Synergistic effects of mineral fibres and cigarette smoke on the production of tumour necrosis factor by alveolar macrophages of rats

Our plain-English summary of Synergistic effects of mineral fibres and cigarette smoke on the production of tumour necrosis factor by alveolar macrophages of rats, by Y. Morimoto, M. Kido, I. Tanaka, et al (British Journal of Industrial Medicine, 1993).

The study

• Authors: Y. Morimoto, M. Kido, I. Tanaka, A. Fujino, T. Higashi, Y. Yokosaki
• Journal: British Journal of Industrial Medicine
• Published: 1993;50(10):955-60
• Cited by: 12 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

The objective of this study was to evaluate the combined effects of mineral fibres and cigarette smoke on the production of tumour necrosis factor (TNF) by alveolar macrophages. Rats were exposed to cigarette smoke in vivo, and production of TNF by alveolar macrophages was measured in the presence of mineral fibres in vitro. For smoke exposure, rats were divided into two groups. Five were exposed to a daily concentration of 10 mg/m3 of cigarette smoke for an eight hour period, and five rats (controls) were not exposed to smoke. Bronchoalveolar lavage was performed after exposure to smoke and the recovered alveolar macrophages were incubated with either chrysotile or ceramic fibres on a microplate for 24 hours. Activity of TNF in the supernatant was determined by the L-929 fibroblast cell bioassay. When alveolar macrophages were not stimulated by mineral fibres, production of TNF by rats exposed to smoke and unexposed rats was essentially the same. When alveolar macrophages were stimulated in vitro by chrysotile or ceramic fibres, production of TNF by alveolar macrophages from rats exposed to smoke was higher than that by alveolar macrophages from unexposed rats. The findings suggest that cigarette smoke and mineral fibres have a synergistic effect on TNF production by alveolar macrophages.

In plain English

This was a laboratory experiment in rats from Japan. Five male Wistar rats were exposed in a chamber to aged sidestream cigarette smoke (40 cigarettes over eight hours, at 10 mg/m3), and five rats were not exposed. The authors then washed cells out of the rats' lungs and cultured the alveolar macrophages (immune cells of the lung) for 24 hours with Canadian chrysotile asbestos or alumina silicate ceramic fibres. They measured tumour necrosis factor (TNF), a signalling protein involved in lung injury and fibrosis. Without fibres, TNF production was essentially the same in both groups. Chrysotile significantly increased TNF production, and the increase was greater in cells from smoke-exposed rats, significantly so at 50 and 100 micrograms per millilitre. With ceramic fibres, cells from smoke-exposed rats produced more TNF at every concentration, but the differences were not statistically significant. Chrysotile stimulated more TNF than ceramic fibres. Smoke-exposed rats had significantly more lung cells recovered. The authors concluded that cigarette smoke and mineral fibres had a synergistic effect on TNF production. In their view, this supports epidemiological evidence that smoking and asbestos exposure interact in lung fibrosis.

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: Animal experiment: rats exposed to cigarette smoke in vivo, then their lung macrophages exposed to mineral fibres in vitro (in the laboratory)
• Who was studied: Ten male Wistar rats, nine weeks old, from Japan: 5 exposed to smoke and 5 unexposed. Their alveolar macrophages were recovered by bronchoalveolar lavage (lung washing).
• Exposure: Aged sidestream cigarette smoke at 10 mg/m3 (40 cigarettes smoked over eight hours; carbon monoxide 79 ppm), followed by 24-hour laboratory exposure of macrophages to Canadian chrysotile (Quebec) or alumina silicate ceramic fibres, at concentrations including 25, 50 and 100 micrograms per millilitre
• Main results:
  • Without fibre stimulation, TNF production by macrophages from smoke-exposed and unexposed rats was essentially the same
  • Chrysotile significantly increased TNF production, and the increase was greater in macrophages from smoke-exposed rats than from unexposed rats
  • Chrysotile increased TNF in a concentration-dependent way. At 50 or 100 micrograms per millilitre, TNF production was significantly greater in smoke-exposed rats than in unexposed rats.
  • With ceramic fibres, TNF production was higher in smoke-exposed rats at all concentrations, but the differences between groups were not statistically significant
  • Chrysotile stimulated greater TNF production than ceramic fibres in both the smoke-exposed and unexposed groups
  • Significantly more total cells were recovered from the lungs of smoke-exposed rats (p less than 0.01). Differential cell counts did not differ significantly, and macrophages made up more than 97% of cells in both groups.
• The authors' conclusion: The authors concluded that cigarette smoke and mineral fibres had a synergistic effect on TNF production by alveolar macrophages. In their view, this supports epidemiological evidence that an interaction between smoking and asbestos exposure affects the incidence of lung fibrosis.

Mines named here

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

• Lake Asbestos of Quebec, Black Lake, Quebec

All asbestos mines

Topics

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

Medical terms in this study, explained in our Lexicon: Synergistic Effect, Necrosis, Alveolar Macrophage, Bronchoalveolar Lavage (BAL), Chrysotile, Fibroblast.

Related studies

• Asbestos fibres and man made mineral fibres: induction and release of tumour necrosis factor-alpha from rat alveolar macrophages — A.G. Ljungman, M. Lindahl, et al. (1994)
• Effects of cigarette smoke and asbestos on airway, vascular and mesothelial cell proliferation — H. Sekhon, J. Wright, et al. (1995)
• Cigarette smoke, asbestos, and small irregular opacities — W. Weiss (1984)
• Cigarette smoke increases the penetration of asbestos fibers into airway walls — D. McFadden, J. Wright, et al. (1986)
• Cigarette smoke makes airway and early parenchymal asbestos-induced lung disease worse in the guinea pig — V. Tron, J.L. Wright, et al. (1987)
• Asbestos-stimulated tumour necrosis factor release from alveolar macrophages depends on fibre length and opsonization — K. Donaldson, X.Y. Li, et al. (1992)

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