Mineralogical features associated with cytotoxic and proliferative effects of fibrous talc and asbestos on rodent tracheal epithelial and pleural mesothelial cells

Our plain-English summary of Mineralogical features associated with cytotoxic and proliferative effects of fibrous talc and asbestos on rodent tracheal epithelial and pleural mesothelial cells, by A.G. Wylie, H.C. Skinner, J. Marsh, et al (Toxicology and Applied Pharmacology, 1997).

The study

• Authors: A.G. Wylie, H.C. Skinner, J. Marsh, H. Snyder, C. Garzione, D. Hodkinson, R. Winters, B.T. Mossman
• Journal: Toxicology and Applied Pharmacology
• Published: 1997;147(1):143-50
• Cited by: 23 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Inhalation of asbestos fibers causes cell damage and increases in cell proliferation in various cell types of the lung and pleura in vivo. By using a colony-forming efficiency (CFE) assay, the cytotoxicity and proliferative potential of three mineral samples containing various proportions of fibrous talc were compared to NIEHS samples of crocidolite and chrysotile asbestos in cell types giving rise to tracheobronchial carcinomas, i.e., hamster tracheal epithelial (HTE) cells, and mesotheliomas, i.e., rat pleural mesothelial (RPM) cells. Characterization of mineralogical composition, surface area, and size distributions as well as proportions of fibers in all mineral samples allowed examination of data by various dose parameters including equal weight concentrations, numbers of fibers >5 micron in length, and equivalent surface areas. Exposure to samples of asbestos caused increased numbers of colonies of HTE cells, an indication of proliferative potential, but fibrous talc did not. RPMs did not exhibit increased CFE in response to either asbestos or talc samples. Decreased numbers of colonies, an indication of cytotoxicity, were observed in both cell types and were more striking at lower weight concentrations of asbestos in comparison to talc samples. However, all samples of fibrous minerals produced comparable dose-response effects when dose was measured as numbers of fibers greater than 5 micron or surface area. The unique proliferative response of HTE cells to asbestos could not be explained by differences in fiber dimensions or surface areas, indicating an important role of mineralogical composition rather than size of fibers.

Copyright 1997 Academic Press.

In plain English

This was a laboratory study of animal cells, not people. The authors compared three New York talc samples containing fibrous talc (FD14, S157 and CPS183) with chrysotile and crocidolite asbestos. They exposed hamster tracheal epithelial (HTE) cells and rat pleural mesothelial (RPM) cells for 7 days and counted cell colonies. In HTE cells, both asbestos types increased colony numbers at the lowest concentrations, which the authors read as increased cell proliferation and/or survival, and reduced them at higher concentrations. RPM cells did not grow more with either asbestos type, but their colony numbers fell at higher asbestos concentrations. Compared at equal weight doses, the talc samples were less cytotoxic (harmful to cells) than asbestos in both cell types. When dose was counted as fibers 5 micrometers or longer, HTE responses differed by mineral type. RPM responses appeared largely independent of it, setting aside a slight cytotoxic effect of FD14 at low concentrations. Surface area did not explain the responses. The authors concluded that mineral type, rather than fiber length itself, shaped the cell responses.

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: In vitro (cell culture) experiment using a colony-forming efficiency (CFE) assay, with cells exposed to mineral samples for 7 days
• Who was studied: An established hamster tracheal epithelial (HTE) cell line, and primary rat pleural mesothelial (RPM) cells taken from the parietal pleura of two weanling male Fischer 344 rats
• Exposure: Three talc samples containing fibrous talc from the Gouverneur Mining District, New York: FD14 (commercial talc), S157 (formerly produced as a fiber talc product) and CPS183 (laboratory concentrate of fibrous talc). These were compared with NIEHS chrysotile (Plastibest 20) and NIEHS crocidolite asbestos at a range of concentrations.
• Main results:
  • Composition of the talc sample FD14: platy talc, true mineral fibers of talc and talc/amphibole, tremolite cleavage fragments, and platy serpentine, with chrysotile absent. The talc samples also contained tremolite and, in S157 and CPS183, anthophyllite.
  • In HTE cells, both chrysotile and crocidolite raised colony numbers at the lowest concentrations (statistically significant, p less than 0.05). The authors read this as increased cell proliferation and/or survival.
  • In HTE cells, colony numbers fell significantly at asbestos concentrations of 0.5 (printed as mg/cm2) and greater. The authors read this as toxicity or growth inhibition.
  • RPM (pleural mesothelial) cells showed no proliferative effect from either asbestos type.
  • In RPM cells, colony numbers fell significantly at asbestos concentrations greater than 0.05 (printed as mg/cm2).
  • At equal weight doses, both cell types were more sensitive to the cytotoxic effects of asbestos than of talc.
  • Among the talc samples, CPS183 was the most toxic, followed by S157 and then FD14.
  • When dose was expressed as the number of fibers 5 micrometers or longer per square centimeter, the authors found that the HTE cell responses depended on mineral type rather than fiber number.
  • When dose was expressed as fibers per square centimeter, RPM cell responses appeared to be independent of mineral type.
  • The authors set aside a slight cytotoxic response to FD14 at low concentrations. With that exception, significant decreases in RPM colonies began between about 10^3 and 10^4 fibers per square centimeter for all samples (printed as '103 and 104' in the scanned text).
  • Surface area of the samples did not explain the cell responses in either HTE or RPM cells.
• The authors' conclusion: The authors concluded that their data point to the importance of mineral type, rather than fiber length itself, in determining cell responses linked to the disease-causing potential of mineral dusts.
• Limitations the authors state:
  • The lack of a proliferative response in RPM cells may reflect the assay design, which exposed single cells rather than confluent layers of cells.
  • The small numbers of cells used in the CFE assay may not produce enough growth factors (cytokines) for mesothelial cells to proliferate.
  • Fiber counts for chrysotile are underestimated because chrysotile is hard to see by scanning electron microscopy.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Talc and vermiculite.

Medical terms in this study, explained in our Lexicon: Talc, Mesothelial Cells, Pleura, Crocidolite, Chrysotile, Carcinoma, Mesothelioma, Dose-response relationship.

Related studies

• Asbestos induces nuclear factor kappa B (NF-kappa B) DNA-binding activity and NF-kappa B-dependent gene expression in tracheal epithelial cells — Y.M. Janssen, A. Barchowsky, et al. (1995)
• Transfection of a manganese-containing superoxide dismutase gene into hamster tracheal epithelial cells ameliorates asbestos-mediated cytotoxicity — B.T. Mossman, P. Surinrut, et al. (1996)
• Effect of mineral particles containing iron on primary cultures of rabbit tracheal epithelial cells: possible implication of oxidative stress — C. Guilianelli, A. Baeza-Squiban, et al. (1993)
• Effects of crocidolite and chrysotile asbestos on cellular uptake and metabolism of benzo(a)pyrene in hamster tracheal epithelial cells — B.T. Mossman, A. Eastman, et al. (1983)
• Cigarette smoke increases amosite asbestos fiber binding to the surface of tracheal epithelial cells — A. Churg, J. Sun, et al. (1998)
• Iron enhances uptake of mineral particles and increases lipid peroxidation in tracheal epithelial cells — B. Keeling, K.Y. Li, et al. (1994)

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