Effects of asbestos on epithelioid cell lines

Our plain-English summary of Effects of asbestos on epithelioid cell lines, by A.I. Neugut, D. Eisenberg, M. Silverstein, et al (Environmental Research, 1978).

The study

• Authors: A.I. Neugut, D. Eisenberg, M. Silverstein, P. Pulkrabek, I.B. Weinstein
• Journal: Environmental Research
• Published: 1978;17(2):256-65
• Cited by: 23 articles, as counted by NIH iCite
• Read it: PubMed · Publisher
• In J-M's library: Johns-Manville's company medical library held a copy.

Abstract

The in vitro effects of asbestos fibers on the growth and viability of CHO cells, an epithelioid cell line derived from Chinese hamster ovary, and on K-22 cells, an epithelial cell line derived from rat liver, have been studied. Relatively low concentrations of asbestos (10 micrograms/ml) were quite cytotoxic to both cell types. A sample of chrysotile asbestos was more toxic than samples of crocidolite or amosite. The toxic factor could not be extracted from the asbestos and toxicity occurred only if there was physical contact between the fibers and the cells. Although the phorbol ester class of tumor promoters induces the synthesis of plasminogen activator in various cell cultures, asbestos did not induce this protease in epithelioid or fibroblast cell cultures. The results obtained are compared to previous in vitro results obtained with fibroblast or macrophage cultures and are discussed in terms of their possible relevance to asbestos-induced fibrosis and tumorigenesis.

In plain English

This laboratory study tested how asbestos fibers affected the growth and survival of two cultured epithelioid cell lines. The first was CHO, from Chinese hamster ovary. The second was K-22, a normal rat liver epithelial line. The authors added UICC chrysotile, amosite or crocidolite asbestos, or glass fibers, generally at 10 micrograms per ml. Chrysotile was extremely toxic to K-22 cells, and amosite was also quite toxic. In CHO cells, glass fibers and amosite were mildly toxic, while crocidolite and chrysotile were extremely toxic. Higher chrysotile doses produced more toxicity, and cell death was delayed rather than immediate. Growth medium that had held chrysotile and was then filtered was not toxic. Chrysotile was also not toxic when the fibers could not touch the cells. Chrysotile did not raise production of the enzyme plasminogen activator in four cell lines, although the authors confirmed that it did so in mouse peritoneal macrophages. The authors concluded that the toxicity was not due to adsorbed impurities and that the fibers must touch or be very close to the cells. They noted the findings might not extend to other asbestos samples.

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 (in vitro) cell culture experiments
• Who was studied: Cultured cell lines: CHO (Chinese hamster ovary, an epithelioid malignant line) and K-22 (normal rat liver epithelial line). For the plasminogen activator tests, also HeLa cells, chick embryo fibroblasts and mouse peritoneal macrophages. Work done at Columbia University, New York; received August 1977.
• Exposure: UICC amosite, crocidolite and chrysotile B asbestos, and glass fibers made from Whatman filters, mostly added at 10 micrograms per ml. Chrysotile was also tested at other doses. The phorbol ester tumor promoter TPA was used for comparison in the enzyme tests.
• Main results:
  • In K-22 cells, chrysotile was extremely toxic, causing cell death, multinucleation, vacuolation and an almost immediate, complete arrest of growth.
  • In K-22 cells, amosite was also quite toxic, even after washing to remove adsorbed impurities.
  • In CHO cells, glass fibers and amosite were mildly toxic, while crocidolite and chrysotile were extremely cytotoxic. Chrysotile stayed highly toxic after extraction of possible impurities, though it seemed somewhat less toxic than before.
  • In CHO cells, increasing chrysotile doses produced increasing toxicity.
  • CHO cells that recovered growth despite continued chrysotile exposure (CHO-R) were not more resistant when exposed again.
  • CHO cells exposed to chrysotile for 24 to 48 hours showed reduced cloning efficiency but still excluded trypan blue. The authors took this to mean that cell death was delayed rather than immediate.
  • Growth medium that had been stirred with chrysotile and then filtered to remove the fibers was not toxic to CHO cells.
  • When flasks were inverted so that the chrysotile settled away from the CHO cells while sharing the same medium, there was no cytotoxicity.
  • Chrysotile did not induce plasminogen activator in epithelioid or fibroblast cultures (CHO, K-22, HeLa, chick embryo fibroblasts). TPA markedly increased it in HeLa and chick embryo fibroblast cultures. The authors confirmed, with their own chrysotile, that asbestos stimulates plasminogen activator in mouse peritoneal macrophages.
• The authors' conclusion: The authors concluded that asbestos's cytotoxic effects on the two epithelioid lines resembled those seen before with macrophages and fibroblasts, with chrysotile the most toxic sample. They concluded the toxicity was not due to adsorbed impurities or extractable material and required physical contact between fibers and cells. They also concluded that plasminogen activator production appeared unrelated to the cytotoxic effects in epithelioid or fibroblast cells.
• Limitations the authors state:
  • The authors stated it is not clear whether the findings would extend to a larger series of asbestos samples, or how far they reflect differences in fiber size or chemical composition.

Topics

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

Medical terms in this study, explained in our Lexicon: Epithelioid, Chrysotile, Crocidolite, Amosite, Fibroblast, Macrophage, Fibrosis, Tumorigenesis.

Related studies

• Expression of plasminogen activator and plasminogen activator inhibitor by rat mesothelioma induced by asbestos — S.P. Lenz, F.H. Green, et al. (1993)
• Gene expression profiles in asbestos-exposed epithelial and mesothelial lung cell lines — P. Nymark, P.M. Lindholm, et al. (2007)
• Utilization of gene profiling and proteomics to determine mineral pathogenicity in a human mesothelial cell line (LP9/TERT-1) — J.M. Hillegass, A. Shukla, et al. (2010)
• Three newly established immortalized mesothelial cell lines exhibit morphological phenotypes corresponding to malignant mesothelioma epithelioid, intermediate, and sarcomatoid types, respectively — T. Sato, H. Nakanishi, et al. (2021)
• Expression of cell adhesion molecules and connexins in gap junctional intercellular communication deficient human mesothelioma tumour cell lines and communication competent primary mesothelial cells — K. Pelin, A. Hirvonen, et al. (1994)
• Strain differences in pleural mesothelial cell reactions induced by potassium octatitanate fibers (TISMO) infused directly into the thoracic cavity — M. Yokohira, Y. Nakano, et al. (2013)

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