Shark-Fin Soup and Methylmercury: To Eat or Not to Eat

Fish are a good, low-cost, low-fat source of nutrition, rich in healthy, omega-3 fatty acids. However, some fish may be contaminated with mercury, a natural and abundant environmental element, and particularly methylmercury, a toxic product biotransformed from mercury by selected bacteria. These and other toxicants from the water from which fish are harvested present health risks to vulnerable populations such as pregnant and lactating women, unborn children, and young children. Exposure to high levels of methylmercury has produced fatalities and devastating neurological damage. In addition, it is a known teratogen.

Large, long-lived, predatory ocean fish, such as tuna, swordfish, king mackerel, and shark, bioaccumulate methylmercury in the edible portions. In fact, methylmercury levels may be 1,000–10,000 times greater in selected seafood and shellfish than in any other foods. From an environmentalist perspective, the combination of the food safety concern and the rather inhumane treatment of sharks—removing dorsal fins and dumping the vulnerable, finless sharks at sea—to prepare shark-fin soup has recently prompted activists to promote a ban on shark finning.

Some local and state agencies have had regulatory programs in effect for more than 20 years. Wisconsin, for example, warns women of childbearing years, nursing mothers, and children under 15 years to eat only one meal of bluegill, sunfish, crappie, yellow perch, or bullheads per week and only one meal of pike, catfish, sturgeon, carp, and bass per month. The Food and Drug Administration has set an advisory limit of 1 ppm for methylmercury in commercial fish.

But are we throwing the baby out with the bath water? Nutritionists have been touting the benefits of eating marine-fish products for decades. After all, fish is a great source of protein and polyunsaturated fatty acids which may be important for normal neurological development in infants and may be cardioprotectants via some anti-inflammatory modulation mechanism. Fish species that accumulate mercury contain many essential nutrients; thus, benefits of avoiding contaminated fish as a short-term solution must be balanced against possible nutritional disadvantages. For some populations, even within the United States, caught fish may be the only good source of protein for a nutritious diet.

The paradox becomes more complicated when we consider that several nutrients—selenium, zinc, and vitamins C and E—have a profound effect on mercury and methylmercury toxicity. For more than 30 years, we have known about the protective effects of selenium against mercury. Many marine organisms that have high tissue levels of mercury also have high tissue levels of selenium or a mercury-to-selenium tissue ratio of 1:1. Thus, the apparent survival of certain species in the midst of mercury intoxication may be related to a detoxification mechanism involving interactions between mercury and selenium. It is noteworthy that European research has demonstrated the usefulness of a remediation process of adding selenium salts to mercury-contaminated lakes. Such work has improved the ecology of such areas, including survival of endogenous aquatic organisms. However, U.S. agencies have not willingly grasped the concept of using a toxic element in the remediation of another toxic element.

Research results suggest that it is important for regulatory agencies, such as the Environmental Protection Agency and FDA, to take actions that will protect vulnerable populations from potential adverse effects of mercury and methylmercury in fish. But they also behoove these agencies not to exclude consideration of possible nutritional adjuvants against mercury, such as selenium.

The regulatory agencies and food scientists must:
• Intensify technical research to reduce, to the greatest possible extent, exposure of pregnant and lactating women, children, and other sensitive general populations to mercury and methylmercury.

• Clarify the effect of selenium on the toxic bioavailability of mercury and organic mercury, e.g., investigate its possible usefulness in the detoxification of heavy metals and consider the role of selenium-sequestered mercury in protecting humans against methylmercury-induced neuropathologies.

• Reassess environmental cleanup technologies and processes that may use substances that are designated as toxicants, e.g., use of selenium in remediation of sites contaminated with mercury.

• Examine the effect of other potential contributing factors—such as nutritional deficiencies and interactions, other pollutants, and polychlorinated biphenyls (PCBs)—on mercury-induced dysfunctions.

• Design and implement regulatory plans to protect the public from contaminants. These plans must consider the total science, including conflicting studies.

There is much more research to be done so that we can develop a better understanding about potential toxicant–dietary interactions and special susceptibilities. There are critical data gaps in exposure and neurological, immunological, and cardiovascular effects resulting from toxicant–nutrient interactions. Such interactions may result in overall better nutrition, health, and ecological stability.

by STANLEY T. OMAYE
Contributing Editor
Professor, Dept. of Nutrition and
the Environmental Sciences & Health Program
University of Nevada, Reno