Page 881 - The Toxicology of Fishes

Reproductive Impairment of Great Lakes Lake Trout by Dioxin-Like Chemicals 861

predicted thresholds, making correlations difficult at best. So, some of these studies do not fully support
a relationship between lake trout egg exposure to HAHs and lake trout recruitment failures.
Field studies that have demonstrated a dose–response relationship between HAHs and lake trout effects
offer the strongest support for the coherency criterion and an association between these factors. Graded
doses of organic extracts from Lake Michigan lake trout were injected into hatchery-derived eggs and
caused blue sac syndrome and mortality in a dose-related fashion (Tillitt and Wright, 1997, Wright and
Tillitt, 1999). Not only did these studies demonstrate the toxicity of the chemicals present in lake trout
from the Great Lakes, but they were also consistent with the additive models of toxicity that had been
developed for HAHs in salmonines (Zabel et al., 1995b,c). As such, they support the coherence criterion
as being consistent with known toxicological models. The retrospective risk assessment of HAHs in
Lake Ontario (Cook et al., 2003) indicated that estimated exposure from HAHs was sufficient to cause
complete mortality in lake trout sac fry from Lake Ontario from approximately 1945 to 1985. This
evaluation was based on the toxicological models of HAH effects that have been confirmed by numerous
laboratories in a variety of species. Again, this study is consistent with toxicological information
regarding the effects of HAHs on lake trout and strongly supports the coherence criterion.

Conclusion
The complexity of an ecosystem as large as the Great Lakes makes simple cause-and-effect relationships
difficult, if not impossible to demonstrate. A relationship between HAHs and the lack of recruitment
observed in lake trout in the lower Great Lakes during the last half of the 20th century is no exception.
This chapter has focused on HAHs and other chemicals as potential causative agents in the lake trout
reproductive failures in the lower Great Lakes, but it would be naïve to think that factors such as predation
by invasive species, genetics, and habitat quality, among others, did not have an influence on lake trout
populations during this period. We have presented multiple lines of evidence of biological field infor-
mation, molecular mechanisms, toxicological models and testing, life history information, and a retro-
spective risk assessment which, together, suggest that HAHs were causally linked to lake trout recruitment
failures in Lake Ontario, Lake Michigan, and likely Lake Huron during the mid- to late 20th century.
Ecoepidemiological criteria also support a causal relationship between HAHs in lake trout and their
failures to reproduce naturally over this period. Biological factors, such as predation of lake trout by
sea lamprey, were important in the initial crashes of adult lake trout populations, and chemical agents
such as DDT were likely affecting lake trout recruitment and the ability to reestablish self-sustaining
lake trout populations. The major lines of evidence, however, suggest that exposure of lake trout to HAH
chemicals with TCDD-like AhR agonist activity was the key causative factor in the recruitment failures
observed in populations of lake trout in the lower Great Lakes for nearly four decades of the 20th century.

Acknowledgments
The authors would like to thank Mark Hahn, Woods Hole Oceanographic Institute, for his review and
assistance with portions of this chapter. We also thank James Fairchild and Michael Mac, Columbia
Environmental Research Center, for their critical review and comments of this chapter.

References
Abnet, C. C., Markwardt, D., Heideman, W., Hahn, M., Pollenz, R., and Peterson, R. (1996). Cloning of the
rainbow trout AhR and Arnt: mechanistic examination of interspecies differences in sensitivity to AhR agonists,
in Proceedings of the 17th Annual SETAC Annual Meeting, November 15–21, Washington, D.C., p. 82.
Abnet, C. C., Tanguay, R. L., Heideman, W., and Peterson, R. E. (1999). Transactivation activity of human,
zebrafish, and rainbow trout aryl hydrocarbon receptors expressed in COS-7 cells: greater insight into
species differences in toxic potency of polychlorinated dibenzo-p-dioxin, dibenzofuran, and biphenyl
congeners. Toxicol. Appl. Pharmacol., 159, 41–51.