The clinical relevance of asbestos-induced pleural fibrosis

Our plain-English summary of The clinical relevance of asbestos-induced pleural fibrosis, by D.A. Schwartz (Annals of the New York Academy of Sciences, 1991).

The study

• Author: D.A. Schwartz
• Journal: Annals of the New York Academy of Sciences
• Published: 1991;643:169-77
• Cited by: 4 articles, as counted by NIH iCite
• Read it: PubMed · Publisher
• In J-M's library: Johns-Manville's company medical library held a copy (J-M no. 004938).

Abstract

Asbestos-induced pleural fibrosis is the most common radiographic abnormality among asbestos-exposed persons. Circumscribed pleural plaques and diffuse pleural thickening account for more than 90% of the asbestos-induced chest wall abnormalities, and their prevalence is expected to increase for the next 15 to 20 years. Several investigators have recently found that pleural plaques and diffuse pleural thickening independently contribute to the development of restrictive lung function. The work presented in this paper indicates that asbestos-induced pleural fibrosis is also associated with evidence of interstitial lung abnormalities, even among those with normal parenchyma on chest X-ray film. These parenchymal abnormalities include an increased percentage of lymphocytes on bronchoalveolar lavage and an increase in the interstitial changes observed on high-resolution chest computerized tomography (HRCT) scan. However, neither a lymphocytic alveolitis nor an interstitial parenchymal fibrosis influenced the relationship between pleural fibrosis and restrictive lung function. We conclude that asbestos-induced pleural disease contributes to the development of restrictive lung function and identify a group of exposed individuals who are at excess risk of asbestosis.

In plain English

This paper summarizes a study published in more detail elsewhere on why asbestos-related scarring of the pleura (the lung lining) is linked to reduced lung function. It included 24 sheet-metal workers, never or former smokers, whose lung tissue looked normal on chest X-ray. Of these, 7 had normal pleura, 9 had circumscribed pleural plaques and 8 had diffuse pleural thickening. All had breathing tests, high-resolution CT scans and lung washing (bronchoalveolar lavage). After adjusting for age, years in the trade and smoking, workers with diffuse pleural thickening scored on average about 27, 25 and 22 percentage points of predicted normal lower than workers with normal pleura on forced vital capacity, total lung capacity and diffusing capacity respectively. The reduction in forced vital capacity with plaques was only marginally significant. Diffuse thickening was also linked to more lavage lymphocytes and more interstitial (lung-tissue) changes on CT (87.5% versus 14.3% of workers). These findings did not change the link between pleural fibrosis and reduced lung function. The author concluded that asbestos-induced pleural disease contributes to restrictive lung function and identifies exposed people at excess risk of asbestosis.

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: Cross-sectional comparison of a small, selected group of workers by type of pleural fibrosis. The paper is a summary of an investigation the author says was published in more detail elsewhere.
• Who was studied: 24 white sheet-metal workers: 7 with normal pleura, 9 with circumscribed plaques and 8 with diffuse pleural thickening. All were never smokers or former smokers with normal-appearing lung tissue (parenchyma) on chest radiograph. The article does not state where or when the study took place.
• Exposure: Work in the sheet-metal trade; no fiber type or dose is given. Workers were compared by type of asbestos-induced pleural fibrosis. Diffuse pleural thickening was defined as requiring obliteration of the costophrenic angle on the involved side, a modification of the ILO classification.
• Main results:
  • Before adjustment, workers with circumscribed plaques tended to have lower forced expiratory volume and forced vital capacity than those with normal pleura, but the differences were not statistically significant. Their lung volumes and diffusing capacity were virtually indistinguishable from those with normal pleura.
  • Before adjustment, workers with diffuse pleural thickening had significantly lower forced expiratory volume, forced vital capacity and total lung capacity than those with normal pleura. Mean forced vital capacity was 76.8 versus 104.9 percent of predicted.
  • After controlling for age, years in the trade and pack-years of smoking, workers with diffuse pleural thickening were lower than workers with normal pleura by about 27 percentage points of predicted forced vital capacity, 25 of predicted total lung capacity and 22 of predicted diffusing capacity. The regression coefficients were -27.1, -24.9 and -21.8. The article's prose describes these as a 27%, 25% and 22% reduction.
  • Workers with circumscribed pleural plaques had a marginally significant reduction in forced vital capacity after adjustment compared with workers with normal pleura. The regression coefficient was -11.0 percentage points of predicted (standard error 5.3), p = 0.06.
  • Lymphocytes made up 15.5% (standard deviation 12.1) of lavage cells in workers with diffuse pleural thickening, compared with 3.9% (standard deviation 3.8) in those with normal pleura and 7.8% in those with plaques. The difference for diffuse thickening versus normal pleura was statistically significant; the difference for plaques was not.
  • Interstitial (parenchymal) abnormalities on high-resolution CT were found in 87.5% of workers with diffuse pleural thickening, 55.6% of those with plaques and 14.3% of those with normal pleura. The difference for diffuse thickening versus normal pleura was statistically significant, and there was a significant trend across the three groups.
  • In combined models, pleural fibrosis (plaques or diffuse thickening) was associated with declines of about 14, 13 and 11 percentage points of predicted forced vital capacity, total lung capacity and diffusing capacity. The article's prose describes these as 14%, 13% and 11% declines. Lavage lymphocytes and interstitial changes on CT added very little to this relationship.
• The authors' conclusion: The author concluded that asbestos-induced pleural disease contributes to the development of restrictive lung function and identifies a group of exposed individuals at excess risk of asbestosis.
• Limitations the authors state:
  • The CT readers could not be blinded to whether pleural fibrosis was present, although they were blinded to its category.

Topics

Medical terms in this study, explained in our Lexicon: Fibrosis, Pleural Plaques, Diffuse Pleural Thickening, Restrictive Lung Disease, Interstitial, Parenchyma, Chest X-Ray, Bronchoalveolar Lavage (BAL).

Related studies

• Clinical relevance of cellular mediators of inflammation in workers exposed to asbestos — D.A. Schwartz, J.R. Galvin, et al. (1993)
• The effect of asbestos-induced pleural fibrosis on pulmonary function: quantitative evaluation — R. Lilis, A. Miller, et al. (1991)
• Relative release of interleukin-1 beta and interleukin-1 receptor antagonist by alveolar macrophages. A study in asbestos-induced lung disease, sarcoidosis, and idiopathic pulmonary fibrosis — J.N. Kline, D.A. Schwartz, et al. (1993)
• A single intratracheal instillation of single-walled carbon nanotubes induced early lung fibrosis and subchronic tissue damage in mice — E.J. Park, J. Roh, et al. (2011)
• Alveolar macrophage cytokine and growth factor production in a rat model of crocidolite-induced pulmonary inflammation and fibrosis — K.E. Driscoll, J.K. Maurer, et al. (1995)
• Bidirectional modulation of TNF-alpha production by alveolar macrophages in asbestos-induced pulmonary fibrosis — S. Ouellet, H. Yang, et al. (1993)

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