By JANET RALOFF
While local communities have decried the loss of their prized lake trout -- one of the top aquatic predators in the Great Lakes -- scientists had until recently all but brushed off the possibility that the fish might have been poisoned. Instead, the majority had attributed the extinction of this trout in most of its range to more conventional causes, principally overfishing, predation by lampreys, and oxygen-depleted water, or eutrophication. |
 Juvenile lake trout in an aquarium. Though these fish take 4 to 5 years to mature, a female doesn't become a prime spawner unitl age 7. (Photo: John G. Shedd Aquarium.) |
Over the past decade, however, teams of aquatic toxicologists headed by Philip M. Cook of the Environmental Protection Agency office in Duluth, Minn., and Richard E. Peterson of the University of Wisconsin-Madison have been investigating a curious coincidence. The lake trout's demise began at about the same time that large amounts of dioxins, polychlorinated biphenyls (PCBs), and their chemical kin were pouring into these lakes. What's more, concentrations of these pollutants peaked around 1970 -- just when fisheries managers began noticing that, although restocked lake trout had reached sexual maturity, their lake-spawned young were not surviving.
Dioxinlike toxicants sabotaged these efforts to reintroduce a self-sustaining population of the fish, Cook and Peterson argue in several studies to be published later this year. They even make the controversial claim that exposure to these pollutants before 1960 "probably contributed to the decline and virtual extinction" of this trout in Lake Ontario and perhaps in the other lakes.
There's good news, however. After more than 25 years of restocking the trout, "we are just beginning to see success," says Clifford P. Schneider, a biologist at the Cape Vincent (N.Y.) Fisheries Station. In Lake Ontario, historically the most dioxin-contaminated of the Great Lakes, "each year now, for the last 4, we've had successful reproduction that's gone beyond the fry stage."
Still, the fish may not be home free. As pollutant concentrations fall, new laboratory tests suggest that less-than-lethal amounts of dioxinlike pollutants may cause harm. Moreover, several newly identified lake contaminants appear at least as harmful to fish as the 2,3,7,8-chlorinated dioxin (TCDD). Until recently, TCDD was considered the most potent dioxinlike toxicant.
The five Great Lakes constitute the world's largest freshwater system. Until midway through this century, the silvery lake trout, which can live to 30 years and grow to more than 30 pounds, reigned as undisputed king.
"The importance of lake trout in the food web cannot be overstated," says Marc Gaden of the Great Lakes Fishery Commission in Ann Arbor, Mich. This trout's collapse "allowed alewife and smelt populations to expand, which set off a disruptive chain reaction." Today, the Great Lakes' fish population is less diverse than it was before the trout's decline, Gaden notes, and species abundances oscillate far less predictably.
Fishers and resource managers have been anxious to understand why commercial catches of lake trout fell so precipitously in Lake Ontario during the 1930s, in Huron during the early 1940s, in Lake Michigan by the end of that decade, and in Superior by the 1950s.
Overfishing and predation by sea lamprey undoubtedly played a role, believes aquatic toxicologist Michael Mac of the U.S. Geological Survey (USGS) in Reston, Va. However, no one realized that toxicants might also have contributed to the decline until Cook began probing the ecological fallout of dioxins released from Superfund sites (SN: 5/31/80, p. 340) around Love Canal in Niagara Falls, N.Y.
Because contaminated sediment and particulates would collect downstream, the EPA team designed a Lake Ontario study in 1987. By 1992, they had strong evidence that lake trout embryos exposed to dioxin could develop a lethal syndrome called blue sac.
  Lake trout fry 4 weeks after hatching. The one on the left is normal; the one on the right exhibits blue sac syndrome from egg exposure to TCDD. (Photo: J.M. Spitsbergen and R.E. Peterson.) |
The yolk sac of healthy trout spawn gives them a rich golden hue. During the month or so after hatching, when the fry rely exclusively on that yolk for nutrients, they become vulnerable to blue sac syndrome. In this disorder, fluid leaks out of the blood vessels and into the yolk sac, which turns milky and slightly blue.
