Chemistry Reference
In-Depth Information
Cell vacuole-based protection mechanisms have
been observed to dominate in leaves of metallophytes,
whereas cell wall-based mechanisms dominate in
roots, which makes sense in relation to the kinetics
of metals in plants. Metals are taken up in roots and
transported in cell sap.
Metallophytes can absorb extensive amounts of
metals, especially in hyperaccumulators, who have
been reported to concentrate metals by factors of 10
to almost 4000, thereby reaching extreme concentra-
tions of tens of grams per kilogram (various metals in
various plant species). This is used for phytoremedia-
tion of metal polluted soils or waters. In special cases,
hyperaccumulator plants can be harvested for use
as fuel and the ashes used for metal refi ning (phyto-
mining).
likely reduced to Cu
+
before or during interaction with
the gill.
Early in the development of ecotoxicology as a
science providing data for risk assessment and risk
regulation, it became clear that in aquatic environ-
ments metal toxicity was poorly correlated to total
metal concentrations, stimulating intense research in
speciation, to identify determinants of toxicity (i.e.,
relations between water chemistry, dominant metal
species, and toxicity). Selective analytic procedures
have been developed to try to quantify labile (bioavail-
able) fractions of total metal. These methods include
voltammetry, ligand competition, and resin equilibra-
tion. At present, the only technique allowing reliable
measurement of free metal concentrations is the use
of ion selective electrodes and only at relatively high
( toxicologically relevant) concentrations.
Accumulating evidence on disproportionality between
concentration and effect led to formulation of the free ion
activity model (FIAM) (Campbell, 1995), which has been
further developed into the biotic ligand-modeling con-
cept (BLM) (Paquin
et al
., 2002), which incorporates metal
speciation in description of toxicity. Like the pure specia-
tion models, various BLMs assume equilibrium.
A BLM is a conceptual framework, describing that
the acute toxicity of metals is associated with bind-
ing of “active” forms of metals (labile complexes or
“free” hydrated metals) to biological structures (biotic
ligands) as proteins, organelles, etc. Accordingly, the
BLM predicts that water chemistry extensively affects
metal toxicity, either through binding the metal (e.g.,
dissolved organic carbon, complexing compounds) or
competing for sites at the biotic ligand (e.g., calcium).
Various authors have developed formal BLM
descriptions allowing calculation of metal toxicity
from metal speciation data acquired from chemical
analysis of water and the speciation models described
previously, in combination with conditional stabil-
ity constants for metal-gill tissue complex formation
measured experimentally. In this sense, the BLMs are
extensions of the previous speciation models including
further compartments, the biotic ligands. The presently
fi nal modeling approach to predict metal toxicity is the
development of a sediment biotic ligand model based
on measurement of sediment concentrations of acid-
soluble metals (simultaneously extracted metals, SEM)
and acid-volatile sulfi de (AVS), modeling metal parti-
tion using the WHAM, and toxicity modeling using a
BLM for metals (Di Toro
et al
., 2005).
The applicability of the various models for predict-
ing metal toxicity is limited by the fact that a central
assumption of all BLMs is that metal uptake is under
5 TO
XICITY OF METALS IN ECOSYST
EMS
Despite the fact that some of the fi rst observations on
the ecotoxicology of metals came from terrestrial stud-
ies on, for example, the toxicity of organomercurials
used in farming, today, by far most experimentation,
data, and mechanistic understanding in ecotoxicology
relates to the aquatic environment, both in general and
specifi cally for metals. Research indicates that the pri-
mary site for toxic actions of most metals in aquatic
organisms is the gill, especially in acute exposures of
freshwater organisms.
The functions of the gill are much more com-
plicated than those of terrestrial lung. Besides gas
transport and acid-base regulation, some kidney
functions (e.g., N-metabolism, water, salt, and
metal homeostasis) are in part regulated by the gill.
These functions are executed by an array of nega-
tively charged gill membrane proteins that bind
cations. This is likely the reason for the high sensi-
tivity of the gill to toxic metals. During acute expo-
sure to toxic metals, extensive histological damage
is rapidly induced in gills, leading to reduced gas
exchange and efflux of essential ions and eventu-
ally mortality.
At lower level chronic exposures, metals, includ-
ing Cd, Cu, Ag, Zn, and others, tend to bind to specifi c
gill structures involved in metal homeostasis: Mono-
valent cations (e.g., Ag
+
and Cu
+
) affect Na
+
transport,
whereas divalent cations (e.g., Cd
++
and Zn
++
) affect
Ca
++
transport. Some metals cross the gill membrane
and exert a toxic effect after systemic distribution (e.g.,
Hg
++
and Pb
++
). Although Cu in aquatic environments
predominantly exists as the divalent Cu
++
ion, it is most
