Effects of cigarette smoke dose and time after smoke exposure on uptake of asbestos fibers by rat tracheal epithelial cells

Our plain-English summary of Effects of cigarette smoke dose and time after smoke exposure on uptake of asbestos fibers by rat tracheal epithelial cells, by A. Churg, J. Hobson, J. Wright (American Journal of Respiratory Cell and Molecular Biology, 1990).

The study

• Authors: A. Churg, J. Hobson, J. Wright
• Journal: American Journal of Respiratory Cell and Molecular Biology
• Published: 1990;3(3):265-9
• Cited by: 10 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

We have previously shown that exposure of excised rat tracheal segments to cigarette smoke followed by exposure to a solution of amosite asbestos increases uptake of asbestos fibers compared to exposure to air followed by asbestos. To learn more about the mechanism of smoke-enhanced fiber uptake, we evaluated the effects of amount of smoke and time delay between smoke exposure and asbestos exposure on fiber penetration into the epithelium. To determine whether amount of smoke exposure affected this process, we exposed tracheal segments to 1, 3, or 6 puffs of smoke and subsequently to 5 mg/ml amosite asbestos for 1 h. The segments were then maintained in organ culture for up to 7 d. Asbestos uptake was evaluated by counting fibers in the epithelium by light microscopy. Exposure to increasing numbers of puffs of smoke produced a dose-related increase in fiber uptake at 1 d, 3 d, and 7 d after exposure. To determine whether asbestos exposure needed to occur immediately after smoke exposure for enhanced uptake of fibers to occur, we exposed tracheal segments to 6 puffs of smoke and then delayed exposure to asbestos for 0 (immediate exposure), 3, 18, or 48 h. Tracheas were again maintained in organ culture for up to 7 d after asbestos exposure. Delayed exposure to asbestos after 6 puffs of smoke produced an increase in fiber uptake, even with an interval as long as 48 h between smoke and asbestos exposure; however, the absolute magnitude of fiber uptake was less than that seen with immediate postsmoke asbestos exposure. If catalase was added to the asbestos solution, the smoke-enhanced uptake was abolished, no matter what the time delay.(ABSTRACT TRUNCATED AT 250 WORDS)

In plain English

This laboratory experiment used small pieces of windpipe (trachea) from male Sprague-Dawley rats, kept alive in culture. The pieces were exposed to smoke from 1, 3 or 6 puffs of a nonfilter cigarette, or to air, then to amosite asbestos. After 1, 3 and 7 days, the authors counted fibers inside the lining cells, sticking out of them into the airway, or lying just beneath the lining. One puff had no effect on fiber uptake, while 3 and 6 puffs increased it. The two higher doses had the same effect at 1 and 3 days; 6 puffs had a significantly greater effect at 7 days. When asbestos exposure was delayed 3, 18 or 48 hours after 6 puffs, smoke still increased uptake at most time points. However, uptake was lower than with immediate exposure, significantly so at 1 and 3 days. Catalase, an enzyme, added to the asbestos at the 18- and 48-hour delays, abolished the smoke effect. Boiled catalase did not. The authors concluded that a single smoke exposure leaves the cells "primed" for increased fiber uptake long after the exposure ends.

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 using tracheal segments from rats kept in organ culture (explants)
• Who was studied: Tracheal segments, each about 2 by 2 mm, from 200-g male Sprague-Dawley rats, studied at the University of British Columbia, Vancouver. At each time point, 6 to 9 segments per test group were examined. The number of rats is not stated.
• Exposure: Whole smoke of 1, 3 or 6 puffs (20 ml each, one per minute, 10 minutes total) from a commercial nonfilter cigarette, or air (sham smoking). This was followed by amosite asbestos at 5 mg/ml for 1 hour, given either immediately or after delays of 3, 18 or 48 hours. In some groups, catalase (1,300 U/ml) or boiled catalase was added to the asbestos.
• Main results:
  • Fiber uptake was measured by counting fibers (longer than 4 micrometres, by light microscopy) that were completely inside epithelial cells, sticking out of epithelial cells into the airway, or lying beneath the epithelial basement membrane. Counts were expressed per millimetre of epithelium.
  • In segments exposed to smoke immediately before asbestos, 1 puff had no effect on fiber uptake, while 3 and 6 puffs increased uptake.
  • At 1 and 3 days of culture, 3 and 6 puffs produced the same enhancement of uptake. At 7 days, 6 puffs produced a significantly greater effect than 3 puffs.
  • With no delay between 6 puffs of smoke and asbestos, uptake was significantly enhanced compared with asbestos alone after 3 and 7 days of culture.
  • With delays of 3, 18 or 48 hours between smoke and asbestos, smoke still significantly increased uptake compared with asbestos alone for most culture periods.
  • Segments with a 3-, 18- or 48-hour delay took up significantly fewer fibers than segments exposed to asbestos immediately after smoke, at 1 and 3 days of culture (reported as P less than 0.01 or greater).
  • At 7 days of culture, the lower uptake in delayed groups was still present but not always statistically significant. The size of the decrease did not appear to correlate with the length of the delay.
  • With 18- and 48-hour delays after 6 puffs, adding catalase to the asbestos solution abolished the smoke-related increase in uptake.
  • Boiled catalase did not have this protective effect.
• The authors' conclusion: The authors concluded that the smoke-related increase in fiber uptake depends on the amount of smoke. They also concluded that a single smoke exposure produces a persistent change in the cells, leaving them "primed" for increased fiber uptake long after smoke exposure ends.
• Limitations the authors state:
  • Only fibers longer than 4 micrometres were counted by light microscopy. The authors state this was for convenience and was not meant to imply that short fibers play no role.
  • The authors had not formally studied whether the effects seen in isolated tracheal segments apply to intact animals and humans. They mention only a few unpublished observations in rats.
  • The authors state it remains to be determined whether smoke makes more fibers stick to the cell surface, increases the rate at which stuck fibers penetrate, or both.
  • 48 hours was the longest delay between smoke and asbestos exposure that was tested.

Topics

Medical terms in this study, explained in our Lexicon: Amosite, Asbestos Exposure, Epithelium.

Related studies

• Effects of cigarette smoke on epithelial uptake of non-asbestos mineral particles in tracheal organ culture — B. Keeling, J. Hobson, et al. (1993)
• Cigarette smoke increases amosite asbestos fiber binding to the surface of tracheal epithelial cells — A. Churg, J. Sun, et al. (1998)
• Active oxygen species mediate asbestos fiber uptake by tracheal epithelial cells — J. Hobson, J.L. Wright, et al. (1990)
• Scavengers of active oxygen species prevent cigarette smoke-induced asbestos fiber penetration in rat tracheal explants — A. Churg, J. Hobson, et al. (1989)
• Iron enhances uptake of mineral particles and increases lipid peroxidation in tracheal epithelial cells — B. Keeling, K.Y. Li, et al. (1994)
• Effects of crocidolite and chrysotile asbestos on cellular uptake and metabolism of benzo(a)pyrene in hamster tracheal epithelial cells — B.T. Mossman, A. Eastman, et al. (1983)

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