Clinical features to stage alveolitis in asbestos workers

Am J Ind Med. 1985;8(6):521-36. doi: 10.1002/ajim.4700080604.

Abstract

To analyze the clinical features of asbestos-induced alveolitis and stage its activity, we evaluated 217 asbestos workers by the usual clinical, radiological, and functional parameters and computerized gallium 67(Ga) lung scan; we obtained bronchoalveolar lavage (BAL) in 33 and lung biopsy in 6. In addition, we scored the profusion of lung rales and correlated it with other parameters of severity of asbestosis. In the 55 workers without asbestosis and normal 67Ga scan, BAL analyses were comparable to those of controls. Of the 56 without asbestosis but increased 67Ga lung uptake, BAL analyses in 8 documented a predominantly macrophagic alveolitis (confirmed on lung biopsy in 3), with the highest levels of BAL fibronectin. In the 106 workers with asbestosis, 67Ga lung uptake was increased in 75; BAL in 17 demonstrated a macrophagic and neutrophilic alveolitis with elevated fibronectin levels. Lung biopsy in 3 of the latter workers documented peribronchiolar fibrosing alveolitis. Rale scores in all workers or in those without asbestosis did not correlate with 67Ga scores; they correlated fairly well with profusion of parenchymal opacities (Rs = 0.42) and rigidity of the lung pressure-volume curve (Rs = 0.39). Thus, 67Ga lung uptake is an early indicator of chronic macrophagic alveolitis in asbestos workers, which usually progresses to asbestosis. In the disease, profusion of lung rales constitutes a simple clinical mode of assessment of disease severity that correlates better with radiological and functional parameters than with parameters of alveolitis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Asbestos / adverse effects*
  • Asbestosis / complications
  • Asbestosis / diagnosis*
  • Biopsy
  • Humans
  • Middle Aged
  • Peptidyl-Dipeptidase A / metabolism
  • Pulmonary Fibrosis / classification
  • Pulmonary Fibrosis / diagnosis
  • Pulmonary Fibrosis / etiology*
  • Respiratory Function Tests
  • Respiratory Sounds
  • Smoking

Substances

  • Asbestos
  • Peptidyl-Dipeptidase A