Biology Reference
In-Depth Information
This guideline of 1000 μg kg -1 dry weight (1000 ng g -1 dry weight) did not incorporate a
safety factor to account for uncertainty in this threshold estimate, as risk analyses often do.
It was a practical value for management decisions that should be protective of estuarine
fish populations and workable from the perspective of sediment remediation and manage-
ment (Johnson et al. 2002).
It would be worth developing a similar approach to protect invertebrates and consum-
ers at higher levels in the food chain. Indeed, invertebrates bioaccumulate pollutants that
may be transferred to their predators via the food chain. After the Erika oil spill (13.2.1),
high levels of PAHs in soft tissues of marine mussels were measured, and a threshold of
total PAHs in seafood had to be defined to protect human health. Lemière et al. (2005b)
showed that ingestion by mammals of mussels contaminated with the Erika oil induced
DNA damage in their hepatocytes, blood cells, and bone marrow. The authors established
that a threshold level of BaP toxic equivalents in food, i.e., mussel tissues, is in the range
of 6-34 μg kg -1 d.w., which would not induce any DNA damage and be safe to consumers.
13.5 Conclusions
Links between genotoxicity at the level of the individual and population effects have
been established retrospectively in several cases and in some situations of severe stress.
It would be useful if future studies explored genomic changes associated not only with
contaminant exposure, but also with tolerance and adaptation (Chapter 14). There is a real
need for integrated studies to better understand mechanisms developed at the population
level, for species to survive and reproduce in unsafe environments, in the field, and over
several generations. Stress conditions that are not too stringent would be worth studying
in order to help determine pollution thresholds that can be accepted in the long term and
be compatible with individual/population fitness.
The present review has shown that several assays are efficient tools to detect genotoxic
impacts in exposed species in situ . In some cases, genotoxicity in somatic cells could be
associated with embryo mortality, decreased viability, and reproduction impairment.
Measuring genotoxicity in early life stages and juveniles may be envisaged to link more
closely genotoxicity in individuals and population dynamics. The comet assay would be
a useful tool to investigate genotoxicity in juveniles, with careful interpretation of the
responses and time-course studies of repair efficiency.
Bearing in mind that the gametes of a number of invertebrates are emitted into the sur-
rounding water and that larvae are in direct contact with pollutants in contaminated envi-
ronments, these critical life stages would be worth studying as targets for genotoxic aquatic
pollutants. Prospects for research on gametes have emerged recently. The significance of such
studies in an ecological perspective is obvious, provided they mimic conditions of exposure
representative of the environment. In invertebrates and vertebrates, it would be worth analyz-
ing the sensitivities of gametes and zygotes at environmental concentrations of contaminants.
In the case of LMW PAHs, it has been demonstrated that exposure at low concentrations
to these congeners may induce cardiac and skeleton abnormalities in embryos that will
have consequences on adult performance. These congeners are considered nongenotoxic
in mammals, but their genotoxicity in embryos is not well known. Whether or not their
mode of action refers to genotoxicity in embryos, it is necessary to have a better knowledge
of the underlying mechanisms of toxicity at the gene level and to understand the network
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