23 healthy controls were exposed in a double-blinded crossover control fashion to both filtered air and diesel exhaust (100 μg/m3 PM10) for 2 h. Airway inflammation was assessed by bronchoscopy 18 h postexposure. In addition, lung function, fraction of exhaled nitric oxide and bronchial reactivity to metacholine were examined in the subjects with asthma.

Results In healthy control subjects a significant increase in submucosal neutrophils (p=0.004) was observed following the diesel challenge. Significant increases in neutrophil numbers (p=0.01), and in the concentrations of interleukin 6 (p=0.03) and myeloperoxidase (p=0.04), were also seen in bronchial wash after diesel, relative to the control air challenge. No evidence of enhanced airway inflammation was observed in the subjects with asthma following the diesel exposure.

Conclusions Exposure to diesel exhaust at concentrations consistent with roadside levels elicited an acute and active neutrophilic inflammation in the airways of healthy subjects. This response was absent in subjects with asthma, as was evidence supporting a worsening of allergic airway inflammation.

  • Inflammation
  • air pollution
  • asthma
  • particulate matter
  • diesel
  • airway epithelium
  • asthma mechanisms

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  • See Editorial, p 4

  • Linked articles 145391.

  • Funding Swedish Heart–Lung Foundation, European Commission HEPMEAP project (QLRT 1999-01582) and Umeå University, Sweden. AB is the holder of the Lars Werkö distinguished research fellowship from the Swedish Heart–Lung Foundation.

  • Competing interests None.

  • Ethics approval This study was conducted with the approval of the research ethics committee at Umea University, Sweden.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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