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Daily variation in fine and ultrafine particulate air pollution and urinary concentrations of lung Clara cell protein CC16
  1. K L Timonen1,
  2. G Hoek2,
  3. J Heinrich3,
  4. A Bernard4,
  5. B Brunekreef2,
  6. J de Hartog2,
  7. K Hämeri5,
  8. A Ibald-Mulli3,
  9. A Mirme6,
  10. A Peters3,
  11. P Tiittanen7,
  12. W G Kreyling8,
  13. J Pekkanen
  1. 1Department of Clinical Physiology and Nuclear Medicine, Kuopio University Hospital and University of Kuopio, Kuopio, Finland
  2. 2Environmental and Occupational Health Unit, University of Utrecht, Utrecht, Netherlands
  3. 3GSF-Institute of Epidemiology, Neuherberg, Germany
  4. 4Unité de Toxicologie Industrielle et de Médicine du Travail, University of Louvain, Brussels, Belgium
  5. 5Department of Physics, University of Helsinki, and Finnish Institute of Occupational Health, Helsinki, Finland
  6. 6University of Tartu, Tartu, Estonia
  7. 7Unit of Environmental Epidemiology, National Public Health Institute, Kuopio, Finland
  8. 8GSF-Institute for Inhalation Biology, Neuherberg, Germany
  1. Correspondence to:
 Ms K L Timonen
 Department of Clinical Physiology and Nuclear Medicine, Kuopio University Hospital, PO Box 1777, FIN-70211 Kuopio, Finland;


Background: Daily variations in ambient particulate air pollution have been associated with respiratory mortality and morbidity.

Aims: To assess the associations between urinary concentration of lung Clara cell protein CC16, a marker for lung damage, and daily variation in fine and ultrafine particulate air pollution.

Methods: Spot urinary samples (n = 1249) were collected biweekly for six months in subjects with coronary heart disease in Amsterdam, Netherlands (n = 37), Erfurt, Germany (n = 47), and Helsinki, Finland (n = 47). Ambient particulate air pollution was monitored at a central site in each city.

Results: The mean 24 hour number concentration of ultrafine particles was 17.3×103 cm−3 in Amsterdam, 21.1×103 cm−3 in Erfurt, and 17.0×103 cm−3 in Helsinki. The mean 24 hour PM2.5 concentrations were 20, 23, and 13 μg/m3, respectively. Daily variation in ultrafine particle levels was not associated with CC16. In contrast, CC16 concentration seemed to increase with increasing levels of PM2.5 in Helsinki, especially among subjects with lung disorders. No clear associations were observed in Amsterdam and Erfurt. In Helsinki, the CC16 concentration increased by 20.2% (95% CI 6.9 to 33.5) per 10 μg/m3 increase in PM2.5 concentration (lag 2). The respective pooled effect estimate was 2.1% (95% CI −1.3 to 5.6).

Conclusion: The results suggest that exposure to particulate air pollution may lead to increased epithelial barrier permeability in lungs.

  • particulate air pollution
  • clara cell protein
  • epidemiology

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