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Cause Found For Great Lakes Trout Reproduction Failure

Date:
February 13, 1997
Source:
University of Wisconsin Sea Grant Institute
Summary:
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.


Story Source:

The above story is based on materials provided by University of Wisconsin Sea Grant Institute. Note: Materials may be edited for content and length.


Cite This Page:

University of Wisconsin Sea Grant Institute. "Cause Found For Great Lakes Trout Reproduction Failure." ScienceDaily. ScienceDaily, 13 February 1997. <www.sciencedaily.com/releases/1997/02/970213133222.htm>.
University of Wisconsin Sea Grant Institute. (1997, February 13). Cause Found For Great Lakes Trout Reproduction Failure. ScienceDaily. Retrieved September 2, 2014 from www.sciencedaily.com/releases/1997/02/970213133222.htm
University of Wisconsin Sea Grant Institute. "Cause Found For Great Lakes Trout Reproduction Failure." ScienceDaily. www.sciencedaily.com/releases/1997/02/970213133222.htm (accessed September 2, 2014).

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