Effects of cigarette smoke on the clearance of short asbestos fibres from the lung and a comparison with the clearance of long asbestos fibres

Our plain-English summary of Effects of cigarette smoke on the clearance of short asbestos fibres from the lung and a comparison with the clearance of long asbestos fibres, by A. Churg, J.L. Wright, J. Hobson, et al (International Journal of Experimental Pathology, 1992).

The study

• Authors: A. Churg, J.L. Wright, J. Hobson, B. Stevens
• Journal: International Journal of Experimental Pathology
• Published: 1992;73(3):287-97
• Cited by: 9 articles, as counted by NIH iCite
• Read it: PubMed · Free full text

Abstract

Long asbestos fibres are generally considered to have greater disease-producing potential than short asbestos fibres. However, recent reports have suggested that short fibre asbestos appears to be as effective an inducer of macrophage growth factors and toxic oxygen species as long fibre asbestos, but that short fibres are readily removed from lung and do not gain access to tissues. Because smoke is believed to impair the clearance of asbestos fibres from lung, we examined the clearance of a short (geometric mean length 1.3 microns) amosite preparation administered by intratracheal instillation to guinea-pigs. Half the animals in each group were exposed to the smoke of 10 cigarettes daily. Animals were sacrificed 1 day, 1 week, or 1 month later, the macrophages recovered by lavage, and fibre concentrations and sizes determined by analytical electron microscopy in macrophages and lung tissue. A 30-fold increase was seen in total numbers of fibres retained in macrophages in smokers compared to non-smokers by 1 month, and there was an eightfold increase in retention of short fibres in the lung tissue by 1 month. By contrast, a long fibre amosite preparation (geometric mean length 8.9 microns) showed approximately the same increase in fibre retention in macrophages, but only a twofold increase in tissue retention. We conclude that (1) cigarette smoke markedly impairs the clearance of short amosite fibres from the lung with enhanced retention of fibres in both macrophages and tissue; (2) the effects of smoke on short fibre tissue retention appear to be greater than those on long fibre retention; (3) with the long fibre preparation, smoke causes increased tissue retention of relatively shorter fibres; (4) for both fibre size experiments, the increase in total fibres in macrophages in smoke-exposed animals reflects an increase in the total number of fibre-containing macrophages, rather than an increase in the number of fibres phagocytized per macrophage; (5) enhanced short fibre retention markedly increases total fibre surface area, a parameter which has been suggested as a measure of fibre toxicity, to the point where short fibres might under some circumstances have roughly the same potential toxicity as long fibres. These observations suggest that short asbestos fibres could play an important role in the pathogenesis of some types of asbestos-related disease in cigarette smokers.

In plain English

This was an animal experiment. Female guinea-pigs had amosite asbestos placed directly into the windpipe (intratracheal instillation). Some received a short-fibre preparation (geometric mean length 1.3 micrometres, 15 mg dose) and others a long-fibre preparation (geometric mean length 8.9 micrometres, 1.5 mg dose). Half the animals were then exposed daily to the smoke of 10 non-filter cigarettes; the rest were sham-smoked with air. Lungs were examined 1 day, 1 week or 1 month later. By 1 month, for both preparations, smoke-exposed animals had 20 to 30 times more fibres in the scavenger cells (macrophages) washed out of their lungs than non-smoke-exposed animals. In lung tissue, smoke-exposed animals had five to eight times the short-fibre concentration at 1 week and 1 month, but only about twice the long-fibre concentration, and only at 1 month. The authors cautioned that the tenfold higher short-fibre dose and the instillation method mean that comparisons between long and short fibres must be treated with considerable caution. They concluded that in cigarette smokers short fibres might have considerable disease-causing potential.

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. Guinea-pigs were given amosite by intratracheal instillation and split into smoke-exposed and sham-smoked (air) groups. Lungs were washed out (lavage) and fibres in macrophages and lung tissue were counted and sized by analytical electron microscopy at 1 day, 1 week and 1 month.
• Who was studied: Female Hartley strain guinea-pigs weighing 400 g, studied in groups of five to seven smoke-exposed or non-exposed animals per time point; Department of Pathology, University of British Columbia, Vancouver.
• Exposure: Amosite asbestos in two preparations: short fibre (geometric mean length 1.3 micrometres, width 0.20 micrometres), 15 mg in 0.5 ml saline; long fibre (geometric mean length 8.9 micrometres, width 0.33 micrometres), 1.5 mg in 0.5 ml saline. Half the animals were also exposed daily, head-only, to the whole smoke of 10 non-filter commercial cigarettes for about 2 hours.
• Main results:
  • At 1 month, significantly more macrophages were recovered from smoke-exposed animals than from non-exposed animals, for both short and long fibres.
  • The total number of fibres in all recovered macrophages was increased in smoke-exposed animals at 1 week and 1 month for both preparations. By 1 month the difference between smokers and non-smokers was 20 to 30-fold.
  • The number of fibres per macrophage was increased only modestly (two to three-fold) and inconsistently in smoke-exposed animals.
  • In lung tissue, smoke-exposed animals given short fibres had a five to eight-fold increase in fibre concentration at 1 week and 1 month. Smoke-exposed animals given long fibres had about a twofold increase, at 1 month.
  • In animals given long fibres, the mean length of fibres in lung tissue at 1 month was significantly shorter in smoke-exposed than in non-exposed animals (P less than 0.01).
  • Smoke exposure increased the total surface area of retained short fibres, in both tissue and macrophages, to about the values found for long fibres.
• The authors' conclusion: The authors concluded that short fibres may be relatively harmless in non-smokers, but in cigarette smokers short fibres might have considerable disease-causing potential.
• Limitations the authors state:
  • The authors deliberately gave ten times the mass dose of short fibres compared with long fibres.
  • Because of differences in dose and in how fibres spread after intratracheal instillation, the authors said comparisons of long versus short fibre retention must be treated with considerable caution.
  • Only fibres inside lavaged macrophages were counted, so the total fibre burden in the air spaces of the lung was underestimated.
  • The dosing method was non-physiologic, and the authors said the experimental system is difficult to compare to any real exposure; the surface-area calculations are only a model of potential effects.
  • The data could not rule out that the higher macrophage fibre totals in smoke-exposed animals reflected recruitment of more macrophages rather than slower clearance.

Topics

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

Medical terms in this study, explained in our Lexicon: Macrophage, Amosite.

Related studies

• Effects of cigarette smoke exposure on retention of asbestos fibers in various morphologic compartments of the guinea pig lung — A. Churg, V. Tron, et al. (1987)
• Rapid short-term clearance of chrysotile compared with amosite asbestos in the guinea pig — A. Churg, J.L. Wright, et al. (1989)
• Effects of cigarette smoke on tissue uptake and retention of iron oxide in the guinea pig — B. Gilks, J. Wright, et al. (1988)
• Cigarette smoke makes airway and early parenchymal asbestos-induced lung disease worse in the guinea pig — V. Tron, J.L. Wright, et al. (1987)
• Inflammation generating potential of long and short fibre amosite asbestos samples — K. Donaldson, G.M. Brown, et al. (1989)
• Smoking inhibits asbestos clearance — D. McFadden, J.L. Wright, et al. (1986)

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