Lymphocyte-macrophage alveolitis in nonsmoking individuals occupationally exposed to asbestos

Our plain-English summary of Lymphocyte-macrophage alveolitis in nonsmoking individuals occupationally exposed to asbestos, by W.N. Rom, W.D. Travis (Chest, 1992).

The study

• Authors: W.N. Rom, W.D. Travis
• Journal: Chest
• Published: 1992;101(3):779-86
• Type of article: Case report
• Cited by: 26 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. 004142).

Abstract

A disordered immunologic activity has been observed in humans and animal models of asbestosis and silicosis. To characterize the lung immunologic response following long-term occupational exposure to asbestos, bronchoalveolar lavage (BAL) was performed on 28 nonsmoking individuals. Increased BAL lymphocytes were observed in one third. Lung lymphocytes were predominantly of the CD4+ helper-inducer subtype with increased CD4+/CD8+ ratio and increased surface expression of DR antigen consistent with the activation phenotype. Histologic evaluation of lung tissue from two individuals with lymphocytic-macrophage alveolitis and asbestos exposure revealed an infiltration of alveolar walls with chronic inflammatory mononuclear cells (lymphocytes). Interferon gamma was spontaneously released by BAL cells from 19 (76 percent) of 25 of the individuals with asbestos exposure and only one of ten normal controls. The release of interferon gamma by BAL cells could be further stimulated with concanavalin A and suppressed by cyclosporine. Although asbestosis is characterized by a predominant alveolar macrophage alveolitis, there is a subgroup with lymphocytic alveolitis and activated lymphocytes participating in the inflammatory response, especially in those without respiratory impairment early in the course of the disease process.

In plain English

This study examined lung cells from 28 men who had worked with asbestos for more than 20 years in the construction trades as insulators, boilermakers, plumbers or sheet metal workers. All were lifelong nonsmokers or had quit more than five years earlier. All had pleural plaques and/or thickening, and their chest X-rays showed irregular opacities. Cells were washed out of the lungs (bronchoalveolar lavage) and compared with cells from 16 controls with no occupational inorganic dust exposure. In 10 of 28 exposed men (36 percent), the share of lymphocytes was above the highest control value. Exposed men had more CD4 helper lymphocytes (20 versus 9 percent of recovered cells) and a higher CD4-to-CD8 ratio (2.9 versus 1.3). Lung cells released interferon gamma in 19 of 25 exposed men and 1 of 10 controls. Exposed men with normal lung function had almost twice the level of interferon gamma of those with restrictive impairment, which affected 13 of 28. Lung biopsies from two men showed lymphocyte-rich inflammation. The authors concluded that a subgroup has lymphocytic alveolitis with activated lymphocytes, especially early in the disease process.

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 laboratory comparison of lung lavage cells from asbestos-exposed workers and unexposed controls, with two case reports of open lung biopsy
• Who was studied: 28 men with more than 20 years of occupational asbestos exposure, all lifelong nonsmokers or ex-smokers for more than five years, all with bilateral pleural plaques and/or thickening. There were 16 controls with normal chest X-rays, normal lung function and no occupational inorganic dust exposure. The article does not state the study location or dates; the authors' affiliation is Bellevue Hospital and New York University Medical Center in New York.
• Exposure: Occupational asbestos exposure for more than 20 years (Table 1 mean 30 years) in the construction trades as insulators, boilermakers, plumbers or sheet metal workers. Fiber types for the workers are not stated. In a laboratory test, chrysotile asbestos was added to lung cells from normal individuals.
• Main results:
  • Among asbestos-exposed men, 36 percent (10/28) had a percentage of lung lymphocytes greater than the highest value among normal controls.
  • Restrictive lung function impairment was found in 13 of 28 (46 percent) asbestos-exposed men.
  • Lung lavage cells spontaneously released interferon gamma in 19/25 (76 percent) of asbestos-exposed men and 1/10 (10 percent) of normal controls. Mean levels were 70 plus or minus 27 units in exposed men and 1.0 plus or minus 1.0 units in controls (p less than 0.01).
  • Asbestos-exposed men had a higher proportion of CD4+ helper/inducer cells than normals (20 versus 9 percent of cells recovered, p less than 0.05). They also had a higher CD4+/CD8+ ratio (2.9 versus 1.3, p less than 0.05).
  • Asbestos-exposed men with normal lung function had almost twice the level of interferon gamma, and half as many negative samples, compared with those with restrictive impairment.
  • In the laboratory, concanavalin A significantly increased interferon gamma release in 11 of 12 asbestos-exposed men, and cyclosporine significantly reduced it (p less than 0.05).
  • Adding chrysotile asbestos in the laboratory to lung cells from normal individuals did not stimulate interferon gamma release at the concentrations tested.
  • Lung cells from 4 of 13 asbestos-exposed men spontaneously released interleukin 2, and 3 of these 4 also released interferon gamma.
  • Case reports: two 44-year-old male plumbers had open lung biopsies showing inflammation that was predominantly lymphocytic. Case 1 was a never smoker. Case 2 was an ex-smoker who quit at age 39 and also had rare non-caseating granulomas.
• The authors' conclusion: The authors concluded that, although asbestosis is characterized mainly by an alveolar macrophage alveolitis, there is a subgroup with lymphocytic alveolitis and activated lymphocytes taking part in the inflammation. They said this was especially so in those without respiratory impairment early in the disease process. They suggested that a longitudinal study of asbestos-exposed workers may help clarify the role of these immune signals.

Topics

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

Medical terms in this study, explained in our Lexicon: Macrophage, Silicosis, Occupational Exposure, Bronchoalveolar Lavage (BAL), Asbestos Exposure, Alveolar Macrophage.

Related studies

• Manifestations of cellular immunity in the rat after prolonged asbestos inhalation. II. Alveolar macrophage-induced splenic lymphocyte proliferation — K. Miller, E. Kagan (1981)
• Neutrophil chemotactic factor release and neutrophil alveolitis in asbestos-exposed individuals — A.A. Hayes, A.H. Rose, et al. (1988)
• Alveolitis of pulmonary asbestosis. Bronchoalveolar lavage studies in crocidolite- and chrysotile-exposed individuals — B.W. Robinson, A.H. Rose, et al. (1986)
• Characterization of the lower respiratory tract inflammation of nonsmoking individuals with interstitial lung disease associated with chronic inhalation of inorganic dusts — W.N. Rom, P.B. Bitterman, et al. (1987)
• Lymphocyte subpopulations in bronchoalveolar lavage fluid in asbestos workers — A.R. Gellert, M.G. Macey, et al. (1985)
• Contrasting effects of alveolar macrophages and neutrophils on asbestos-induced pulmonary epithelial cell injury — D.W. Kamp, M.M. Dunn, et al. (1994)

Browse more research in Chest, or return to medical research.