Increased incidence of DNA double-strand breaks and anti-ds DNA antibodies in blood of workers occupationally exposed to asbestos

Our plain-English summary of Increased incidence of DNA double-strand breaks and anti-ds DNA antibodies in blood of workers occupationally exposed to asbestos, by B. Marczynski, A.B. Czuppon, W. Marek, et al (Human & Experimental Toxicology, 1994).

The study

• Authors: B. Marczynski, A.B. Czuppon, W. Marek, G. Reichel, X. Baur
• Journal: Human & Experimental Toxicology
• Published: 1994;13(1):3-9
• Cited by: 26 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Asbestos, proven to be carcinogenic in humans and animals, is reported to have no genotoxic effect. Asbestos workers have an increased risk of lung cancer, mesothelioma, and other tumours. Earlier findings showed that crocidolite can induce DNA strand breaks in cultured rat embryo cells as assessed by nick translation. We investigated DNA double-strand breaks in white blood cells (WBC) of ten workers occupationally exposed to asbestos. According to our results, obtained with neutral filter elution, individuals who had been exposed to asbestos fibres showed two to four times more DNA double-strand breaks (dsb) in white blood cells than ten non-exposed persons. The induced DNA fragments are of about 250 kb (compared to chromosomal DNA of Saccharomyces cerevisiae standard marker). Using additionally the chromosomal DNA protective method of agarose-plugs, DNA fragments in the range of 200 to 1000 kb have been found in the white blood cells of the same ten workers occupationally exposed to asbestos. In the white blood cells of non-exposed subjects no DNA fragments could be detected with this method. Compared to 51 non-exposed persons, elevated anti-ds DNA antibody concentrations were found in ten workers occupationally exposed to asbestos. The fact that workers occupationally exposed to asbestos have distinctly more double-strand breaks and anti-ds DNA antibodies could mean that an increased incidence of DNA-fragments may be an important indicator in the chronic effect of asbestos-associated carcinogenesis. Apparently, the chronic effects of asbestos observed here do not seem to be identical with that of previously reported acute in vitro effects.

In plain English

This laboratory study, from a research institute in Bochum, Germany, looked for DNA damage in the white blood cells of ten workers occupationally exposed to mixed asbestos fibres. They were compared with ten healthy men never exposed to asbestos at work. Four of the workers and seven of the controls were smokers, and two workers had also been exposed to coal dust. The authors reported that the workers' white blood cells had two to four times more DNA double-strand breaks than the controls' (26-46% versus under 10%). With a second method, the workers' DNA showed fragments of 200 to 1000 kb, while control samples showed a single peak indicating more intact DNA. Antibodies against double-stranded DNA averaged 140 U/ml in the ten workers and 64 U/ml in 51 unexposed men, a statistically significant difference (p less than 0.05). Neither measure was statistically correlated with how long workers had been exposed. The authors concluded that occupational asbestos exposure could be associated with white blood cell DNA damage. They said it was unclear whether the damage came directly from asbestos in the lung or from impaired blood-cell formation.

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 comparison of blood samples from asbestos-exposed workers and non-exposed controls. DNA double-strand breaks were measured by neutral filter elution and pulsed-field gel electrophoresis, and anti-double-stranded DNA antibodies by enzyme-linked immunosorbent assay.
• Who was studied: Ten workers occupationally exposed to asbestos fibres (four smokers) and ten healthy male volunteers never occupationally exposed to asbestos. Serum from a further 41 healthy unexposed male volunteers was also analysed for antibodies; the antibody comparison was against 51 non-exposed men. The authors are based at a research institute in Bochum, Germany. Dates of sampling are not given.
• Exposure: Occupational exposure to mixed asbestos fibres. The authors assumed all had been exposed to both serpentine and amphibole asbestos. Two workers (no. 4 and 7) had also been exposed to coal dust. No doses or job titles are given in the text.
• Main results:
  • Measured by filter elution and densitometry, the ten exposed workers' white blood cells had two to four times more DNA double-strand breaks than those of the unexposed controls.
  • The percentage of DNA double-strand breaks was 26-46% in the exposed workers and less than 10% in the controls.
  • DNA fragments released by filter elution were about 250 kb in size.
  • Using the agarose-plug method, the exposed workers' DNA showed fragments between 200 and 1000 kb from multiple double-strand breaks at random sites.
  • In the healthy volunteers shown, the agarose-plug method gave only one peak, which the authors read as more intact DNA.
  • The mean anti-double-stranded DNA antibody concentration in the 51 unexposed men was 64 U/ml.
  • The ten exposed workers had a significantly higher mean anti-double-stranded DNA antibody concentration, 140 U/ml, than the 51 non-exposed controls (p less than 0.05, t-test and Kruskal-Wallis test).
  • There was no statistical correlation between duration of asbestos exposure and either the percentage of double-strand breaks or antibody concentration.
• The authors' conclusion: The authors concluded that occupational asbestos exposure could be associated with white blood cell DNA damage. They also concluded that the increased incidence of DNA fragments can be an indicator of a chronic effect of asbestos-associated carcinogenesis.
• Limitations the authors state:
  • The authors said it was unclear whether the DNA damage was directly due to chronic exposure to asbestos fibres in the lung or to impaired blood-cell formation (haemopoiesis).
  • The authors noted that handling the DNA (ultrafiltration) could itself cause additional breaks.
  • The authors said the finding should be further studied with regard to smoking, alcohol consumption, X-ray examinations and medications.

Topics

Medical terms in this study, explained in our Lexicon: Carcinogenic, Lung Cancer, Mesothelioma, Crocidolite, Carcinogenesis.

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• DNA double-strand breaks by asbestos, silica, and titanium dioxide: possible biomarker of carcinogenic potential? — Z. Msiska, M. Pacurari, et al. (2010)
• Asbestos causes DNA strand breaks in cultured pulmonary epithelial cells: role of iron-catalyzed free radicals — D.W. Kamp, V.A. Israbian, et al. (1995)
• Modulation of DNA single-strand breaks by intracellular glutathione in human lung cells exposed to asbestos fibers — A. Puhakka, T. Ollikainen, et al. (2002)
• Iron mobilization from crocidolite asbestos greatly enhances crocidolite-dependent formation of DNA single-strand breaks in phi X174 RFI DNA — L.G. Lund, A.E. Aust (1992)

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