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In 2004, and again in 2007, the issue of mercury in seafood rose its head as it had in 1972. This time, a coalition of top scientists from private groups and federal agencies had more information to work with and made the correct decision. Now it is up to the food regulators in USDA and EPA. I had participated in formulating the Government response to the 1972 scare and forwarded my recollections to the NOAA/National Marine Fisheries Service (NMFS) people working the issue and to the United States Tuna Foundation in the spring of 2004. Finally, the news is out of the bag and it is safe to eat fish, and it is healthy to eat fish - again.The following information was provided in 2004. It is clear, just from this, that there could be no other conclusion.
In 1972, there was very poor lab capability for mercury analysis. We did a test of about 6-10 NOAA and external labs on the same fish samples and the results ranged from not a trace amount to very high levels (perhaps even lethal) on the identical samples of blended fish. A couple labs had similar results and they seemed to be what was expected (more in larger fish), so we used their results as the standard for our NMFS labs to strive towards.
In the hysteria of the moment in 1972, we found a study (or did a study - can't remember) of the mercury content of fishermen’s hair on Japanese longline fishing vessels, which catch the larger fish. The mercury was beyond the perceived lethal concentration for the oldest crew members, yet they were apparently healthy. This evidence of non-toxicity was a major factor in our fighting those who wanted to have the standard tighter than 0.5 ppm (parts per million). At the time, we thought that the presence of elevated selenium (which we also found in the high mercury samples), must be having a salubrious, offsetting impact. We did not know the mechanism. We thought then that eating marine fish containing natural mercury (with selenium and perhaps other things), was very different than eating fish with man-made/introduced mercury in freshwater, or in a polluted estuary. This sounds remarkably like the “News” of October 2007.
Before bringing my recollections to the attention of Government and industry, I wanted to see if this was credible, so I reviewed about 400 articles available on the web. After doing so, the proposition appeared to me to be factually based and now scientifically supportable, yet I saw nothing where the Government nor industry was pursuing it. In the literature review below, I was particularly taken by the Japanese report (at the end) on the high concentrations of mercury in marine mammals that has been rendered non hazardous by processes that I suspect are mammalian in general. While the total mercury in fish is nearly 100% toxic methyl mercury, the marine mammals have converted it into relatively innocuous variants. It also goes on in rats, also reported below, when selenium is added to their diets, so it probably happens in humans when eating marine fish. Since we are taught that Earth’s animal life rose from the sea, and we know that mercury in the oceans pre-dates industrialization, it is logical that there must be a mechanism in our bodies, just as in dolphins, whales, and rats to deal with it.
I suspected the current generation of mercury/fish gurus may not realize that the wheel is going around again.... And the old files have all been boxed up and archived or destroyed. For NMFS it likely happened when NMFS was still housed at the Interior Building, then Wisconsin Ave, then Conn. Ave, then Silver Spring, Maryland.
I'm still eating my tuna!
Dr. John T. Everett, President
Ocean Associates, Incorporated
While searching for selenium/mercury relationships, in order to test the value of my own recollections before forwarding the materials to the National Marine Fisheries Service and the United States Tuna Foundation, some other relevant materials were also found and included, just in case they might be of interest to scientists. About 400 of 25,600 Google hits for “mercury selenium fish” were reviewed and searched for key words. This was done "gratis" out of personal interest.
The scientific credibility of the sources below, in several cases, are without merit. However, this does not mean the original source (unknown to me, but perhaps obtainable) is not credible. In many cases, though, scientifically credible sources say similar things and some are likely the sources for the lay articles.
Items are roughly organized by topic. In each case the source citation comes first. Extraneous materials have been excised, but the links to the source items are provided to assure anyone that the text is not being taken out of context. Remarkably, there is little evidence of opposing results to these citations below.
Source http://www.inchem.org/documents/jecfa/jecmono/v004je02.htm WHO Food Additives Series, 1972, No. 4
Some of the larger specimens of predatory species may contain high levels, apparently derived from natural sources since the same levels are found in museum specimens caught 50-100 years ago.
Research done on museum fish show fish had these same mercury levels over 100 years ago, so this is not a new issue, although industrial pollution does effect certain near-land areas more than others.
Museum collections provide evidence for temporal increases in mercury in wild birds. Mercury levels in the feathers of sea birds from the North Atlantic Ocean were higher in the 1980s than they were during the period 1850-1950. Furthermore, mercury in eggs of sea birds nesting in the Canadian arctic increased between 1975-1998. There is evidence for food chain biomagnification of mercury in aquatic ecosystems, suggesting that predatory species, especially fish-eating birds and mammals, may be at greatest risk from increases of mercury in the environment. In birds and mammals, a large proportion of the total body burden of mercury occurs in feathers and hairs, respectively. Dietary mercury as well as that stored in liver, kidney and other organs can be deposited in growing feathers and hairs. This is an important “detoxification” pathway, because once mercury is deposited in feathers or hairs it is inert and non-toxic.