Though many conditions can cause blue sac, it has usually been linked to incubating fish eggs at too warm a temperature. In collaboration with Peterson's group, Cook's team has now confirmed that lake trout fry fall prey to blue sac syndrome if their eggs possess dioxinlike chemicals.
At concentrations of just 60 parts per trillion (ppt), TCDD kills 50 percent of lake trout fry -- making this fish the most vulnerable known. The same mortality in rainbow trout requires 400 ppt.
Eleven types of PCBs exhibit dioxinlike toxicity, as do 6 other chlorine-containing dioxins and 10 of the 135 different chlorinated furans emitted by combustion (SN: 9/24/94, p. 206). Though none of these related compounds matches TCDD in potency, Peterson's group has demonstrated over the past year that their presence adds to any blue sac risk posed by TCDD.
Based on calculations of former concentrations of these dioxinlike chemicals in Lake Ontario, Cook told Science News, "you end up with a pretty significant period when exposures to lake trout embryos would have been 2.5 times greater than would cause 100 percent mortality."
What's more, certain brominated dioxins, furans, and biphenyls, though less persistent in the environment, are even more toxic than their chlorinated counterparts. For instance, the 2,3,7,8-brominated dioxin poses a higher risk of blue sac than TCDD does, and certain brominated biphenyls are 10 times more potent than PCBs, Peterson's group finds.
Since most of these brominated compounds come from the burning of flame-retardant materials -- and the use of flame retardants is increasing -- the pollutants may pose a growing risk to wild fish, Peterson and his colleagues concluded in the October 1996 Toxicology and Applied Pharmacology.
In December, Peterson and Erik W. Zabel, also of Wisconsin, reported finding a component of paper mill waste (2,3,6,7-tetrachloroxanthene) that is about as potent as TCDD at inducing blue sac in trout. They worry that it may pose a risk to wild fish "even at low concentrations."
An even more arcane blue sac threat has just been identified by government scientists in Canada. This dioxin, present in a lamprey-killing compound used in the Great Lakes, contains not only a chlorine atom but also three fluorine atoms and several other chemical groups. Its discovery "shocked the pants off of us," says Mark R. Servos of Environment Canada in Burlington, Ontario.
While this pollutant does not appear to pose a major risk now, observes Cook, "it does suggest how, by doing something in the name of improving the lakes and their trout, we could actually risk aggravating the problem."
Since tough pollution control laws went into effect during the early 1970s, dioxinlike pollutants in the Great Lakes have been falling -- generally to concentrations below which blue sac mortality might be expected. This has prompted many researchers to begin investigating possible sublethal effects.
Dioxinlike chemicals have long been known to retard growth, but studies in EPA's Duluth facility also indicate that sublethal exposures to TCDD can induce lethargy and a failure to avoid light -- changes that might further compromise a fry's ability to evade predators, Cook notes.
Donald E. Tillitt of the USGS laboratory in Columbia, Mo., and his colleagues find that dioxins foster programmed cell death in vascular and neural tissue. One of Tillitt's students has just begun studying whether sublethal exposures might cause nerve damage that impairs behavior.
Meanwhile, John P. Giesy's team at Michigan State University in East Lansing has begun investigating immune function. George Noguchi there has preliminary evidence that certain PCBs damage infection-fighting T cells. PCB-induced suppression of immunity could have contributed to the large number of fish deaths from bacterial kidney disease in 1989, Giesy now believes.
"The real shocker from Peterson and Cook's work is that by 1940, levels of 2,3,7,8,-TCDD in Lake Ontario may have been so high that none of the lake trout were hatching," says Michael Gilbertson of the International Joint Commission in Windsor, Ontario.
Many others, like Mac and Giesy, argue that there are not and probably never will be sufficient data to indict pollutants as a major cause of the lake trout's extinction. Still, they share Cook and Peterson's concern that sublethal effects of chlorinated and brominated pollutants may continue to compromise the health of Great Lakes fish -- and perhaps the wildlife and people that eat them.
