Fish are good for you - except when they're bad. How a legacy of environmental contamination continues to haunt one of our healthiest foods, and what we can do to fix it.
If every writer has a muse, then Nancy Langston’s is surely Lake Superior. An environmental historian who has written three books about people’s connection to natural places, Langston fell in love with the lake’s shimmering blue expanse while house-sitting for a colleague several summers ago. Within a month she’d begun looking for her own lakeside retreat, and soon found it in a 10- by 20-foot shed, to which she and her husband added insulation and a floor. Here she has spent every summer since, drawing inspiration from the rare beauty of her surroundings: the vast, unbroken forests, the beaches of polished stones, the serenity of her kayak slicing through the waves. And, of course, the fish—succulent, fresh-caught lake trout so alive with flavor they could be a muse all on their own. Her days often ended with a trip to the market for a few fresh fillets to cook for dinner.
But Langston doesn’t eat lake trout nearly as often anymore. Despite its divine flavor and undeniable health benefits—including a wallop of omega-3 fatty acids—she fears that her habit of eating trout three or four times a week was doing harm to her body. One concern is toxaphene, a pesticide sprayed extensively on cotton fields in the 1960s and ’70s that has found its way into Lake Superior waters. A member of the infamous “dirty dozen” organic chemicals outlawed in 2004 by the international Stockholm Convention—along with PCBs, DDT and dioxins—toxaphene has been linked to kidney and liver problems and increased risk of cancer. Still more troubling is how toxaphene levels have risen over time in large, predatory Lake Superior fish such as lake trout, even as traces of other banned chemicals have declined.
Langston, a professor with UW’s Nelson Institute for Environmental Studies and CALS’ Department of Forest and Wildlife Ecology, had never heard of toxaphene before reading chemist Melvin Visser’s 2007 book Cold, Clear and Deadly, which chronicled the history of the pollutant in the Great Lakes. Visser’s tale put an abrupt end to her love affair with lake trout.
“Now I know enough that I mostly eat whitefish,” she says. “It’s lower on the food chain so it’s less high in contaminants. But it’s also less abundant in healthy fats. And it just doesn’t taste as good.”
In her dilemma over fish, Langston is hardly alone. Consumers are told repeatedly that fish is among the healthiest sources of protein in our diets. Eating fish twice a week can help stave off heart attacks and lower cholesterol. Doctors encourage women to eat more fish during pregnancy to prevent early delivery and foster fetal brain development. But looming over these benefits is a dark warning about toxic chemicals with the potential to cause cancer, neurological problems and reproductive dysfunction. Worse still, the dangers are rarely clear, varying greatly among fish species and location, making it tough for consumers to know how to protect themselves.
“It’s a real quandary for anybody: Can you eat the fish? Is it healthy to eat fish?” says Marty Kanarek, an environmental epidemiologist in the UW-Madison School of Medicine and Public Health who has studied contaminants in fish and their impacts on people. “You know, when you go to the grocery store, the price per unit (on foods) is marked carefully, the calories are labeled, all kinds of ingredients are labeled. But the labels don’t tell you which fish is safe and which isn’t.”
How did we reach this place, where one of our healthiest foods has grown so complicated? As is true of many contemporary questions, the answers lie in the past, Langston says. In her latest book, Toxic Bodies, she delves into a 70-year history of industrialization and environmental pollution that begins to explain why we’re facing a problem with fish. But the story is much more than that. Mostly, it’s about us—us and the unbreakable tie to the world around us, a connection that is at once obvious and easy to forget.
It was not a fish, but an endangered bird, that first drew Langston’s attention to the influence of humans in ecosystems. As a graduate student pursuing her Ph.D. in ecology, she traveled to Zimbabwe to observe bird populations in a national park, but she quickly found herself more interested in an unfolding human story. A flood of refugees from neighboring Zambia had stirred fears about poaching, leading park officials to warn that any African caught inside the park would be shot on sight. At the same time, Zimbabwe’s own agricultural lands were shifting heavily toward commodity crops such as sugarcane, creating pressure to open parklands to settlement and farming. Langston soon became convinced that the real driving factor in environmental change was human culture. Understanding and reversing environmental decline, she realized, required watching more than birds. It meant observing people.
After returning home, she refocused her research on environmental history, the study of the shared history of people and the land. Her first book, published in 1995, explored the root causes of the failing health of forests in the western United States. She followed with an examination of riparian zones, showing how scientific and cultural ideas about nature triggered often-contentious disagreements about how to manage these areas.
