Pulmonary function in asbestosis and asbestos-related pleural disease

Our plain-English summary of Pulmonary function in asbestosis and asbestos-related pleural disease, by A. Miller (Environmental Research, 1993).

The study

• Author: A. Miller
• Journal: Environmental Research
• Published: 1993;61(1):1-18
• Type of article: Review
• Cited by: 20 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

This review begins with the classic physiologic syndrome of interstitial lung disease (ILD) described in established asbestosis in the 1950s: reduced VC and pulmonary compliance, maintenance of airflow (measured indirectly), decreased diffusing capacity (a laborious undertaking in those years), and hyperventilation, increased dead space (VD/VT), and desaturation on exercise. Small airways dysfunction (SAD) was recognized in the 1960s and 1970s as the physiologic counterpart of the early peripheral bronchiolar inflammatory and fibrotic narrowing reported in experimental animals and in asbestos workers. SAD is nonspecific and is often overshadowed by more severe obstruction caused by smoking or by the countervailing effects of increased lung recoil caused by interstitial fibrosis. Airtrapping secondary to SAD may explain some of the reduction in VC in asbestos exposed workers whose FEV1/FVC is normal. There may be a greater frequency of obstructive airways disease in asbestos workers who smoke than in other smokers, suggesting an interaction between these two noxious inhalants. An interaction is seen in the greater frequency and severity of radiographic asbestosis in smokers at equivalent durations of exposure and in the greater reduction in FVC in smokers at equivalent ILO profusion scores. The functional importance of PT is well documented by lower values for FVC at equivalent profusions of parenchymal disease. This is true of circumscribed PT but much more so of diffuse PT, which can occasionally result in ventilatory failure and death. Incremental exercise testing often reveals evidence of excessive ventilation and abnormal gas exchange (VD/VT) attributable to ILD, when standard tests of pulmonary function and chest radiography are normal. These abnormalities help explain dyspnea in such patients.

In plain English

This article was a review by an author at the Mount Sinai School of Medicine in New York of research on lung function in asbestosis and asbestos-related pleural thickening. It often drew on Mount Sinai studies of asbestos workers, mostly insulators. It described an early study (Bader et al., 1961) of 17 patients who made amosite-containing insulation. Vital capacity was reduced in 8, and after 10 years of observation 8 of the 17 had died. A North American insulator study showed the impact of pleural disease on lung function. In a related analysis, forced vital capacity fell as a pleural index rose with circumscribed pleural thickening; with diffuse thickening, even the lowest index was associated with a near-maximum reduction. In insulators 30 to 39 years from first exposure, radiographic asbestosis was reported in 60% of smokers versus 40% of nonsmokers. Current smokers had lower FEV1 than nonsmokers. In an exercise study of 53 patients with asbestos-related pleural disease but without asbestosis, 17 had an excessive ventilatory response on exercise. The author's group reported that diffuse pleural thickening may cause respiratory failure and death.

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: Review of published studies of pulmonary function in asbestosis and asbestos-related pleural disease, emphasizing work from the Mount Sinai group
• Who was studied: Not a single study population. The review covered studies of asbestos-exposed workers, many of them Mount Sinai studies of insulation workers, including a survey of long-term insulators.
• Exposure: Occupational asbestos exposure, mainly among insulation workers. One early study reviewed was of workers making amosite-containing insulation.
• Main results:
  • In the early study by Bader et al. of 17 patients making amosite-containing insulation, vital capacity was reduced in 8.
  • In the follow-up of the same patients, 8 of the 17 original subjects were dead after 10 years of observation.
  • The author stated that the North American insulator study showed the impact of pleural disease on lung function.
  • In workers with circumscribed pleural thickening, there was an inverse relationship between an index of pleural abnormality and percentage predicted FVC.
  • In workers with diffuse pleural thickening, there was no such relationship; the lowest index was associated with a near-maximum reduction in FVC.
  • In insulators 30 to 39 years from onset of exposure, radiographic asbestosis (ILO readings of 1.0 or more) was reported in 60% of smokers, in contrast with 40% of nonsmokers.
  • Severe asbestosis (readings of 1.5 or more) was reported in 10% of all smokers, in contrast with 4% of nonsmokers.
  • Mean FEV1 was far more reduced in current smokers than in nonsmokers (75.3% vs 82.4% predicted).
  • In a Mount Sinai exercise study of 53 patients with asbestos-related pleural disease but without asbestosis, 17 (32%) had an excessive ventilatory response.
  • In an early study of 288 insulators, reduction in vital capacity came 10 to 15 years before 'extensive' radiographic abnormality.
• The authors' conclusion: The author stated that the Mount Sinai group had shown that diffuse asbestos-related pleural thickening may cause severe ventilatory impairment, resulting in respiratory failure and death.
• Limitations the authors state:
  • The author noted that the review would frequently refer to Mount Sinai investigations.
  • For the early study of 288 insulators, the author noted that the frequency of reduced vital capacity may have been underestimated, partly because the cutoff for abnormal vital capacity was low.

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, Interstitial Lung Disease, Diffusing Capacity (DLCO), Interstitial Fibrosis, FEV1/FVC Ratio, Dyspnea.

Related studies

• 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)
• Signs of asbestosis and impaired pulmonary function in women who worked in shipyards — K.H. Kilburn, R. Warshaw, et al. (1985)
• Libby Amphibole Disease: Pulmonary Function and CT Abnormalities in Vermiculite Miners — A. Miller, J. Szeinuk, et al. (2018)
• Asbestos-related lesions of the pleura: parietal plaques compared to diffuse thickening studied with chest roentgenography, computed tomography, lung function, and gas exchange — G. Hillerdal, P. Malmberg, et al. (1990)
• 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)
• Respiratory muscle function in patients with asbestos-related pleural disease — N.A. Jarad, M.P. Carroll, et al. (1994)

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