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Coinhibition of viral interferon induction by benzo\[a\]pyrene and chrysotile asbestos

Our plain-English summary of Coinhibition of viral interferon induction by benzo[a]pyrene and chrysotile asbestos, by N. Hahon, J.A. Booth (Environmental Research, 1986).

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The study

Abstract

Benzo[a]pyrene (B[a]P) and its noncarcinogenic analog, benzo[e]pyrene (B[e]P), each in combination with chrysotile, were studied for their inhibitory effects on interferon (IFN) induction by influenza virus in rhesus monkey kidney (LLC-MK2) cell monolayers. B[a]P alone had no adverse effect on IFN induction; however, from 60 to 70% inhibition of IFN production occurred when B[a]P was enzymatically activated by rat liver S9. Chrysotile's inhibitory effect on the IFN process was similar in magnitude to that of activated B[a]P. The combination of activated B[a]P with chrysotile resulted in coinhibition of IFN induction which significantly exceeded (P less than 0.05) the inhibitory activity of the reagents tested alone or in other combinations. B[e]P alone or with S9 neither affected IFN induction nor was it capable of further enhancing chrysotile's inhibition of IFN synthesis. These findings provide further evidence of enhanced deleterious action by the combination of asbestos and activated B[a]P on a biological defense mechanism and further support the discriminatory power and credibility of the inhibition IFN induction assay for evaluating potential carcinogens.

In plain English

This laboratory study used cell cultures, not people. It tested whether chrysotile asbestos and the chemical benzo[a]pyrene (B[a]P) together interfere with interferon, a substance cells make to defend against viruses. Rhesus monkey kidney cells were exposed for 24 hours to chrysotile, to B[a]P, or to a related chemical the authors call noncarcinogenic, benzo[e]pyrene (B[e]P). These were used alone or combined, with or without a rat liver extract (S9) that chemically activates B[a]P. The cells were then stimulated with inactivated influenza virus. B[a]P alone did not reduce interferon production, but B[a]P activated by S9 reduced it by 60 to 70%. Chrysotile alone reduced it by a similar amount. Activated B[a]P plus chrysotile reduced it by 88.0% and 86.9% at the two dose levels tested, significantly more (P less than 0.05) than the agents alone. B[e]P had no appreciable effect and did not add to chrysotile's effect. The authors concluded this was further evidence that asbestos combined with activated B[a]P harms a biological defense mechanism. They said the mechanism was unclear and might be purely additive.

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 (in vitro) cell culture experiment, performed in duplicate
  • Who was studied: Rhesus monkey kidney (LLC-MK2) cell monolayers of about 2 x 10^7 cells per flask, used for interferon induction; human Chang conjunctival cells were used to measure interferon. Work was done at the U.S. Public Health Service Appalachian Laboratory for Occupational Safety and Health and West Virginia University, Morgantown. No people were studied.
  • Exposure: Chrysotile asbestos from the Diablo Range, California (0.1 or 0.5 mg), combined with benzo[a]pyrene or benzo[e]pyrene (0.0039 or 0.039 micromole), with or without rat liver S9 fraction, for 24 hours at 35 degrees C before stimulation with ultraviolet-inactivated influenza virus
  • Main results:
    • B[a]P alone did not reduce interferon production. When B[a]P was activated by S9, interferon production was inhibited by 60 to 70%, depending on the amount (70.2% at 0.039 micromole; 61.3% at 0.0039 micromole).
    • Chrysotile alone, with or without S9, inhibited interferon production by a similar amount (for example 70.5% with 0.5 mg and 65.0% with 0.1 mg, without S9).
    • Activated B[a]P plus chrysotile inhibited interferon production by 88.0% (0.039 micromole B[a]P with 0.5 mg chrysotile) and 86.9% (0.0039 micromole with 0.1 mg). This was significantly greater (P less than 0.05) than the reagents alone or in other combinations.
    • B[e]P, with or without S9, had no appreciable adverse effect on interferon induction. Chrysotile markedly depressed interferon production (77.6% with 0.5 mg alone), but adding B[e]P or S9 did not increase this.
    • In cell viability tests, B[e]P appeared more toxic to cells than B[a]P. Cells tolerated at least ten times more B[a]P (0.039 micromole) than B[e]P (0.0039 micromole).
  • The authors' conclusion: The authors concluded that the findings give further evidence of enhanced harmful action by the combination of asbestos and activated B[a]P on a biological defense mechanism. They also said the findings support the interferon-inhibition test as a way to evaluate potential carcinogens.
  • Limitations the authors state:
    • The authors said the mechanism of the combined effect is not clear, and that it may be a purely additive effect with each agent acting on different targets in the cell.
    • The authors said a lack of information at the host, cellular and molecular levels limits understanding of the interferon system's role in the combined cancer-promoting potential of B[a]P and asbestos.

Topics

Medical terms in this study, explained in our Lexicon: Chrysotile.

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How to cite it

Cite the study

N. Hahon, J.A. Booth. Coinhibition of viral interferon induction by benzo[a]pyrene and chrysotile asbestos. Environmental Research 1986;40(1):103-9. doi:10.1016/s0013-9351(86)80086-x. PMID: 2423322.

Cite our summary

“Coinhibition of viral interferon induction by benzo[a]pyrene and chrysotile asbestos.” AsbestosClaims.Law Library. https://asbestosclaims.law/library/research/coinhibition-of-viral-interferon-induction-by-benzoapyrene-and.

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