Page 877 - The Toxicology of Fishes

Reproductive Impairment of Great Lakes Lake Trout by Dioxin-Like Chemicals 857

of this monitoring called for the removal of “deformed fry” from the cultures (Willford et al., 1981),
which may have confounded the fry survival data. The temporal aspects of lake trout hatch and fry
survival studies from Lake Ontario also support this criterion. The New York Department of Environ-
mental Conservation monitored lake trout sac fry mortality associated with blue sac syndrome from
1977 to 1984 (Cook et al., 2003). The decrease in blue-sac-related fry mortality during this period was
consistent with the decreases in TEQs and predicted toxicity over this period (Figure 21.8) (Cook et al.,
2003). Thus, the reports of signs of blue sac symptoms in lake trout sac fry and subsequent mortality
rates from the mid-1970s to the late 1980s followed a temporal trend consistent with general declines
of HAHs (Lake Michigan) and predicted toxicity, based on TEQs in lake trout (Lake Ontario). In each
case, the time-order criterion is supported. Data are not available for either contaminant concentrations
or blue sac syndrome in lake trout from Lake Huron.

Strength of Association
This criterion refers to the strength to which there is an association between the putative causal agent and
the effect across wide geographic areas. This criterion also refers to the magnitude in differences in effects
observed in exposed vs. non-exposed populations. Was there a coincidence between HAHs in lake trout
populations across the Great Lakes and symptoms of blue sac syndrome or reproductive failure? The
evidence for this comes from comparisons of concentrations of dioxin-like contaminants in lake trout over
the past 50 years. Clearly, lake trout and other fish from the lower Great Lakes (Michigan, Ontario, and
Huron) had greater concentrations of HAHs as compared to lake trout from Lake Superior (Baumann and
Whittle, 1988; DeVault et al., 1986, 1989; Hickey et al., 2006). This difference in chemical contamination
of the Great Lakes continues even today, with Lake Superior having smaller concentrations of PCBs, as
well as a number of other persistent organic pollutants, as compared to Lakes Michigan, Ontario, and to
a lesser extent Lake Huron (Hickey et al., 2006). There was a consistent pattern of the incidence of blue
sac syndrome in lake trout during the late 1970s into the 1980s when fry rearing studies were conducted
(Cook et al., 2003; Mac et al., 1985). Little or no blue-sac-related mortality was observed in lake trout
fry from Lake Superior, while elevated amounts of this syndrome were observed in fry from Lake Michigan
(Mac et al., 1985). This is consistent with the elevated HAH chemicals observed at the time in lake trout
from Lake Michigan and HAHs at concentrations below known thresholds of toxicity in lake trout from
Lake Superior. The most complete and compelling evidence for the strong association among lake trout
exposure to dioxin-like chemicals (HAHs), predicted toxicity, and degree of observed blue-sac-related
mortality comes from the retrospective risk analysis for Lake Ontario (Cook et al., 2003). In that example,
we saw that estimated exposure of lake trout to dioxin-like PCBs, PCDDs, and PCDFs was high over a
four-decade period, from roughly 1945 to 1985. Predicted toxicity of TEQs derived from the PCBs,
PCDDs, and PCDFs in lake trout eggs (TEQ ) was sufficient to cause complete lake trout sac fry mortality
egg
and lack of recruitment in lake trout inhabiting Lake Ontario over this period. Consistent with that premise,
no recruitment was observed over that period in lake trout populations from Lake Ontario.
The geographic distribution of dioxin-like pathologies observed in lake trout and other salmonines
of the Great Lakes supports the strength of association between HAH exposure and HAH-induced
toxicity in lake trout. The most consistent of the dioxin-like responses observed in both lake trout adult
and sac fry from contaminated areas was induction of CYP1A activity. AhR-mediated induction of
CYP1A is a biomarker of exposure to TCDD-like AhR agonists and can be measured catalytically as
AHH or EROD activity (Stegeman and Hahn, 1994). Induction of CYP1A was observed in lake trout
sac fry from Lake Michigan during the late 1970s (Binder and Lech, 1984). EROD was also induced
in Chinook salmon from Lake Michigan in the mid-1980s (Ankley et al., 1989), and, most significantly,
a direct comparison demonstrated up to 60-fold greater AHH induction in lake trout from Lake Ontario
compared to those collected in Lake Superior (Luxon et al., 1987). A histological finding that is consistent
with dioxin-like toxicity and has been observed in Great Lakes salmonines was thyroid hyperplasia
(Moccia et al., 1981) and altered thyroid hormones (Leatherland and Sonstegard, 1981); however, a
geographic distribution of thyroid pathologies in salmonines from the Great Lakes was not found to be
linked to chemical contamination (Leatherland, 1992, 1993; Moccia et al., 1977). Although a thyroid
abnormality known to be associated with HAH-induced toxicity was present in Great Lakes salmonines