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Measuring Mercury

Measuring Mercury


Volume 104, Number 8, August 1996 - Environmental Health Perspectives

Measuring Mercury
Mercury from natural and man-made sources

Element of destruction. Mercury from natural and man-made sources is released into air, soil, and water. Bacteria convert mercury to methylmercury, which accumulates in fish that are eaten by humans and may cause adverse health effects.

Mercury is ubiquitous in the environment. Spewing from volcanoes, evaporating off bodies of water, and rising as gas from the Earth's crust, the poisonous, metallic element floats in the air as vapor or binds to particles. Eventually it falls to the Earth to settle in sediment, oceans, and lakes, or reenters the atmosphere by evaporation. The "hand of man" has contributed to this outpouring as well. Since the late 18th century and the dawn of the Industrial Revolution, mercury has been used in products such as lightbulbs, batteries, thermometers and barometers, pesticides, and paint. It is released from the burning of fossil fuels in municipal and hospital incinerators, coal combusting powerplants, lead smelters, and chlorine producers. Because it can dissolve metals, and particularly because it can separate gold from impurities, it has long been used heavily in mining, and is found in tailings around the world. Even crematoria contribute mercury to the environment as mercury is released when dental amalgams melt.

Once in water, mercury accumulates in fish. As a result, the consumption of fish becomes the primary pathway by which humans are exposed to methylmercury (another form of mercury). At elevated levels, poisoning can occur. Fetuses are particularly at risk and can suffer damage to the central nervous system, mental retardation, and a lack of physical development as a result of mercury exposure. Effects on adults can also be severe and include both sensory and motor skills damage.

Because it cuts across both environmental and public health concerns, two federal agencies with two different (though often overlapping) mandates--the EPA must safeguard human health through protecting the environment, while the FDA must safeguard human health through regulation of foods and drugs--have responsibility for regulating exposure to methylmercury. Right now, the agencies disagree on how best to fulfill these mandates and set standards for safe levels of methylmercury as they continue to examine the same data from two different perspectives. How the issue will be resolved is not clear, but interested parties, including industry and fishing lobbyists, consumer groups, and environmentalists, are working to influence the decisions of the two agencies.

Where and How Much

The World Health Organization estimates that approximately 10,000 tons of mercury are released worldwide from both natural and manmade sources each year. Initially, it floats into the atmosphere, mostly in the form of mercury vapor (Hg). Eventually, rainwater washes it back down to the Earth, where the process is repeated in what is described as a "ping-pong" effect. "As with any of the chemical elements, mercury exists as part of the Earth," says Kathryn Mahaffey, a senior scientist with the EPA. "As an element, it's not going to be created or destroyed, but its chemical form can always change." Over time, the ultimate sink for mercury is in the sediments of the Earth's oceans and lakes. There, microorganisms convert the inorganic mercury to methylmercury, the form that is potentially harmful to humans.

Methylmercury is produced by methanogenic (TK) bacteria (that produce methane), some of the oldest living cells known, says Tom Clarkson, a toxicologist at the University of Rochester. When mercury is methylated through ingestion by microorganisms, a carbon atom is added on to the mercury atom. This additional atom is what changes mercury's properties, allowing it to be readily accumulated in fish.

Exactly why the microorganisms methylate mercury isn't clear, says Clarkson. "Generally, inorganic mercury is more toxic to the organism, so it may be they convert it to get rid of it." Once it's methylated, mercury leaves the microorganism and moves up the aquatic food chain. "So what's good for them," says Clarkson, "becomes bad for us."

Once released from microorganisms, methylmercury rapidly diffuses, binding to proteins in aquatic biota. From there it marches up the food chain in a process known as biomagnification. Simply put, smaller fish absorb the methylmercury from water as it passes over their gills and as they feed on methylmercury-tainted flora and fauna. In turn, these fish are eaten by bigger fish, which is why the highest concentrations of methylmercury are found in fish at the top of the aquatic food chain. Large, predatory species like tuna, swordfish, and shark in ocean waters and trout, pike, walleye, and bass in fresh waters contain more methylmercury in their tissues than smaller, nonpredatory fish. Also, the older the fish, the more time methylmercury has to accumulate.

