Cellular ingestion, toxic effects, and lesions observed in human bronchial epithelial tissue and cells cultured with asbestos and glass fibers

Our plain-English summary of Cellular ingestion, toxic effects, and lesions observed in human bronchial epithelial tissue and cells cultured with asbestos and glass fibers, by A. Haugen, P.W. Schafer, J.F. Lechner, et al (International Journal of Cancer, 1982).

The study

• Authors: A. Haugen, P.W. Schafer, J.F. Lechner, G.D. Stoner, B.F. Trump, C.C. Harris
• Journal: International Journal of Cancer
• Published: 1982;30(3):265-72
• Cited by: 44 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Although exposure to asbestos has been shown in previous epidemiological studies to synergistically increase the risk of bronchogenic carcinoma for cigarette smokers, the pathobiological mechanism(s) responsible for the cocarcinogenic action of asbestos is not known. Therefore, the effects of asbestos fibers on normal human tracheobronchial epithelium are of interest. Asbestos fibers, i.e., amosite, crocidolite and chrysotile (UICC samples) and glass fibers were initially assayed for their cytotoxicity. Bronchial epithelial cells exposed to either asbestos or glass fibers displayed inhibition of cell growth as a function of fiber concentration. When compared to glass fibers, asbestos fibers caused a statistically significant (p<0.05) decrease in cell population doubling rate. Chrysotile was approximately 10 times more cytotoxic than either amosite or crocidolite and more than 100 times more cytotoxic than the glass fibers. Epithelial cells were 10 to 15 times more sensitive to the cytotoxic effects of asbestos fibers than bronchial fibroblasts from the same donor. Using electron microscopy, asbestos fibers were seen to be ingested by epithelial cells. After exposure for 2 h short fibers (<12 µm) were found both in the cytoplasm and within phagosomes. High-voltage electron microscopy combined with stereo-microscopy revealed asbestos fibers in the cytoplasmic matrix. A single exposure to amosite asbestos (100-1000 µg/ml) was found to induce focal hyperplasia and epidermoid metaplasia with cellular atypia in human tracheobronchial explants. Surface fine structure observations revealed asbestos fibers protruding from these lesions. Intra-cytoplasmic and intranuclear fibers of amosite were identified in these focal lesions using X-ray microanalysis in combination with transmission electron microscopy. With increasing time, fibers were also seen deposited within the submucosa of the explants. The preferential cytotoxicity of asbestos for epithelial cells and the metaplastic response of bronchial epithelium may be important in the cocarcinogenic action of asbestos.

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

In plain English

This laboratory study, not a study of people, exposed cultured human bronchial (airway) cells to standard samples of chrysotile, amosite and crocidolite asbestos and to glass fibers, and exposed small pieces of human bronchial tissue obtained at autopsy to amosite only. All fiber types slowed the growth of bronchial lining (epithelial) cells, more so at higher concentrations, and asbestos slowed growth statistically significantly more than glass fibers. Chrysotile was about 10 times more toxic than amosite or crocidolite and more than 100 times more toxic than glass fibers. Epithelial cells were about 10 to 15 times more sensitive to asbestos than connective-tissue cells (fibroblasts) from the same donor. Electron microscopy showed short fibers inside cells after 2 hours. In the tissue pieces, a single amosite exposure was followed from 2 weeks on by areas of abnormal cell growth (hyperplasia, epidermoid metaplasia, cell atypia), with fibers inside cells and their nuclei. Control tissue looked essentially normal. The authors concluded these effects may be important in asbestos's cocarcinogenic action, while noting that the relevance of such tissue changes to cancer had not been established.

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) experiment using cultured human bronchial cells and bronchial tissue explants, examined by cell-growth assays and electron microscopy
• Who was studied: Human bronchial tissue explants obtained at 'immediate autopsy', plus bronchial epithelial cells and bronchial fibroblasts grown from the explants. Four explants per group were examined at 2, 4 and 8 weeks. The number of donors is not stated.
• Exposure: UICC standard reference samples of Canadian chrysotile B, crocidolite and amosite, plus glass fibers made from homogenized Whatman glass-fiber filters, were tested on cultured cells at various concentrations for 3 days. Tissue explants were exposed only to amosite, once, at suspensions of 10, 100 or 1,000 per ml (the unit symbol is garbled in the scan), and fibers were removed after 24 h.
• Main results:
  • Bronchial epithelial cells exposed to asbestos or glass fibers showed growth inhibition that increased with fiber concentration. Compared with glass fibers, asbestos caused a statistically significant (p less than 0.05) decrease in cell population doubling rate.
  • In epithelial cells, chrysotile was approximately 10 times more cytotoxic than amosite or crocidolite and more than 100 times more cytotoxic than glass fibers.
  • Bronchial fibroblasts from the same donor were about 10- to 15-fold more resistant to asbestos than epithelial cells. Glass fibers had no significant toxic effect on fibroblasts.
  • Epithelial cells ingested asbestos fibers. After 2 h, short fibers (under 12 micrometres) were found in the cytoplasm and within phagosomes.
  • In bronchial explants, a single amosite exposure induced focal hyperplasia and epidermoid metaplasia with cellular atypia. Lesions were seen as early as 2 weeks after exposure.
  • Amosite fibers were identified inside the cytoplasm and inside the nuclei of cells in these lesions, using X-ray microanalysis with transmission electron microscopy.
  • In heavily ciliated areas of the explants, most fibers were removed by ciliary action.
  • Control (sham-exposed) tissue was essentially normal, with only rare areas of metaplasia.
• The authors' conclusion: The authors concluded that asbestos's preferential toxicity to epithelial cells, and the metaplastic response of bronchial epithelium, may be important in the cocarcinogenic action of asbestos.
• Limitations the authors state:
  • The authors state that the relevance of these tissue changes to the cancer process has not been established.
  • The authors note there is no direct correlation between in vitro cytotoxicity and carcinogenesis, since all major asbestos types can cause respiratory cancer.

Topics

Medical terms in this study, explained in our Lexicon: Bronchogenic Carcinoma, Epithelium, Amosite, Crocidolite, Chrysotile, UICC, Fibroblast, Transmission Electron Microscopy (TEM).

Related studies

• DNA repair in human bronchial epithelial cells — A.J. Fornace, J.F. Lechner, et al. (1982)
• Asbestos induces tissue factor in Beas-2B human lung bronchial epithelial cells in vitro — A. Iakhiaev, U. Pendurthi, et al. (2004)
• Asbestos exposure increases human bronchial epithelial cell fibrinolytic activity — T.J. Gross, S.M. Cobb, et al. (1993)
• Malignant transformation of immortalized human bronchial epithelial cells by asbestos fibers — T.K. Hei, L.J. Wu, et al. (1997)
• Cytotoxicity, oxidative stress and genotoxicity induced by glass fibers on human alveolar epithelial cell line A549 — V. Rapisarda, C. Loreto, et al. (2015)
• Multi-walled carbon nanotubes directly induce epithelial-mesenchymal transition in human bronchial epithelial cells via the TGF-β-mediated Akt/GSK-3β/SNAIL-1 signalling pathway — M. Polimeni, G.R. Gulino, et al. (2016)

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