Page 873 - The Toxicology of Fishes

Reproductive Impairment of Great Lakes Lake Trout by Dioxin-Like Chemicals 853

2000
Sub-
Lethal Mortality 100% Mortality
Effects
1990 Core LO87–20
1980

1970 > 500

1960
1950

1940
2378 TCDD 2378 TCDF
1930 PCB 126 Other
23478 PeCDF Measured in
lake trout
12378 PeCDD
1920 Estimated from
123478 HxCDF TCDD in herring
PCB 77 gull eggs
1910
0 50 100 150 200 250 300
TEQs in Lake Trout Eggs (pg/g ww)
FIGURE 21.8 TEQs in lake trout eggs determined retrospectively from analysis of radionuclide-dated, 1-cm sections of
a sediment core (LO87-20) from eastern Lake Ontario. The concentrations of each AhR agonist times the appropriate BSAF
values for lake trout eggs and fish TEF equate to the contribution of each chemical to the TEQs in the eggs that may be
related to mortality expected from acute and chronic toxicity in Lake Ontario lake trout sac fry. Predicted TEQs in eggs
are compared to measured TEQs in eggs of lake trout (diamonds) and lake trout egg TEQs estimated from TCDD
concentrations measured in herring gull eggs (circles). (From Cook, P.M. et al., Environ. Sci. Technol., 37, 3867–3877,
2003. With permission.)

present, TCDD-associated toxicity would have impacted the lake trout population in Lake Ontario for
at least four decades (1940 to 1980) and would have caused complete reproductive failure for nearly
three decades (1945 to 1975). These predictions could underestimate impacts to the extent some AhR
agonists were present and unaccounted for in the assessment.
The resulting estimates of early-life-stage mortality predicted over this time period were then compared
to known rates of fry mortality and observation of population trends in Lake Ontario (Figure 21.9). The
minimum toxicity model had thresholds as listed above. The maximum toxicity model incorporated the
precept that sublethal toxic effects, which occur during development, would result in losses from the
population at later life stages. Sublethal effects of HAHs in salmonine fry most certainly could affect
juvenile fitness and their ability to compete in natural environments; therefore, predictions of maximum
toxicity presented in their risk assessment were based on a TCDD threshold for mortality of 5 pg/g and
100% mortality occurring at 50 pg/g in the lake trout eggs. Their choice of a maximum toxicity threshold
of 5 pg/g was also based on the fact that lake trout from Lake Superior had similar exposures during the
1960 and 1970s, yet there were no associated reductions in native trout populations (Hansen et al., 1995).
The predicted lake trout early-life-stage toxicities were compared with the observed sac fry mortality
rates in lake trout collected by the New York Department of Environmental Conservation (Cook et al.,
2003). The observations of blue-sac-related mortality compared well with the predicted estimates based
on the additive 2,3,7,8-TCDD toxicity equivalence model over the period from 1978 to 1991 (Figure
21.9). Additive toxicity of HAHs had previously been demonstrated with binary mixtures, synthetic
mixtures, and complex environmental mixtures, so the 2,3,7,8-TCDD toxicity equivalence approach was
supported and again appeared to accurately reflect the toxicity of HAH congeners in an environmental
mixture.