Clara cell protein (CC-16) and surfactant-associated protein A (SP-A) in asbestos-exposed workers

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 A(2) (PLA(2)), CC-16 and SP-A are putative candidates for controlling lung inflammatory events. Both were measured with PLA(2) 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 mu g/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 PLA(2) activity was slightly enhanced in Asb (p