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et al. (1996) found that germinal mutations were two times higher at three minisatellite
loci in a human population living around Chernobyl compared to a reference population
living in England. Ellegren et al. (1997) highlighted higher germinal mutations in swal-
lows (
Hirundo
rustica
) whose parents had reproduced in the radionuclide-contaminated
zones of the Chernobyl region compared to reference swallows; they noted higher germi-
nal mutations not only in noncoding regions of the DNA (especially microsatellites) but
also in coding regions such as mutations causing albinism. Herring gulls (
Larus argentatus
)
nesting near steel mills on the Great Lakes were shown to have higher germline muta-
tion rates at minisatellite DNA loci than those at rural sites (Yauk and Quinn 1996), and
mutation frequency increased with colony proximity to integrated steel mills (Yauk et al.
2000). The authors postulated that inhaled airborne contaminants emitted from steel mills,
such as polycyclic aromatic compounds, were largely responsible for mutation induction
(Yauk et al. 2000). To address this issue, mice were exposed
in situ
to ambient air in a pol-
luted industrial area near steel mills. Heritable mutation frequency at tandem-repeat DNA
loci in mice exposed 1 km downwind from two integrated steel mills was 1.5- to 2-fold
elevated compared with those at a reference site 30 km away (Somers et al. 2002).
14.4.1.2 Indirect Effects
Indirect effects of pollutants on genomes may be due to:
• A massive reduction of the size of the population due to mortality
• A selection of alleles or genotypes associated with “tolerance” in contaminated
areas and an elimination of the most “sensitive” genotypes
Only a few studies have highlighted the existence of genetic erosion due to a massive
reduction of the size of populations in contaminated sites. For example, Demarais et al.
(1993) concluded that the modifications of genetic structure of populations of the fresh-
water fish (
Gila
seminuda
) observed after an acute accidental exposure to the insecticide
rotenone, were probably due to a genetic bottleneck caused by a high mortality. Murdoch
and Herbert (1994) suggested the same hypothesis to explain the weak mitochondrial
genetic diversity observed in populations of catfish (
Ameiurus nebulosus
) from contami-
nated sites. Facemire et al. (1995) have also hypothesized that the mixture of contaminants
[mercury, polychlorobiphenyls (PCBs), etc.] occurring in Florida induced mortalities in
Florida panther
Puma concolor
populations, leading to a loss of genetic diversity in these
populations. In a more recent study, Matson et al. (2006) observed a general reduction of
the haplotype and nucleotide diversities in marsh frog (
Rana ridibunda)
populations in the
highly contaminated industrial sector of Sumgayit, Azerbaijan, compared to uncontami-
nated reference sites.
Numerous studies have been conducted over the last three decades trying to identify
associations or correlations between the level of contaminant exposure and genotypic
and/or allelic frequency variations. The first studies deal essentially with allozyme mark-
ers and field populations, considering simple contamination, with metals (Nevo et al.
1984), radionuclides (Gillepsie and Guttman 1989), and pesticides (Tanguy et al. 1999). For
example, Gillepsie and Guttman (1989) detected significant changes in allelic frequencies
at the PGM (phosphoglucomutase) locus between fish populations (
Campostoma anomalum
)
from upstream sites (less contaminated) and fish from downstream sites (with high radio-
nuclide concentrations). These changes occurred within 500 meters from the original site
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