The transference of mercury from emissions to fish is nothing new. "Methylmercury has probably been in fish as long as fish have been on this planet," notes Clarkson. What is new is that people are eating more fish; in 1992 it was estimated that in today's supposedly more health conscious United States, fish consumption has risen 25% in the last ten years as people seek to benefit from fish's high protein and low unsaturated fatty acids, calories, and cholesterol, all of which may prevent heart disease and have other beneficial health consequences.

But scientists say that eating too much fish may have adverse impacts on health because of the increased intake of highly toxic methylmercury. "No one is arguing whether or not there are neurobehavorial effects of mercury on children exposed in utero," says Mahaffey. "Mercury is one of the most firmly established neurotoxins there is." If exposed in the womb, children can later develop a whole host of problems, ranging from delays in speech or walking to severe brain damage. FDA officials stress, however, that these effects have only been seen in populations exposed to high levels of methylmercury.

"It came as a shock to us in 1969 when Swedish scientists first discovered that methylmercury could accumulate in fish," says Clarkson. "In fact, there was a near-panic among people when high levels were found in fish near Detroit. People thought they were going to be poisoned." This good fish-bad fish conundrum is what the FDA and EPA are trying to resolve. "We've been wrestling with this issue for some time now," says Michael Bolger, a toxicologist and chief of the contaminants section for the FDA.

FDA Advisories

In 1979, the FDA established an "action level" of 1.0 part per million (ppm) to regulate methylmercury in commercial fish. The level serves a two-fold purpose. As the agency that oversees the safety of commercial fish in interstate commerce, the FDA uses this measure to make recommendations for legal action when a sample of the fish in a given shipment contains levels of methylmercury in excess of 1.0 ppm in the edible portion. This level is also used to assess risk to human health. As part of their normal diet, 1.0 ppm is the maximum level of methylmercury in fish that humans should eat on a frequent and consistent basis, but Bolger adds that such a number by itself is not helpful without taking other factors into consideration, such as how much fish people eat and what particular species they consume. "There's a problem with having a single number for a heterogeneous food like fish," says Bolger, "because unlike beef and poultry, which are consumed in fairly consistent amounts, there are pronounced differences between what species of fish are consumed, in what amounts, and how often. Looking at a single, safe level in a fish doesn't tell you anything about how much and how often that fish is consumed."

For instance, swordfish and shark, two big fish that are high up on the food chain, have methylmercury levels over 1.0 ppm. Yet most people eat these two fish on an occasional basis only. Thus, the FDA states that swordfish and shark "are safe, provided they are eaten infrequently (no more than once a week) as part of a balanced diet." Another complication is that levels of methylmercury vary between species. Canned tuna, for example, the number-one consumed fish in the United States, has fairly low levels of mercury--about 0.2 ppm, says Bolger. But certain species of very large tuna, which are not used in canned tuna but are typically sold as fresh steaks or sushi, can have levels over 1.0 ppm. Again, though, most people only eat tuna steak infrequently, so an occasional meal of it is probably okay.

Still other differences depend on who's doing the eating. Due to the fact that fetuses are especially vulnerable to methylmercury's effects, the appropriate levels for women of child-bearing age to consume may not be the same as for other people. In the womb, says Bolger, humans are susceptible to the effects of high methylmercury exposure because of the sensitivity of the developing nervous system. "Methylmercury easily crosses the placental barrier," he says. What the FDA didn't know when the action level was established, and still doesn't know, is the effect on the fetus of "normal" methylmercury exposures seen with fish consumption. The question, Bolger says, is whether effects on fetuses can occur with levels of exposure lower than those associated with adverse effects on adults seen in poisoning episodes.

