Page 867 - The Toxicology of Fishes

Reproductive Impairment of Great Lakes Lake Trout by Dioxin-Like Chemicals 847

concentrations in plasma have been depressed. Yet, when salmon from the Great Lakes were fed to rats,
the rats developed thyroid hyperplasia, hypothyroidism, and goiters (Sonstegard and Leatherland, 1979).
The same mechanism for thyroid toxicity in mammals is thought to occur in fish (Brown et al., 2004a;
Kohn, 2000). Rats are known to be sensitive to PCB-induced thyroid dysfunction (Bastomsky, 1977;
Bowers et al., 2004), so species sensitivity differences may account for the apparent lack of coherence
in thyroid pathologies among fish and rodents. Conversely, fish-eating birds in the Great Lakes have had
thyroid pathologies that corresponded with contaminant exposure (Rolland, 2000). We simply are not
certain if HAHs had a bearing on the thyroid pathologies in Great Lakes lake trout and salmon that
occurred in the 1970s to 1980s.
Histopathological lesions in the livers of afflicted lake trout from Lake Michigan were also consistent
with an exposure and response to HAHs. Mac (1986) observed liver pathologies in fry from Lake
Michigan collected during the late 1970s. These fry also had induced mixed function oxidases and
depletion of liver glycogen, possibly indicative of the wasting syndrome that is a hallmark of HAH
toxicity (Mac, 1986; Mac and Edsall, 1991).
Altered levels of vitamin A and its metabolites are another known effect of the dioxin-like toxicity of
HAHs (Zile, 1992). Reduced or lowered amounts of vitamin A have been observed in fish collected
from polluted waters of the Great Lakes (Rolland, 2000). White suckers (Catostomus commersoni) and
lake sturgeon (Acipenser fulvescens) collected from the Ottawa River near Montreal also had reduced
concentrations of vitamin A storage forms (retinyl palmitate and dehydroretinyl palmitate), and lake
sturgeon had reduced concentrations of storage forms of vitamin A in the intestines (Branchaud et al.,
1995; Ndayibagira et al., 1995). Unfortunately, no studies reported concentrations of retinoids in lake
trout or other salmonines from the Great Lakes during the 20th century, so inferences from these other
species are all we have to draw upon for field assessments of vitamin A levels. Laboratory studies with
fish, mammals, and birds have all demonstrated that HAHs reduce plasma and storage levels of retinoids
(Rolland, 2000; Simms and Ross, 2000). Specifically in salmonines, HAHs alter retinoid homeostasis
in both adults (Gilbert et al., 1995; Ndayibagira et al., 1995; Palace and Brown 1994) and in developing
embryos (Carvalho and Tillitt, 2004). Induction of monooxygenases in the liver, intestines, vasculature,
and other organs by HAHs causes increased metabolism of retinoids (Branchaud et al., 1995; Simms
and Ross, 2000; Zile, 1992). In conjunction with increases in phase I metabolism of retinoids, HAHs
induce retinoid conjugation by glucuronyltransferases and enhance excretion of retinoids (Simms and
Ross, 2000). These mechanisms for HAH-related reductions in retinoids are thought to be conserved
across vertebrate species, including fish. Thus, vitamin A and its metabolites are known to respond to
HAH exposure in fish, and reduced concentrations of vitamin A have been observed in Great Lakes
fishes. Unfortunately, no direct measurements of retinoids in salmonine species from the Great Lakes
exist for the period when HAH exposures were greatest.

Role of Other Stressors in Limitations of
Great Lakes Lake Trout Recruitment
Chemical Contaminants Other Than HAHs
The other chemical contaminant that has been strongly considered and investigated as a potential factor
in the lack of recruitment of lake trout in some of the Great Lakes is DDT. Generally, DDT fed in the
diet has little effect on adult fishes. The threshold for toxic effects in brook trout eggs (Salvelinus
fontinalis) is approximately 1.5 mg/kg ww, based on its effects in developing embryos and fry (Macek,
1968). There was generally little effect on the survival or hatching of eggs, but fry died at the swim-up
stage. The threshold toxic concentration of DDT in lake trout eggs has been estimated to be approximately
5 mg/kg ww (Burdick et al., 1964). It should be noted that this was a field study and that it is unknown
whether the concentrations of DDT present actually caused the adverse effects on egg viability and fry
survival. The threshold to cause lethality of rainbow trout (Oncorhynchus mykiss) embryos is approxi-
mately 1.5 mg/kg, of egg (Hopkins et al., 1969). In studies of brook, brown (Salmo trutta), and lake
trout, the thresholds for lethality of eggs and fry ranged from 5.8 to 11.9 mg/kg ww (Burdick et al.,