longer influence sac-fry and possibly contribute to subse-
When compared to the dose-response relationship for
quent recruitment problems.
overt early life-stage toxicity of TCDD to lake trout, the
resulting TEC eggs predict an extended period during which
Dr. Don Tillitt, Columbia Environmental Research Center of
lake trout sac fry survival was negligible.
the U.S. Geological Survey, reported to the SAB’s Work
Beginning in 1940, following more than a decade of
Group on Ecosystem Health, the findings of recently
completed work on the sublethal consequences of TCDD
population decline attributable to reduced fry stocking and
contamination to rainbow trout sac fry. To investigate this,
loss of adult lake trout to commercial fishing, Dr. Cook’s
behavioral methods based on the optomotor response
model predicts increased sac fry mortality and possible
were performed to achieve preliminary evaluations of
sublethal consequences due to TCDD-mediated effects
such that from 1950, early life-stage toxicity alone explains
visual/motor function of viable swim-up trout developing
from eggs exposed to graded doses of TCDD.  Preliminary
the subsequent loss of the species.  After 1980, reduced fry
results indicate that significant deficits compared to the
survival, associated with lethal and sub-lethal adverse
“normal” group in terms of detail discrimination (visual
effects, possibly complicated by other environmental
acuity), motion detection (flicker fusion thresholds) and
factors, have probably contributed to a lack of reproductive
success of stocked trout despite gradually declining TEC eggs
prey capture occurred at one-third the lethal
These effects also were associated with a
consentration 50.
Since 1995 there has been evidence of limited natural
reduction in the density of retinal ganglion cells.  These
reproduction.  Current day exposures to TCDD and TCDD-
results show that factors other than overt mortality may
like chemicals are likely near the most probable no
contribute to recruitment failures and imply that sac fry
observable adverse effect concentration (NOAEL TEC egg = 5
survivors of TCDD exposures above the no-observable-
pg TCDD toxicity equivalence/g egg).  However all the
effects-level for overt egg mortality exhibit adverse effects
potential sub-lethal consequences to chronic low-level
that may impact subsequent survival and recruitment.  The
exposure to TCDD-like contaminants and other factors that
results also support the contention that current egg TCDD
may impact feral lake trout recruitment have not been fully
toxicity equivalence concentrations of 5 pg/g egg in lake
elucidated.  Dr. Cook concludes that other less sensitive
trout from Lake Ontario are likely near the most probable
fish species were probably also affected when the highest
no-observable-adverse-effect concentration and that the
exposure levels were reached.
continued present day low-level of recruitment observed
for feral lake trout must also be associated with other
Assuming no new loadings of persistent bioaccumulative
contributory factors.
chemicals with TCDD-like toxicity, further reduction in
TCDD-like toxicity risk will occur with declines in concen-
Early mortality syndrome is the term used to describe an
trations of PCDDs, PCDFs, and PCBs in the surficial
embryonic mortality affecting the offspring of all salmonids
sediments.  Therefore, it seems most certain that not only
(coho salmon, chinook salmon, steelhead trout, brown
did the persistent TCDD-like contaminants contribute to
trout and lake trout) in lakes Michigan and Ontario and to a
the historical extirpation of an economically valuable
lesser extent lakes Huron and Erie.  Clinical symptoms of
fishery resource in Lake Ontario, until very recently, these
early mortality syndrome include loss of equilibrium,
contaminants have also thwarted extensive restoration
swimming in a spiral pattern, lethargy, hyper excitability,
efforts.  The work by Dr. Cook and his colleagues also
hemorrhage and death occurring between hatch and first
shows that successfully curbing the inputs of persistent
feeding.  Before 1993, mortality rates due to early mortality
TCDD-like chemicals has improved conditions in Lake
syndrome in Lake Michigan coho salmon offspring were
Ontario to the extent that overt early life-stage mortality
around 20 percent.  Beginning in 1993, early mortality
due to TCDD-like chemicals is no longer viewed as a
syndrome mortality in coho salmon rose dramatically and,
limiting factor for the restoration of self-sustaining lake
with the exception of 1997 and 1998, has proved to be
trout populations.
problematic for both coho and chinook stocks for the last
10 years. The extent of early mortality syndrome in lake
Curbing the direct inputs of 2,3,7,8-tetrachlorodibenzo-p-
trout from lakes Ontario and Michigan has ranged from 5 to
dioxin (TCDD) and TCDD-like contaminants into the Great
70 percent averaging near 30 percent over the past 10
Lakes has met with considerable success.  Concentrations
years.  Low egg thiamine levels and enhanced survival
of PCBs and TCDD have declined in lake trout eggs to the
following thiamine treatments are common characteristics
extent that there is no longer concern that overt mortality
of early mortality syndrome.  In the past few years, there
contributes to loss of sac fry.  However, this decline in the
have been significant developments in early mortality
concentration of persistent contaminants has slowed
syndrome research on Great Lakes species.
considerably in recent years.  There is a need to firmly
establish the exposure conditions under which sublethal
effects of TCDD and TCDD–like contaminants will no
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