Immunology and asbestos

Our plain-English summary of Immunology and asbestos, by M.M.F. Wagner (1980).

The study

• Author: M.M.F. Wagner
• Published: Pages 247-249 of a proceedings volume on asbestos (the volume title is not shown on these pages); the preceding reference list is from a Sébastien et al. paper. (1980)
• Type of article: Conference paper
• Our copy: from Johns-Manville's own medical library. The article is still under copyright, so we describe it here rather than post it.

In plain English

This short article by M.M.F. Wagner mostly summarized findings the author's group published elsewhere, plus animal experiments. About 140 Devonport dockyard workers (Plymouth, UK), chosen from jobs likely to involve very heavy asbestos exposure, were examined twice yearly for four years, mainly by blood immune-cell tests. The aim was to spot men who might develop tumours or fibrosis, or whose fibrosis was progressing. With no unexposed men nearby, men with normal X-rays served as comparison. Smokers with fibrosis on X-ray had a slightly higher percentage of E rosettes, a T lymphocyte test, though overall significance was not great. The author attributed this to fewer late-rosetting cells rather than more early-rosetting ones. Lymphocytes from men with fibrosis or pleural changes responded less to phytohaemagglutinin, especially in nonsmokers. Tissue typing (HLA) showed no consistent associations. In rats given asbestos into the chest cavity, thymus removal did not change the tumour rate, but a sham operation at four days of age reduced it to 7%. The author suggested that a smoking- and asbestos-linked autoimmune process might help flag people likely to develop fibrosis, and that macrophages may help control mesothelioma.

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: Brief overview of a longitudinal immunological study of dockyard workers, with animal (rat) experiments. Most results are summarized from other publications or from unpublished data of the author's group.
• Who was studied: Approximately 140 asbestos-exposed men working at the Devonport dockyard, Plymouth, UK, examined twice yearly for four years. They were grouped by X-ray category: no exposure or normal X-ray, pulmonary fibrosis (small opacities), and pleural changes. Rats were used in the experimental work.
• Exposure: Occupational asbestos exposure in the dockyard. Men were chosen from occupations where they were most likely to have been very heavily exposed. The fiber type was not stated for the men. In the rat experiments, chrysotile or crocidolite was injected into the pleural cavity.
• Main results:
  • In a tissue-typing study cited as Darke et al. (1979), one HLA antigen (its name is unreadable in the scan) was twice as frequent in men with pulmonary fibrosis and diffuse pleural thickening as in 64 asbestos workers with no chest abnormality. This difference was not statistically significant.
  • When these HLA data were analysed together with four other studies, no consistent associations were found.
  • Peripheral blood leucocyte counts and E binding rosettes were measured on five separate occasions.
  • As reported by Wagner et al. (1979), smokers with radiological evidence of fibrosis had a small increase in the percentage of E rosettes. Overall significance was not great, but the increase was found on each occasion it was measured. Three smokers who had recently developed pulmonary fibrosis showed the increase even while their X-ray was still normal.
  • The author stated that the percentage difference appeared to be due to a smaller number of late-rosetting T lymphocytes. There was no real increase in early-rosetting cells.
  • Smoking had the greatest effect, particularly on total leucocyte count, which was higher in smokers. Absolute T lymphocyte numbers did not differ between smokers with normal X-rays and smokers with pulmonary fibrosis.
  • As reported by Campbell et al. (1980), men with X-ray evidence of either pulmonary fibrosis or pleural change showed a significantly depressed lymphocyte response to phytohaemagglutinin. This was much more marked in nonsmokers.
  • In unpublished rat experiments, injecting chrysotile or crocidolite into the pleural cavity led to the production of lysosomal enzymes, particularly by giant cells in asbestos-induced granulomas.
  • In rats with mesotheliomas, there was very little evidence of any collection of lymphocytes.
  • In unpublished experimental work, giving carrageenan after asbestos was injected into the pleural cavity increased the tumour rate in rats to over 70%.
  • In rats injected intrapleurally with asbestos, thymectomy did not alter the tumour rate (Wagner, 1979). Sham thymectomy, carried out at the age of four days, reduced the rate to 7%. The starting rate is garbled in the scan, which prints it as 'over 501'.
• The authors' conclusion: The author suggested that there is probably an autoimmune situation associated with smoking and asbestos. In the author's view it is weakly reflected in the peripheral blood and may help recognize people who will later develop progressing pulmonary fibrosis. From the animal work, the author suggested that macrophages may play a role in controlling mesothelioma.
• Limitations the authors state:
  • No men who had not been exposed to asbestos could be found nearby, so the comparison group included men with normal X-rays.
  • When all results were considered together, the significance of the E rosette increase was not great.
  • There was not yet any evidence linking the immunological findings in the asbestos-exposed population to the development of mesotheliomas.

Topics

Medical terms in this study, explained in our Lexicon: Asbestos Exposure, Fibrosis, Macrophage, Mesothelioma.

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