Cigarette smoke increases amosite asbestos fiber binding to the surface of tracheal epithelial cells

Our plain-English summary of Cigarette smoke increases amosite asbestos fiber binding to the surface of tracheal epithelial cells, by A. Churg, J. Sun, K. Zay (The American Journal of Physiology, 1998).

The study

• Authors: A. Churg, J. Sun, K. Zay
• Journal: The American Journal of Physiology
• Published: 1998;275(3):L502-8
• Cited by: 11 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Binding of asbestos fibers to the cell surface appears to be important in the initiation of intracellular signaling events as well as in initiation of particle uptake by the cell. We have previously shown that cigarette smoke increases the uptake of asbestos fibers by tracheal epithelial cells in explant culture. Whether smoke acts by increasing surface binding of fibers is not known. In this study, we exposed rat tracheal explants to air or cigarette smoke and then to a suspension of amosite asbestos. Explants were harvested after 1 or 24 h of dust exposure and washed by repeated dips in culture medium to remove loosely bound fibers, and the number of fibers adhering to the apical cell surfaces was determined by scanning electron microscopy. Smoke-exposed explants retained significantly more surface fibers than air-exposed explants. After four washes, binding levels were similar at 1 and 24 h. The smoke effect was still present when incubations were carried out at 4 degrees C, but binding was decreased approximately 25%. Preincubation of the asbestos fibers with iron chloride to increase surface iron increased fiber binding in both air- and smoke-exposed explants, whereas preincubation of the fibers with the iron chelator deferoxamine decreased binding after air exposure and completely eliminated the smoke effect. Inclusion of mannitol or catalase in the medium or preincubation of the explants with GSH produced decreases in binding of 10-25% in air-exposed explants and generally greater decreases in smoke-exposed explants. We conclude that 1) amosite binding is a very rapid process that does not require active cellular metabolism, 2) cigarette smoke increases adhesion of fibers to the epithelial surfaces, and 3) iron on the asbestos fiber appears to play an important role in binding, probably through an active oxygen species-mediated process.

In plain English

This was a laboratory experiment on pieces of rat windpipe (tracheal explants), not a study of people. Explants were exposed for 10 minutes to room air or cigarette smoke, then soaked for 1 hour in an amosite asbestos suspension. After gentle washing, the authors used scanning electron microscopy to measure how much of the cell surface was covered by fibers that stayed attached. Smoke-exposed explants kept significantly more fibers than air-exposed explants; at 24 hours the difference was two- to threefold. Cooling to 4 degrees Celsius lowered binding by about 25%, but the smoke effect remained. Adding iron to the fibers increased binding. Treating the fibers with the iron-binding drug deferoxamine reduced binding and completely removed the smoke effect. Antioxidant treatments generally reduced binding more after smoke than after air. The authors concluded that binding is very rapid, that cigarette smoke increases amosite fiber adhesion, and that iron on the fiber appears to play an important role in binding. They noted the results apply only to amosite and probably crocidolite.

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 experiment on rat tracheal tissue in organ culture (explants)
• Who was studied: Tracheal explants (windpipe segments) from 250-g Sprague-Dawley rats; each test group had four or five segments. The work was done at the Department of Pathology, University of British Columbia, Vancouver; no study dates are given.
• Exposure: Explants were exposed for 10 minutes to room air or to cigarette smoke (five 20-ml puffs of whole smoke) in a 2-liter chamber. All were then submerged for 1 hour in a 5 mg/ml suspension of UICC (Union Internationale Centre le Cancer) amosite asbestos in serum-free medium. In some experiments, surface iron on the fibers was changed, oxygen-radical scavengers were added, tissue glutathione (GSH) levels were changed, or exposure was done at 4 degrees C.
• Main results:
  • Smoke-exposed explants had significantly more adherent amosite fibers than air-exposed explants. At 1 hour this held after two or four washes; at 24 hours it held after one, two and four washes.
  • The difference between smoke-exposed and air-exposed explants was more apparent at 24 hours, ranging from two- to threefold.
  • After four washes, the number of bound fibers in air-exposed explants differed very little between 1 hour and 24 hours.
  • Exposure at 4 degrees C reduced binding by about 25% in both air- and smoke-exposed explants, and smoke still increased binding.
  • Loading fibers with iron raised surface iron from 110 plus or minus 6.0 to 250 plus or minus 6.0 micrograms per gram of dust (mean plus or minus SD). It increased adherent fibers by 30% in air-exposed explants and by 42 to 47% in smoke-exposed explants.
  • Treating fibers with the iron chelator deferoxamine decreased bound fibers by approximately 25% in air-exposed explants and approximately 70% in smoke-exposed explants, completely abolishing the smoke effect.
  • Mannitol (a hydroxyl radical scavenger) reduced adhesion by approximately 20% in air-exposed explants and by 20 to 25% in smoke-exposed explants.
  • Catalase had minimal effects in air-exposed explants (a 15% decrease at 24 hours and a 4% increase at 1 hour) and produced a 20 to 25% decrease in smoke-exposed explants.
  • Raising tissue GSH (close to 10-fold) produced less than a 10% decrease in fiber adhesion in air-exposed explants and about a 25% decrease in smoke-exposed explants.
  • Depleting GSH with diethylmaleate lowered GSH to undetectable levels but had no effect on fiber adhesion.
• The authors' conclusion: The authors concluded that amosite binding is a very rapid process that does not require active cellular metabolism, that cigarette smoke increases adhesion of fibers to the epithelial surfaces, and that iron on the asbestos fiber appears to play an important role in binding.
• Limitations the authors state:
  • Defining a 'bound' fiber as one that resists removal by washing may be criticized as arbitrary.
  • Tracheal explants are not a direct model of particle uptake in the alveoli (the air sacs of the lung).
  • The authors cautioned that their conclusions about surface iron and active oxygen species must be viewed with caution.
  • Active oxygen species can only partly explain fiber binding: scavengers and iron chelators never reduced binding below about 75% of control values after air exposure.
  • The results apply only to amosite and probably crocidolite. Whether smoke increases chrysotile binding is not known.
  • It is unclear why lowering cellular GSH did not have the opposite effect to raising it.

Topics

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

Medical terms in this study, explained in our Lexicon: Amosite, Scanning Electron Microscopy (SEM).

Related studies

• Iron enhances uptake of mineral particles and increases lipid peroxidation in tracheal epithelial cells — B. Keeling, K.Y. Li, et al. (1994)
• Effects of cigarette smoke dose and time after smoke exposure on uptake of asbestos fibers by rat tracheal epithelial cells — A. Churg, J. Hobson, et al. (1990)
• Effects of cigarette smoke on epithelial uptake of non-asbestos mineral particles in tracheal organ culture — B. Keeling, J. Hobson, et al. (1993)
• Relationship of fiber surface iron and active oxygen species to expression of procollagen, PDGF-A, and TGF-beta(1) in tracheal explants exposed to amosite asbestos — J. Dai, A. Churg (2001)
• Active oxygen species mediate asbestos fiber uptake by tracheal epithelial cells — J. Hobson, J.L. Wright, et al. (1990)
• Effects of cigarette smoke and asbestos on airway, vascular and mesothelial cell proliferation — H. Sekhon, J. Wright, et al. (1995)

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