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Inhalation carcinogenesis from various forms of asbestos

Our plain-English summary of Inhalation carcinogenesis from various forms of asbestos, by A.L. Reeves, H.E. Puro, R.G. Smith (Environmental Research, 1974).

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The study

Abstract

Rats, rabbits, guinea pigs, gerbils, and mice were exposed to the inhalation of chrysotile, crocidolite, or amosite for 2 years. Mean atmospheric concentrations were 47.9-50.2 mg/m³, but only 0.08-1.82% of the dusts retained fibrous morphology during the dissemination procedure which involved hammer milling. Trace contamination especially by chromium and nickel was also increased. Light microscopic fiber counts per ml chamber air were 54 (chrysotile), 1105 (crocidolite), and 864 (amosite). A fibrogenic response to these dusts was observed in all five animal species, the severity corresponding to the extent of exposure (with reaction to chrysotile frequently very slight). Gerbils developed frequent alveolar proteinosis. Mice developed spontaneous papillary carcinomas in the lungs. Disregarding the latter species, carcinogenic response to asbestos inhalation was restricted to rats and occurred in all three exposure groups. There were 2 lung cancers and 1 pleural mesothelioma after chrysotile inhalation; 4 lung cancers after crocidolite inhalation; and 1 lung cancer and 2 pleural mesotheliomas after amosite inhalation. These cases constituted 7-9% incidence of malignancy among rats with adequate survival record. Hypotheses of asbestos carcinogenesis are reviewed and it is suggested that different etiologic principles may be involved in the causation of lung cancer and of pleural mesothelioma.

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

In plain English

In this animal experiment, the authors exposed rats, rabbits, guinea pigs, gerbils and mice to air containing chrysotile, crocidolite or amosite asbestos for 2 years. Mean dust levels were 47.9 to 50.2 mg/m3. However, after the milling used to spread it, only 0.08 to 1.82% of the dust looked fibrous under the light microscope, though most particles appeared fibrous under the electron microscope. Fiber counts per ml of chamber air were 54 for chrysotile, 1105 for crocidolite and 864 for amosite. Grinding also added chromium and nickel to the dusts. All five species developed lung scarring (fibrosis), with the reaction to chrysotile often very slight. The authors regarded lung tumors in mice as spontaneous. Apart from those, cancers occurred only in rats: 2 lung cancers and 1 pleural mesothelioma after chrysotile, 4 lung cancers after crocidolite, and 1 lung cancer and 2 pleural mesotheliomas after amosite. This was a 7-9% incidence of malignancy among rats with adequate survival. The authors concluded that, under the conditions of this experiment, there was no important difference in cancer-causing capacity among the three minerals.

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 inhalation experiment (chronic exposure in walk-in dust chambers)
  • Who was studied: 715 animals of both sexes at Wayne State University, Detroit. There were 207 rats, 96 guinea pigs, 60 rabbits, 90 mice and 204 gerbils, divided evenly among the amosite, crocidolite and chrysotile chambers. A smaller number (10-12 of each species) were kept as unexposed controls. The animals were 3-6 weeks old when shipped.
  • Exposure: Inhalation of ball-milled, hammer-milled amosite, crocidolite or chrysotile dust (Johns-Manville samples). Exposure ran 4 hours/day, 4 days/week, for 2 years, totalling 1480 exposure hours. Mean concentrations were roughly 48-50 mg/m3 in each chamber.
  • Main results:
    • Only 0.08-1.82% of the dusts kept a fibrous shape (by light microscopy) during the dissemination procedure, which involved hammer milling.
    • The authors stated that the great majority of fibers visible under the light microscope were destroyed, or were transformed into submicronic fibrils or apparently nonfibrous crystals.
    • A similar loss of fibrous structure was not seen under the electron microscope, where most particles appeared fibrous.
    • Light microscopic fiber counts per ml of chamber air were 54 for chrysotile, 1105 for crocidolite and 864 for amosite.
    • Grinding introduced chromium into amosite (3 times) and crocidolite (9 times), and nickel into crocidolite (5 times).
    • All five species showed a fibrogenic (scarring) response whose severity matched the extent of exposure. The reaction to chrysotile was frequently very slight.
    • Lung weight/body weight ratio, crocidolite versus control: the difference was significant in gerbils (t = 3.14, 99.5% confidence level) and in rats (t = 2.36, 95% confidence level). In the other species, differences were of low or borderline significance.
    • Cancers in rats by fiber:
  • Chrysotile: 2 lung cancers and 1 pleural mesothelioma.
  • Crocidolite: 4 lung cancers.
  • Amosite: 1 lung cancer and 2 pleural mesotheliomas.
    • These rat cases made up a 7-9% incidence of malignancy among rats with adequate survival.
    • One additional amosite-exposed rat had a lung osteosarcoma, which the authors judged was probably a spread from a primary bone tumor. The authors excluded it from the count of asbestos-related tumors.
    • Mice developed papillary carcinomas of the lung that the authors described as spontaneous. There were 2 in crocidolite-exposed mice and 1 in a control mouse.
    • Leaving mice aside, cancer after asbestos inhalation was restricted to rats and occurred in all three exposure groups. Rabbits, guinea pigs and gerbils had no malignancies. Gerbils frequently developed alveolar proteinosis.
  • The authors' conclusion: The authors concluded that, under the conditions of this experiment, there was no important difference in carcinogenic capacity among the three minerals, including amosite.
  • Limitations the authors state:
    • Milling destroyed the fibrous structure of a large proportion of particles, which was not intended.
    • Dust preparation introduced heavy metal contamination.
    • 25-30 rats were lost for unexplained reasons during the fourth half-year of exposure.
    • The X-ray diffraction estimates of crystallinity loss were uncorrected and only approximate.

Topics

Medical terms in this study, explained in our Lexicon: Carcinogenesis, Chrysotile, Crocidolite, Amosite, Fibrogenic, Carcinoma, Carcinogenic, Lung Cancer.

Browse more research in Environmental Research, or return to medical research.

Cited on this site

How to cite it

Cite the study

A.L. Reeves, H.E. Puro, R.G. Smith. Inhalation carcinogenesis from various forms of asbestos. Environmental Research 1974;8(2):178-202. doi:10.1016/0013-9351(74)90050-4. PMID: 4455505.

Cite our summary

“Inhalation carcinogenesis from various forms of asbestos.” AsbestosClaims.Law Library. https://asbestosclaims.law/library/research/inhalation-carcinogenesis-from-various-forms-of-asbestos.

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