July/August 1997
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July/August 1997 |
by Sarah Coomber
Although fish managers have been stocking lake trout in the Great Lakes for 30 years, they have failed to re-establish self-sustaining populations of the fish in four of the five Great Lakes. University of Wisconsin Sea Grant researcher Richard Peterson says he has a possible explanation for the problem: toxic chemicals.
Peterson, a University of Wisconsin-Madison toxicologist, has been studying Great Lakes contamination and its effect on fish for nearly two decades. He acknowledges that the failure of the lake trout population to recover could be due to other environmental and biological factors but says,"Toxic contaminants are the closest we've got to a smoking gun so far."
Peterson has found that lake trout are very sensitive to TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin), the most toxic form of dioxin, and they are most vulnerable in their early life stages. Dioxins, and similar chemicals, are unwanted byproducts of chemical manufacture, burning and other processes.
"It's a combination of several chemicals that are very persistent in the environment," Peterson said. "They're resistant to degradation and they bioaccumulate, or build up, in these lake trout. When the lake trout spawn, these particular chemicals get transferred to the eggs, where they go on to affect the development of the lake trout."
Even though stocked lake trout live in the Great Lakes and reproduce, their offspring don't live long enough to join the adult population, except in some areas of Lake Superior. The embryos survive their eight- to 10-weeklong development, but one week before hatching, the trouble begins.
"If you look at the embryos up until then, they appear to be normal in every way whatsoever," Peterson said. "It's only when they reach that particular point in their development that one first begins seeing signs of toxicity, and then it escalates during the next two to three weeks."
The eggs hatch, but the young fish that are affected by the contaminants die within a few weeks.
Peterson has found that TCDD levels above 30 parts per trillion in lake trout eggs cause an increase in sac fry mortality. TCDD levels of 100 parts per trillion and above kill 100 percent of the sac fry. Newly hatched trout are called sac fry because they receive their nourishment from a yolk sac. The young fish die from an accumulation of excess fluid in the yolk sac and around the heart, obstructed blood flow, hemorrhaging and skull malformations -- conditions resembling blue sac disease, a fatal condition normally seen in a very small percentage of wild trout sac fry.
Today TCDD levels in Lake Ontario lake trout eggs are at five parts per trillion and the equivalent of 10 parts per trillion when related chemicals that act like TCDD are included. Between 1966 and 1970, these concentrations were about 20 times higher, according to Philip Cook, acting chief of the Ecological Toxicology Branch of the U.S. Environmental Protection Agency's National Health and Environmental Effects Research Laboratory in Duluth, Minnesota.
Currently Peterson and Cook are preparing a paper that includes a retrospective risk assessment, or historical analysis, based on sediment core samples taken from Lake Ontario. Using the sediment record, Cook determined lake contamination levels from the 1930s to the present.
"You see an increase in contaminants until 1970," he said. "Then things start coming down pretty fast."
By pairing sediment data with the lake trout dioxin studies, the researchers found that levels of dioxin and related chemicals in Lake Ontario were high enough from 1945 to 1975 to have resulted in no survival of lake trout sac fry, Peterson said.
Lake trout was once the dominant species in the Great Lakes, but populations collapsed during the 1940s due to overfishing and the invasion of parasitic sea lampreys. By the mid-1950s, the species was considered extinct in the Great Lakes except for a few isolated Lake Superior populations.
After the sea lamprey was brought under control in the 1960s, state and federal fishery managers began stocking the Great Lakes with an average of 4 million lake trout annually. Although the stocked fish reached sexual maturity and produced fertilized eggs, the recruitment of yearling lake trout into the adult population has been negligible in all of the Great Lakes except Lake Superior, which is the cleanest lake in the chain.
Some people question Peterson's dioxin diagnosis. William Horns, Wisconsin Department of Natural Resources' Great Lakes fisheries specialist, says there have been a number of studies of lake trout in Lake Michigan that show it is possible to take their eggs and raise them successfully in the lake or laboratory.
"It's not to say that contaminants aren't playing a role," Horns said. "But there's pretty good reason to believe there must be other factors involved."
There are a number of theories that could explain the survival problems of lake trout. Some people say stocking practices are the source of the problem. When it is time for the stocked fish to reproduce, there is evidence that they return to the place where they were released, and often that habitat is unsuitable for spawning.
Another possibility is that the genetic strains of the stocked lake trout are unsuitable for the lakes in which they're being placed. Some people point to exotic species. Daniel Thomas, president of the Great Lakes Sport Fishing Council, sits on numerous state committees concerning nonindigenous species, including the Aquatic Nonindigenous Species National Task Force and the U.S. Fish and Wildlife Service Ruffe Control Committee. He says the introduction of nonindigenous species to the Great Lakes ecosystem has created an imbalance.
"What we have today is largely an exotic predator base feeding on a largely exotic prey base," he said. "Because there's such an imbalance out there, (lake trout) become preyed upon by other fishes."
Great Lakes Fishery Commission senior scientist Randy Eshenroder said that although Peterson's findings might help explain the decimated lake trout populations in Lake Ontario, they do not provide a reason to alter lake trout stocking efforts.
"We can't say (contaminants) are not a problem," Eshenroder said. "But the current ambient levels (in the Great Lakes) are lower than the levels shown to cause effects in the lab."
Lake trout are considered an important indicator of the health of the Great Lakes ecosystem. One specific objective in the Great Lakes Water Quality Agreement is to maintain Lake Superior "as a balanced and stable oligotrophic ecosystem with lake trout as the top aquatic predator of a cold-water community."
There is no guarantee that everyone will one day agree on what is troubling lake trout in the Great Lakes.
"You can find reason to believe and reason not to believe -- for each hypothesis," Horns said.
Sarah Coomber is the science writer for the University of Wisconsin Sea Grant Institute. For further information about the effects of toxic chemicals on Lake Trout, contact Richard Peterson at University of Wisconsin-Madison, School of Pharmacy, 5203 Chamberlin Hall, Madison, WI 53706. (608)263-5453, rep@pharmacy.wisc.edu.
Sommaire
Même si l'on ensemence les Grands Lacs en touladis (truites de lac) depuis 30 ans, on n'a pas réussi, dans quatre des cinq lacs, à rétablir les populations de l'espèce à un niveau où elles peuvent se maintenir . Richard Peterson, chercheur du programme Sea Grant de l'Université du Wisconsin, attribue le problème aux substances chimiques toxiques.
M. Peterson, toxicologue à l'Université du Wisconsin à Madison, étudie la contamination des Grands Lacs et ses effets sur les poissons depuis une vingtaine d'années. Il reconnaît que l'échec des mesures de rétablissement des populations de touladi pourrait s'expliquer par d'autres facteurs environnementaux et biologiques, mais il estime que les contaminants constituent la cause la plus évidente jusqu'à présent.
Ce chercheur a constaté que le touladi est très sensible au
TCDD (2,3,7,8-tétrachlorodibenzo-p-dioxine), la forme la plus toxique de la dioxine, à laquelle l'espèce est très vulnérable au début de son cycle biologique.
Revised: July 7, 1997
Maintained by Kevin McGunagle,
mcgunaglek@ijc.wincom.net