Her interest in environmental pollutants was sparked by conversations with one of her graduate students, a native of Wisconsin named Maria. Growing up on the shores of the Fox River, Maria spent her summers swimming in the Green Bay waters where the Fox River empties. Friday feasts of local fish were a family tradition. Only years later did she realize the river was choked with PCBs, released over decades by paper mills lining its banks. The Fox River became a Superfund site, and Maria became an environmental scientist. She became keenly aware of the dangers of PCBs, which can collect in the body, causing cancer and disturbing hormonal activity.
By 2000, Maria confronted a difficult choice. Pregnant with her first child, she worried about whether to breastfeed her baby, knowing that the PCBs she’d accumulated during her childhood could flow into her baby with breast milk. At the same time, how could she not breastfeed her baby, considering all the benefits it provided?
Maria’s dilemma haunted Langston. It also left her curious. What in our history could explain why such painful decisions were necessary, and how might our past end up shaping the future?
“Part of what interests me is that we eat fish in the here-and-now, but fish have the traces, the legacies, of the past five decades of industrialization,” says Langston. “And our children and grandchildren will continue to bear those legacies.”
In her research for Toxic Bodies, Langston went back to the days just after World War II, when advances in the manufacture of synthetic chemicals spawned an array of new industries. In the decades since, synthetic fertilizers, pesticides and pharmaceuticals have flooded the U.S. consumer market, bringing with them scores of benefits. The products have boosted yields of the nation’s most important food crops, kept pests at bay and ushered in an age of better living through chemistry. But we know now that many of these wonder chemicals have a dark side: Their use can exact a devastating toll on the environment and the health of people and animals. And as Langston argues, we often continue to feel the impact of chemicals even decades after they were used.
The focus of her book is diethylstilbestrol, or DES, a hormone-mimicking chemical approved by the then fledgling Food and Drug Administration in 1941. A potent form of synthetic estrogen, DES was shown in early tests to cause cancer and disrupt sexual development in laboratory animals. Nevertheless, the FDA first sanctioned it as a hormone replacement for women during menopause and later as a treatment for pregnant women to prevent miscarriage. DES found further use in the livestock industry, which deployed it to increase meat in chickens, turkeys and cattle without increasing feed. Millions of women were prescribed DES, and millions more were exposed to residues of the chemical through meat and polluted runoff from farms Yet the FDA didn’t fully ban the chemical until the early 1970s.
Why the agency approved DES and then failed to restrict it for so long is central both to Langston’s book and to the situation we face with many other contaminants. Langston explains that since the 1920s, debate has raged over whether chemicals should be regulated based on their potential to cause harm or evidence of actual harm. In many instances through history, the latter argument won out: Regulators agreed to approve use of chemicals where the effects on humans were unknown or unclear.
And there’s the rub. Demonstrating that chemicals will harm us is tough because such lab tests can’t be carried out on people. Typically, the best evidence of a chemical’s effects come from studies on lab animals, but scientists are far from unanimous about how well those studies predict what might happen in human populations. Even extrapolating lab studies to wild animals is tricky. For one, environmental levels of toxins are typically much lower than the doses employed in toxicology tests, says Bill Karasov, a colleague of Langston’s in forest and wildlife ecology who has studied the effects of contaminants on fish-eating birds, including loons and bald eagles. Animals also vary tremendously in their vulnerability to different toxins. Some species may be worse than others at clearing a chemical once they consume it, for example, or they may harbor especially sensitive target sites in the body.
Nothing, therefore, is assumed. Along with laboratory experiments, regulatory agencies usually require proof of harm from both studies of wildlife and epidemiological research on people—where exposure to a contaminant is correlated to health problems—before banning or restricting a chemical.
“Our society demands a lot of evidence before we take policy actions,” says Karasov, “and that goes for protecting human life and wildlife.”
But others worry that the level of certainty required to ban a chemical creates a wedge for manufacturers, who can argue that the clear economic and social benefits of using chemicals outweigh the potential threats. “It’s precautionary to assume that if a chemical causes harm to other animals then it could be harmful to people,” says Langston. “But each time there’s political pressure, that caution gets eroded.”
One chemical whose toxic effects are undisputed is mercury. In its silvery, elemental form, mercury is relatively harmless. But the metal can also take an organic form, called methylmercury, that can accumulate in tiny organisms and the larger animals who eat them, sometimes with tragic results.
That is what happened in the 1950s in the Japanese town of Minimata, where a factory had begun dumping mercury-laden wastewater into a nearby bay. Unbeknownst to the company or townspeople, the waste mercury wasn’t washing out to sea, but was instead accumulating as methylmercury inside bay fish, a chief source of food in the local diet. The result was a public health disaster.
