Plausible Cause Found for Great Lakes
Lake Trout Reproduction Failure
by Stephen Wittman
SEATTLE (2/13/97) -- For 30 years, efforts to re-establish self-sustaining populations of lake trout in four of the five Great Lakes have failed. Now a University of Wisconsin Sea Grant researcher thinks he knows why: toxic chemicals.
The levels of dioxin and related chemicals in Lake Ontario were high enough from 1945 to 1975 to have resulted in zero survival of lake trout sac fry, according to Richard E. Peterson, a toxicology professor at the UW-Madison School of Pharmacy.
Female fish accumulate dioxin-like chemicals in their bodies and transfer some of these toxins to their eggs, he said. At high enough concentrations, Peterson said these contaminants can cause all of the fish's offspring to die within three weeks of hatching. The highest concentrations of dioxins and similar toxic industrial contaminants generally are found in the Great Lakes' largest trout and salmon, especially in the long-lived lake trout.
Peterson's findings are based on two decades of laboratory research supported by the National Sea Grant College Program and recently completed studies in collaboration with Philip M. Cook, a researcher at the Mid-Continent Ecology Division of the U.S. Environmental Protection Agency's National Health and Environmental Effects Research Laboratory, in Duluth, Minn.
"Our data suggest that dioxins and related chemicals may have contributed to the extinction of lake trout in Lake Ontario prior to 1960 and to the recruitment failure of stocked lake trout since then," Peterson announced today in Seattle at a briefing organized by the Sea Grant Media Center. "But the good news is that declining levels of these contaminants and signs of general ecosystem recovery suggest that significant recruitment of lake trout through natural reproduction may start occurring in Lake Ontario and the other Great Lakes in the near future."
Once the dominant species in the Great Lakes, native lake trout populations collapsed during the 1940s under the one-two punch of over-fishing and predation by parasitic sea lampreys. By the mid-1950s, the species was deemed extinct in all of the lakes except for a few isolated remnant populations in Lake Superior.
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 four million lake trout annually, and they banned commercial harvest of the fish except by tribal operations. Although the stocked fish reached sexual maturity and produced fertilized eggs, the recruitment of yearling lake trout into the population has been negligible in each of the Great Lakes except Superior, the uppermost and most pristine lake in the chain.
The reasons for this recruitment failure could include other environmental and biological factors, the UW-Madison researcher said, "but toxic contaminants are the closest we've got to a smoking gun so far."
Of the Great Lakes fish Peterson tested, he found lake trout were the most sensitive to TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin), the most toxic form of dioxin. He discovered that TCDD levels in lake trout eggs as low as 30 parts per trillion (ppt) caused observable increases in sac fry mortality, and 100 percent mortality occurred at TCDD levels above 100 ppt. The sac fry die from an accumulation of excess fluid in the yolk sac (yolk sac edema) and around the heart (pericardial edema), obstructed blood flow (ischemia), hemorrhaging, and a deformed skull (craniofacial malformations) -- conditions resembling blue sac disease, a fatal disease usually seen in only a very small percentage of wild trout sac fry.
TOP -- Normal lake trout sac fry (Salvelinus namaycush).
BOTTOM -- Lake trout sac fry exhibiting blue sac disease symptoms after exposure to dioxin (TCDD) in laboratory tests. Note deformed skull and excess fluid in yolk sac. Hemorrhaging is also evident as dark blotches in the fry's body.
While contaminant levels have dropped dramatically over the last decade, lake trout and other sport fish in the Great Lakes -- as well as those in most other U.S. lakes and rivers -- still contain detectable levels of TCDD and related toxins, including various forms of PCDD (polychlorinated dibenzo-p-dioxin), PCDF (polychlorinated dibenzofuran) and PCB (polychlorinated biphenyl). Peterson's research shows that, in the early stages of life, fish are particularly vulnerable to the toxic effects of these chemicals, which he found act in an additive fashion.
A notable spin-off of Peterson's Sea Grant research was his determination, with EPA support, of TCDD Toxicity Equivalence Factors (TEFs) for individual dioxin-like chemicals, based on their ability to cause fish embryo mortality. TEF values permit an accurate evaluation of the cumulative risks to the early development of fish posed by low concentrations of dioxin-like chemicals in their eggs, he said, adding that the EPA is proposing to adopt the TEF approach to more precisely assess the risks these chemical pose to wild fish populations.
Peterson developed the TEF method as a way to convert the concentrations of several different dioxin-like chemicals found in Lake Ontario lake trout eggs to the equivalent concentration of TCDD. EPA's Cook then estimated the historical concentrations in the eggs based on the concentrations of these chemicals found in Lake Ontario bottom sediment cores covering the 1930 to 1987 period.
The EPA analysis showed that contamination of Lake Ontario by TCDD-like chemicals began in the 1930s and peaked in the late 1960s. Sac fry hatched from the lake trout eggs collected from Lake Ontario, the last lake in the Great Lakes chain, continued to exhibit blue sac disease-like symptoms up to the middle 1980s, Peterson said.
While no blue sac symptoms were evident in fry hatched from Lake Ontario lake trout eggs in 1991, Peterson said that "even at sub-lethal levels, TCDD and similar chemical contaminants may be compromising the survival of swim-up fry in the environment." He noted that dioxins and PCBs have been identified as possible endocrine disrupters -- chemicals that alter the action of natural hormones and interfere with normal reproduction and development in animals -- the focus of Peterson's current Sea Grant research.
However, a hopeful sign was last year's declaration by the U.S.- Canadian Great Lakes Fishery Commission that self-sustaining lake trout populations had been restored to most waters of Lake Superior. As a result, lake trout from federal hatcheries are no longer being stocked in that lake.
Created in 1966, Sea Grant is a national network of 29 university-based programs of research, outreach and education dedicated to the protection and sustainable use of the United States' coastal, ocean and Great Lakes resources. The National Sea Grant Network is a partnership of participating coastal states, private industry and the National Sea Grant College Program , National Oceanic & Atmospheric Administration , U.S. Department of Commerce . The University of Wisconsin Sea Grant College Program is administered by the Sea Grant Institute on the UW-Madison campus in Madison, Wisconsin.
Posted 13 February 1997 by S. Wittman
All contents copyright 1997 University of Wisconsin Sea Grant Institute
Laboratory research photographs by Jan Spitsbergen, School of Pharmacy, University of
Wisconsin-Madison.
www.seagrant.wisc.edu/research/ResearchNews.html
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