For years, we have probably eaten tuna and swordfish with mercury levels above FDA's limit without harmful effects. Analysis of museum specimens of tuna caught from 1879 to 1909 reveal that they contain levels of mercury as high as those in fish being caught today. Scientists therefore conclude that mercury levels in tuna, and probably swordfish, have not changed in the past 100 years...Researchers found that some fish, including tuna, can block and reduce the toxicity of mercury in their tissues. This research may explain how we have safely eaten fish containing levels of mercury higher than allowed by FDA.
Source: WHO http://www.inchem.org/documents/jecfa/jecmono/v004je02.htm
When rats were maintained on a purified basal diet containing 20% casein or the same diet supplemented with 0.5 mg/kg selenium, with various concentrations of methylmercury in the drinking water all rats fed 10 mg/kg mercury without selenium died, but those fed diet with selenium were still alive at the end of week 6 (Ganther et al., 1972).
http://www.chem.unep.ch/mercury/Report/ Final report/chapter5.pdf
361. In particular, the ability of birds to demethylate methylmercury (which may be related to their dietary preference – fish diet versus vegetable diet) has important implications for avian risk assessment since most tests have been conducted on non-fish-eating species. In addition, the confounding effects of co-exposure to selenium on methylmercury toxicity should be mentioned, as selenium has been shown in laboratory studies to elicit protective and in some cases antagonistic effects on mallards depending on the life stage (US EPA, 1997).
Source National Institute for Minamata Disease
The effect of selenium compound for the toxicity of the methylmercury was examined in rats. Male rats of 10 11 weeks-old were used as experimental animals. Methyl mercury was administered to male rats at proportion of 5mgHg/B.W.-kg/day for 12 days. These rats died all within 2 weeks after the end of the administration. The selenomethionine was administered with methylmercury to the rats of the other group at the proportion of 1mgSe/Kg or 5mgSe/Kg. The rats that both of methyl mercury and selenomethionine were administered were also weak on the lowering of the body weight, and survived over 30th all. In addition, only the methylmercury is continuously administered to the rats of next group at proportion of 5mgHg/B.W.-Kg/day for 12 days, and selenomethionine was administered at proportion of 1mgSe/B.W.-Kg/day from the 13th. Intake of bait and water gently rose, when the selenomethionine was administered to these rats, and the body weight was also recovered, and then it began to increase. The rat over 80% survived over 30th. As above, it was clarified that the selenomethionine suppressed very strongly methylmercury toxicity for rats.
However, very high concentrations of mercury were found in tissue samples of the Saimaa ringed seal collected in the 1960s (Helminen et al. 1968, Henriksson et al. 1969). It is generally accepted that the toxicity of mercury for ringed seals is reduced by immobilisation of mercury to the liver by selenium (Smith and Armstrong 1978, Kari and Kauranen 1978). Thus, it was considered relevant (IV) to assess the possible impact of mercury on the well-being of Saimaa ringed seals...
In an experimental study it was found that selenium in the diet of an adult seal reduced mercury concentrations in hair. It is also noteworthy that when this experimental seal was released back to its native habitat, the level of mercury in hair soon increased back to the initial level (IV).
There is, however, some evidence that selenium tends to antidote the toxicity of mercury, at least within certain limits. Nevertheless, there is no reason to panic over mercury poisoning on the basis of the very skimpy and equivocal evidence of its environmental hazard to date.
The most toxic form of mercury, methyl mercury in an industrial waste that has been dumped into some water supplies. It is unsafe to eat fish taken from some areas because of their high mercury content. Mercury concentrates especially in fish liver. Larger, older fish tend to accumulate more mercury. Most swordfish should not be eaten. In tuna, albacore and skipjack are usually better than yellow fin and big eye.
The fish seem to be protected if they have a high enough level of selenium. This combines with mercury to form mercury selenate which is not toxic. Senenium is an immune system protectant that protects against cancer.
Vitamin E works with the mineral selenium to neutralize mercury
Source http://www.netl.doe.gov/publications/proceedings/03/ valuing-ext/posters/Ralston poster.pdf
Interesting slide presentation. Only last page copied here.