“Babies were born with a terrible cerebral palsy-type condition where they were virtually helpless, and they had all kinds of neurological problems,” says Kanarek, who has studied mercury exposure in Wisconsin communities that depend on fishing. Children and adults in Minimata lost the ability to walk or speak. Some shook violently. The strange ailment afflicted entire families, and it soon was dubbed Minimata disease.
Thinking the condition was contagious, the community isolated the victims and disinfected their homes. But people eventually suspected a different cause. Cats were behaving strangely after eating fish tossed from boats returning from the bay. “The cats would do this dance in the air and then drop dead,” says Kanarek. “That’s when people first began realizing that maybe fish were causing the problem.”
Although concentrated sources of mercury pollution are virtually nonexistent today, methylmercury in fish remains a public health threat in many parts of the world, including Wisconsin. Released into the atmosphere primarily through coal burning and small gold-mining operations, mercury can travel anywhere from a few miles to halfway around the globe before falling to earth. When it reaches lakes and oceans, microorganisms convert it into methyl form, which then gets stuck in small organisms like plankton. Plankton is eaten by fish, which in turn are eaten by larger fish, passing mercury contamination up the food chain. As a result, “tiny quantities in water end up being hundreds of thousands of times more concentrated in fish,” says Henry Anderson, the State of Wisconsin’s chief medical officer for environmental and occupational health. “Then we’re at the top of the chain, so it accumulates in people.” The same mechanism explains how toxins such as PCBs and toxaphene reach unsafe levels.
It’s the job of Anderson’s department to help people reduce their exposure, which it does first by monitoring a host of contaminants in fish—everything from older banned chemicals, like DDT, to newer ones, such as flame retardants. The group then issues consumption guidelines for fish caught in Wisconsin lakes and sold in grocery stores.
But the advice grows quickly complicated. For one, species from the same lake often contain different amounts of toxins; a walleye, for example, typically has four times the methylmercury of a bluegill. This means that warnings to merely stay away from certain lakes are too simple.
There are other complexities, as well. Methylmercury does slowly leave the body, for instance. So if a woman wants to get pregnant, she can reduce her mercury level by half if she stops eating contaminated fish for two months. PCBs are another story. “You just accumulate them over your lifetime,” Anderson says. At the same time, since PCBs build up exclusively in fat, a diner can cut exposure to PCBs by as much as half simply by trimming away a fish’s skin and belly fat. The same trick does nothing to lower methylmercury, however, which settles in muscle tissue throughout the body.
It’s enough to make one swear off eating seafood altogether. But Anderson contends that being informed about fish isn’t different from learning how to limit our intake of saturated fat or salt. The basic guidelines are simple, he suggests: Know where your fish come from, and eat a variety of types, especially smaller, short-lived species low on the food chain, such as bluegills, yellow perch and small rainbow trout. And most Wisconsinites consume fish once a week or less, hardly enough to worry about.
“Most people don’t eat that much fish,” he says. “They could probably stand to eat more.”
This may be true for many Wisconsin families, but it’s hardly the case for Mic Isham. A leader of the Lac Courte Oreilles band of Ojibwe in northern Wisconsin, Isham and his family follow a traditional lifestyle that revolves around Ojibwe customs, encompassing language, culture and spirituality. Tribal members gather and hunt indigenous foods such as wild rice, berries, venison and fish, which form a significant portion of their diets. The serving of these traditional foods is also required at feasts, funerals and other tribal ceremonies. And in northern Wisconsin, any traditional feast is bound to include plenty of walleye—ogaa in Ojibwe. This means that when the ogaa spawn in the spring waters around Lac Courte Oreilles, the Ojibwe fish. And fish. And fish.
“We harvest them,” says Isham. “We get 300 fish, we put them in the freezer, and we’re eating a lot of meals a week with our children and our families.”
The Lac Courte Oreilles alone take between 1,900 and 2,500 fish during spring spear-fishing season, says Isham, who helps manage the annual harvest for his band. Yet cherished as the tradition may be, it too has been touched by modern day concerns about chemicals. When Isham chooses the 15 or so lakes where the band will spear, for example, he takes a step his ancestors never did: He consults a set of maps issued by the Great Lakes Indian Fish and Wildlife Commission, detailing which lakes carry the highest risk of methylmercury exposure. At the same time, tribal members are encouraged to catch and eat mostly smaller fish, both during the spear-fishing season and throughout the year. Because families freeze so many fish to eat later, they’re also taught to label each bag with the weight and species of fish, along with where it was caught, to help them monitor their families’ exposure to methylmercury and other contaminants.
