Genetic ecotoxicology of asbestos pollution in the house mouse Mus musculus domesticus

Our plain-English summary of Genetic ecotoxicology of asbestos pollution in the house mouse Mus musculus domesticus, by R. Ben-Shlomo, U. Shanas (Environmental Science and Pollution Research International, 2011).

The study

• Authors: R. Ben-Shlomo, U. Shanas
• Journal: Environmental Science and Pollution Research International
• Published: 2011;18(8):1264-9
• Cited by: 5 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Purpose: We tested the genetic diversity in wild mice (Mus musculus domesticus) inhabiting the asbestos-polluted area as a model for the long-term mutagenic effect of asbestos. Hazardous effects of deposited asbestos persist in the environment because of low rate of fiber disintegration. The upper layers of the soil in the vicinity of a former asbestos factory are nearly "saturated" with asbestos fibers and dust. Natural populations of mice dwell in this area and are constantly exposed to asbestos fibers.

Methods: We measured the microsatellites genetic diversity of wild mice (Mus musculus domesticus) inhabiting the asbestos-polluted area as a model for the long-term mutagenic effect of this environmental toxin.

Results: The six tested microsatellites were highly polymorphic, revealing 111 different alleles for the two sampled populations. Effective number of alleles was slightly higher in the polluted population relative to the control population, while observed heterozygosity was lower. The chromatographic profile of the polluted population exhibited a significantly higher number of bands, probably resulting from somatic mutations, in addition to the ordinary microsatellite band profiles.

Conclusions: Long-term exposure to asbestos fibers significantly elevates the level of somatic mutations. It also leads to a relatively high level of observed homozygosity, a phenomenon that may be associated with loss of heterozygosity. Based on the mice population, our data suggest elevated health risks for humans living in an asbestos-polluted area.

In plain English

This study compared the genetics of two groups of wild house mice in northern Israel. The authors trapped 24 mice within 250 m of a former asbestos factory in Nahariya, which operated from 1952 to 1997, and 68 mice at an agricultural site in Tivon, 50 km away, where no asbestos had been reported. An earlier survey cited by the authors found soil near the factory containing up to 35% crocidolite and 25% chrysotile. The authors analysed six DNA markers called microsatellites from tail, toe or ear tissue. Mice from the polluted site had lower observed heterozygosity than control mice (0.63 versus 0.72, p=0.043) and a higher inbreeding value (0.255 versus 0.146). The authors also counted extra DNA bands, which they considered probably the result of somatic mutations. These bands were significantly more frequent in the polluted group for four of the six markers. Twenty-two of 24 polluted-site mice showed them, compared with 37 of 68 control mice. The authors concluded that long-term asbestos exposure significantly elevates somatic mutations, and suggested elevated health risks for humans living in asbestos-polluted areas.

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: Field study comparing the population genetics (microsatellite DNA markers) of wild mice from an asbestos-polluted site and an unpolluted control site
• Who was studied: Wild house mice (Mus musculus domesticus) in northern Israel: 24 trapped in Nahariya within 250 m of a former asbestos factory, and 68 trapped in Tivon, an agricultural site with no reported asbestos. The mice were released after a small tissue sample was taken.
• Exposure: Environmental asbestos in soil near the former 'Isasbest/Eitanit' factory, which operated 1952 to 1997. An earlier 2002 survey cited by the authors (not measured in this study) found the soil there contained up to 35% crocidolite and 25% chrysotile. The authors describe exposure as mostly by ingestion but also by inhalation.
• Main results:
  • The effective number of alleles was slightly but not significantly higher in the polluted population (p=0.152). Observed heterozygosity was lower in the polluted population (p=0.043).
  • Observed heterozygosity was 0.63 in the polluted population and 0.72 in the control population.
  • The fixation index, which the authors read as a higher level of inbreeding, was 0.255 in the polluted population and 0.146 in the control population (p=0.049).
  • 90% of genetic variance was within populations and 10% was between the two populations.
  • The polluted population had significantly more extra bands, interpreted as probable somatic mutations, in four of the six microsatellites tested.
  • There were 92 extra bands among the 24 polluted-area mice and 85 extra bands among the 68 unpolluted-area mice.
  • 22 of 24 polluted-area mice (more than 90%) and 37 of 68 unpolluted-area mice (less than 55%) showed extra bands in at least one locus.
• The authors' conclusion: The authors concluded that long-term exposure to asbestos fibers significantly elevates the level of somatic mutations and leads to relatively high observed homozygosity, which may be associated with loss of heterozygosity. Based on the mice, they suggested elevated health risks for humans living in an asbestos-polluted area.
• Limitations the authors state:
  • The authors stated that the possible link between the low observed heterozygosity and loss of heterozygosity caused by asbestos, and whether it is causal, needs further testing.

Topics

Medical terms in this study, explained in our Lexicon: Somatic Mutation.

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