•MECHANISM OF MERCURY TOXICITY MAY INVOLVE INHIBITION OF SELENIUM DEPENDENT PHYSIOLOGY
•SELENIUM STATUS MAY INFLUENCE VULNERABILITY OF MERCURY EXPOSED POPULATIONS
•IN-SILICO, IN-VITRO AND IN-VIVO STUDIES FOCUSED ON EXAMINING THE SELENIUM-MERCURY INTERACTION ARE NEEDED TO CLARIFY TOXICITY MECHANISM/S
•POPULATION STUDIES NEED TO INCLUDE EXAMINATION OF SELENIUM STATUS IN RELATION TO MERCURY EXPOSURE
Research project 6: Interactions of mercury and selenium in bioaccumulation processes
The possible interactions among different elements affecting mercury accumulation by aquatic biota are poorly known. An antagonistic effect of selenium (Se) on mercury (Hg) accumulation was observed some thirty years ago. Although a number of studies have been published since, most were performed in restricted laboratory conditions with unrealistically high concentrations of selenium and/or mercury and inadequate exposure times. Although a reduction of Hg assimilation in the presence of Se was frequently observed under such conditions, many controversies about the possible interaction between these two elements still exist. Due to excessive concentrations of both elements, the death of fish and other organisms were occasionally noticed even in the short period of laboratory experiments. We think that under these acute and much simplified conditions, the normal processes of bioaccumulation and elemental interaction were seriously affected or modified. Therefore the validity of the results is open to question.
That's an excellent reference to the species-dependent mercury exposure. The lower down the food chain you eat is probably better, but even tuna and swordfish may be safe, if the selenium content is there.
The heavy metals mercury and cadmium accumulate mainly in the liver, whereas POPs accumulate in fatty tissue. No effects on people from heavy metals or POPs have been found in Greenland.
One of the very few thorough studies of Greenlanders' diet was carried out in Disco Bay in the mid-1990s. It showed a mixed diet - the Greenlandic diet supplemented by imported western food products. "We concentrated on the Greenlandic part of the diet, not the imported part," says Poul Johansen, who has spent many years researching the routes followed by heavy metals and POPs in living organisms. Some of the research, which is cofunded by Dancea, is carried out at Denmark's National Environmental Research Institute in Roskilde.
Quantitatively, the diet of Greenlanders in Disco Bay consists mainly of fish and seal meat. The absolutely dominant source of the diet's content of the heavy metals mercury and cadmium is seal liver. Seal liver constitutes only a small part of the diet, but is the main source of the diet's content of heavy metal.
In terrestrial animals, the levels of heavy metals are generally low. There are exceptions, however. For example, ptarmigan have high concentrations of cadmium in the liver, the only explanation for which must be that ptarmigan have naturally developed an ability to accumulate cadmium in their bodies - and live happily with that.
Poul Johansen says, "Many people who eat the Greenlandic diet ingest more cadmium and mercury than international limit values, and people who eat a lot of birds can reach lead concentrations around the limit value." However, there are no documented effects from heavy metals on human health in Greenland.
Selenium is interesting because there seems to be a relationship between selenium and mercury, with the selenium binding to the mercury so that it is not absorbed. Selenium binds to mercury in the ratio 1:1. So it is important where selenium is found and where mercury occurs. The main source of selenium is mattaq - whale skin - but selenium is also plentiful in other marine food. How does selenium get into the mattaq? Nobody knows - all one can say is: "that's nature!" Specific substances are concentrated in specific places in food. The fact is that there is a sufficiently large content of selenium in the Greenlandic diet to eliminate the current content of mercury.
Do Vitamin E and Selenium lower mercury toxicity? YES. Several studies in both humans and cats have proven that low levels of E & selenium prevent toxic effects in even high levels of mercury. E & selenium are anti-oxidants so they act not to decrease the mercury, but to prevent oxidation thereby lessening the damage from it.
In spite of being obese and sedentary, and having high levels of mercury in their own blood and hair, all 117 Inuit living in the town of Salluit had very healthy cholesterol levels, says Belanger, who adds that mortality from heart disease among the Inuit is 50% less than the overall rate for Quebec. That's probably because their favorite snack, maktaaq, or beluga skin, is very rich in omega-3 fatty acids and selenium. The omega-3 lowers their blood cholesterol levels, and the selenium protects against the effects of the mercury, says Belanger
"I don't want the Inuit to be afraid to continue eating their traditional foods," says Ms Belanger, who worked with colleagues at Laval University to see whether mercury contamination was having any ill effects on the Inuit after studies from Finland linked heart disease with the pollutant. "I looked at their levels of oxidized low density lipoprotein, or LDL (the LDL contaminated with oxygen), because oxidized LDL causes atherosclerosis, but I found there is no link in the Inuit. Also, their oxidized LDL levels were lower than those of healthy Caucasians, probably because of the omega 3 fatty acids and selenium which protect them."
