Skip to main content
NCBI home page
Thorax logoLink to Thorax
. 1984 Oct;39(10):752–758. doi: 10.1136/thx.39.10.752

Asbestos related pleuropulmonary lesions and the erythrocyte sedimentation rate.

G Hillerdal
PMCID: PMC459913  PMID: 6495243

Abstract

Asbestos related lesions of the lung parenchyma and the pleura can be divided into three main types: parietal pleural plaques, diffuse interstitial fibrosis ("classical asbestosis"), and a third type of reaction affecting both the pleura and the lung parenchyma. The last type includes such lesions as acute pleurisy, diffuse pleural thickening, and rounded atelectasis. Among 1344 patients with asbestos related pleural lesions, 1190 had pleural plaques, 29 of whom also had pulmonary fibrosis (asbestosis); 83 had unilateral sequelae of pleurisy, of whom nine had asbestosis; and 71 had bilateral sequelae of pleurisy, of whom 23 also suffered from asbestosis. The erythrocyte sedimentation rate (ESR) was measured in 184 patients--79 with pleural plaques, 44 with unilateral sequelae of pleurisy, and 61 with bilateral sequelae. In patients with pleural plaques with or without asbestosis the ESR was usually normal, the mean being 9.6 mm in one hour. Among patients with sequelae of pleurisy, however, many had a raised ESR. The mean ESR was 25.7 mm in one hour in those with bilateral changes and 13.2 in those with unilateral changes. Statistical analysis showed that in this group of subjects the presence of sequelae of pleurisy was a highly significant determining factor for the ESR (p less than 0.0001). Asbestosis alone was not a significant determining factor but there was a low grade of significance for the combined effect of asbestosis and sequelae of pleurisy (p less than 0.05). These findings suggest that the pathogenesis of the various changes is different.

Full text

PDF
752

Images in this article

754Image
on p.754
755Image
on p.755
755Image
on p.755
756Image
on p.756

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Campbell M. J., Wagner M. M., Scott M. P., Brown D. G. Sequential immunological studies in an asbestos-exposed population. II. Factors affecting lymphocyte function. Clin Exp Immunol. 1980 Jan;39(1):176–182. [PMC free article] [PubMed] [Google Scholar]
  2. Hahon N., Eckert H. L. Depression of viral interferon induction in cell monolayers by asbestos fibers. Environ Res. 1976 Feb;11(1):52–65. doi: 10.1016/0013-9351(76)90110-9. [DOI] [PubMed] [Google Scholar]
  3. Hanke R. Rundatelektasen (Kugel- und Walzenatelektasen). Ein Beitrag zur Differentialdiagnose intrapulmonaler Rundherde. Fortschr Geb Rontgenstr Nuklearmed. 1971 Feb;114(2):164–183. [PubMed] [Google Scholar]
  4. Hillerdal G., Baris Y. I. Radiological study of pleural changes in relation to mesothelioma in Turkey. Thorax. 1983 Jun;38(6):443–448. doi: 10.1136/thx.38.6.443. [DOI] [PMC free article] [PubMed] [Google Scholar]
  5. Hillerdal G., Hemmingsson A. Pulmonary pseudotumours and asbestos. Acta Radiol Diagn (Stockh) 1980;21(5):615–620. doi: 10.1177/028418518002100507. [DOI] [PubMed] [Google Scholar]
  6. Hillerdal G., Hillerdal O., Nöu E. Radiologically visible pleural plaques in a one-year material from a health survey in 1976 a cross-sectional study. Eur J Respir Dis Suppl. 1980;107:89–98. [PubMed] [Google Scholar]
  7. Hillerdal G., Lindgren A. Pleural plaques: correlation of autopsy findings to radiographic findings and occupational history. Eur J Respir Dis. 1980 Dec;61(6):315–319. [PubMed] [Google Scholar]
  8. Hillerdal G. Non-malignant asbestos pleural disease. Thorax. 1981 Sep;36(9):669–675. doi: 10.1136/thx.36.9.669. [DOI] [PMC free article] [PubMed] [Google Scholar]
  9. Hillerdal G. Pleural plaques in a health survey material. Frequency, development and exposure to asbestos. Scand J Respir Dis. 1978 Oct;59(5):257–263. [PubMed] [Google Scholar]
  10. Huuskonen M. S., Räsänen J. A., Härkönen H., Asp S. Asbestos exposure as a cause of immunological stimulation. Scand J Respir Dis. 1978;59(6):326–332. [PubMed] [Google Scholar]
  11. Kagan E., Solomon A., Cochrane J. C., Kuba P., Rocks P. H., Webster I. Immunological studies of patients with asbestosis. II, Studies of circulating lymphoid cell numbers and humoral immunity. Clin Exp Immunol. 1977 May;28(2):268–275. [PMC free article] [PubMed] [Google Scholar]
  12. Kang K., Sera Y., Okochi T., Yamamura Y. Letter: T lymphocytes in abestosis. N Engl J Med. 1974 Oct 3;291(14):735–736. doi: 10.1056/NEJM197410032911414. [DOI] [PubMed] [Google Scholar]
  13. Lange A. An epidemiological survey of immunological abnormalities in asbestos workers. I. Nonorgan and organ-specific autoantibodies. Environ Res. 1980 Jun;22(1):162–175. doi: 10.1016/0013-9351(80)90128-0. [DOI] [PubMed] [Google Scholar]
  14. Mackenzie F. A., Harries P. G. Changing attitudes to the diagnosis of asbestos disease. J R Nav Med Serv. 1970 Spring;56(1):116–123. [PubMed] [Google Scholar]
  15. Mintzer R. A., Cugell D. W. The association of asbestos-induced pleural disease and rounded atelectasis. Chest. 1982 Apr;81(4):457–460. doi: 10.1378/chest.81.4.457. [DOI] [PubMed] [Google Scholar]
  16. Turner-Warwick M., Parkes W. R. Circulating rheumatoid and antinuclear factors in asbestos workers. Br Med J. 1970 Aug 29;3(5721):492–495. doi: 10.1136/bmj.3.5721.492. [DOI] [PMC free article] [PubMed] [Google Scholar]

Articles from Thorax are provided here courtesy of BMJ Publishing Group

RESOURCES