Large predatory fish such as Lake Trout can accumulate many toxic chemicals, making fish consumption an important source of human exposure. Even after these chemicals are banned, levels may continue to rise in lakes, fish, and people. In the late 1990s, Canadians noticed that levels of a persistant organic pollutant named toxaphene were rising in the fish of Lake Superior, even though the chemical had not been used anywhere near Lake Superior for decades. High toxaphene levels were startling because, along with other POPS, toxaphene had been banned in the 1980s. But levels of toxaphene were for some reason extraordinarily high. When researchers looked, it was clear that people who ate fish from the Great Lakes were accumulating significant levels of banned toxic chemicals. During pregnancy and breastfeeding, women passed those chemicals to their developing fetuses, at their most vulnerable stages of development. The legacies of the past were becoming the body burdens of future generations.
Lake Superior, on the border between Canada and US, is cold, vast, and distant from most industrial development. Of all the Great Lakes, it is easily the cleanest, and in many ways it seems almost pristine. So why would toxaphene be highest in this particular lake, in a region where the chemical had never been produced and had hardly even been used? What might that contamination mean for one of the great recovery stories of modern conservation: the restoration of Lake Superior fisheries? Even more pressing, what might that contamination mean for Ojibwe bands trying to restore culturally significant foods such as lake fish to their diets?
The name toxaphene refers to a group of turpentine-smelling chemicals made from pine oil and chlorine--two natural chemicals combined into a synthetic substance. First introduced in 1945 by Hercules Co. (Wilmington, DE), toxaphene was immediately found to be toxic to fish, birds, and mammals. In the late 1940s, research was published showing its toxicity, and over the next 2 decades, studies showed it to be mutagenic and carcinogenic in mammals. Even though much of this research was published well before DDT was banned, soon after the ban on DDT in the early 1970s, toxaphene manufacturers began promoting toxaphene as a safe alternative to DDT--safe because it was made from nature's own building blocks. Soon it was being mass produced and widely used as an insecticide, particularly in the cotton-growing industry in the American South.
Toxaphene became one of the most heavily used pesticides ever--as much as 46 million pounds a year during the height of its use in the 1970s, according to the U.S. Agency for Toxic Substances and Disease Registry. In the United States, most of that was sprayed on cotton and soybeans in the South, but it was registered for use in more than 800 products--for everything from tick control on livestock to the killing of unwanted fish species in lakes and ponds.
After research showed it to be carcinogenic, mutagenic, and teratogenic, its use was banned in the US and Canada in the 1980s. But instead of destroying existing stocks of the chemical, manufacturers shipped them overseas, and soon began marketing the chemical worldwide. Throughout Russia, China, and Africa, the chemical found its widest use.
In the 1950s, lake trout in the Great Lakes had been driven to the verge of extinction. With intensive fishing harvests, invasion by sea lampreys and alewives, and accumulation of persistent organic pollutants that affected reproductive health, the cumulative effects had led to a collapse of lake trout populations, with economic, cultural, and health consequences for Native peoples and for whites alike. But, in one of the great recovery stories of conservation, commercial fishing restrictions and the banning of many persistant organic pollutants led to a substantial recovery. By the late 1980s, breeding populations appeared to have recovered in Lake Superior. So the finding, a decade later, that lake trout were newly contaminated with toxaphene, unsettled fisheries biologists deeply. Where was that toxaphene coming from?
Researchers initially suspected the culprit was pulp mills lining the Canadian shores of Lake Superior near Thunder Bay, where deforestation of regional boreal forests had begun in the 1980s. The harvests supplied a growing paper industry, which dumped pulp mill wastes directly into Lake Superior. Those wastes contained chlorine and pine oils, which could combine under certain natural conditions to form toxaphene. But even in inland lakes such as Lake Siskiwit on Isle Royale--unaffected by toxins directly carried over from Thunder Bay--contamination was high.
Evidence suggests that the chemical continues to be volatized from old cotton fields in the American South, and that global wind currents may also be transporting toxaphene still used in Africa into Lake Superior and other boreal lakes—where it finds its way into fish, and eventually into the people eating that fish. Once it falls into Lake Superior, it tends to concentrate, for the lake never gets warm enough to allow much toxaphene to go airborne again. Canadian researcher Terry Bidleman of the Atmospheric Environment Service has documented toxaphene as far north as the polar ice cap, stored in the fat of marine mammals, fish, and northern peoples.
