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Eur Respir J 2002; 20:1152-1161
Copyright ©ERS Journals Ltd 2002


Serum levels of CC16, SP-A and SP-B reflect tobacco-smoke exposure in asymptomatic subjects

M. Robin1, P. Dong2, C. Hermans1, A. Bernard1, A.D. Bersten2 and I.R. Doyle2

1 Industrial Toxicology and Occupational Medicine Unit, Faculty of Medicine, Catholic University of Louvain, Brussels, Belgium. 2 Depts of Human Physiology and Critical Care Medicine, School of Medicine, Flinders University, Adelaide, Australia

CORRESPONDENCE: I.R. Doyle, Dept of Human Physiology, Flinders University, Bedford Park, South Australia, Australia, 5042. Fax: 61 882045768. E-mail: Ian.Doyle@flinders.edu.au

Keywords: alveolocapillary leakage, Clara cell secretory protein, Clara cell toxicity, surfactant protein-A, surfactant protein-B, tobacco smoke

Received: November 2, 2001
Accepted June 12, 2002

This work was supported by the National Fund for Scientific Research (FNRS), the Belgian Government Association (CT DD/MD006) and the European Commission (QLK 4-1308), the National Health and Medical Research Council of Australia and Autogen Research Pty Ltd.

Since the 16-kDa bronchiolar Clara cell protein (CC16) and the alveolar surfactant-associated proteins (SP)-A and -B leak into the circulation when parenchymal health is disturbed, the aim of this study was to determine whether their serum levels could serve as early peripheral markers of tobacco smoke-induced epithelial injury.

Sixty-nine (51 yrs (32–54) median (25–75th percentile)) nonsmokers and 54 (42 yrs (31–53)) asymptomatic smokers were enrolled in the study.

Serum levels of SP-A did not differ between subjects (270 (208–389) versus 259 (168–392) µg·L–1), however, CC16 levels decreased (10.6 (8.7–14.6) versus 7.6 (6.0–11.2) µg·L–1) and SP-B levels increased (2,529 (2,091–2,943) versus 3,053 (2,613–4,188) µg·L–1) in the smokers. When tobacco smoke exposure, serum creatinine (renal index), age and sex were used as independent variables, CC16 was negatively influenced by cumulative smoking and positively influenced by age. SP-A and -B were negatively influenced by creatinine and positively influenced by cumulative smoking. Serum SP-B was inversely correlated with forced expiratory volume in one second/vital capacity, suggesting an association between obstructive disease and parenchymal lung health.

The authors suggest that serum surfactant-associated proteins-A and -B reflect increased alveolocapillary leakage whereas Clara cell secretory protein 16 reflects tobacco smoke-induced Clara cell toxicity. Their evaluation may allow the effects of tobacco smoke on different levels of the respiratory tract, cellular toxicity and epithelial leakage to be distinguished.




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