Kerosene soot genotoxicity: enhanced effect upon co-exposure with chrysotile asbestos in Syrian hamster embryo fibroblasts

Our plain-English summary of Kerosene soot genotoxicity: enhanced effect upon co-exposure with chrysotile asbestos in Syrian hamster embryo fibroblasts, by M. Lohani, E. Dopp, D.G. Weiss, et al (Toxicology Letters, 2000).

The study

• Authors: M. Lohani, E. Dopp, D.G. Weiss, D. Schiffmann, Q. Rahman
• Journal: Toxicology Letters
• Published: 2000;114(1-3):111-6
• Cited by: 9 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Epidemiological and experimental studies have suggested an enhancement of asbestos-induced bronchogenic carcinoma by cigarette smoke. Further, our recent experimental and epidemiological studies have indicated that besides smoking, several other compounds including kerosene soot may accelerate disease processes in asbestos-exposed animals as well as in the humans. Incomplete combustion of kerosene oil generates large volumes of soot, which contains various polycyclic aromatic hydrocarbons and aliphatic compounds. As reported earlier, exposure to kerosene soot is known to cause biochemical and pathological changes in the pulmonary tissue, which may cause cardiopulmonary disorders. In this study we investigated genotoxic effects caused by kerosene soot and chrysotile asbestos as well as co-exposure of kerosene soot and chrysotile using Syrian hamster embryo fibroblasts (SHE). The micronucleus assay revealed a significant increase of induced micronuclei (MN), (P</=0.05) in SHE cells after treatment with kerosene soot (0.5-1.0 microg/cm(2)) for 66 h (36 MN/1000 cells). Combined treatment with chrysotile and soot induced up to 110 MN/1000 cells (chrysotile alone: 80 MN/1000 cells; concentrations: 1 microg/cm(2), exposure times: 66 h). Kinetochore staining revealed mainly clastogenic effects in all cases (soot: 21.3% CRMN(+); chrysotile: 27%; soot+chrysotile: 27.6%; control: 20.8%). This is the first study showing that kerosene soot is not only genotoxic but it can also elevate the genotoxic potential of chrysotile asbestos. This information may be of importance for workers occupationally exposed to asbestos and domestically exposed to kerosene soot.

In plain English

This laboratory study tested whether kerosene soot, chrysotile asbestos, or both cause genetic damage in cultured Syrian hamster embryo fibroblasts. The soot came from burning kerosene in a pressure stove; the asbestos was Rhodesian chrysotile (UICC standard). Cells were checked for micronuclei after 24 to 72 hours with soot, and after 48 or 66 hours with chrysotile or both. Micronuclei are small extra nuclei that reflect chromosome damage or loss of whole chromosomes. Soot alone produced at most 36 micronuclei per 1000 cells (5.0 micrograms per square centimeter, 66 hours). Chrysotile alone produced up to 87 per 1000 cells, about four times the control level of 22. Both together, at 1.0 microgram per square centimeter of each, produced 104 (48 hours) and 111 (66 hours) per 1000 cells, against 21 in untreated cells. In this combined-exposure experiment, the authors reported that the differences between treated and untreated cells were statistically significant. Further staining pointed mainly to chromosome breakage. The authors concluded that kerosene soot is a relatively weak but effective genotoxic agent and that combined exposure had additive effects. These were hamster cells, not people.

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: In vitro laboratory experiment (micronucleus assay with kinetochore staining) in cultured Syrian hamster embryo cells
• Who was studied: Syrian hamster embryo (SHE) fibroblasts isolated from 13-day-old embryos. Each data point was the mean of at least three independent experiments, with 2000 nuclei evaluated in each. The work was done by laboratories in Lucknow, India and Rostock, Germany.
• Exposure: Rhodesian chrysotile (UICC standard) and kerosene soot, made by burning kerosene oil in a pressure stove, each alone and in combination. Doses were 0.5, 1.0, 5.0 and 10.0 micrograms per square centimeter; the scan prints the unit as 'mg/cm2' because the micro sign is misread as 'm'. Soot was tested at 24, 48, 66 and 72 hours. Chrysotile and the combination were tested at 48 and 66 hours.
• Main results:
  • Kerosene soot alone: the maximum number of micronuclei was a mean of 36 per 1000 cells, at 5.0 micrograms per square centimeter after 66 hours of exposure.
  • Kerosene soot alone: at higher concentrations the number of micronuclei decreased, which the authors attributed probably to increased cytotoxicity.
  • Chrysotile alone: the maximum was a mean of 87 micronuclei per 1000 cells, at 5.0 micrograms per square centimeter after 48 hours. This was about four-fold the control level (22 per 1000 cells at 48 hours; 22.5 per 1000 cells at 66 hours).
  • Chrysotile plus soot at 1.0 microgram per square centimeter of each: a mean of 104 micronuclei per 1000 cells at 48 hours and 111 per 1000 cells at 66 hours. This was up to five times untreated controls (21 per 1000 cells). At 0.5 of each, the means were 90 per 1000 cells at 48 hours and 95 per 1000 cells at 66 hours.
  • In the co-exposure experiment, the differences between treated and untreated cells were reported as statistically significant (p less than 0.001) in all cases.
  • Chrysotile alone induced a significantly higher number of micronuclei than kerosene soot at similar concentrations.
  • Kinetochore staining: the percentage of kinetochore-positive micronuclei was not significantly increased after soot exposure (21.3% versus 20.1% in controls). Chrysotile-treated cells showed 26.9% and co-exposed cells 27.6%; the table marks these as not significant. The authors concluded that loss of whole chromosomes is involved, but that mainly clastogenic (chromosome-breaking) events produce the micronuclei.
• The authors' conclusion: The authors concluded that kerosene soot is a relatively weak but effective genotoxic agent that induces micronuclei mainly through clastogenic events. They also concluded that co-exposure of kerosene soot and chrysotile asbestos results in additive genotoxic effects.
• Limitations the authors state:
  • The authors stated that the whole mechanism still needs detailed study.
  • The authors stated that further studies are needed to show a statistically relevant influence of kerosene soot on bronchogenic carcinoma in asbestos-exposed people.

Topics

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

Medical terms in this study, explained in our Lexicon: Genotoxicity, Chrysotile, Fibroblast, Bronchogenic Carcinoma, Micronuclei.

Related studies

• Mineral fibers induce apoptosis in Syrian hamster embryo fibroblasts — E. Dopp, B. Nebe, et al. (1995)
• Effect of kerosene and its soot on the chrysotile-mediated toxicity to the rat alveolar macrophages — J.M. Arif, S.G. Khan, et al. (1997)
• Mitotic disturbances and micronucleus induction in Syrian hamster embryo fibroblast cells caused by asbestos fibers — E. Dopp, J. Saedler, et al. (1995)
• Effect of coexposure to asbestos and kerosene soot on pulmonary drug-metabolizing enzyme system — J.M. Arif, S.G. Khan, et al. (1994)
• In vitro cytotoxicity and transforming potential of industrial carbon dust (fibers and particles) in syrian hamster embryo (SHE) cells — C. Darne, F. Terzetti, et al. (2010)
• Cytotoxicity and multinucleate giant cell formation in Chinese hamster lung fibroblast caused by crocidolite and chrysotile — Y.C. Hong, S.S. Choi (1997)

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