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
trout became commercially 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 1986.
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.
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.
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.
to right: Lake trout sac fry develop a characteristic set
of syndromes when exposed to TCDD. Damage includes a yolk
sac edema, hemmoraging and malformations in the skull.
from Cook et al.
analysis rests on three different sets of data:
trends in adult lake trout in Lake Ontario, based on fish capture
impacts of dioxin and dioxin-like contaminants on young trout
reconstruction of dioxin levels in Lake Ontario from sediment
cores and from fish samples.
findings are important because they reveal the powerful population-level
impact that low-level but highly toxic contaminants can have on
commercially important fish.
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.
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.
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.
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 century.
graph below summarizes the scientists' results. Lake trout numbers
plummeted from the 1920's onward, reaching commercial extinction
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%.
mortality (available for several years since 1978) tracks
between predicted minimum and maximum mortalities.
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.
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.
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.