A retired shipyard worker with rapidly progressive pulmonary interstitial fibrosis

Our plain-English summary of A retired shipyard worker with rapidly progressive pulmonary interstitial fibrosis, by E.V. Moy, H. Hu, D.C. Christiani (Environmental Health Perspectives, 1999).

The study

• Authors: E.V. Moy, H. Hu, D.C. Christiani
• Journal: Environmental Health Perspectives
• Published: 1999;107(4):321-7
• Type of article: Case report
• Cited by: 1 article, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

We present a case of progressive interstitial fibrosis in a retired shipyard worker who was exposed to asbestos during the postwar era of the late 1940s and 1950s, when asbestos exposures in the workplace were not regulated. Forty years later, at 63 years of age, the patient presented with restrictive lung disease. The patient was diagnosed with asbestos-related pleural disease and parenchymal asbestosis. He remained stable for the next 7 years, but then he began to manifest rapid clinical progression, which raised the possibility of an unusual variant of asbestosis, a concomitant interstitial process, or an unrelated disease. Lung biopsy was not undertaken because of the patient's low pulmonary reserve and limited treatment options. An empiric trial of oral steroids was initiated, but his pulmonary status continued to deteriorate and he died of pulmonary failure at 72 years of age. Many diseases result in pulmonary interstitial fibrosis. Ideally, open lung biopsy should be performed, but this procedure inevitably causes complications in many patients with end-stage restrictive lung disease. Furthermore, while the presence of asbestos bodies in tissue sections is a sensitive and specific marker of asbestos exposure, neither this finding nor any other charge is a marker indicative of asbestosis or the severity of asbestosis. With the enactment of the Asbestos Standard in the United States, asbestos exposures have been decreasing in this country. However, industries that produce asbestos products and wastes continue to expand in developing countries. Prevention of asbestos-related lung disease should be a global endeavor, and asbestos exposures should be regulated in both developed and developing countries.

In plain English

This article is a case report of one retired shipyard worker, followed by a review-style discussion. The man was a former carpenter. He began shipyard work in 1948 on the construction, repair and demolition of vessels, often below deck, where he was exposed to visible clouds of asbestos dust. The asbestos fiber type involved in his exposure was not specified. He was referred in 1988 at age 63. His chest X-ray showed pleural plaques on both sides and mild interstitial fibrosis, and breathing tests showed a moderate restrictive defect. He was diagnosed with asbestos-related pleural plaques and asbestosis. His forced vital capacity fell from 2.34 liters (61% of predicted) in 1988 to 1.89 liters (52%) in 1992 and 1.25 liters (35%) in 1996. His diffusing capacity, at first 85% of predicted, later dropped to 59%. No lung biopsy was done because of his low lung reserve and limited treatment options. He was given prednisone, 60 mg per day, but continued to deteriorate and died of pulmonary failure. The authors judged the progression more rapid than usual for asbestosis. They suggested either a variant of asbestosis or a process unrelated to asbestos exposure.

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 report (single patient) with a review-style discussion of asbestosis and other interstitial lung diseases
• Who was studied: One man, a 63-year-old former carpenter and shipyard worker, referred in 1988 to the Center for Occupational and Environmental Medicine at the Massachusetts Respiratory Hospital, Braintree, Massachusetts, and followed until his death
• Exposure: Shipyard work beginning in 1948: construction, repair and demolition of vessels, often below deck in enclosed spaces, with visible clouds of asbestos dust. The fiber type involved in his exposure is not specified.
• Main results:
  • At referral, the patient's chest X-ray showed pleural plaques on both sides and mild diffuse interstitial fibrosis
  • Initial breathing tests showed a moderate restrictive defect with a normal diffusing capacity
  • He was diagnosed with asbestos-related pleural plaques and asbestosis, based on his occupational history, chest X-ray and breathing tests
  • His forced vital capacity fell from 2.34 liters (61% of predicted) in 1988 to 1.89 liters (52%) in 1992 and 1.25 liters (35%) in 1996
  • His total lung capacity fell from 3.61 liters (60% of predicted) in 1988 to 3.22 liters (55%) in 1992 and 2.33 liters (40%) in 1996. The 40% figure is confirmed by Table 1.
  • His diffusing capacity was normal at 85% of predicted from 1988 to 1992, then dropped sharply to 59% of predicted
  • During exercise oximetry, his oxygen saturation dropped to 88% after he walked 1,100 feet in 6 minutes
  • Despite an empiric trial of prednisone, 60 mg per day, his pulmonary status continued to deteriorate
  • He died of pulmonary failure
• The authors' conclusion: The authors judged that the progression after 1995 was more rapid than usual for asbestosis. In their view, this suggested either a variant of asbestosis or a process unrelated to asbestos exposure.
• Limitations the authors state:
  • No lung biopsy was performed, because of the patient's low pulmonary reserve and limited treatment options, so the diagnosis was not confirmed by tissue examination
  • No autopsy was performed

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis.

Medical terms in this study, explained in our Lexicon: Interstitial Fibrosis, Asbestos Exposure, Restrictive Lung Disease, Asbestos-Related Pleural Disease, Interstitial, Biopsy, Asbestos Bodies.

Related studies

• Asymmetric rapidly progressive lung fibrosis: a cause of pseudotumour in asbestosis — W.O. Cookson, J.J. Glancy, et al. (1985)
• Asbestosis: interstitial pulmonary fibrosis and pleural fibrosis in a cohort of asbestos insulation workers: influence of cigarette smoking — R. Lilis, I.J. Selikoff, et al. (1986)
• Interstitial pulmonary fibrosis in an automobile body shop worker — A. Fischbein, A.N. Rohl, et al. (1985)
• Pulmonary function, smoking habits, and high resolution computed tomography (HRCT) early abnormalities of lung and pleural fibrosis in shipyard workers exposed to asbestos — S. Neri, P. Boraschi, et al. (1996)
• Mica-associated pulmonary interstitial fibrosis — S.K. Landas, D.A. Schwartz (1991)
• Diffusing capacity and forced vital capacity in 5,003 asbestos-exposed workers: relationships to interstitial fibrosis (ILO profusion score) and pleural thickening — A. Miller, R. Warshaw, et al. (2013)

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