Clara Cell Protein (CC-16) and Surfactant-Associated Protein A (SP-A) in Asbestos-Exposed Workers

¹ From the Unité de Recherche Pulmonaire, Université de Sherbrooke, Québec, Canada
² From the Unité de Toxicologie Industrielle et Médecine du Travail, Université Catholique de Louvain, Bruxelles, Belgium

Asbestos-exposed workers (Asb) can sometimes develop lung impairments resembling idiopathic pulmonary fibrosis (IPF). Smoking is often a troubling confounder in the natural history of these lung diseases. Distal airspace epithelial cells, which are also altered in asbestosis, secrete Clara cell protein (CC-16, also designated CC-10) and surfactant-associated protein A (SP-A). By inhibiting phospholipase A₂ (PLA₂), CC-16 and SP-A are putative candidates for controlling lung inflammatory events. Both were measured with PLA₂ activity in alveolar fluids (and sera for CC-16) of smoker and nonsmoker Asb and compared with smoking-matched normal subjects (N). CC-16 (in mg/L) was slightly increased in Asb and affected by smoking: nonsmoker Asb: 3.1±0.5 vs nonsmoker N: 1.9±0.2 (p<0.05), smoker Asb: 1.7±0.3 vs smoker N: 0.6±0.1 (p<0.05). SP-A (in µg/mL) was enhanced in Asb but not affected by smoking: 5.4±1.5 in Asb vs 1.6±0.4 in N (p<0.05), whereas SP-A to phosphorus ratio was increased in Asb but affected by smoking. CC-16 to albumin and CC-16 in serum to alveolar fluid ratios were altered by cigarette consumption in Asb (p<0.05 vs N). Secretory PLA₂ activity was slightly enhanced in Asb (p<0.05 vs N). All data were similar between stages of disease. In summary, alveolar CC-16, SP-A, and secretory PLA₂ activity were increased in Asb. Smoking affected several parameters. By this habit, Asb might reinforce lung profibrotic factors and increase their risk in developing lung alterations resembling IPF.

Key Words: asbestosis • epithelium • phospholipase A₂ • surfactant-associated protein

Submitted on May 19, 1995
Accepted on August 30, 2007

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