Environmental Engineering Reference
In-Depth Information
significant amounts of Hg and that location, age-specific
feeding habits, and size of individuals were important
factors contributing to the observed variability in Hg
levels. Moreover, Kahn and Tansel (2000) reported that
in the Florida Everglades, where atmospheric deposition
of inorganic Hg is believed to be a major source of Hg
contamination, Hg bioconcentration factors (relative to
Hg in the water column) for adult American alligators
were extremely high (39.9
3
10
7
for liver, and 32.9
3
10
7
for kidney), whereas in juveniles they were lower (liver,
10.55
3
10
7
; kidney, 9.34
3
10
7
). Although Hg bioaccumula-
tion studies in American alligators have been published,
the long-term toxicity of Hg in this species (e.g., possible
reproductive impairment) is unknown.
Although the use of snakes as bioindicators of environ-
mental contaminants, such as pesticides, was proposed over
30 years ago (Bauerle, 1975; Stafford, 1976; Burger, 1992), very
little is known about Hg bio-accumulation and short-term
or low-level long-term MeHg toxicity in snakes (Heinz et al.,
1980.) Burger et al. (2005) measured Hg in a variety of water
snake eggs, testes, kidney, liver, muscle, and skin and blood
samples. This study also evaluated the use of skin and blood
as nonlethal indicators of Hg contamination and reported
that this species was a reliable indicator because they are
widely distributed top-level predators and because skin was
shown to be predictive of internal exposure in this species.
In conclusion, amphibian and reptile Hg ecotoxicology has
focused primarily on exposure studies, whereas, in general,
studies of mechanistic effects are still lacking. In addition,
the effects of Hg exposure in the context of multiple stressors,
such as exposure to metal mixtures, the presence or absence
of predators, varying food web structure, and spatiotemporal
habitat complexities related to ecosystem sensitivity to Hg
methylation are in need of further study. Future Hg ecotox-
ciology research should focus on the mechanistic effects of
MeHg at molecular, individual, and population scales and
should use ecologically realistic concentrations and routes of
exposure to reflect actual environmental conditions.
wildlife following MeHg exposure. In an early account,
cats, birds, and fish exhibited a range of neurologic symp-
toms in the vicinity of MeHg-contaminated Minamata
Bay, Japan, in the 1950s (Harada, 1995; Eto 1997). From
the 1960s through the 1980s, several reports of MeHg-
associated neurobehavioral toxicity were reported in vari-
ous species of wildlife, including mink (
Mustela vison
), river
otter (
Lontra canadensis
), and predatory and seed-eating
birds, across Europe and North America (Borg et al., 1967;
Wobeser and Swift, 1976; Fimreite, 1979; Wren, 1985). Most
of these cases of MeHg intoxication resulted from short-
term exposures to high dietary levels of MeHg derived from
point sources of contamination. Although legacy Hg con-
tamination around some industrial sites remains problem-
atic, many of the once-common sources of environmental
Hg contamination (e.g., releases to the environment from
the chlor-alkali industry; and organomercurials used as
antifungal seed dressings) have been eliminated or greatly
restricted. currently, fish and wildlife are much less often
exposed to MeHg under short-term exposure scenarios that
were more common in the past, but are instead exposed
to lower levels of dietary MeHg on a more continual basis
over the long term. Nevertheless, tissue Hg concentrations
in several wildlife species continue to be within an order of
magnitude of levels associated with overt toxicity (USEPA,
1997; Basu
et al., 2007a). New analytical tools and bio-
marker strategies are being developed to characterize the
subclinical and early health effects associated with such
environmentally relevant exposures.
Prior to the onset of toxicant-induced structural and
functional damage to the nervous system, significant
changes in brain neurochemistry occur (Manzo
et al.,
1996). “Brain neurochemistry” refers to neurotransmit-
ters, receptors, enzymes, and transporters that mediate
neuronal signaling throughout the nervous system. In
experimental studies using laboratory rodents, MeHg was
shown to affect several neurochemical receptors, enzymes,
and transporters (e.g., Brookes and Kristt, 1989, castoldi
et al., 1996). Monitoring specific changes in brain chem-
istry (neurochemical biomarkers) thus represents a novel
method to identify early cNS effects associated with MeHg
exposure.
Measurement of neurochemical biomarkers has proven
successful in recent years for characterizing early cNS
effects of MeHg on several fish-eating wildlife species.
In one of the earliest studies, brain tissues were obtained
from wild mink trapped across canada (yukon Territory,
Ontario, and Nova Scotia), and a significant positive cor-
relation was found between levels of brain MeHg and the
density of muscarinic cholinergic receptors (Basu et al.,
2005a). In a subsequent study on these same wild mink, a
significant negative correlation was found between brain
MeHg and levels of
N
-methyl-
d
-aspartate (NMDA) recep-
tor densities (Basu
et al., 2007b). Studies of fish-eating
birds (common loons and bald eagles) reported similar
associations—positive correlations between brain MeHg and
Effects of Methylmercury in Wild birds
and Mammals
The toxic effects of MeHg ingestion in wild birds and mam-
mals have been studied for many years, and much research
has been published relative to most other taxa, such as fish,
amphibians, and invertebrates. Major advances in MeHg
toxicology in birds and mammals have focused on early
neurochemical changes,
in ovo
toxicity (birds), and effects
on reproductive success in wild populations. In addition,
new information on the important interactions between
Hg and Se in various tissues has been published.
effects on neurochemistry
The central nervous system (cNS) has long been known as
a major target organ for MeHg toxicity, and numerous stud-
ies have demonstrated overt neurotoxicity in fish-eating
