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Cytogenetic studies on chrysotile asbestos

Our plain-English summary of Cytogenetic studies on chrysotile asbestos, by K.S. Lavappa, M.M. Fu, S.S. Epstein (Environmental Research, 1975).

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The study

Abstract

The cytogenetic effects of chrysotile asbestos (chrysotile A) in vivo in Rhesus monkeys and Swiss albino mice, and in vitro in embryonic hamster cells were investigated. Single oral dosages of chrysotile, 100 or 500 mg/kg, failed to induce chromosome aberrations in bone marrow cells of Rhesus monkeys. Similarly, oral or intraperitoneal administration of chrysotile over a dose range from 0.4 to 400 mg/kg. failed to induce micronuclei formation in bone marrow cells of mice. However, chrysotile induced a significant and dose-related increase in chromosome aberrations and a dose-related inhibition of the mitotic index of cultured Syrian hamster embryo cells.

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

In plain English

This preliminary laboratory study tested whether chrysotile asbestos (Rhodesian chrysotile A) damages chromosomes. Male Rhesus monkeys were fed chrysotile in cookies: six at 100 mg/kg, three at 500 mg/kg, and two controls without chrysotile. In bone marrow, one cell with a chromatid gap was found among 441 examined in the 100 mg/kg group, and one among 209 in the 500 mg/kg group (Table 1 says 219); controls had none. Female Swiss albino mice, two per dose, received chrysotile twice, 24 hours apart, by mouth or abdominal injection, at 0.2 to 200 mg/kg each time (0.4 to 400 mg/kg total). They showed no significant increase in bone marrow micronuclei, a sign of chromosome damage. In cultured Syrian hamster embryo cells, chrysotile produced a dose-related increase in chromosome aberrations, from 0.9% at the lowest concentration to 1.66% at the highest, against 0.1% in untreated controls (p less than 0.01). It also reduced cell division at the three higher concentrations. The authors suggested the negative animal results may reflect poor chrysotile access to bone marrow in the short test, or cell resistance.

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: Laboratory experiments described by the authors as preliminary: in vivo tests in monkeys and mice, and an in vitro test in cultured hamster embryo cells
  • Who was studied: Male Rhesus monkeys weighing 5-8 kg: six given 100 mg/kg, three given 500 mg/kg, and two controls. Female Swiss albino mice in groups of two per dose. Syrian hamster embryo cell cultures. The work was done at Case Western Reserve University, Cleveland, Ohio; Table 1 lists dosing dates in 1973-1974.
  • Exposure: Rhodesian chrysotile A asbestos. Monkeys received it by mouth in cookies (100 or 500 mg/kg). Mice received it twice by gavage or by intraperitoneal injection, at 0.2, 2, 20 or 200 mg/kg per dose, 24 hours apart. The tables list these as totals of 0.4, 4, 40 and 400 mg/kg. Hamster cell cultures were exposed to 0.1, 1, 10 or 100 micrograms per milliliter.
  • Main results:
    • Monkeys given 100 mg/kg (six animals, 72 days before sacrifice): 1 cell with a chromatid gap among 441 bone marrow metaphases examined.
    • Monkeys given 500 mg/kg (three animals, 24 hours before sacrifice): 1 cell with a chromatid gap among 209 metaphases (Table 1 gives 219). The aberration frequency in control monkeys was zero.
    • Mice given chrysotile orally or intraperitoneally showed no significant increase in bone marrow micronuclei. Mice in the mitomycin C positive control group showed a significant increase (0.7%).
    • Hamster embryo cells, overall incidence of chromosome aberrations: 0.9% at 0.1, 1.38% at 1, 1.67% at 10 and 1.66% at 100 micrograms per milliliter, against 0.1% in untreated controls. The differences were statistically significant (p less than 0.01) at all four concentrations.
    • Hamster embryo cells, mitotic index (share of dividing cells): 2% at 0.1 micrograms per milliliter against 1.96% in controls. It fell to 1.56%, 1.3% and 0.30% at 1, 10 and 100 micrograms per milliliter (each p less than 0.01).
  • The authors' conclusion: The authors concluded that, under their test conditions, oral chrysotile did not induce chromosome aberrations in monkey bone marrow, and oral or intraperitoneal chrysotile did not induce micronuclei in mouse bone marrow. In contrast, it induced dose-related chromatid gaps and breaks in cultured hamster embryo cells. They suggested the reduced cell division could be interpreted as due to the cytotoxic nature of chrysotile.
  • Limitations the authors state:
    • The authors noted that the negative bone marrow results may reflect problems with chrysotile reaching bone marrow cells during the short test period, or resistance of those cells to chrysotile.
    • The authors stated that the mechanism by which chrysotile induced the aberrations is unclear.
    • The authors described the work as preliminary.

Topics

Medical terms in this study, explained in our Lexicon: Chrysotile, Micronuclei, Mitotic Index.

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Cited on this site

How to cite it

Cite the study

K.S. Lavappa, M.M. Fu, S.S. Epstein. Cytogenetic studies on chrysotile asbestos. Environmental Research 1975;10(2):165-73. doi:10.1016/0013-9351(75)90080-8. PMID: 811459.

Cite our summary

“Cytogenetic studies on chrysotile asbestos.” AsbestosClaims.Law Library. https://asbestosclaims.law/library/research/cytogenetic-studies-on-chrysotile-asbestos.

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