Neutrophil chemotactic factor release and neutrophil alveolitis in asbestos-exposed individuals

Our plain-English summary of Neutrophil chemotactic factor release and neutrophil alveolitis in asbestos-exposed individuals, by A.A. Hayes, A.H. Rose, A.W. Musk, et al (Chest, 1988).

The study

• Authors: A.A. Hayes, A.H. Rose, A.W. Musk, B.W. Robinson
• Journal: Chest
• Published: 1988;94(3):521-5
• Cited by: 25 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Alveolar neutrophil accumulation occurs in asbestosis. To evaluate a possible role for release of neutrophil chemotactic factor (NCF) in the pathogenesis of asbestosis, spontaneous NCF release from alveolar macrophages obtained by bronchoalveolar lavage (BAL) in eight individuals with asbestosis, 13 asbestos-exposed individuals without asbestosis, and five control subjects has been studied. Alveolar macrophages were incubated in medium (four hours; 37 degrees C), and neutrophil responses to the supernatants were assayed in a microchemotaxis chamber. Alveolar macrophages from subjects with asbestosis released more NCF (97 +/- 19 neutrophils per high-power field [N/HPF]) than controls (3 +/- 1 N/HPF; p less than 0.01). Alveolar macrophages from individuals with asbestos exposure and increased BAL neutrophil proportions (n = 7) released more NCF (93 +/- 24 N/HPF) than individuals with asbestos exposure and normal BAL neutrophil proportions (n = 6; 11 +/- 6 N/HPF; p less than 0.02). The results show that spontaneous NCF release occurs in asbestosis and that NCF release is associated with neutrophil alveolitis in asbestos-exposed individuals without asbestosis, suggesting a pathogenic role for NCF in mediating this neutrophil alveolitis. The results of the study also suggest that the presence of crackles is a better predictor of the presence of neutrophil alveolitis than is an abnormal chest x-ray film.

In plain English

This Western Australian study examined lung cells collected by bronchoalveolar lavage (washing out part of the lung through a bronchoscope) from 21 asbestos-exposed men and five controls with no asbestos exposure. Twenty men had been exposed to crocidolite while mining at Wittenoom and one to chrysotile in manufacturing. Eight had asbestosis on chest X-ray. Of the 13 without it, seven had raised proportions of neutrophils (a white blood cell) in the lavage fluid and six had normal proportions. The authors measured how much neutrophil chemotactic factor (NCF), a signal that attracts neutrophils, the lung's macrophage cells released on their own. Average release, counted as neutrophils per high-power microscope field, was 97 ± 19 in the asbestosis group, 93 ± 24 in exposed men with raised neutrophils, 11 ± 7 in exposed men with normal neutrophils, and 3 ± 1 in controls. Six of the seven men with raised neutrophils had lung crackles, and none of the six with normal neutrophils did. The authors concluded that locally released NCF may drive neutrophil buildup in asbestos-exposed people, and that crackles may identify this inflammation more reliably than X-ray changes.

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 study comparing lung lavage cells from asbestos-exposed men and unexposed controls
• Who was studied: 21 asbestos-exposed men in Western Australia: 8 with radiographic asbestosis, and 13 with normal chest X-rays (7 with raised and 6 with normal lavage neutrophil proportions). Also 5 control subjects with no asbestos exposure: 4 being investigated for localized lung lesions and 1 normal volunteer.
• Exposure: Crocidolite in 20 men, from asbestos mining at Wittenoom, Western Australia. Chrysotile in 1 man, from manufacture of asbestos-containing products. Mean exposure duration in years was 9 ± 4 in the asbestosis group, 3 ± 1 in the raised-neutrophil group and 2 ± 1 in the normal-neutrophil group.
• Main results:
  • Control subjects' alveolar macrophages released negligible NCF on their own (3 ± 1 neutrophils per high-power field, mean ± SEM). When stimulated with opsonized zymosan, a known trigger, they released 113 ± 25.
  • Alveolar macrophages from the 8 subjects with asbestosis released 97 ± 19 neutrophils per high-power field spontaneously, rising to 125 ± 20 with opsonized zymosan. The comparison with controls was reported as p less than 0.01.
  • Alveolar macrophages from the 7 asbestos-exposed subjects with normal X-rays but raised lavage neutrophil proportions released 93 ± 24 neutrophils per high-power field spontaneously, and 148 ± 15 with opsonized zymosan.
  • Alveolar macrophages from the 6 asbestos-exposed subjects with normal lavage neutrophil proportions did not spontaneously release significant NCF (11 ± 7 neutrophils per high-power field, similar to controls), and 101 ± 17 with opsonized zymosan. The comparison with the raised-neutrophil group was reported as p less than 0.02.
  • Among asbestos-exposed subjects with normal chest X-rays, 6 of the 7 with raised lavage neutrophil proportions had crackles on listening to the chest. None of the 6 with normal neutrophil proportions had crackles.
  • Subjects with asbestosis had been exposed longer and had more impaired lung function. Lung function in the raised-neutrophil group without X-ray abnormality fell between the asbestosis group and the normal-neutrophil group.
• The authors' conclusion: The authors concluded that the findings suggest locally released NCF mediates the neutrophil accumulation seen in asbestos-exposed individuals. They also concluded that crackles may be a more reliable way of identifying alveolitis than chest X-ray changes.

Mines named here

Asbestos mines this study is about. Each mine's page says who ran it, when it worked, and what it produced.

• Wittenoom, Western Australia

All asbestos mines

Topics

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

Medical terms in this study, explained in our Lexicon: Alveolar Macrophage, Bronchoalveolar Lavage (BAL), High-Power Field, Asbestos Exposure, Chest X-Ray.

Related studies

• Asbestos-induced release of a human alveolar macrophage-derived neutrophil chemotactic factor — A.A. Hayes, T.J. Venaille, et al. (1990)
• Pleural mesothelial cells stimulated by asbestos release chemotactic activity for neutrophils in vitro — V.B. Antony, C.L. Owen, et al. (1989)
• Alveolitis of pulmonary asbestosis. Bronchoalveolar lavage studies in crocidolite- and chrysotile-exposed individuals — B.W. Robinson, A.H. Rose, et al. (1986)
• Time course of chemotactic factor generation and the corresponding macrophage response to asbestos inhalation — D.B. Warheit, L.H. Hill, et al. (1986)
• Lymphocyte-macrophage alveolitis in nonsmoking individuals occupationally exposed to asbestos — W.N. Rom, W.D. Travis (1992)
• Role of alveolar macrophages in asbestosis: modulation of neutrophil migration to the lung after acute asbestos exposure — C.I. Schoenberger, G.W. Hunninghake, et al. (1982)

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