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Great Lakes Article:

Dioxins drove Great Lakes trout levels down
From Our Stolen


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 1986.

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 century.

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.

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