The Canadian government advises citizens to avoid eating Lake Superior trout altogether because of toxaphene contamination. Across the border in the United States, levels are equally high, but no advisories warn against consumption of fish contaminated with toxaphene. Nevertheless, because the present concentrations in fish are high enough to be causing reproductive problems for the fish themselves, researchers are concerned that human health may also be at risk.
Among those most concerned are indigenous communities who live along the shores of Lake Superior. Fish is particularly important for the health of fetuses and young children, and eating fish is of great cultural significance. But its potential contamination forces communities to make trade-offs between their beliefs and possible harm to themselves. How much fish do you eat when it’s culturally important? How much do you eat when you’re pregnant?
Many tribal health departments are urging members to eat much more traditional or country food, wild food, to reduce the risks of diabetes, heart disease, and obesity from high-fructose corn syrup, white flour, trans fats that make up the average American diet. But much traditional food, such as lake trout, is at the top of long food chains, and therefore quite high in contaminants that have bioaccumulated in the fat of prey species. As the writer Paul Rauber notes, "Like dead fish rising to the surface, poisons dumped down drains or pumped into the wind return again--often on the plates of the poor." Rauber reports on a visit to the Red Cliff Band of Lake Superior, where the biologist and tribal member Judy Pratt-Shelley told him: “We don't need people to tell us,`Don't eat the fish,'" ...'This is a guaranteed, federally reaffirmed right that we retained in our treaties when we ceded this territory: the right to hunt, fish, and gather.....What we need is for the laws to change so that those [chemicals] aren't allowed in the ecosystem to begin with. That's the only way they're not going to end up in our breast milk.' Giving up local fish would mean giving up her culture, and while the effects of eating tainted fish are chronic, subtle, and often hard to separate from the manifold ailments of poverty, the effects of losing one's culture are there for anyone to see: alcoholism, broken families, drifting children....In the end, the only problem fish advisories solve is that of informed consent. People have a right to know the risks involved in what they eat, but they have an even more fundamental right not to face those risks in the first place."
Melvin J. Visser, Cold, Clear, and Deadly: Unraveling a Toxic Legacy 14 ( 2007).
 H J de Geus et al., Environmental occurrence, analysis, and toxicology of toxaphene compounds, 107 Suppl 1 Environmental Health Perspectives 115-144 (1999).
 Id. See also S. Fields, Great Lakes Resource at Risk, 113 (3) Environ Health Perspect A164-173 (2005), http://www.ncbi.nlm.nih.gov.ezproxy.library.wisc.edu/pmc/articles/PMC1253773/ (last visited Nov 17, 2009).
 V. Monks, How Did the Poison Get into the Trout, National Wildlife 36 (1998), http://www.nwf.org/nationalwildlife/article.cfm?issueID=19&articleID=157 (last visited Nov 17, 2009).
 Derek C.G. Muir et al., Bioaccumulation of Toxaphene Congeners in the Lake Superior Food Web, 30 Journal of Great Lakes Research 316-340 (2004).
 A popular discussion of this work can be found at Monks, "How Did the Poison Get into the Trout." The research includes:
Bidleman, T. F., and C. E. Olney. "Long Range Transport of Toxaphene Insecticide in the Atmosphere of the Western North Atlantic." Nature 257, no. 5526 (1975): doi:10.1038/257475a0. http://dx.doi.org/10.1038/257475a0.
Bidleman, T. F., and G. W. Patton. "Toxaphene and Other Organochlorines in Arctic Ocean Fauna: Evidence for Atmospheric Delivery." Arctic 42, no. 4 (1989): 307-313.
Bidleman, Terry F., and Andi Leone. "Soil-air Relationships for Toxaphene in the Southern United States."Environmental toxicology and chemistry / SETAC 23, no. 10 (2004): doi:10.1897/03-405.
Bidleman, T F, and A Leone. "Soil-air Relationships for Toxaphene in the Southern United States."Environmental toxicology and chemistry 23, no. 10 (2009): 2337-2342.
Jantunen, L M, and T F Bidleman. "Air—water Gas Exchange of Toxaphene in Lake Superior."Environmental toxicology and chemistry 22, no. 6 (2003): 1229-1237.
 Susan T. Glassmeyer et al., Toxaphene in Great Lakes Fish: A Temporal, Spatial, and Trophic Study, 31 Environmental Science & Technology 84-88 (1997).
 P. Rauber, "Fishing for Life: Thousands of Americans Face the Choice of Eating Contaminated Fish or Not Eating at All," Sierra Magazine Nov/Dec 2001, http://www.sierraclub.org/sierra/200111/fishing.asp (last visited Nov 17, 2009).