Page 842 - The Toxicology of Fishes
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822                                                        The Toxicology of Fishes


                       over the last half of the 20th century (Cook et al., 2003). Trout express the aryl hydrocarbon receptor
                       (AhR) and its dimerization partner, aryl hydrocarbon nuclear translocator (ARNT) and therefore have
                       the capacity to respond to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related chemicals (Abnet et
                       al., 1996; Pollenz et al., 1996). PCDDs, PCDFs, and the planar PCB congeners present in the Great
                       Lakes ecosystem are approximate isostereomers of TCDD and are capable of causing signs of early-
                       life-stage toxicity in trout identical to TCDD (Walker and Peterson, 1991, 1994a; Zabel et al., 1995a).
                       Among fish species studied, lake trout are the most sensitive to TCDD-induced early-life-stage mortality,
                       with LD  values in the environmentally relevant range of 58 to 80 pg TCDD per g egg (Spitsbergen et
                             50
                       al., 1991; Walker et al., 1991, 1994), and mixtures of the dioxin-like PCB, PCDD, and PCDF AhR
                       agonists present in Lake Michigan lake trout eggs interact in an additive fashion to cause trout early-
                       life-stage mortality (Walker et al., 1996; Wright and Tillitt, 1999; Zabel et al., 1995b). Taken together,
                       these and other findings presented in this chapter support the contention that HAH contamination in the
                       Great Lakes has led to decreased recruitment in select populations of lake trout (Cook and Burkhard,
                       1998; Cook et al., 1997, 2003).
                        Numerous adverse effects have been associated with sustained AhR activation caused by dioxin-like
                       PCBs, PCDDs, and PCDFs. These include  carcinogenesis,  wasting syndrome,  endocrine disruption,
                       altered lipid metabolism,  porphyria, hepatotoxicity, dermal toxicity, immunotoxicity, developmental
                       toxicity, and reproductive toxicity (Colborn et al., 1993; Safe, 1994). In this chapter on lake trout, we
                       focus on developmental toxicity because early life stages of vertebrates, including fish, represent the life
                       stage most sensitive to the toxicity of PCBs, PCDDs, and PCDFs (ASTDR, 1996; Cook et al., 1993;
                       Eisler and Belisle, 1996; Peterson et al., 1993; USEPA, 1995; Walker and Peterson, 1994a). Planar PCB
                       congeners, PCDDs, and PCDFs are the most potent with regard to causing AhR-mediated toxicity to
                       early life stages of trout (Walker and Peterson, 1991, 1994a; Zabel et al., 1995a) and have occurred at
                       great enough concentrations in eggs of feral lake trout to result in early-life-stage mortality (Cook and
                       Burkhard, 1998; Cook et al., 1997).
                        The goal of this chapter is to review the evidence for contaminant-related effects on lake trout
                       populations in the Great Lakes. The history of lake trout populations is presented. The concentrations
                       of HAHs and other persistent organic pollutants (POPs) observed in lake trout and other top predator
                       fishes in the Great Lakes are reviewed. We also review the toxicity of HAHs to fish. Field and laboratory
                       studies of chemical exposure in lake trout and other related species indicate that salmonines are partic-
                       ularly sensitive to dioxin-like chemicals. Field studies related to chemical contamination of Great Lakes
                       salmonines are reviewed, and a case study of HAH contamination in lake trout from Lake Ontario is
                       provided. Finally, the causative relationship between chemical pollutants and the lack of successful
                       reproduction of Great Lakes lake trout is evaluated through a set of the criteria developed for ecoepi-
                       demiology (Fox, 1991).



                       Historical Aspects of the Great Lakes Lake Trout Fishery

                       Lake trout were historically the key top predatory fish species in the Great Lakes (Balon, 1980). Lake
                       trout have been an important species to humans for commercial purposes, recreation, and sustenance,
                       in the case of Native Americans. Ecologically, the lake trout represents the endemic salmonine atop the
                       food chain, and they have served the role of “keystone predator” in the balance of the Great Lakes
                       ecosystem. This critical role was no more apparent than in the mid-1950s, when populations of lake
                       trout severely declined and the overabundance of forage fish resulted in massive die-offs. The dead
                       forage fish, mainly alewives, filled the shorelines of Lake Michigan, causing problems associated with
                       the odor, public health, and the recreational economy. They are a long-lived species of trout, with life
                       spans of over 20 years in the lakes and 30 years in hatcheries. Lake trout are a member of the charr
                       family and have temperature preferences of 8 to 12°C (Balon, 1980). The lake trout is slow growing
                       and takes approximately 6 years to become reproductively active. The high fat content observed in lake
                       trout (8 to 18%), presumably facilitating their survival in colder water temperatures, has also made them
                       a favorite for human consumption.
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