In vivo pulmonary toxicity of cellulose in rats

Our plain-English summary of In vivo pulmonary toxicity of cellulose in rats, by E. Tátrai, M. Brozik, Z. Adamis, et al (Journal of Applied Toxicology, 1996).

The study

• Authors: E. Tátrai, M. Brozik, Z. Adamis, K. Merétey, G. Ungváry
• Journal: Journal of Applied Toxicology
• Published: 1996;16(2):129-35
• Cited by: 20 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Cellulose after a single intratracheal dose (15 mg per animal) brought about fibrosing granulomatous alveobronchiolitis and an increase of IgA production in the bronchoalveolar lavage. Fibrosing alveolitis showed moderate progression as a function of time. With different morphological methods, injury of type I pneumocytes and the incomplete repair of type II pneumocytes were detected. The damage of the alveolar epithelium initiated and activated a series of processes that led to definite pulmonary alterations: pulmonary fibrosis leading to the disintegration of the alveolo-capillary morphological functional unit.

In plain English

This animal experiment tested whether cellulose dust, an organic fibre, harms the lungs of male Sprague-Dawley rats. Rats received a single 15 mg dose of respirable cellulose placed directly into the windpipe. Control rats received salt solution with penicillin. At 6 months, the cellulose-treated rats showed granulomatous inflammation narrowing the small airways and air sacs, signs of damage to type I lung lining cells, and enlargement of type II cells. At 12 months, the inflammation persisted, fibrous tissue had increased, and collagen had built up in the walls of the air sacs and capillaries. The authors rated the scarring as degree III on the Belt-King system for classifying experimental fibrosis. Control lungs showed no changes at 12 months. A second experiment, lasting two weeks, used crocidolite asbestos (1 mg) as a comparison. Blood antibody levels did not change significantly. In fluid washed from the lungs, IgA fell significantly in asbestos-treated rats after 1 day and rose significantly in cellulose-treated rats by the end of the second week. The authors concluded that damage to the lung lining set off processes leading to pulmonary fibrosis.

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 experiment (two experiments: a 6- and 12-month lung pathology study, and a 2-week immune response study with saline and crocidolite comparison groups)
• Who was studied: Male Sprague-Dawley rats weighing 230-260 g. In the first experiment, four groups of 13 animals received cellulose. Light microscopy used 10 animals per group and electron microscopy three animals per group. Serum testing in the second experiment used five animals per group.
• Exposure: Single intratracheal dose of 15 mg of respirable cellulose (Cellulosepulver MN 300) in 1 ml saline. Controls received saline with penicillin. In the second experiment, crocidolite (1 mg per animal) was given as a positive control.
• Main results:
  • At 6 months, cellulose-treated rats developed granulomatous inflammation in the lung interstitium that narrowed the bronchioles and alveoli.
  • At 6 months in cellulose-treated rats, RCA reactivity on alveolar surfaces weakened or disappeared, indicating damage to type I pneumocytes. MPA reactivity became more intense, pointing to hypertrophy of type II cells.
  • At 12 months in cellulose-treated rats, alveolar walls were thickened, granulomatous inflammation persisted, and argyrophilic fibres had increased compared with 6 months.
  • At 12 months, electron microscopy of cellulose-treated rats showed collagen fibres accumulated in the walls of alveoli and capillaries.
  • Control rats at 12 months showed no histological alterations in the lungs or regional lymph nodes.
  • By the end of the first year, fibrosing alveobronchiolitis in cellulose-treated rats reached degree III on the Belt-King classification system.
  • Serum IgG, IgA and IgM levels did not change significantly over time.
  • In bronchoalveolar lavage fluid, IgA decreased significantly in asbestos-treated rats after 1 day.
  • In bronchoalveolar lavage fluid, IgA increased significantly in cellulose-treated rats by the end of the second week. IgM and IgG did not change.
• The authors' conclusion: The authors concluded that cellulose damaged the alveolar epithelium, which set off processes leading to pulmonary fibrosis and disintegration of the alveolo-capillary unit. They described the rise in lung-fluid IgA as a local immune response to cellulose.

Topics

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

Medical terms in this study, explained in our Lexicon: Bronchoalveolar Lavage (BAL), Epithelium, Pulmonary Fibrosis.

Related studies

• Pulmonary toxicity of wollastonite in vivo and in vitro — E. Tátrai, Z. Kováciková, et al. (2004)
• Gender differences in murine pulmonary responses elicited by cellulose nanocrystals — A.A. Shvedova, E.R. Kisin, et al. (2016)
• Comment on Shvedova et al. (2016), "gender differences in murine pulmonary responses elicited by cellulose nanocrystals" — J.A. Shatkin, G. Oberdörster (2016)
• Pulmonary response of mice to fiberglass: cytokinetic and biochemical studies — I.Y. Adamson, H. Prieditis, et al. (1995)
• Enhanced lipid peroxidation and lysosomal enzyme activity in the lungs of rats with prolonged pulmonary deposition of crocidolite asbestos — J. Jajte, I. Lao, et al. (1987)
• Tumorigenicity of cellulose fibers injected into the rat peritoneal cavity — R.T. Cullen, B.G. Miller, et al. (2002)

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