References:
Cantrell, S.M. . . .D.E. Tillitt, and M. Hannink. 1996. Embryotoxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD): The embryonic vasculature is a physiological target to TCDD-induced DNA damage and apoptotic cell death in Medaka (Orizias latipes). Toxicology and Applied Pharmacology 141(November):23.
Cook, P.M., E.W. Zabel, and R.E. Peterson. In press. The TCDD toxicity equivalence approach for characterization of trout early life stage mortality risks associated with exposures to TCDD and related chemicals. In Chemically Induced Alterations in the Functional Development and Reproduction of Fishes, R.M. Roland, ed. Pensacola, Fla.: SETAC Press.
Giesy, J.P., L.L. Feyk, and E.M. Snyder. In press. Xenobiotic modulation of endocrine function in fish. In Principles and Processes for Evaluating Endocrine Disruptors in Wildlife, R.J. Kendall, et al., ed. Pensacola, Fla.: SETAC Press.
Guiney, P.D. . . .R.E. Peterson, and J.J. Stegeman. 1997. Correlation of 2,3,7,8-tetrachlorodibenzo-p-dioxin induction of cytochrome P4501a in vascular endothelium with toxicity in early life stages of lake trout. Toxicology and Applied Pharmacology 143(April):256.
Hahn, M.E. . . .J.J. Stegeman. 1994. Photoaffinity labeling of the Ah Receptor: Phylogenetic survey of diverse vertebrate and invertebrate species. Archives of Biochemistry and Biophysics 310(April)218.
Henry, T.R. . . .R.E. Peterson. 1997. Early life stage toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin in zebrafish (Danio rerio). Toxicology and Applied Pharmacology 142(January):56.
Hewitt, L. Mark. 1996. Use of an MFO-directed toxicity identification evoluation to isolate and characterize bioactive impurities from a lampricide formulation. Environmental Toxicology & Chemistry 15:894.
Hornung, M.W., E.W. Zabel, and R.E. Peterson. 1996. Toxic equivalency factors of polybrominated dibenzo-p-dioxin, dibenzofuran, biphenyl and polyhalogenated diphenyl ether congeners based on rainbow trout early life stage mortality. Toxicology and Applied Pharmacology 140(October):227.
Schlezinger, J.J., R.D. White, and J.J. Stegeman. 1997. Oxidative inactivation of CYP1A1 by 3,3',4,4'-tetrachlorobiphenyl and release of active oxygen from hepatic microsomes stimulated by slow CYP1A1 substrates. The Toxicologist 36(March):Abstract 692.
Walker, M.K., P.M. Cook. . . .E. Peterson. 1996. Potency of a complex mixture of polychlorinated dibenzo-p-dioxin, dibenzofuran, and biphenyl ocngeners compared to 2,3,7,8-tetrachlorodibenzo-p-dioxin in causing fish early life stage mortality. Fundamental and Applied Toxicology 30:178.
Zabel, E.W., and R.E. Peterson. 1996. TCDD-like activity of 2,3,6,7-tetrachloroxanthene in rainbow trout early life stages and in a rainbow trout gonadal cell line (RTG-2). Environmental Toxicology & Chemistry 15(December):2305.
Zabel, E.W., R. Pollenz, and R.E. Peterson. 1996. Relative potencies of individual polychlorinated dibenzo-p-dioxin, dibenzofuran, and biphenyl congeners and congener mixtures based on induction of cytochrome P450aA mRNA in a rainbow trout gonadal cell line (RTG-2). Environmental Toxicology & Chemistry 15(December):2310.
Further Readings:
Guiney, P.D., P.M. Cook. . . .R.E. Peterson. 1996. Assessment of 2,3,7,8-tetrachlorodibenzo-p-dioxin induced sac fry mortality in lake trout (Salvelinus namaycush) from different regions of the Great Lakes. Canadian Journal of Aquatic Sciences 53:2080.
