Occupational and Environmental Factors Enhancing the Genotoxicity of Asbestos

Our plain-English summary of Occupational and Environmental Factors Enhancing the Genotoxicity of Asbestos, by Q. Rahman, E. Dopp, M. Lohani, et al (Inhalation Toxicology, 2000).

The study

• Authors: Q. Rahman, E. Dopp, M. Lohani, D. Schiffmann
• Journal: Inhalation Toxicology
• Published: 2000;12 Suppl 3:157-65
• Cited by: 7 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Epidemiological and experimental studies have suggested the enhancement of asbestos-induced disease processes by simultaneous exposure to kerosene, its soot, and cigarette smoke in asbestos-exposed animals as well as in humans. To determine the influence of these factors on the genotoxic potential of asbestos, a micronucleus test was performed in Syrian hamster embryo fibroblasts (SHE) and human lymphocytes. To observe the specific chromosomal damages, multicolor fluorescence in situ hybridization (FISH) was done in the lymphocytes from smokers and nonsmokers exposed in vitro to asbestos. Significantly higher numbers of micronuclei were observed in SHE cells after combined treatment with chrysotile and kerosene soot (111 micronuclei/1000 cells) in comparison to chrysotile and kerosene soot separately. Kinetochore staining revealed mainly clastogenic effects in all the cases. In human lymphocytes exposed in cultures to chrysotile and crocidolite the numbers of micronuclei were found higher in smokers than nonsmokers. Multicolor FISH assay suggested that asbestos fibers inflict high damage within 1q12 and in the region between 1cen and 1q12 of chromosome 1. In the exposed population of an asbestos cement factory, the highest genetic damage was found in the blood lymphocytes of exposed smokers. The study suggests that smokers occupationally exposed to asbestos and domestically to kerosene soot are at higher risk for the early development of asbestos-induced diseases.

In plain English

This laboratory study tested whether kerosene soot and cigarette smoking increase the genetic damage caused by asbestos. The authors used the micronucleus test, which counts small extra nuclei that signal chromosome damage, in Syrian hamster embryo cells and human blood cells. They also used a chromosome-labeling method (FISH) on chromosome 1. In hamster cells, combined treatment with chrysotile and kerosene soot produced about double the micronuclei, roughly the sum of what each agent produced alone. The authors reported no additive effect for crocidolite with soot. In volunteers' blood cells exposed in the laboratory to chrysotile and crocidolite, smokers' cells had more micronuclei than nonsmokers' cells. Chromosome 1 breaks rose significantly with asbestos. In blood from asbestos cement factory workers (six smokers, six nonsmokers) and 12 unexposed people, micronuclei per 1000 cells were 76.36 in exposed smokers, 60.52 in exposed nonsmokers, 39.05 in unexposed smokers and 24.90 in controls. The authors concluded that smokers exposed to asbestos at work and to kerosene soot at home are at higher risk for early development of asbestos-induced diseases.

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 experiments in hamster embryo cells and human blood cells, plus a small comparison of blood cells from asbestos cement workers and unexposed people
• Who was studied: Syrian hamster embryo fibroblasts; blood from healthy smoker and nonsmoker volunteers (six per group); blood from six smoking and six nonsmoking asbestos-exposed workers of an asbestos cement factory and six smokers and six nonsmokers not exposed to asbestos, matched for age, sex and socioeconomic conditions
• Exposure: Rhodesian chrysotile (UICC standard), crocidolite, and kerosene soot made by burning kerosene in a pressure stove. Hamster cells received 0.5 and 1.0 micrograms per square centimeter. Human blood cells received 10 and 50 micrograms per milliliter of chrysotile or crocidolite. Cigarette smoking was compared through smokers' versus nonsmokers' cells, and the workers had occupational asbestos exposure.
• Main results:
  • In hamster cells, combined exposure to chrysotile and kerosene soot produced about double the micronuclei.
  • In hamster cells, combined treatment with crocidolite and kerosene soot gave no additive effect (data not shown).
  • Kinetochore staining indicated the micronuclei in hamster cells were mainly clastogenic, meaning they came from chromosome breakage. The share of kinetochore-positive micronuclei was 21.3% for soot, 26.9% for chrysotile and 27.6% for the combination, against 20.1% in controls, each marked nonsignificant.
  • In volunteers' blood cells, untreated cells from smokers had significantly more micronuclei than untreated cells from nonsmokers. After exposure to chrysotile and crocidolite, smokers' cells had more micronuclei than nonsmokers' cells (data not shown).
  • In the FISH assay, breaks and hyperdiploidy in chromosome 1 were slightly higher in smokers' than nonsmokers' untreated cells, but not significantly.
  • Breaks and hyperdiploidy were significantly higher in all asbestos-exposed cells from both nonsmokers and smokers. The largest effect was in smokers' blood exposed to 50 micrograms per milliliter crocidolite: total breaks were 42.12 per 1000 cells, against 33.87 for nonsmokers.
  • In asbestos cement factory workers and unexposed people, micronuclei per 1000 blood cells were 76.36 in exposed smokers, 60.52 in exposed nonsmokers, 39.05 in nonexposed smokers and 24.90 in the control group.
• The authors' conclusion: The authors concluded that smokers exposed to asbestos at work and to kerosene soot at home are at higher risk for early development of asbestos-induced diseases.
• Limitations the authors state:
  • The authors stated that further studies are needed to show a statistically relevant influence of kerosene soot and cigarette smoke on the development of bronchogenic carcinoma (lung cancer) in asbestos-exposed people.
  • The authors stated that the mechanism behind the increased genotoxicity is not yet understood.

Topics

Medical terms in this study, explained in our Lexicon: Genotoxicity, Fibroblast, Damages, Fluorescence In Situ Hybridization (FISH), Micronuclei, Chrysotile, Crocidolite, Asbestos-Cement.

Related studies

• Host and environmental factors enhancing carcinogenesis in the respiratory tract — P. Nettesheim, D.C. Topping, et al. (1981)
• Kerosene soot genotoxicity: enhanced effect upon co-exposure with chrysotile asbestos in Syrian hamster embryo fibroblasts — M. Lohani, E. Dopp, et al. (2000)
• Smoking enhances asbestos-induced genotoxicity, relative involvement of chromosome 1: a study using multicolor FISH with tandem labeling — M. Lohani, E. Dopp, et al. (2002)
• Diallylsulfide attenuates asbestos-induced genotoxicity — M. Lohani, S. Yadav, et al. (2003)
• Occupational and environmental risk factors for idiopathic pulmonary fibrosis in Australia: case-control study — M.J. Abramson, T. Murambadoro, et al. (2020)
• Environmental and occupational risk factors for lung cancer — I. Brüske-Hohlfeld (2009)

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