Cigarette smoke increases the penetration of asbestos fibers into airway walls

Our plain-English summary of Cigarette smoke increases the penetration of asbestos fibers into airway walls, by D. McFadden, J. Wright, B. Wiggs, et al (The American Journal of Pathology, 1986).

The study

• Authors: D. McFadden, J. Wright, B. Wiggs, A. Churg
• Journal: The American Journal of Pathology
• Published: 1986;123(1):95-9
• Cited by: 46 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. 000421).

Abstract

For study of the penetration of asbestos fibers into airway walls, guinea pigs were given amosite asbestos by intratracheal instillation. Half of the animals were also exposed to cigarette smoke. Animals were sacrificed at 1 week and 1 month, and numbers of fibers in airway walls were counted in histologic sections. In both smoke-exposed and nonexposed groups, numbers of fibers per square millimeter of airway wall increased from 1 week to 1 month in the respiratory bronchioles. At each time period, smoke-exposed animals had significantly higher numbers of fibers in the airway walls, compared with nonexposed animals. It is concluded that 1) continued transport of fibers into interstitial tissues may be the reason that asbestosis can progress after cessation of exposure; 2) cigarette smoke increases the penetration of fibers into airway walls. This effect may play a role in the increased incidence of disease seen in smoking, compared with nonsmoking, asbestos workers.

In plain English

In this animal experiment, 20 female guinea pigs were split into two groups. Half breathed whole smoke from nonfilter cigarettes (10 cigarettes a day, 5 days a week) for 2 weeks before and throughout the experiment; half did not. All received one 1 mg dose of UICC amosite asbestos placed into the windpipe. Five animals per group were killed at 1 week and five at 1 month, and fibers longer than 5 micrometers were counted in small-airway walls by light microscopy. In respiratory bronchioles, smoke-exposed animals had more fibers per square millimeter of wall at both times (p less than 0.01), and fiber numbers rose from 1 week to 1 month in both groups. The share of these airways with any fibers was 13% and 30% without smoke versus 37% and 49% with smoke (1 week and 1 month). No differences appeared in membranous bronchioles or in fibers within the airway lining (epithelium). The authors suggested that increased fiber penetration may be one way smoking worsens asbestos disease, and noted that dosing by instillation is artificial.

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: guinea pigs given asbestos, with and without cigarette smoke exposure, examined at two time points
• Who was studied: Twenty 400-g Hartley strain female guinea pigs. Half were smoke-exposed and half were not. Five smoke-exposed and 5 non-exposed animals were killed 1 week after asbestos, and the remaining 5 in each group at 1 month (University of British Columbia, Vancouver)
• Exposure: A single dose of 1 mg UICC amosite asbestos in 0.5 ml saline given by intratracheal instillation. The smoke group received whole smoke of 10 nonfilter cigarettes per day (200 puffs total), 5 days a week, for 2 weeks before the asbestos dose and for the rest of the experiment
• Main results:
  • A total of 167 membranous bronchioles and 800 respiratory bronchioles were examined
  • In respiratory bronchioles, smoke-exposed animals had greater numbers of fibers per square millimeter of airway wall than non-exposed animals at both 1 week and 1 month (P less than 0.01 in Table 1). The authors called the difference highly significant
  • In respiratory bronchioles, fibers per square millimeter increased from 1 week to 1 month in both smoke-exposed and non-exposed animals (P less than 0.01). The rate of increase did not differ statistically between the two groups
  • Percentage of respiratory bronchioles with any fibers in their walls: not smoke-exposed 13% at 1 week and 30% at 1 month; smoke-exposed 37% at 1 week and 49% at 1 month
  • In membranous bronchioles there were no differences between smoke-exposed and non-exposed groups at either time, and no differences between the two time points
  • Fibers were readily found in the airway epithelium of both airway types. Their numbers showed no difference by smoking status or by time
• The authors' conclusion: The authors suggested that continued transport of fibers into airway walls after a single dose could help explain why asbestosis can progress after exposure stops. They also suggested that increased fiber penetration caused by smoke may be one of the mechanisms by which smoking potentiates asbestos disease
• Limitations the authors state:
  • Intratracheal instillation is an artificial way of giving asbestos and tends to spread particles unevenly compared with inhalation
  • The airway lining may react differently to masses of instilled fibers than to inhaled fibers. The method of administration should be borne in mind when comparing the results to humans
  • The authors did not systematically evaluate tissue changes in the animals
  • Only fibers easily visible by light microscopy were counted, a crude technique that detects a minority of fibers. Electron microscopy might show differences for smaller fibers
  • The authors considered it likely, but not proved, that fibers also pass through the airway lining in humans

Topics

Medical terms in this study, explained in our Lexicon: Amosite, Interstitial.

Related studies

• Cigarette smoke makes airway and early parenchymal asbestos-induced lung disease worse in the guinea pig — V. Tron, J.L. Wright, et al. (1987)
• Effects of cigarette smoke and asbestos on airway, vascular and mesothelial cell proliferation — H. Sekhon, J. Wright, et al. (1995)
• Cigarette smoke, asbestos, and small irregular opacities — W. Weiss (1984)
• Synergistic effects of mineral fibres and cigarette smoke on the production of tumour necrosis factor by alveolar macrophages of rats — Y. Morimoto, M. Kido, et al. (1993)
• Retinoid signaling and activator protein-1 expression in ferrets given beta-carotene supplements and exposed to tobacco smoke — X.D. Wang, C. Liu, et al. (1999)
• Cigarette smoke increases amosite asbestos fiber binding to the surface of tracheal epithelial cells — A. Churg, J. Sun, et al. (1998)

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