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Copyright ©ERS Journals Ltd 2003
Clara cell protein as a biomarker for ozone-induced lung injury in humans
1 Dept of Respiratory Medicine and Allergy, University Hospital, 3 Environmental and Occupational Medicine, Dept of Public Health and Clinical Medicine, Umeå University, and 4 National Institute for Working Life, Umeå, Sweden. 2 School of Health and Life Sciences, King's College London, London, UK. 5 Industrial Toxicology Unit, Faculty of Medicine, Catholic University of Louvain, Brussels, Belgium.
CORRESPONDENCE: A. Blomberg, Dept of Respiratory Medicine and Allergy, University Hospital, SE-901 85, Umeå, Sweden. Fax: 46 90141369. E-mail: anders.blomberg@lung.umu.se
Keywords: air pollution, biomarkers, Clara cell protein, lung permeability, ozone
Received: May 1, 2003
Accepted July 16, 2003
This study was supported by the European Commission HELIOS project (QLK4CT-1999-01308), the Swedish Heart-Lung Foundation, Umeå University, the Swedish Environmental Protection Agency and the Swedish Research Council for Environment, Agricultural Sciences and Spatial Planning (FORMAS), Sweden.
Exposure to ozone (O3) impairs lung function, induces airway inflammation and alters epithelial permeability. Whilst impaired lung function and neutrophilia have been observed at relatively low concentrations, altered lung epithelial permeability is only seen after high-dose challenges. The appearance of Clara cell protein (CC16) in serum has been proposed as a sensitive marker of lung epithelial injury. Here, the use of CC16 as an injury biomarker was evaluated under a controlled exposure to O3 and the relationship between this marker of lung injury and early lung function decrements was investigated.
Subjects (n=22) were exposed on two separate occasions to 0.2 parts per million O3 and filtered air for 2 h. Blood samples were drawn and lung function assessed at 2 h pre-exposure, immediately before and immediately after exposure as well as 2 and 4 h postexposure.
O3 increased CC16 serum concentrations at 2 h (12.0±4.5 versus 8.4±3.1 µg·L–1) and 4 h postexposure (11.7±5.0 versus 7.9±2.6 µg·L–1) compared with air concentrations. Archived samples from O3 studies utilising the same design indicated that this increase was sustained for up to 6 h postexposure (9.1±2.6 versus 7.1±1.7 µg·L–1) with concentrations returning to baseline by 18 h (7.7±2.9 versus 6.6±1.7 µg·L–1). In these studies, the increased plasma CC16 concentration was noted in the absence of increases in traditional markers of epithelial permeability. No association was observed between increased CC16 concentrations and lung function changes.
To conclude, Clara cell protein represents a sensitive and noninvasive biomarker for ozone-induced lung epithelial damage that may have important uses in assessing the health effects of air pollutants in future epidemiological and field studies.
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