Formation of the asbestos body. A comparative study with three types of asbestos

Our plain-English summary of Formation of the asbestos body. A comparative study with three types of asbestos, by Y. Suzuki, J. Churg (Environmental Research, 1970).

The study

• Authors: Y. Suzuki, J. Churg
• Journal: Environmental Research
• Published: 1970;3(2):107-18
• Cited by: 40 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

.Asbestos bodies were produced experimentally in the lungs of hamsters by intratracheal instillation of three types of asbestos: soft chrysotile, harsh chrysotile, and amosite. Though some differences were noted, harsh chrysotile and amosite fibers were converted into asbestos bodies by the same snccessive steps that were prrvion\ly described for soft chrysotilr: [ 1) phagocytosis of asbestos by alveolar nlac ophages and other phagocytic cells and incorporation into phagolysosomes; (2) accumulation of iron micelles around the fibers, possibly by fusion of asbestos-containing phagosomes with hemosiderin granules; and (3) compaction of the micelles and clearing of the peripheral zone, to form a mature asbestos body. Formation of asbestos bodies seems to be a continuous process with old bodies growing in thickness and uncoated fibers being converted into bodies months 01 !.rars after instillation of asbestos. Possible origins of hemosiderin granules are discussed. Striking hyperplasia of cell organelles was fonntl. presm~lably intlicativr of their participation in the tlc~vclopment of the asbestos bodies.

PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

In plain English

This was an animal experiment in which the authors used electron microscopy to compare how three types of asbestos (soft chrysotile, harsh chrysotile and amosite) are turned into asbestos bodies, which are fibers coated with iron, in hamster lungs. Five hamsters each received a single 1 mg dose of soft chrysotile into the windpipe and were killed 6, 12 and 24 months later. One received 1.5 mg of harsh chrysotile and was killed after 12 months. One received 2.5 mg of amosite monthly, 25 mg in total, and was killed 10 months after the last dose. Although the fibers differed in structure, the process was quite similar for all three. A lung scavenger cell (macrophage) engulfed the fiber into a small sac, iron particles gathered around and inside the sac, and these packed tightly to form a mature body. Destruction of lung air sacs was seen especially in the amosite animal. The authors concluded that the process is basically similar for chrysotile and amosite, and that the iron most likely comes from the body's own cells. They noted that the number of animals was small.

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; comparative light and electron microscopy study of hamster lungs after asbestos was instilled into the windpipe
• Who was studied: Male Syrian hamsters: five given soft chrysotile, one given harsh chrysotile, one given amosite, and three controls. Place and dates are not stated beyond the authors' New York institutions.
• Exposure: Intratracheal instillation of soft chrysotile (single 1 mg dose), harsh chrysotile (single 1.5 mg dose, killed after 12 months) or amosite (2.5 mg monthly, 25 mg total, killed 10 months after the last dose)
• Main results:
  • Despite differences in fiber structure, asbestos body formation was quite similar with soft chrysotile, harsh chrysotile and amosite.
  • Chrysotile fibers in the lungs tended to break into short thin bundles and individual unit fibers. Amosite fibers were solid rather than tubular.
  • Iron particles (micelles) clustered around the cell sacs (phagosomes) that contained asbestos.
  • A mature asbestos body was marked by many tightly packed iron particles inside a membrane-enclosed space.
  • Maturation of the body did not depend on fiber length.
  • In some areas the air sacs (alveoli) were destroyed, especially in the animal given amosite.
  • Adenomatous proliferation of the terminal bronchioles became prominent 12 to 24 months after first exposure.
  • In the five soft chrysotile animals the changes were virtually identical, apart from fibrosis gradually progressing with time.
• The authors' conclusion: The authors concluded that asbestos body formation is basically similar for serpentine asbestos (soft and harsh chrysotile) and amphibole asbestos (amosite). They also concluded that the iron in the bodies is more likely of cellular origin than derived from the fibers.
• Limitations the authors state:
  • The number of animals was small.
  • Amosite fibers were readily dislodged during sectioning of the tissue.
  • The authors did not measure the enzyme activity of acid hydrolases.
  • The mechanism and significance of the iron-free outer layer of the bodies have not been established.

Topics

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

Medical terms in this study, explained in our Lexicon: Asbestos Body Formation, Asbestos Bodies, Chrysotile, Amosite, Phagocytosis, Phagolysosome.

Related studies

• Structure and development of the asbestos body — Y. Suzuki, J. Churg (1969)
• Asbestos-body formation in the lungs of rats and guinea-pigs after inhalation of anthophyllite — S.K. Botham, P.F. Holt (1972)
• Asbestos body formation and iron accumulation in mouse peritoneal granulomas after the introduction of crocidolite asbestos fibers — H.K. Koerten, J. Hazekamp, et al. (1990)
• The enigmatic asbestos body: its formation and significance in asbestos-related disease — A. Morgan, A. Holmes (1985)
• The mechanism of formation of asbestos bodies — S.K. Botham, P.F. Holt (1968)
• Proceedings: The recognition of various types of asbestos as minerals, and in tissues — F.D. Pooley (1974)

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