Respiratory muscle function in patients with asbestos-related pleural disease

Our plain-English summary of Respiratory muscle function in patients with asbestos-related pleural disease, by N.A. Jarad, M.P. Carroll, C. Laroche, et al (Respiratory Medicine, 1994).

The study

• Authors: N.A. Jarad, M.P. Carroll, C. Laroche, N. Poulakis, J. Moxham, M. Green, R.M. Rudd
• Journal: Respiratory Medicine
• Published: 1994;88(2):115-20
• Cited by: 5 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The effect of asbestos-related pleural disease (ARPD) on the generation of maximum respiratory pressure was investigated in 11 male patients with ARPD mean age 57 years, range 45-74, and mean duration of asbestos exposure of 9.9 years, range 5-16. There were three smokers, seven ex-smokers and one non-smoker. Breathlessness ranged from grade 1-3 on the MRC score. The extent of pleural disease was calculated using a score based on the ILO score for pleural disease. Full respiratory function tests, global respiratory muscle strength and diaphragmatic strength were assessed. Respiratory muscle strength, including diaphragm strength, was normal. Recoil pressure was high or at the upper limit of normal in four patients and correlated with chest radiograph score for pleural disease (r = 0.65, P < 0.02). There was no difference in either global respiratory muscle or diaphragmatic strength between patients with and without involvement of one or both costophrenic angles or between patients with mild or severe breathlessness. We conclude that respiratory muscle strength is not importantly reduced in ARPD, and it is unlikely that weakness contributes to breathlessness in these patients. By contrast reduced chest wall compliance is likely to be an important factor in breathlessness in some cases.

In plain English

This study tested whether asbestos-related pleural disease (thickening of the lining around the lungs) weakens the breathing muscles, including the diaphragm. The authors examined 11 breathless male patients, aged 45 to 74, exposed to asbestos for an average of 9.9 years in insulation product factories, dockyards or the building trade. All had diffuse pleural thickening, and none had interstitial lung disease. The authors judged breathing-muscle strength normal in most patients and possibly mildly reduced in two. Strength did not differ between patients with mild and more severe breathlessness, or between those with and without pleural disease at the costophrenic angles (the lower corners of the chest). Lung recoil pressure was high in two patients and at the upper limit of normal in two more, and it correlated with the chest X-ray score for pleural disease (r = 0.65, P < 0.02). The authors concluded that muscle weakness is unlikely to contribute to breathlessness, and that reduced compliance may contribute in some patients.

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: Clinical physiological study of a small group of patients with no control group. Patients' breathing-muscle measurements were compared with published normal values.
• Who was studied: 11 male patients with asbestos-related pleural disease and a plain chest radiograph profusion score of less than 1/0. Mean age was 57 (range 45-74). There were three current smokers, seven ex-smokers and one non-smoker. All were breathless (MRC grade 1-3). All had diffuse pleural thickening and pleural disease involving the diaphragm. Eight had circumscribed plaques, five had pleural calcification, and none had interstitial lung disease. The authors were at the London Chest Hospital and the Royal Brompton National Heart and Lung Hospital, London. Study dates were not stated.
• Exposure: Asbestos exposure for a mean of 9.9 years (range 5-16 years). Jobs were in insulation product factories (five patients), dockyards (five patients) or the building trade (one patient). Fiber types were not stated.
• Main results:
  • In general, the patients had a restrictive ventilatory defect. Mean FEV1/FVC ratio was 96% and mean total lung capacity 86% of predicted values, with preserved or increased KCO (mean 110% of predicted).
  • Oesophageal sniff pressure, a measure of overall inspiratory muscle strength, was normal in all 11 patients.
  • Maximum expiratory mouth pressure ranged from 70 to 155 cm H2O (mean 125; normal above 80) and was abnormally low in two patients.
  • Sniff transdiaphragmatic pressure (diaphragm strength) ranged from 70 to 147 cm H2O (mean 116; normal above 100). It was below the lower limit of normal in two patients and at the lower limit in two more.
  • Overall, the authors judged respiratory muscle strength normal in most of the 11 patients and possibly mildly reduced in two.
  • Mean maximum elastic recoil pressure was 36 cm H2O (range 20-60; normal 20-40). It was high in two patients and at the upper limit of normal in two more.
  • Maximum elastic recoil pressure correlated with the chest radiograph score for pleural disease (r = 0.65, P < 0.02, Spearman's rank test). In their conclusion the authors described this as a weak correlation.
  • Chest radiograph score correlated negatively with vital capacity (r = -0.90, P < 0.005).
  • Patients with mild breathlessness (MRC grades 1 and 2) and patients with moderate to severe breathlessness (grade 3) did not differ in chest radiograph scores, lung function tests, or respiratory muscle and diaphragm strength tests.
  • Respiratory muscle and transdiaphragmatic pressure measurements did not differ between patients with and without pleural disease involving one or both costophrenic angles.
• The authors' conclusion: The authors concluded that in asbestos-related pleural disease, global inspiratory muscle strength is well preserved and weakness is unlikely to contribute to breathlessness. They found recoil pressure mildly increased and weakly correlated with the extent of pleural disease. They concluded that reduced compliance may be a contributory factor in the breathlessness of some patients.
• Limitations the authors state:
  • Transdiaphragmatic pressure measured at total lung capacity is a relatively insensitive test, so mild to moderate diaphragm weakness could have been missed by that test.
  • One patient (patient 9) had values so low on static manoeuvres that the authors questioned whether the patient performed the test properly.
  • No single test of respiratory muscle strength is a gold standard, so a battery of tests was used.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis, Pleural plaques and thickening.

Medical terms in this study, explained in our Lexicon: Asbestos-Related Pleural Disease, Asbestos Exposure, Diaphragm, Chest X-Ray, Costophrenic angle.

Related studies

• Pleural plaques and respiratory function — B. Järvholm, A. Sandén (1986)
• Cardiorespiratory responses to incremental exercise in patients with asbestos-related pleural thickening and normal or slightly abnormal lung function — A. Miller, A. Bhuptani, et al. (1993)
• Exercise training for asbestos-related and other dust-related respiratory diseases: a randomised controlled trial — M.T. Dale, Z.J. McKeough, et al. (2014)
• Asbestos-related pleural disease due to tremolite associated with progressive loss of lung function: serial observations in 123 miners, family members, and residents of Libby, Montana — A.C. Whitehouse (2004)
• Pulmonary function in asbestosis and asbestos-related pleural disease — A. Miller (1993)
• Abnormal lung function associated with asbestos disease of the pleura, the lung, and both: a comparative analysis — K.H. Kilburn, R.H. Warshaw (1991)

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