Genotoxic effects of asbestos in humans

Our plain-English summary of Genotoxic effects of asbestos in humans, by M. Dusinská, A. Collins, A. Kazimírová, et al (Mutation Research, 2004).

The study

• Authors: M. Dusinská, A. Collins, A. Kazimírová, M. Barancoková, V. Harrington, K. Volkovová, M. Staruchová, A. Horská, L. Wsólová, A. Kocan, J. Petrík, M. Machata, B. Ratcliffe, S. Kyrtopoulos
• Journal: Mutation Research
• Published: 2004;553(1-2):91-102
• Cited by: 87 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Risks of carcinogenic and non-carcinogenic effects from asbestos continue owing to the persistence of the fibres in building materials and other products. For this reason, epidemiological and mechanistic research on the toxic effects of asbestos and mineral fibres is still needed. The present molecular epidemiological study was conducted in a former asbestos cement plant in Slovakia. Altogether 82 subjects were investigated, 61 exposed subjects (24 smokers and 37 non-smokers), and 21 factory controls (8 smokers and 13 non-smokers). Workers were exposed to asbestos for between 5 and 40 years. Though the exposure to asbestos during past 40 years was relatively high, at the time of sampling the concentrations of asbestos in the production hall exceeded the Slovak occupational limit (0.001 fibre/cm3) by a factor of only 3-5. The office area levels were below this limit. Biomarkers of exposure, effect and individual susceptibility were measured, including DNA damage (strand breaks [SBs], base oxidation and alkylation, using the comet assay); cytogenetic parameters; and individual DNA repair capacity (incision at 8-oxoguanine measured using a modified comet assay). Oxidised pyrimidines were significantly higher in exposed men compared with non-exposed (P = 0.04). There was also a positive association between SBs (P = 0.04) and age, and alkylation damage to DNA (P = 0.04) and age. Moreover, oxidised pyrimidines (P = 0.01) and alkylated bases (P = 0.001) strongly correlated with years of occupational exposure. Micronucleus frequency did not differ between exposed and control subjects. Repair capacity overall did not show any effect of exposure, though female controls had higher incision rates than did female exposed subjects. However, exposed asbestos workers had significantly higher numbers of chromosomal aberrations (P = 0.01) compared with control group. This finding is consistent with the known association of chromosome aberrations with cancer-risk.

In plain English

This molecular epidemiological study examined blood cells from workers at a former asbestos cement plant in Nitra, Slovakia. Samples were taken in September 2000, after asbestos production had stopped at the end of 1999. The study included 61 workers exposed to asbestos for 5 to 40 years and 21 factory controls. Past fibre levels were much higher than at sampling, when levels in the production hall were 3 to 5 times the Slovak limit of 0.001 fibre/cm3. The authors wrote that their hypothesis of increased oxidative DNA damage in lymphocytes received little support. Exposed men had more oxidised pyrimidines, a type of DNA damage, than control men (P = 0.04). In men, this damage and alkylation damage rose with years of exposure. Overall, DNA repair capacity and micronucleus frequency did not differ between exposed workers and controls. Cells with chromosome aberrations were about twice as common in exposed workers (P = 0.01), and among exposed workers they were more common in smokers. The authors concluded that this finding is consistent with the known link between chromosome aberrations and cancer risk.

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: Molecular epidemiological study comparing biomarkers in asbestos-exposed workers and factory controls
• Who was studied: 82 people from a former asbestos cement plant in Nitra, Slovakia, sampled in September 2000: 61 exposed workers (24 smokers, 37 non-smokers) and 21 factory controls (8 smokers, 13 non-smokers)
• Exposure: Occupational asbestos exposure in production of asbestos-based building materials, lasting 5 to 40 years. The article does not specify fibre types. At sampling, production-hall levels were 3 to 5 times the Slovak limit of 0.001 fibre/cm3; past levels were much higher (for example 2 to 11 fibre/cm3 in 1978 to 1990).
• Main results:
  • The authors reported that their hypothesis of increased oxidative DNA damage in lymphocytes from asbestos exposure received little support.
  • Oxidised pyrimidines (endonuclease III-sensitive sites) were higher in exposed men (116 ± 9, n = 42) than in control men (77 ± 14, n = 11), P = 0.04.
  • Exposed non-smokers had higher DNA strand break levels than control non-smokers.
  • Alkylation damage (AlkA-sensitive sites) was significantly lower in exposed smokers than in control smokers.
  • In men, oxidised pyrimidines correlated with duration of exposure (r = 0.383, P = 0.01, n = 42).
  • In men, alkylated bases correlated with duration of exposure (r = 0.495, P = 0.001, n = 43).
  • DNA strand breaks and alkylation sites correlated positively with age, but only in men.
  • Overall, DNA repair capacity showed no effect of exposure, but female controls had higher incision rates than exposed women.
  • Micronucleus frequency did not differ between exposed and control subjects.
  • Exposed workers had significantly more chromosomal aberrations than controls (P = 0.01); the percentage of aberrant cells was about twice as high in exposed workers.
  • Within the exposed group, smokers had more chromosome aberrations than non-smokers. Multivariate analysis showed no interaction between smoking and exposure.
• The authors' conclusion: The authors concluded that chromosome aberrations were elevated in asbestos-exposed workers, especially smokers, and that this is consistent with the known association of chromosome aberrations with cancer risk.
• Limitations the authors state:
  • The authors noted that the lack of a repair-capacity effect may reflect the time elapsed since the last asbestos exposure.
  • The authors stated that the alkylation damage findings by smoking status were difficult to explain.

Topics

Medical terms in this study, explained in our Lexicon: Carcinogenic, Asbestos-Cement, Biomarker, Comet Assay, Occupational Exposure.

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• Validity of the Lymphocyte Cytokinesis-Block Micronucleus Assay (L-CBMN) as biomarker for human exposure to chemicals with different modes of action: A synthesis of systematic reviews — M. Kirsch-Volders, M. Fenech, et al. (2018)
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