Dioxins drove Great Lakes trout
From Our Stolen Future.org
Cook, P, JA Robbins, DD Endicott, KB Lodge, PD Guiney,
MK Walker, EW Zabelo and RE Peterson. 2003. Effects of
Aryl Hydrocarbon Receptor-Mediated Early Life Stage Toxicity
on Lake Trout Populations in Lake Ontario during the 20th
Century. Environmental Science and Technology. DOI: 10.1021/es034045m
Lake trout became extinct in Lake Ontario by the 1960s.
Their decline has been attributed largely to excessive
commercial fishing and predation by the sea lamprey. But
there were hints that these might not be the real explanation.
For example, other fish declined, including some species
not subjected to fishing pressure. Then determined efforts
to decrease lamprey numbers had little impact on lake
trout numbers. And re-stocking efforts using year-old
fish that started in 1971 succeeded in creating a small
population of adults, but no successful breeding until
With this paper, Cook et al. make a persuasive case that
lake trout were eliminated not by the factors that received
so much attention over these past several decades, but
instead because of dioxin and dioxin-like pollution in
Lake Ontario and its high toxicity to embryos and very
young trout just after hatching. The breeding recovery
that has been occurring since 1985 has taken place as
dioxin levels gradually decreased to beneath the concentrations
that caused complete mortality in young fish.
The key toxicological findings that pointed to dioxin's
impact (and other dioxin-like contaminants) were a series
of studies demonstrating that lake trout sac fry are extremely
sensitive to dioxin's most powerful form, TCDD.
Transfer of TCDD from the mother trout to her eggs kill
the fry at dioxin levels above 30 picograms/gram (parts
per trillion). By 100 ppt, all fry die. Other contaminants
that act via the same molecular mechanisms as TCDD, the
aryl hydrocarbon receptor, interact additively with TCDD.
Hence the impact has not been due to just one chemical,
but to a mixture all of which together affect survival
of young fish. To date, lake trout are the most sensitive
fish species to TCDD impacts during the early life of
fry that has been found.
Their analysis rests on three different sets of data:
population trends in adult lake trout in Lake Ontario,
based on fish capture records;
toxicological impacts of dioxin and dioxin-like contaminants
on young trout mortality;
a reconstruction of dioxin levels in Lake Ontario from
sediment cores and from fish samples.
Their findings are important because they reveal the powerful
population-level impact that low-level but highly toxic
contaminants can have on commercially important fish.
What did they do? Cooke et al. compiled data on fish
contamination and sediment from samples that had been
taken since the 1970s. The fish samples allowed direct
measurement of contamination levels. For the years before
1971, when no tissue or eggs were available either from
lake trout or similar species, the scientists estimated
contamination levels by measurements of contamination
in sediments, combined with information about how those
levels relate to what is found in fish.
The sediment studies allowed them to reconstruct the
build-up of contaminants in Lake Ontario during the 20th
century. Sediment gradually accumulates on the lake bottom,
so in places where it has not been disturbed, deeper parts
of the cores are from older time periods. They used trace
patterns of radioactivity to help determine at what year
a given layer of sediment was deposited.
They then determined when dioxin contamination would
have reached levels that would harm larval fish, the most
delicate part of the life cycle of lake trout, and they
looked at the relationship between those data and when
lake trout went extinct.
What did they find? Cook et al.'s indicate that all lake
trout sac fry in Lake Ontario would have been killed by
dioxin for several decades during the middle of the 20th
Based on their calculations of exposure to dioxin/dioxin-like
contaminants, virtually all lake trout fry would have
been killed by 1950, when the minimum predicted level,
in blue, reaches 100%.
Observed mortality (available for several years since
1978) tracks between predicted minimum and maximum mortalities.
What does it mean? This compelling documentation of the
extirpation of a commercially- and recreationally-exploited
fish population caused by dioxin-related contamination
took an extraordinary scientific effort, spanning years
of work and a sophisticated combination of laboratory
and field studies. The findings contradict long-held assumptions
about what had driven lake trout in Lake Ontario to extinction,
assumptions that were used to justify a series of costly
and ultimately ineffective interventions.
One of the central messages of this work is that different
parts of the life cycle of an organism are not equally
vulnerable to contamination, but that the bottleneck created
by a single life-cycle stage's vulnerability can affect
population size profoundly. Annual stocking of yearling
trout, beginning in 1973, was successful in establishing
a population of adults, with no outward sign of dioxin-related
adult toxicity, but a population incapable of breeding
because of effects on reproduction and larval survival.
Cook et al. cite research showing that adult female lake
trout showed no overt signs of toxicity to TCDD levels
3x that sufficient to cause 100% mortality in their offspring.
These females also failed to ovulate. Then as Lake Ontario
dioxin levels fell in the 80s through to 1994, fecundity
of lake trout rose 8-fold.
Few commercial fish species have been studied as thoroughly,
from a toxicological perspective, as Lake Ontario lake
trout. Indeed most fish species have received very little
attention. This study raises unanswered questions about
the contribution of contamination to declines in other
fishing stocks, particularly those whose larval nurseries
are in contaminated estuaries, or anadromous fish whose
migrations may take them into contaminated watersheds.