But these are far from the most significant changes the tribe has seen. “Cleaning up certain things, like mercury in a lake, is really, really hard. The obvious way to go is to prevent any further contamination,” says Isham. “So now we’re really environmentally active.” The Ojibwe have been vocal in calling for regulation of mercury emissions from coal-burning plants, for example. But they work on many other issues, as well, including mining, shoreline development, forestry practices and dealing with invasive species.
Why cast such a wide net when the target is contaminated fish?
“It’s all connected,” Isham says. “That’s how we try to educate our youth, so that the next generation is smarter than we are when it comes to contaminants and other things.” He explains how the tribe understands that activities far outside their community affect the health of fisheries and forests, just as the actions on their reservation spill over to the lands outside. Likewise, the philosophy with chemicals, he says, is to understand that by using them in the wider world “basically you’re putting them into your own body.”
This is the ultimate message of Langston’s work, and it leaves us with an ultimate choice. Are we satisfied with making personal decisions about which fish to eat and how often? Or do we want to work toward a future where such decisions aren’t required anymore? Because the way the world is now wasn’t inevitable, says Langston. It, too, was built of choices.
“For me, that’s one of the most valuable lessons about history,” she says. “We’re not constrained by the way the present looks today. There were other paths we could have taken (in the past) and that means there are other choices we can make here and now.”
As we consider this, we may want to remember the Ojibwe, who not only believe the health of people and the water are inextricably linked, but that each is also the caretaker of the other. Thus, they say that when human life is sick, the water will flush it away.
And when the water is sick, it is up to us to flush it away.
SIDEBAR — Grow Fish
If wild fish turn unhealthy, can farmed stocks swim to the rescue?
With many wild fish stocks in decline from overfishing and other threats, aquaculture—the managed cultivation of fish—has taken on a larger role in feeding the nation’s growing appetite for seafood. But are farmed fish really any freer from contamination than wild ones?
That all depends, says Jeff Malison, director of the CALS aquaculture program in the Department of Animal Sciences.
“No fish is going to be pollutant-free,” he says. “But yes, farmed fish can have much lower levels (of contaminants) than wild fish—at least they have that potential.”
Because farmed fish accumulate toxins from the environment and their food just like wild fish do, the key to producing a “clean animal” is to grow it in fresh, unpolluted water and feed it a diet free of toxic ingredients, Malison says. But farmed fish also have a fin up on their wild kin: They grow much faster, which means they have considerably less time to collect pollutants during their short lives. Pond-raised rainbow trout, for example, are usually big enough for the dinner plate by one year old, whereas wild trout of the same size might be three to four years old.
Wisconsin happens to be among the top 10 producers of farmed rainbow trout in the country. But before consumers rush out to buy farm-raised filets of other popular Midwest fish, such as yellow perch and walleye, they should know that fish farming is hardly routine. Malison points out that we raise only about six to 10 bird and mammal species for meat, but we eat around 200 species of fish, each with its own set of environmental needs and tolerances. And with the exception of a few species, most fish have yet to be bred for captivity.
“Even though it was practiced in China 4,000 to 5,000 years ago,” says Malison, “aquaculture is still relatively young as a technological industry.”
The aquaculture program has been working since the 1970s to improve two critical factors that limit the production of fish: reproduction in captivity and the costs of raising juveniles. The diminutive yellow perch is a prime example. Because it takes many perch to make a meal, farmers need to grow lots of them. “And when you need lots of them you’ve got to make sure the cost of the babies is really, really low to develop a profitable industry,” says Malison. “So we’ve been doing a lot of research on reproduction to try to reduce the cost of fingerling production.”
CALS researchers have also studied walleye, but for a very different reason. Carnivorous and aggressive, “it’s really kind of a rascal in captivity,” Malison says, noting that farmed walleye have a tendency to attack their own mates. To solve this problem, his group is now using Wisconsin Department of Agriculture, Trade and Consumer Protection funds to breed the brutish walleye with a closely related fish, called the sauger. The result is a much more docile fish that also grows faster.
The success of these projects will surely expand the choices consumers have at the grocery store. But another goal is to expand the state’s aquaculture industry, which also encompasses bait fish and fish for stocking lakes and rivers. And as Malison notes, Wisconsin has plenty to bring to the table—water resources, farming expertise and, of course, the market. Fish fry, anyone?This article was posted in Communities, Cover Story, Environment, Features, Health, Main feature, Summer 2010 and tagged Animal health, Animal science, Food science, Grow Fish, Human-wildlife interactions, Jeff Malison, sidebar, Wildlife ecology.
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