Brief inhalation of asbestos compromises superoxide production in cells from bronchoalveolar lavage

Our plain-English summary of Brief inhalation of asbestos compromises superoxide production in cells from bronchoalveolar lavage, by J.M. Petruska, J. Marsh, M. Bergeron, et al (American Journal of Respiratory Cell and Molecular Biology, 1990).

The study

• Authors: J.M. Petruska, J. Marsh, M. Bergeron, B.T. Mossman
• Journal: American Journal of Respiratory Cell and Molecular Biology
• Published: 1990;2(2):129-36
• Cited by: 28 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Production of superoxide (O-.2) was measured in alveolar macrophages (AM) exposed to asbestos in vitro and in cells obtained from bronchoalveolar lavage (BAL) of rats inhaling asbestos. Steady state levels of O-.2 released by AM in vitro were dose and time dependent in response to crocidolite, chrysotile, and opsonized zymosan, a particulate used to trigger O-.2 generation. In contrast, an inhalation exposure for 1 h to crocidolite or for 6 days to either crocidolite or chrysotile asbestos resulted in a decreased production of O-.2 by BAL cells. Likewise, BAL cells from rats inhaling chrysotile for 1 h or crocidolite for 9 days exhibited a diminished capacity to secrete O-.2 when challenged with the particulate opsonized zymosan. Diminished generation of O-.2 by asbestos occurred in BAL cell populations containing either significantly increased numbers of polymorphonuclear leukocytes and lymphocytes (6- and 9-day exposures) or 99% AM (1-h exposure). Thus, these novel observations suggest that short-term inhalation of asbestos compromises the ability of BAL cells to produce O-.2 in the presence or absence of an additional phagocytic stimulus.

In plain English

This laboratory study in rats and cultured cells measured superoxide, a reactive form of oxygen released by lung defense cells. First, the authors exposed alveolar macrophages from unexposed rats to crocidolite or chrysotile asbestos in culture dishes. Superoxide release rose with dose and time. Asbestos added before a yeast-particle stimulus (opsonized zymosan) did not significantly change the cells' response. Second, young male Fischer 344 rats breathed crocidolite or chrysotile dust 6 hours a day, 5 days a week; lung-wash cells were collected after 1 hour and 1, 3, 6 and 9 days. Compared with sham-exposed rats, baseline superoxide was lower after 1 hour of crocidolite and after 6 days of either fiber. It was unchanged at other times. With the zymosan stimulus, superoxide was lower after 1 hour of chrysotile and after 9 days of crocidolite. From day 1 the lung cells shifted toward more polymorphonuclear leukocytes, and from day 3 toward more lymphocytes. The authors concluded that brief asbestos inhalation compromises superoxide release by these cells, which may have implications for occupationally exposed people. They noted that the exposure was brief.

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: cell-culture (in vitro) study of rat alveolar macrophages plus an animal inhalation experiment with sham-exposed controls
• Who was studied: Male Fischer 344 rats, 8 to 9 weeks old, studied at the University of Vermont. Lung-wash (bronchoalveolar lavage) cells were taken from asbestos-exposed and sham-exposed rats. Alveolar macrophages from control rats were used for the dish experiments. The total number of rats is not stated; group sizes in the inhalation superoxide experiments were n = 2 to 9. Study dates are not given.
• Exposure: Dish experiments used UICC reference crocidolite and Rhodesian chrysotile. The doses chosen for further work were 10 micrograms per square centimeter of crocidolite and 3 micrograms per square centimeter of chrysotile. Inhalation experiments used N.I.E.H.S. crocidolite or chrysotile at about 10 mg per cubic meter of air, 6 hours a day, 5 days a week. Rats were sampled at 1 hour and at 1, 3, 6 and 9 days. Opsonized zymosan (yeast particles) was used as an additional stimulus.
• Main results:
  • In dishes, rat alveolar macrophages exposed to crocidolite, chrysotile or opsonized zymosan showed dose- and time-dependent increases in superoxide production. The increases were more striking with zymosan than with either type of asbestos.
  • In dishes, macrophages exposed to chrysotile or crocidolite before opsonized zymosan showed no significant differences in superoxide generation compared with cells not exposed to asbestos.
  • In rats, baseline superoxide production by lung-wash cells was lower than in sham controls after a 1-hour crocidolite exposure and after a 6-day exposure to either crocidolite or chrysotile.
  • At all other time points, inhalation of asbestos produced no change in baseline superoxide release compared with sham controls.
  • When stimulated with opsonized zymosan, lung-wash cells from rats exposed to chrysotile for 1 hour or crocidolite for 9 days produced significantly less superoxide than cells from sham controls (p less than 0.05).
  • Total numbers of cells recovered by lung wash did not differ significantly among sham, crocidolite-exposed and chrysotile-exposed rats.
  • After 1 day of exposure to either type of asbestos, the percentage of alveolar macrophages fell and the percentage of polymorphonuclear leukocytes rose. Lymphocyte percentages increased significantly after 3 days and remained elevated. The authors report that the changes were more pronounced with crocidolite than with chrysotile.
  • The lowered superoxide occurred both when lung-wash cells were about 99% alveolar macrophages (1-hour exposure) and when they included 10 to 20% polymorphonuclear leukocytes and 2 to 3% lymphocytes (6-day exposure).
• The authors' conclusion: The authors concluded that a brief inhalation of asbestos compromises superoxide release by lung-wash cells. They suggested this may have health-related implications for people occupationally exposed to asbestos who are later challenged with other particles.
• Limitations the authors state:
  • The fiber samples used in the dish experiments (UICC) and in the inhalation experiments (N.I.E.H.S.) are chemically similar, but their size distributions may differ.
  • Adding asbestos to cells in dishes probably gives a higher fiber-to-cell ratio than inhalation does.
  • The duration of asbestos exposure in this study was brief.

Topics

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

Medical terms in this study, explained in our Lexicon: Superoxide, Bronchoalveolar Lavage (BAL), Alveolar Macrophage, Crocidolite, Chrysotile.

Related studies

• Asbestos effects on superoxide production. An in vitro study of hamster alveolar macrophages — B.W. Case, M.P. Ip, et al. (1986)
• Enhanced lipid peroxidation in lung lavage of rats after inhalation of asbestos — J.M. Petruska, K.O. Leslie, et al. (1991)
• IgG specifically enhances chrysotile asbestos-stimulated superoxide anion production by the alveolar macrophage — R.K. Scheule, A. Holian (1989)
• Detection of lipid peroxidation in lung and in bronchoalveolar lavage cells and fluid — J.M. Petruska, S.H. Wong, et al. (1990)
• The effects of chrysotile and crocidolite asbestos on the lower respiratory tract: analysis of bronchoalveolar lavage constituents — E. Kagan, Y. Oghiso, et al. (1983)
• Dehydroepiandrosterone inhibits the spontaneous release of superoxide radical by alveolar macrophages in vitro in asbestosis — W.N. Rom, T. Harkin (1991)

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