Inflammation generating potential of long and short fibre amosite asbestos samples

Our plain-English summary of Inflammation generating potential of long and short fibre amosite asbestos samples, by K. Donaldson, G.M. Brown, D.M. Brown, et al (British Journal of Industrial Medicine, 1989).

The study

• Authors: K. Donaldson, G.M. Brown, D.M. Brown, R.E. Bolton, J.M. Davis
• Journal: British Journal of Industrial Medicine
• Published: 1989;46(4):271-6
• Cited by: 85 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Previous studies have shown that long thin asbestos fibres are more pathogenic in in vivo and more active in in vitro assays than short fibre samples. In the present study a long fibre amosite asbestos sample and a short fibre sample prepared from it were tested for ability to cause inflammation in the peritoneal cavity of the mouse; a UICC sample intermediate in fibre size and an inert compact dust, TiO2, were also tested. The ability of the dust samples to cause inflammation, as judged by macrophage and neutrophil recruitment, was ranked in the order long fibre greater than UICC greater than short fibre greater than TiO2. Ability of amosite samples to cause inflammation was therefore related to the proportion of long fibres. The enhanced ability of long fibres to cause inflammation and cause macrophage activation is probably a key factor in the ability of long fibres to cause pulmonary fibrosis and may also be important in fibre carcinogenesis.

In plain English

This was an animal experiment in mice. The authors injected dust into the abdominal (peritoneal) cavity of male C57B16 mice, in groups of three, at 50, 500 or 2500 micrograms, plus 5 micrograms for two samples. They compared long fibre amosite (commercial milled South African amosite), a short fibre sample made by grinding it, the standard UICC amosite sample, and titanium dioxide, used as a low-activity comparison dust. Fibres longer than 10 micrometres made up 10-12% of the long sample, 2-3% of UICC amosite and 0.1-0.2% of the short sample. Inflammation was measured by counting two kinds of white blood cells, macrophages and neutrophils, washed out two or four days later. At virtually all doses and times, long amosite caused the most inflammation, then UICC, then short amosite, then titanium dioxide. At 5 micrograms, long amosite still caused marked inflammation while short amosite was virtually inactive. The authors concluded that inflammation correlated with the proportion of long fibres. They said this probably helps explain lung fibrosis from long fibres and may matter for fibre-related cancer.

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: dusts injected into the peritoneal (abdominal) cavity of mice, followed by washing out the cavity (lavage) and counting inflammatory cells
• Who was studied: Syngenic male C57B16 mice aged 10-12 weeks at injection, in groups of three mice per dust and dose
• Exposure: Long fibre amosite (commercially available, milled South African amosite), a short fibre amosite sample prepared from it by ball-milling, UICC amosite of intermediate fibre length, and rutile titanium dioxide as a negative control. Doses were 50, 500 or 2500 micrograms, and also 5 micrograms for long and short amosite. Fibres longer than 10 micrometres made up 0.1-0.2% of the short sample, 10-12% of the long sample and 2-3% of the UICC sample.
• Main results:
  • Across virtually all doses and times, titanium dioxide caused the least response. Short amosite caused more, but its response was not substantial even at the higher dose. UICC amosite was more active than short amosite, and long fibre amosite caused by far the greatest inflammation.
  • Macrophage recruitment compared with titanium dioxide: on day 2, the amosite samples caused significantly more recruitment in 12 of 18 comparisons. On day 4, there were no differences in 13 of 18 comparisons.
  • Neutrophil recruitment: short and UICC amosite caused significant increases over titanium dioxide in 8 of 12 comparisons. Long amosite showed the most consistent, highly significant increases over titanium dioxide, in 6 of 6 comparisons.
  • Long amosite was significantly more active than short amosite in 10 of 12 comparisons.
  • Two days after a 5 microgram dose, mice given long amosite had 23.25 (SEM 3.56) million macrophages and 13.28 (SEM 3.71) million neutrophils. Mice given short amosite had 4.65 (SEM 0.56) million macrophages and 0.20 (SEM 0.02) million neutrophils. The difference was significant (p less than 0.001).
  • Four days after a 50 microgram dose, macrophages from mice given long amosite spread to 17.38 (SD 7.08) micrometres on glass, a sign of activation. The figure was 10.93 (SD 5.01) for short amosite and 10.90 (SD 1.93) for saline controls. Long amosite differed significantly from both (p less than 0.001).
• The authors' conclusion: The authors concluded that the ranking of the amosite samples by ability to cause inflammation correlated with their proportion of long fibres. In their view, the greater ability of long fibres to cause inflammation and activate macrophages is probably a key factor in their ability to cause pulmonary fibrosis and may also be important in fibre carcinogenesis.
• Limitations the authors state:
  • The UICC amosite sample was sized in an earlier study under slightly different rules: only fibres longer than 0.6 micrometres were counted, against 0.4 micrometres for the long and short samples.

Topics

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

Medical terms in this study, explained in our Lexicon: Inflammation, Amosite, Peritoneal Cavity, UICC, Macrophage, Pulmonary Fibrosis, Carcinogenesis.

Related studies

• Biological activity of respirable industrial fibres treated to mimic residence in the lung — K. Donaldson (1994)
• Differential release of superoxide anions by macrophages treated with long and short fibre amosite asbestos is a consequence of differential affinity for opsonin — I.M. Hill, P.H. Beswick, et al. (1995)
• Gadolinium-based compounds induce NLRP3-dependent IL-1β production and peritoneal inflammation — C. Schmidt-Lauber, L. Bossaller, et al. (2015)
• Distinct Pro-Inflammatory Mechanisms Elicited by Short and Long Amosite Asbestos Fibers in Macrophages — R. Leinardi, J.R. Petriglieri, et al. (2023)
• Effects of cigarette smoke on the clearance of short asbestos fibres from the lung and a comparison with the clearance of long asbestos fibres — A. Churg, J.L. Wright, et al. (1992)
• Long and short fiber amosite asbestos alters at a different extent the redox metabolism in human lung epithelial cells — C. Riganti, E. Aldieri, et al. (2003)

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