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News Release (8K)



NEWS RELEASE
For Release: Thursday, 13 February 1997


CAUSE FOUND FOR GREAT LAKES TROUT REPRODUCTION FAILURE
Researcher says toxic chemicals are 'smoking gun' in 30-year-old mystery


FOR MORE INFORMATION:
Richard Peterson, University of Wisconsin-Madison -- (608) 263-5453
Stephen Wittman, UW-Madison Sea Grant Institute -- (608) 263-5371
Web page: http://www.seagrant.wisc.edu/research/ResearchNews.html


SEATTLE (2/13/97) -- For 30 years, efforts to re-establish reproducing
populations of lake trout in four of the five Great Lakes have failed. Now a
University of Wisconsin-Madison 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 more than a decade of laboratory research
supported by the National Sea Grant College Program and recently completed
studies in collaboration with Philip M. Cook of the U.S. Environmental
Protection Agency (EPA).

"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 at
a national Sea Grant news briefing today in Seattle. "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 species of 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.

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 fish -- 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.

# # # #
POSTED BY:
Stephen Wittman
Assistant Director for Communications
University of Wisconsin Sea Grant Institute
1800 University Ave. * Madison, WI 53705-4094
====================================
 Phone: (608) 263-5371 * Fax: (608) 263-2063
 E-mail: swittman@seagrant.wisc.edu
 URL: http://www.seagrant.wisc.edu
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