Alveolitis of pulmonary asbestosis. Bronchoalveolar lavage studies in crocidolite- and chrysotile-exposed individuals

Our plain-English summary of Alveolitis of pulmonary asbestosis. Bronchoalveolar lavage studies in crocidolite- and chrysotile-exposed individuals, by B.W. Robinson, A.H. Rose, A. James, et al (Chest, 1986).

The study

• Authors: B.W. Robinson, A.H. Rose, A. James, D. Whitaker, A.W. Musk
• Journal: Chest
• Published: 1986;90(3):396-402
• Cited by: 48 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. 000429).

Abstract

Bronchoalveolar lavage (BAL) findings in 27 individuals with crocidolite- or chrysotile-induced asbestosis were compared to BAL findings in 29 unexposed control subjects. Alveolitis, defined as an increase in the proportions and/or absolute numbers of inflammatory cells present in BAL fluid compared to values in control subjects, was present in 26 (96 percent) subjects with asbestosis. Most exhibited a neutrophil-eosinophil alveolitis, with neutrophil proportions increased to 7.4 +/- 0.7 percent and eosinophil proportions increased to 2.2 +/- 0.4 percent, compared to 2 +/- 0.5 percent and 0.4 +/- 0.01 percent, respectively, in control subjects (p less than 0.01 for both neutrophils and eosinophils). An increase in the total number of neutrophils and eosinophils per ml of lavage fluid was also seen (neutrophils 23 +/- 5 and eosinophils 13 +/- 4 per ml; p less than 0.05 compared to control subjects). Severity of the alveolitis, defined by the neutrophil or eosinophil proportions, was independent of a history of exposure to cigarette smoke. The pattern and severity of alveolitis in crocidolite- and chrysotile-induced asbestosis were similar. There was a significant correlation between duration of exposure to asbestos and neutrophil proportions (p less than 0.01). No significant difference in the severity of the alveolitis was observed between individuals with radiologic and physiologic evidence of asbestosis compared to those with asbestos exposure and crackles alone, suggesting that, in asbestosis as in other chronic interstitial lung diseases, radiologic and physiologic parameters do not reflect the severity of the alveolitis. This study demonstrates that a neutrophil-eosinophil alveolitis is present in individuals with crocidolite- and chrysotile-induced asbestosis, that this alveolitis is independent of cigarette smoking, and that the severity of the BAL changes is not reflected in radiologic and physiologic changes.

In plain English

This Western Australian study used bronchoalveolar lavage, rinsing part of the lung with saline through a bronchoscope and counting the recovered cells. It compared 27 patients with asbestosis with 29 unexposed control subjects having bronchoscopy for localized lung lesions. Twenty patients had been exposed to crocidolite, five to chrysotile, and two to an uncertain fiber type. Alveolitis, defined as increased proportions and/or absolute numbers of inflammatory cells compared with controls, was found in 26 of the 27 patients (96 percent). Mean neutrophil proportions were 7.4 percent in patients and 2 percent in controls. Mean eosinophil proportions were 2.2 and 0.4 percent. Neutrophil and eosinophil proportions did not differ significantly between crocidolite- and chrysotile-exposed patients. They also did not differ significantly between patients with crackles alone and those with X-ray or lung-function changes. Mean neutrophil proportions did not differ significantly by smoking history, but eosinophil proportions were higher in smokers with asbestosis. Among nine crocidolite-exposed patients with crackles, radiologic asbestosis and restrictive lung-function results, neutrophil proportions correlated with exposure duration. The authors concluded that most patients had a neutrophil-eosinophil alveolitis whose severity did not correlate with X-ray or lung-function 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: Clinical comparison study: bronchoalveolar lavage (BAL) cell counts in patients with asbestosis compared with control subjects, with subgroup comparisons by fiber type, smoking history, and radiologic and physiologic findings
• Who was studied: 27 patients with asbestosis (26 male, 1 female; 14 current smokers, 9 ex-smokers, 4 nonsmokers) referred to an Occupational Lung Diseases clinic in Nedlands, Western Australia. The comparison group was 29 control subjects (16 smokers, 7 ex-smokers, 6 nonsmokers; 24 males, 5 females; aged 52 ± 4 years) undergoing bronchoscopy for localized pulmonary lesions, with no evidence of diffuse airway or parenchymal disease. Study dates are not given.
• Exposure: Exposure by fiber type:
• Crocidolite: 20 patients. All had been employed in the Wittenoom asbestos industry, except the one woman, who was exposed while laundering asbestos workers' clothes.
• Chrysotile: 5 patients, from manufacture of asbestos-containing products or insulation.
• Uncertain fiber type: 2 patients.

