Asbestos exposure results in increased lung procoagulant activity in vivo and in vitro

Our plain-English summary of Asbestos exposure results in increased lung procoagulant activity in vivo and in vitro, by K.S. Callahan, D.E. Griffith, J.G. Garcia (Chest, 1990).

The study

• Authors: K.S. Callahan, D.E. Griffith, J.G. Garcia
• Journal: Chest
• Published: 1990;98(1):112-9
• Cited by: 11 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Enhanced fibrin deposition is a common histologic finding in fibrotic lung disorders including asbestosis and may be an important mechanism by which fibroblast proliferation is modulated. Asbestos-induced activation of lung interstitial cells may result in enhanced expression of procoagulant activity which contributes to the inflammatory response resulting in subsequent fibrin deposition. The current study examines procoagulant activity in bronchoalveolar lavage fluid from patients with clinically diagnosed asbestosis, patients with asbestos exposure without asbestosis, and normal, control subjects. Results indicated that asbestos exposure resulted in increased lung procoagulant expression in vivo, and furthermore, suggested that both endothelial cells and alveolar macrophages represented lung parenchymal cells which may contribute to this activity. This imbalance in coagulation homeostasis may be important in the regulation of fibrotic responses observed in asbestosis.

In plain English

This study measured procoagulant (clot-promoting) activity in fluid washed from the lungs (bronchoalveolar lavage) of 9 patients with clinically diagnosed asbestosis, 80 patients with occupational asbestos exposure but no asbestosis, and 13 normal nonsmoking volunteers. Fluid from the volunteers took significantly longer to clot, meaning less activity, than fluid from either patient group. The asbestosis group showed the most activity, even when compared within the same smoking habits. Exposed patients who had never smoked (17 people) did not differ significantly from the volunteers. Lung immune cells (alveolar macrophages) from 5 asbestosis patients showed significantly more activity. Those from 9 exposed patients without asbestosis did not differ significantly from those of controls. In laboratory experiments, amosite asbestos raised tissue factor, a clotting trigger, in human umbilical vein endothelial cells in a dose-dependent way. Latex beads did not. The authors concluded that the increased activity suggests a change that could potentially promote fibrin deposition in the lung. They noted that clot-dissolving activity was not measured, that the controls were younger and all nonsmokers, and that macrophage samples were few.

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 of lung lavage fluid and cells from three groups of people, combined with laboratory (in vitro) experiments on cultured human cells
• Who was studied: 89 patients with a history of occupational asbestos exposure: 9 with clinically diagnosed asbestosis (group 1) and 80 exposed without asbestosis (group 2). Also 13 normal, nonsmoking, unexposed volunteers aged 20 to 44 (group 3). Authors were at the University of Texas Health Center at Tyler. Study dates are not given. Laboratory work used human umbilical vein endothelial cells.
• Exposure: Patients: occupational asbestos exposure, with fiber type not specified. Laboratory: endothelial cells were incubated with amosite asbestos for two to seven hours, at concentrations from 25 to 250 micrograms per ml (up to 500 in one figure).
• Main results:
  • Lung fluid from normal control subjects had significantly longer clotting times (less procoagulant activity) than fluid from asbestos-exposed subjects and subjects with asbestosis (p = 0.0002 for asbestosis versus controls). Exposed and asbestotic patients also differed significantly.
  • Asbestosis patients had significantly increased procoagulant activity compared with the exposed group and the normal subjects, even when matched for smoking habits.
  • Among asbestos-exposed patients without asbestosis, former and current smokers had significantly increased activity compared with nonsmoking controls.
  • Nonsmoking asbestos-exposed patients (n = 17) were not statistically different from the control subjects.
  • In the 80 exposed subjects, clotting time was not significantly related to age (r = 0.08, p = 0.229).
  • Alveolar macrophages from 9 exposed patients without asbestosis had clotting times of 85.5 plus or minus 2.7 seconds and 462 plus or minus 38 tissue factor units. These were not statistically different from macrophages of control subjects.
  • Alveolar macrophages from 5 asbestosis patients had significantly shorter clotting times (71.4 plus or minus 8.3 seconds), meaning higher activity.
  • Amosite asbestos produced a dose-dependent reduction in clotting times of endothelial cells, with significant differences at or above 125 micrograms per ml.
  • Tissue factor activity on endothelial cells peaked five to seven hours after asbestos exposure.
  • Latex beads, which the cells also take up, had no effect on tissue factor expression.
  • Catalase, an oxidant scavenger, inhibited the asbestos-induced activity by only 6.2 percent (plus or minus 0.2 percent).
  • The authors judged that the increased tissue factor expression in amosite-exposed endothelial cells appears to be independent of oxidant production.
• The authors' conclusion: The authors concluded that finding increased procoagulant activity in both asbestos-exposed and asbestotic subjects suggests that procoagulant expression is altered in a way that could potentially promote fibrin deposition in the lung.
• Limitations the authors state:
  • Fibrinolytic (clot-dissolving) capacities were not assessed.
  • Control subjects were all nonsmokers and considerably younger than the patients, which may have contributed to the differences.
  • Only a limited number of alveolar macrophage samples were available.
  • The specific role of asbestos in the increased macrophage activity in asbestosis patients could not be determined.
  • Whether asbestos and smoking combined had an additive or synergistic effect was not addressed. The authors also noted that the nonsmoking exposed subgroup was small.

Topics

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

Medical terms in this study, explained in our Lexicon: Asbestos Exposure, Deposition, Fibroblast, Interstitial, Bronchoalveolar Lavage (BAL), Alveolar Macrophage.

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