Page 869 - The Toxicology of Fishes

Reproductive Impairment of Great Lakes Lake Trout by Dioxin-Like Chemicals 849

that have been increasing in the aquatic environment of the Great Lakes during the last decade of the
20th century and first decade of the 21st century (Hites, 2004; Zhu and Hites, 2004). Concentrations of
PBDEs in lake trout from the Great Lakes have been doubling every 3 years over the period from 1975
to 2005 (Zhu and Hites, 2004). The concentrations of total PBDEs are currently near 1000 ng/g lipid
in lake trout collected from all of the five Great Lakes. The threshold concentrations for effects of PBDEs
in lake trout, particularly with regard to reproductive function or developmental toxicity, are not known.

Loss of Breeding Habitat
The physical and chemical structure of the spawning habitat is another potential factor that could
contribute to the loss of reproductive success in Great Lakes lake trout. Many factors need to be aligned
for adult lake trout to return to the appropriate areas at the appropriate time and spawn. The spawning
habitats must have proper substrate (size and shape), including interstitial spaces (depth); be at the correct
water column depth; have suitable nursery areas nearby; and be of the correct size and water temperatures
at spawning (Marsden et al., 1995). Lake trout spawn on reefs in the Great Lakes at depths from 5 to
80 meters (Goodyear et al., 1982). The spawning reefs have not been physically disturbed and continue
to attract adult lake trout of spawning age in Lakes Michigan, Ontario, and Huron (Fitzsimons, 1995;
Kelso et al., 1995; Marsden et al., 1995). Additionally, the hydrological conditions and temperature
profiles that exist at these spawning areas were not thought to be a limitation for lake trout spawning at
these areas in the Great Lakes for the last five decades of the 20th century (Marsden et al., 1995).
Although pheromones and other olfactory cues were not understood well enough to evaluate (Marsden
et al., 1995), the fact that large numbers of adult lake trout in spawning condition arrive annually at
spawning reefs suggests that homing cues are not a limiting factor for their reproduction. The loss of
spawning habitat, then, is not thought to constitute a significant factor in the rehabilitation of lake trout
populations in the lower Great Lakes.

Predation
Parasitism of adult lake trout by the invasive sea lamprey was a key factor in the initial population
crashes in the mid-20th century. The susceptibility of larval and juvenile age lake trout to parasitism
has been considered an important factor in the inability to establish naturally reproducing lake trout
populations in the Great Lakes. Since the population crashes of lake trout in the 1950s, the greatest
amount of effort toward rehabilitation of lake trout in the Great Lakes has been focused on the control
of sea lamprey populations (Selgeby, 1995). The success of the sea lamprey control program coupled
with stocking programs resulted in large numbers of adult lake trout in the lower Great Lakes (Elrod et
al., 1995; Holey et al., 1995); however, predation on early life stages of lake trout by forage fishes can
cause significant mortalities and may be an important factor that is limiting lake trout populations today.
In particular, alewife (Alosa pseudoharengus) prey on lake trout fry and are present on spawning reefs
and nursery areas when fry emerge and swim up. As a result, they could limit recruitment of Great Lakes
lake trout (Krueger et al., 1995); however, alewife populations have declined in Lake Michigan over the
past four decades (Fleischer et al., 2000) and there are still no signs of recruitment in lake trout. Thus,
the predation of early life stages of lake trout by forage fish, including alewife, may have been a
contributing factor in lake trout recruitment failures, but probably not the most significant factor.

Thiamine Deficiency
A compelling argument can be made for the role of thiamine deficiency as a contributing or causal factor
in the reproductive problems of lake trout in the Great Lakes from the 1980s to the present (Brown et
al., 2005). Thiamine (vitamin B ) is an essential nutrient required as a cofactor in glycolysis, the Krebs
1
cycle, and the pentose pathway. Thiamine concentrations below approximately 1 nmol/g in eggs of lake
trout result in early mortality syndrome (EMS) in the resultant fry (Fitzsimons, 1995). EMS is charac-
terized by mortality of the fry at swim-up. Prior to death, the fry are hyperexcitable in response to
external stimuli, have a loss of equilibrium, lay on their sides, swim in spiral patterns, are lethargic, and