Page 870 - The Toxicology of Fishes

850 The Toxicology of Fishes

generally show symptoms of neurological deficits (Marcquenski and Brown, 1997). The symptoms of
EMS can be observed during incubation of lake trout eggs and fry collected from the Great Lakes (Brown
et al., 2005). Other salmonines in the Great Lakes, such as Coho salmon (Oncorhynchus kisutch) and
Chinook salmon (Oncorhynchus tshawytscha) also exhibit varying degrees of thiamine deficiency and
subsequent EMS in their offspring (Brown et al., 2005). In fact, some of the best data tracking the
occurrence of EMS in Great Lakes salmonines can be found in Coho salmon reared as part of the re-
stocking program of the Michigan Department of Natural Resources (Brown et al., 2005). Coho salmon
fry, collected from adults spawning in the Platte River in Michigan, have been monitored since 1972
for mortality from hatch to feeding. The rates of fry mortality were <20% until 1979, when the rates of
fry mortality increased and began to fluctuate but generally increased until this century (Brown et al.,
2005). The EMS observed in Coho salmon from Lake Michigan during the late 1990s has been highly
correlated with the thiamine content of the eggs (Wolgamood et al., 2005). This same extensive moni-
toring data for EMS is not available for other species or for the other Great Lakes; however, similar
symptoms of EMS and low thiamine have been reported in salmonines from Lake Huron (Wolgamood
et al., 2005) and Lake Ontario (Fitzsimons, 1995). The presumed cause of the thiamine deficiency in
Great Lakes salmonines is a diet rich in thiaminase (Brown et al., 2005). Thiaminase is an enzyme that
hydrolyzes thiamine and is present in large amount in alewife, a major food component of Great Lakes
salmonines (Tillitt et al., 2005).

Case Study: Assessment of the Effects of AhR Agonists on
Reproduction and Survival of Lake Trout in Lake Ontario

Application of toxicology data in actual ecological risk assessments can provide many insights. On the
one hand, retrospective assessments can validate the applicability of data and models for assessment of
both exposure and toxicity. Alternatively, the risk assessment process can facilitate refinements of the
data and models, as well as revealing unanticipated uncertainties requiring further research. Examples
of truly prospective toxicity risk assessments that are later validated are quite rare; however, the ultimate
goal of ecotoxicological research is to develop a risk prediction capability that can be used to prevent
damage to fish and wildlife populations in the future. Studies of the presence of persistent bioaccumu-
lative toxicants such as polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), and dibenzo-
furans (PCDFs) in aquatic food webs in sufficient concentrations to have impacted fish populations
through AhR-mediated toxicities that affect the reproductive cycle can provide opportunities for vali-
dating toxicity risk prediction models and water quality criteria. A complete retrospective assessment
must combine relevant toxicity and exposure data with integrated exposure, bioaccumulation, and
chemical mixture toxicity models to predict population responses that are independently consistent with
the species’ population histories for the ecosystem.
The most complete evaluation of the potential for application of AhR-mediated toxicity data and
models to fish is provided by a retrospective study of the extirpation of lake trout (Salvelinus namaycush)
in Lake Ontario which occurred around 1960 (Cook et al., 2003). Toxicological models of AhR agonists
have been rigorously developed and tested for salmonines and even specifically for lake trout. The
sensitivity of lake trout has been established (Table 21.2), and the additivity of HAHs to cause dioxin-
like toxicity in early life stages of salmonines has been confirmed through a number of different
approaches. The relative potency factors (REPs) used to derive the WHO toxicity equivalency factors
(TEFs) for the AhR agonists were almost solely based on rainbow trout early-life-stage mortality studies
associated with concentrations in embryos, so direct application to lake trout embryos should provide
good estimates of potency of the congeners. Moreover, there have been numerous signs of dioxin-like
toxicity in both adult and early life stages of lake trout from the Great Lakes, particularly Lakes Michigan
and Ontario. Cook et al. (2003) chose to relate lake trout early-life-stage mortality to dose measured as
the 2,3,7,8-TCDD toxicity equivalence concentration in lake trout eggs (TEQ ) for known AhR agonists:
egg
TEQ = ∑(C ) (TEF) i
egg i
egg