Hahn, M.E., and S.I. Karchner. 1995. evolutionary conservation of the vertebrate Ah (dioxin) receptor: Amplification and sequencing of the PAS domain of a teleost Ah receptor cDNA. Biochemistry Journal 310:383.
Hornung, M.W., E.W. Zabel, and R.E. Peterson. 1996. Additive interactions between pairs of polybrominated dibenzo-p-dioxin, dibenzofuran, and biphenyl congeners in a rainbow trout early life stage mortality bioassay. Toxicology and Applied Pharmacology 140(October):345.
Raloff, J. 1996. Lamprey: A taste treat from prehistory, and Westward ho the lamprey. Science News Online(Aug. 10).
______. 1996. Dioxins: New attempts to smoke them out. Science News 149(June 22):390.
______. 1995. Did evolution really anticipate dioxin? Science News 147(May 6):277.
______. 1994. The problem with tallying 'dioxin'. Science News 146(Sept. 24):206.
______. 1992. Perinatal dioxin feminizes male rats. Science News 141(May 30):359.
______. 1988. This 'nontoxic' dioxin isn't. Science News 133(April 23):269.
Schmidt, K.F. 1992. Dioxin's other face. Science News 141(Jan. 11):24.
Thomas, V.M., and T.G. Spiro. 1996. The U.S. dioxin inventory: Are there missing sources? Environmental Science & Technology 30(February):82A.
Walker, M.K., R.S. Pollenz, and S.M. Smith. 1997. Expression of the aryl hydrocarbon receptor (AhR) and AhR nuclear translocator during chick cardiogenesis is consistent with 2,3,7,8,-tetrachlorodibenzo-p-dioxin-induced heart defects. Toxicology and Applied Pharmacology 143(April):407.
Wilson, P.J., and D.E. Tillitt. 1996. Rainbow trout embryotoxicity of a complex contaminant mixture extracted from Lake Michigan lake trout. Marine Environmental Research 42:129.
Zabel, E.W. . . .R.E. Peterson. 1995. Interactions of polychlorinated dibenzo-p-dioxin, dibenzofuran, and biphenyl congeners for producing rainbow trout early life stage mortality. Toxicology and Applied Pharmacology 134:204.
Sources:
Philip M. Cook
National Health and Environmental Effects Research Laboratory
Mid-Continent Ecology Division
U.S. Environmental Protection Agency
6201 Congdon Boulevard
Duluth, MN 55804
Marc Gaden
Great Lakes Fishery Commission
2100 Commonwealth Boulevard, Suite 209
Ann Arbor, MI 48105
John P. Giesy
Department of Fisheries and Wildlife
Institute for Environmental Toxicology
Pesticide Resesarch Center
Michigan State University
East Lansing, MI 48824-1222
E-mail: jgiesy@aol.com
Michael Gilbertson
International Joint Commission
P.O. Box 32869
Detroit, MI 48232
Mark E. Hahn
Biology Department, MS-32
Woods Hole Oceanographic Institution
Woods Hole, MA 02543-1049
Michael Mac
United States Geological Survey National Center
M.S. 301
12201 Sunrise Valley Drive
Reston, VA 20192
Richard E. Peterson
School of Pharmacy
5293 Chamberlin Hall
425 N. Charter Street
University of Wisconsin-Madison
Madison, WI 53706
Clifford P. Schneider
New York State Department of Environmental Conservation
Cape Vincent Fisheries Station
P.O. Box 292
Cape Vincent, NY 13618
Mark R. Servos
Environment Canada
National Water Research Institute
867 Lakeshore Road
Burlington, ON L7R 4A6
Canada
John J. Stegeman
Biology Department, M.S. 32
Woods Hole Oceanographic Institution
Woods Hole, MA 02543
Donald E. Tillitt
Midwest Science Center
U.S. Geological Survey
Biological Resource Division
4200 New Haven Road
Columbia, MO 65201
References
- all articlesSources - all articles
Table of Contents -- May 17, 1997
