Page 874 - The Toxicology of Fishes

854 The Toxicology of Fishes

150 120

100
Lake Trout Commercial Catch (number in thousands) 60 % Sac Fry Mortality
100
80

50
Adult population trend
Predicted min sac fry mortality
Observed min sac fry mortality 40
20
Predicted max mortality
0 0
1910 1920 1930 1940 1950 1960 1970 1980 1990
Year

FIGURE 21.9 Integrated sediment core analysis and toxicity model predicted lake trout sac fry mortality (acute and chronic
toxicity related) in comparison to lake trout population decline prior to extirpation around 1960 and blue sac syndrome
mortality observed for sac fry raised from fertilized eggs collected from stocked fish between 1976 and 1990. (From Cook,
P.M. et al., Environ. Sci. Technol., 37, 3867–3877, 2003. With permission.)

There was an observed concordance between population fluctuations in the numbers of adult lake trout
and stocking rates of a unique lake trout fry stocking program (Figure 21.10). A lake trout fry stocking
program (Elrod et al., 1995) could account for increases in lake trout prior to 1925 and the dramatic
decline in lake trout numbers recorded after 1925 through the 1940s (Figure 21.10). Most interesting
from an epidemiological perspective was the appearance of several strong year classes of adult lake trout
that appear to be associated with earlier peaks in numbers of stocked fry. The last peak of these strong
year classes of lake trout was observed around 1939 and indicates that lake trout reproductive success
occurred as late as 1934. The epidemiological evidence for natural reproduction was consistent with the
predicted maximum toxicity risk analysis (Figure 21.9) presented by Cook et al. (2003). Finally, the first
signs of natural reproduction observed in 1986 (Marsden et al., 1988) are also consistent with the
maximum AhR-mediated toxicity risk model for reproductive success of lake trout in Lake Ontario
(Figure 21.9). A remaining uncertainty is whether AhR-mediated effects on lake trout fecundity may
have further impacted reproductive success during the long HAH exposure history in Lake Ontario.
This retrospective risk assessment provides strong evidence along multiple lines of evidence that
HAHs had impacts on populations of lake trout in the Great Lakes in the latter half of the 20th century.
Predictions of toxicity agree with observations of sac fry mortality from the late-1970s to mid-1980s
(Figure 21.9), are consistent with lake trout population estimates for Lake Ontario (Figure 21.9), and
match up well with exposure metrics estimated from other monitoring programs (Figure 21.8).

Summary
The history of lake trout populations in the Great Lakes during the 20th century is certainly a complex
story of human disturbance, exotic invasive species, and changes in water quality. The dynamic interaction
of these stressors on populations of lake trout has been difficult to assess and has lent itself to a variety
of interpretations. The evidence for effects of overfishing and sea lamprey predation on lake trout population
crashes experienced in the mid-century has been assumed to be conclusive by fisheries scientists;
however, we have summarized information regarding the plausibility of chlorinated hydrocarbons, in