Pathologic changes in the small airways of the guinea pig after amosite asbestos exposure

Our plain-English summary of Pathologic changes in the small airways of the guinea pig after amosite asbestos exposure, by D. Filipenko, J.L. Wright, A. Churg (The American Journal of Pathology, 1985).

The study

• Authors: D. Filipenko, J.L. Wright, A. Churg
• Journal: The American Journal of Pathology
• Published: 1985;119(2):273-8
• Cited by: 17 articles, as counted by NIH iCite
• Read it: PubMed · Free full text
• In J-M's library: Johns-Manville's company medical library held a copy (J-M no. 000472).

Abstract

To determine whether asbestos dust produces pathologic changes in the small airways, and to determine where the anatomic lesions of asbestosis commence, the authors examined lungs from guinea pigs exposed to 10 or 30 mg of amosite asbestos by intratracheal instillation and sacrificed 6 months later. Measurement of airway wall thickness revealed that membranous and respiratory bronchioles of all sizes in exposed animals were significantly thicker than those of controls. Amosite fibers were found embedded in the walls of bronchi and in membranous and respiratory bronchioles; where these fibers penetrated the airway walls, an interstitial inflammatory and fibrotic reaction (asbestosis) occurred. It is concluded that 1) amosite asbestos produces diffuse abnormalities throughout the noncartilagenous airways and possibly the cartilagenous airways as well; 2) this effect is independent of interstitial fibrosis of the parenchyma (classical asbestosis); 3) asbestosis, at least that induced by amosite, commences at any site in the parenchyma to which the asbestos fibers can gain access, either by deposition in alveoli and alveolar ducts or by direct passage of fibers through the walls of all types and sizes of small airways.

In plain English

In this animal experiment, twelve guinea pigs were split into three groups of four. One group had two instillations into the windpipe totalling 30 mg of UICC amosite asbestos, another 10 mg in total, and a control group saline only. The animals were killed 6 months after the second instillation. Among 785 small airways (membranous and respiratory bronchioles) measured in the control and 10 mg groups, walls were significantly thicker in the 10 mg group than in controls in every size range. Lungs from the 30 mg group were accidentally overinflated, so only their overall averages were compared, and these were also significantly thicker than control values. Amosite fibers were embedded in airway walls. Where fibers passed through the walls, an inflammatory and fibrotic reaction appeared in the adjoining lung tissue. Classic interstitial fibrosis was seen only in localized areas. The authors concluded that amosite produces widespread small-airway changes independent of classical asbestosis, and that asbestosis can start wherever fibers reach the lung tissue. They cautioned that instillation results may not apply directly to humans, or to chrysotile.

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 (intratracheal instillation in guinea pigs, with saline-treated controls)
• Who was studied: 12 Hartley strain guinea pigs bred in the University of British Columbia colony, each about 800 g, divided into three groups of 4 (amosite 30 mg, amosite 10 mg, saline control); killed 6 months after the second instillation
• Exposure: UICC amosite asbestos given as two intratracheal instillations totalling 30 mg ("amosite 30") or 10 mg ("amosite 10") in saline, given 7 days apart; controls received saline only
• Main results:
  • A total of 785 airways were measured in the control and amosite 10 groups: 147 membranous bronchioles in controls and 142 in the amosite 10 group, and 257 respiratory bronchioles in controls and 238 in the amosite 10 group
  • In the amosite 10 group, the walls of both membranous and respiratory bronchioles were significantly thicker than in controls in each size range. Membranous bronchiole wall thickness in the amosite 10 group was about 0.09 to 0.11 mm across size ranges, versus about 0.02 to 0.04 mm in controls (table partly garbled by scanning)
  • In the amosite 30 group (overinflated lungs), 201 membranous and 434 respiratory bronchioles were measured. Their overall mean wall thickness was 0.06 mm for membranous and 0.05 mm for respiratory bronchioles, which was statistically greater than control values (P < 0.001)
  • Amosite fibers were found embedded in the walls of respiratory and membranous bronchioles, and occasionally in the walls of bronchi
  • An interstitial inflammatory and fibrotic reaction occurred where fibers penetrated the nonalveolated walls of respiratory and membranous bronchioles and reached the adjacent alveolar tissue
  • Diffuse interstitial fibrosis was occasionally found in the amosite 30 animals, only in very localized areas next to alveolar ducts; minor degrees were seen in the amosite 10 group
• The authors' conclusion: The authors concluded that amosite produces diffuse abnormalities throughout the small airways, independent of interstitial fibrosis of the parenchyma (classical asbestosis). They concluded that asbestosis, at least that induced by amosite, starts anywhere fibers enter the alveolar spaces and interstitium. They suggested that the diffuse airway changes may be responsible for airflow obstruction in asbestos workers.
• Limitations the authors state:
  • Results from intratracheal instillation should be extrapolated to humans with care. Instillation concentrates particles in the airways, which may not reflect the human situation.
  • The mechanism by which these changes occur may be different in humans
  • Only amosite was used; results might not be the same with chrysotile
  • The amosite 30 lungs were accidentally inflated at a higher pressure, which prevented some intended comparisons
  • A relatively small number of animals was examined
  • The observation about where asbestosis starts was not yet confirmed by formal analysis of fiber numbers and reaction pattern

Topics

The National Library of Medicine indexes this study under subjects our site covers: Amosite, Asbestosis.

Medical terms in this study, explained in our Lexicon: Amosite, Asbestos Exposure, Bronchus, Interstitial, Interstitial Fibrosis, Parenchyma, Deposition, Alveoli.

Related studies

• Morphology of small-airway lesions in patients with asbestos exposure — J.L. Wright, A. Churg (1984)
• Severe diffuse small airways abnormalities in long term chrysotile asbestos miners — J.L. Wright, A. Churg (1985)
• Cigarette smoke makes airway and early parenchymal asbestos-induced lung disease worse in the guinea pig — V. Tron, J.L. Wright, et al. (1987)
• Rapid short-term clearance of chrysotile compared with amosite asbestos in the guinea pig — A. Churg, J.L. Wright, et al. (1989)
• Biochemical changes in guinea pig lungs due to amosite asbestos — V. Misra, Q. Rahman, et al. (1978)
• Lung cell reactions in guinea pigs after inhalation of asbestos (amosite) — M. Sjöstrand, R. Rylander, et al. (1989)

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