Mean duration of exposure was 7 ± 3 years. Mean time since first exposure was 28 ± 2 years. Exposure histories were obtained retrospectively from occupational records.

• Main results:
  • Alveolitis, defined as increased proportions and/or absolute numbers of inflammatory cells compared with control subjects, was present in 26 of 27 patients with asbestosis (96 percent).
  • Mean neutrophil proportion in BAL fluid was 7.4 ± 0.7 percent in patients with asbestosis versus 2 ± 0.5 percent in control subjects (p less than 0.01).
  • Mean number of neutrophils per ml of lavage fluid was 26.4 ± 5.8 in patients with asbestosis versus 5.2 ± 1.5 in control subjects (p less than 0.05).
  • Mean eosinophil proportion was 2.2 ± 0.4 percent in patients with asbestosis versus 0.4 ± 0.01 percent in control subjects (p less than 0.01).
  • Mean number of eosinophils per ml of lavage fluid was 14.1 ± 4.2 in patients with asbestosis versus 0.3 ± 0.1 in control subjects (p less than 0.01).
  • Among patients with asbestosis, 70 percent had raised neutrophil proportions and 56 percent had raised neutrophil numbers. For eosinophils, 52 percent had raised proportions and 72 percent had raised numbers.
  • When matched for smoking history, total BAL cell numbers were not significantly higher in patients with asbestosis than in control subjects.
  • Asbestos bodies were seen in BAL samples from 66 percent of the individuals studied.
  • Neutrophil and eosinophil proportions were not significantly different between patients with crocidolite-induced asbestosis (n = 20) and chrysotile-induced asbestosis (n = 5).
  • Among patients with asbestosis, mean neutrophil proportions did not differ significantly between current smokers, ex-smokers and nonsmokers.
  • All nonsmokers with asbestosis had raised neutrophil proportions.
  • Eosinophil proportions were higher in smokers with asbestosis than in ex-smokers and nonsmokers with asbestosis (p less than 0.05).
  • All seven patients with neutrophil proportions above 8 percent, and all eight with eosinophil proportions above 2 percent, had been exposed to cigarette smoke.
  • In crocidolite-exposed patients with crackles plus radiologic asbestosis and restrictive lung function, neutrophil proportion correlated with duration of exposure (correlation coefficient 0.61, p less than 0.01). Those with 7 percent or fewer neutrophils (n = 4) had a mean exposure of 1.2 ± 0.2 years. Those with more than 7 percent (n = 5) had a mean exposure of 3.8 ± 1.1 years.
  • Neutrophil and eosinophil proportions did not differ significantly between patients with crackles alone and those with radiologic and/or physiologic changes. There was a trend toward slightly higher proportions in those with such changes.
• The authors' conclusion: The authors concluded that a neutrophil-eosinophil alveolitis is present in most individuals with crocidolite- or chrysotile-induced asbestosis. They stated that these changes were independent of degree of and time since exposure, fiber type and cigarette exposure, and that the pattern and severity of the alveolitis did not correlate with the presence or absence of radiologic or physiologic changes of asbestosis.
• Limitations the authors state:
  • The authors stated that the significance of finding a similar alveolitis in patients with crackles alone, with regard to the risk of disease progression, requires further study.
  • The authors noted that the role of BAL in diagnosing asbestosis among patients with diffuse interstitial lung disease has not been evaluated.
  • Cell numbers per ml were available for fewer subjects than cell proportions, because total cell numbers were not routinely recorded early in the study.

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, Chrysotile, Crocidolite.

Medical terms in this study, explained in our Lexicon: Asbestosis, Bronchoalveolar Lavage (BAL), Crocidolite, Chrysotile, Asbestos Exposure, Interstitial Lung Disease.

Related studies

• The effects of chrysotile and crocidolite asbestos on the lower respiratory tract: analysis of bronchoalveolar lavage constituents — E. Kagan, Y. Oghiso, et al. (1983)
• Neutrophil chemotactic factor release and neutrophil alveolitis in asbestos-exposed individuals — A.A. Hayes, A.H. Rose, et al. (1988)
• Asbestosis: assessment by bronchoalveolar lavage and measurement of pulmonary epithelial permeability — A.R. Gellert, J.A. Langford, et al. (1985)
• Biochemical components of bronchoalveolar lavage in early experimental asbestosis of the sheep: phospholipase A2 activity, prostaglandin E2 and proteins — P. Sirois, G. Drapeau, et al. (1983)
• Assessment of progression of asbestosis in the sheep model by bronchoalveolar lavage and pulmonary function tests — R. Bégin, M. Rola-Pleszczynski, et al. (1983)
• Brief inhalation of asbestos compromises superoxide production in cells from bronchoalveolar lavage — J.M. Petruska, J. Marsh, et al. (1990)

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