Seafood, except some fish, is believed to be the best source of selenium. Mercury compounds found in some fish bind the selenium thereby making it unavailable to humans. However, some speculate that the selenium content of fish containing only traces of mercury is also low (13). Animal sources of selenium also appear to be higher due to a greater homeostatic control of the element during a wide variety of exposure conditions.
MERCURY, FISH CONSUMPTION AND THE RISK OF CARDIOVASCULAR DISEASES IN INUIT OF NUNAVIK
Concern has been expressed regarding the effects of exposure of human population to methylmercury through fish consumption. Lipid peroxidation is regulated by the level of free radicals, the availability of pro-oxidative catalytic transition metals as well as antioxidative defense including seleno-gluthatione peroxidase (seleno-GPx) and glutathione reductase (GR).
RESULTS:Hair Hg and blood Se were respectively 15- and 7-fold higher than reported in the general population. Their lipoprotein profiles (M/F 35/82, age 45±13 y, BMI 29.4±6.6 kg/m2, mean ± SD) were found to be normal:C 5.52±1.11 mM, Tg 1.23±0.58 mM, LDL-C 3.16±0.95 mM and HDL-C 1.42±0.41 mM. OxLDL was significantly lower than normal (1.6X, p<0.0001). Erythrocyte n-3 fatty acids were 2 to 6 fold higher than Caucasian controls whereas GPx and GR activities were increased (p<0.0001).
CONCLUSION:Despite the high exposure to Hg, high
prevalence of obesity and smoking, the mortality rate of CVD remains extremely
low among Inuits of Nunavik, most likely because of their traditional diet
rich in n-3 fatty acids and Se. IRST and Health Canada.
DNC. This project was supported by IRST and Health Canada.
Mercury is a heavy metal that collects in the human body over the years. Up to 8% of women of childbearing years have enough mercury in their bodies to harm a fetus. How can you remove it?
Elson M. Haas M.D. (Excerpted from Staying Healthy with Nutrition: The Complete Guide to Diet and Nutritional Medicine)
In the early 1970s, the "mercury in the fish" scare spread across the United States. Swordfish, tuna, and other large fish were the subjects of concern, and, in some areas, were measured with higher than acceptable levels of mercury. Caused by industrial contamination, the problem was not as widespread as the concern. Currently, most fish do not contain toxic or problematic levels of mercury, though further contamination could certainly raise the possibility.
Pectin and algin can decrease absorption of mercury, especially inorganic mercury. Selenium binds both inorganic and methyl mercury; mercury selenide is formed and excreted in fecal matter. Selenium is, for many reasons, an important nutrient for all of us, and in an amount of at least 100-200 mcg., it does seem to protect against heavy metal toxicity.
Nearly 100% of the mercury in upper trophic-level fish over three years of age is methylmercury . Total mercury is a conservative surrogate for methylmercury concentration in fish and shellfish. Because of the higher cost of methylmercury analyses, the USEPA recommends that states determine total mercury concentrations in fish and that to be most protective of human health states assume that all mercury in fish or shellfish is methylmercury.
In the marine environment, almost all of the Hg present in fish and squid is methylated (Caurant et al., 1996; Das et al., 2000). However, the major part of Hg accumulated in marine mammal internal organs, especially in the liver, exists as inorganic mercury (I–Hg), suggesting the demethylation of methyl mercury (M–Hg) occurs in their livers (Caurant et al., 1996; Holsbeek et al., 1998; Wagemann et al., 1998; Meador et al., 1999). The high correlation between Hg and selenium (Se) in the organs of marine mammals is well known (Itano et al., 1984; Wagemann et al., 1998; Meador et al., 1999; Das et al., 2000). The formation of the Hg–Se complex appears to be the last step of the detoxification process through the demethylation of M–Hg, leading to the fossilization of Hg and Se in the form of non-biodegradable compounds (Caurant et al., 1996). Metallothioneins (MTs) are well-known proteins, which are important in the detoxification of non-essential elements, such as cadmium (Cd), and I–Hg. In spite of a strong affinity for MTs, only a small part of I–Hg in the liver and kidney of mammals is bound to MTs (Das et al., 2000). According to literature (Caurant et al., 1996; Das et al., 2000), Se plays a key role in M–Hg detoxification processes in marine-mammals, and hence MTs would appear to play only a minor role, probably limited to the detoxification of I–Hg.
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