Respiratory function changes after asbestos pleurisy

Our plain-English summary of Respiratory function changes after asbestos pleurisy, by P.H. Wright, A. Hanson, L. Kreel, et al (Thorax, 1980).

The study

• Authors: P.H. Wright, A. Hanson, L. Kreel, L.H. Capel
• Journal: Thorax
• Published: 1980;35(1):31-6
• Type of article: Case report
• Cited by: 69 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text
• In J-M's library: Johns-Manville's company medical library held a copy (J-M no. 002066).

Abstract

Six patients with radiographic evidence of diffuse pleural thickening after industrial asbestos exposure are described. Five had computed tomography of the thorax. All the scans showed marked circumferential pleural thickening often with calcification, and four showed no significant evidence of intrapulmonary fibrosis (asbestosis). Lung function testing showed reduction of the inspiratory capacity and the single-breath carbon monoxide transfer factor (TLCO). The transfer coefficient, calculated as the TLCO divided by the alveolar volume determined by helium dilution during the measurement of TLCO, was increased. Pseudo-static compliance curves showed markedly more negative intrapleural pressures at all lung volumes than found in normal people. These results suggest that the circumferential pleural thickening was preventing normal lung expansion despite abnormally great distending pressures. The pattern of lung function tests is sufficiently distinctive for it to be recognised in clinical practice, and suggests that the lungs are held rigidly within an abnormal pleura. The pleural thickening in our patients may have been related to the condition described as "benign asbestos pleurisy" rather than the interstitial fibrosis of asbestosis.

In plain English

This was a report of six men with marked diffuse pleural thickening after industrial asbestos exposure, seen at East Ham Chest Clinic and the London Chest Hospital. Jobs included lagging, asbestos factory work, grinding and bagging asbestos fibre, welding, and wood machining in a car-battery factory filled with asbestos dust. Fiber types were not specified for these patients. All six continued to smoke. Five had CT scans, which showed circumferential pleural thickening, often with calcification; four showed no significant evidence of asbestosis. In all six, vital capacity averaged 69% of predicted and carbon monoxide transfer factor 70% of predicted, while the transfer coefficient (Kco) was raised, averaging 118%. In four men given further tests, total lung capacity averaged 64% of predicted, and lung pressure-volume curves lay outside the normal range. The authors concluded that severe pleural thickening, enough to cause marked loss of lung function and breathlessness, can occur in asbestos workers without detectable fibrosis inside the lung; they suggested the lungs are held rigidly within an abnormal pleura. They noted doubt about oesophageal pressure readings in severe pleural disease.

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: case series of six patients (clinical review plus lung function testing and CT)
• Who was studied: Six men with marked pleural thickening. Four came from some 70 patients with asbestos-related disease at East Ham Chest Clinic, London. Two more were found in the records of the London Chest Hospital lung function laboratory.
• Exposure: Industrial asbestos exposure in varied jobs: lagger (heavily exposed), wood machinist in a car-battery factory filled with asbestos dust, asbestos factory process worker, blacksmith and welder (welding rods have been coated with asbestos), six months grinding and bagging asbestos fibre, and dockyard fitter and lagger. Fiber types were not specified for these patients.
• Main results:
  • CT scans (five patients) showed marked circumferential pleural thickening, often with calcification. Four of these scans showed no significant evidence of intrapulmonary fibrosis (asbestosis).
  • Six patients, mean % predicted: vital capacity 69 (range 65-78, P less than 0.001); TLCO 70 (range 56-78, P less than 0.005); Kco 118 (range 102-131, P less than 0.025); FEV1 62 (range 59-72); FEV% 96 (normal, not significant).
  • Four patients, mean % predicted: TLC 64 (p less than 0.02); RV 56 and FRC 71 (not significant). The loss of vital capacity came from reduced inspiratory capacity. Static compliance averaged 40% (p less than 0.05) and specific compliance 34% (p less than 0.02).
  • In the four patients tested, pressure-volume (compliance) curves lay outside the normal range, with markedly more negative intrapleural pressures than in normal people.
• The authors' conclusion: The authors concluded that severe pleural thickening, enough to cause marked loss of lung function and dyspnoea, can occur in asbestos workers without detectable intrapulmonary fibrosis. They suggested the lungs are held rigidly within an abnormal pleura, and that the thickening may relate to 'benign asbestos pleurisy' rather than to asbestosis.
• Limitations the authors state:
  • The authors noted doubt about the exact meaning of oesophageal pressure recordings in the presence of gross pleural disease.
  • The authors noted that other workers have reported different results (abnormally high intrapleural pressures) in patients with presumed pleural restriction.

Topics

Medical terms in this study, explained in our Lexicon: Pleurisy, Diffuse Pleural Thickening, Asbestos Exposure, Thorax, Pleural Thickening, Fibrosis, Pleura, Interstitial Fibrosis.

Related studies

• Ventilatory failure due to asbestos pleurisy — A. Miller, A.S. Teirstein, et al. (1983)
• An outbreak of pleural mesothelioma and chronic fibrosing pleurisy in the village of Karain/Urgüp in Anatolia — Y.I. Baris, A.A. Sahin, et al. (1978)
• Evidence of a role for mesothelial cell-derived interleukin 8 in the pathogenesis of asbestos-induced pleurisy in rabbits — A.M. Boylan, C. Rüegg, et al. (1992)
• Pathogenesis of pleurisy, pleural fibrosis, and mesothelial proliferation — A. Herbert (1986)
• The diagnosis of desmoplastic malignant mesothelioma and its distinction from fibrous pleurisy: a histologic and immunohistochemical analysis of 31 cases including p53 immunostaining — W.E. Mangano, P.T. Cagle, et al. (1998)
• Benign asbestos pleurisy — H.B. Eisenstadt (1965)

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