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

Our plain-English summary of Clara cell protein (CC-16) and surfactant-associated protein A (SP-A) in asbestos-exposed workers, by O. Lesur, A.M. Bernard, R.O. Bégin (Chest, 1996).

The study

• Authors: O. Lesur, A.M. Bernard, R.O. Bégin
• Journal: Chest
• Published: 1996;109(2):467-74
• Cited by: 39 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

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 microgram/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.

In plain English

This study measured two proteins made by deep-lung lining cells, Clara cell protein (CC-16) and surfactant-associated protein A (SP-A), in lung-wash (bronchoalveolar lavage) fluid. It also measured the activity of an enzyme, secretory phospholipase A2. The authors compared 34 asbestos-exposed workers examined in Sherbrooke, Quebec, with 39 healthy volunteers, and split each group into current smokers and non-current smokers (never-smokers and ex-smokers pooled). Workers were staged from A (no diagnostic criteria for asbestosis) to C (advanced asbestosis). CC-16 was higher in workers than volunteers: 3.1 versus 1.9 mg/L among non-current smokers, and 1.7 versus 0.6 mg/L among current smokers. Current smokers had lower CC-16. SP-A was 5.4 micrograms per mL in workers versus 1.6 in volunteers and was not significantly affected by smoking. Enzyme activity was slightly higher in workers. Levels were similar across disease stages. Blood CC-16 did not differ significantly between groups. The authors concluded that this profile differs from what they had previously published for idiopathic pulmonary fibrosis and may be of diagnostic value, and that smoking must be taken into account. They called for larger and longitudinal studies.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Comparison study: lung-wash (bronchoalveolar lavage) fluid and blood from asbestos-exposed workers were compared with fluid and blood from healthy volunteers, with subjects grouped by smoking habit
• Who was studied: 34 asbestos-exposed workers (33 male, 1 female; mean age 60) investigated for lung symptoms, chest X-ray abnormalities or suspected asbestosis over the previous 8 years at two medical centres in Sherbrooke, Quebec, Canada. Among them were two lung cancers and two mesotheliomas (type not stated). They were compared with 39 healthy volunteers (30 male, 9 female; mean age 31). Workers were 7 nonsmokers, 11 ex-smokers and 16 current smokers. For the comparisons, never-smokers and ex-smokers were pooled into one subset, which the article labels 'nonsmokers'.
• Exposure: Occupational asbestos exposure. The article does not name fiber types, jobs or doses. Workers were staged as A (exposed, without diagnostic criteria for asbestosis; 12 workers), B (early asbestosis; 6 workers) or C (advanced asbestosis; 16 workers).
• Main results:
  • Among non-current smokers (never-smokers and ex-smokers pooled; the article calls them 'nonsmokers'), CC-16 in lung-wash fluid was 3.1 plus or minus 0.5 mg/L in asbestos-exposed workers versus 1.9 plus or minus 0.2 mg/L in normal subjects (p less than 0.05). Values are means plus or minus standard error.
  • Among current smokers, CC-16 in lung-wash fluid was 1.7 plus or minus 0.3 mg/L in asbestos-exposed workers versus 0.6 plus or minus 0.1 mg/L in normal subjects. CC-16 was lower in current smokers overall.
  • SP-A in lung-wash fluid was 5.4 plus or minus 1.5 micrograms per mL in asbestos-exposed workers versus 1.6 plus or minus 0.4 in normal subjects (p less than 0.05). It was not significantly affected by smoking.
  • CC-16 was similar in stage A workers (2,255 plus or minus 588 micrograms per liter) and in stage B and C workers combined (2,195 plus or minus 227 micrograms per liter).
  • SP-A was similar in stage A workers (4.8 plus or minus 1.4 micrograms per mL) and in stage B and C workers (5 plus or minus 1.1 micrograms per mL).
  • When CC-16 was adjusted for albumin, the difference between non-current-smoker workers and non-current-smoker normal subjects disappeared, but the difference between the current-smoker groups became larger.
  • The ratio of SP-A to surfactant phosphorus was increased in asbestos-exposed workers compared with both nonsmoker and smoker normal subjects. The ratio was lower in current smokers.
  • CC-16 in blood serum was 13.6 plus or minus 1.8 micrograms per liter in asbestos-exposed workers versus 10.8 plus or minus 1.5 in normal subjects. The difference was not statistically significant.
  • Smoking sharply increased the ratio of serum CC-16 to lung-wash CC-16 in normal subjects but not in asbestos-exposed workers.
  • Secretory phospholipase A2 activity in lung-wash fluid was slightly higher in asbestos-exposed workers than in normal subjects (1.1 plus or minus 0.3 versus 0.5 plus or minus 0.2 percent fatty acid release, p less than 0.05). It was not significantly affected by stage of disease or smoking.
• The authors' conclusion: The authors concluded that several features of the lung-fluid profile in asbestos-exposed workers differ from those they had previously published for idiopathic pulmonary fibrosis, and that this may be of value as a diagnostic tool. They also concluded that smoking is a frequent confounding factor that should be taken into account.
• Limitations the authors state:
  • The authors stated that larger samples of patients and a longitudinal study are needed to establish that values do not fluctuate with severity of asbestosis, and to evaluate whether they vary with outcome.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis.

Medical terms in this study, explained in our Lexicon: Idiopathic, Pulmonary Fibrosis, Habit.

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• Changes in surfactant in bronchoalveolar lavage fluid after hemithorax irradiation in patients with mesothelioma — M. Hallman, P. Maasilta, et al. (1990)
• Two dimensional protein patterns of bronchoalveolar lavage fluid from non-smokers, smokers, and subjects exposed to asbestos — M. Lindahl, T. Ekström, et al. (1996)
• Effect of air pollutants on the pulmonary surfactant system — B. Müller, C. Seifart, et al. (1998)
• Additional proteins in BAL fluid of Metsovites environmentally exposed to asbestos: more evidence of "protection" against neoplasia? — V. Galani, S. Constantopoulos, et al. (2002)

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