To allow for such variation, the FDA has issued suggested guidelines for eating fish. FDA consumer literature states that eating a variety of types of fish does not put anyone in danger of methylmercury poisoning. Pregnant women and women of child-bearing age, though, are advised by the FDA to limit their consumption of shark and swordfish to no more than one portion a month. The literature also says that for persons other than pregnant women and women of child-bearing age who may become pregnant, regular consumption of fish species with methylmercury levels around 1.0 ppm should be limited to about 7 ounces per week (about one serving) to stay below the acceptable daily intake for methylmercury.

Part of the problem in establishing guidelines has been the lack of good data. To arrive at their current action level, the FDA looked at data from several studies of methylmercury poisoning and at the amount of fish consumed by the U.S. population--the best available data at the time. Two of the worst poisoning incidents occurred in Minamata and Niigata, Japan. In the 1950s, 111 people died or suffered from nervous system damage in Minamata, while 120 people were poisoned in Niigata. Both incidents were caused when people ate fish--often daily over extended periods--from waters that were severely polluted with mercury from local industrial discharge. In particular, 23 children in Minamata had severe psychomotor retardation resulting from their mothers' eating contaminated fish while pregnant. Yet the mothers themselves showed only mild manifestations of poisoning or no damage at all.

The studies also showed that harm caused by methylmercury poisoning, particularly neurological symptoms, can progress over a period of years after exposure has ended. The average methylmercury content of fish samples from both areas ranged from 9.0 to 24 ppm, although in Minamata, some fish had levels as high as 40 ppm. Because methylmercury accumulates in the hair of exposed individuals, its concentration can be measured in newly-formed hair and is proportional to the concentration of methylmercury in the blood. Although methylmercury levels in the Minamata mothers were not recorded, toxicologists learned that the lowest methylmercury level in adults associated with toxic effects was 50 ppm in hair. By comparison, the average concentrations of total methylmercury in nonexposed people, according to the FDA, is about 2.0 ppm in hair. "Obviously, these children were grossly compromised," says Bolger, "but those were at levels of exposure that were much higher than the lower dosages associated with minimal effects in adults."

More confusion and controversy arose regarding the potential danger to fetuses with the publication of a study in the mid-1980s led by Clarkson. In the study, based on 81 infant-mother pairs, Clarkson investigated an outbreak of poisoning in Iraq that occurred in the early 1970s when seed grain that had been treated with a methylmercury fungicide was ingested. "The interesting thing we found in Iraq," says Clarkson, "was that the level of methylmercury we found in the mother was predicative of adverse effects in their offspring. We looked at kids about two to two-and-a-half years old and found certain neurological effects, delayed development, and delayed motor effects. It was the first time anybody had shown this."

From the analysis, says Clarkson, estimates were made that levels of methylmercury in the mother's hair that were somewhere between 10 and 20 ppm were associated with roughly a 5% risk of adverse effects in her offspring.

But there were several problems with the study. One was a significant uncertainty in the estimates due to the low numbers of people in the study. Clarkson was also concerned about whether the results could be applied to a fish-eating population in the United States--"After all, people living in the middle of a desert weren't eating fish," he notes--and the fact that the Iraqi poisoning came from contaminated bread, not fish. He then decided to conduct another study, one of a primarily fish-eating population.

Conducting such a study was easier said than done. It took Clarkson more than two years of literally searching the world until in 1980, he found the right population in terms of size and birth rate (among other factors), in the Seychelle Islands in the Indian Ocean. "We needed a birthrate of 1,000 a year; that would give us the 800 infant-mother pairs we needed to check the 5% risk factor from Iraq," Clarkson said. Clarkson and colleagues followed two groups in the Seychelles in an initial pilot study that examined about 750 children up to five-and-a-half years old, followed by a main longitudinal study of 740 children nearly two-and-a-half years old. Both studies evaluated mental and physical development.

Initial results, reported in the Winter 1995-1996 issue of Neurotoxicology, were positive. "We weren't able to find major health problems," says Clarkson. "Children seemed to be developing normally, and in the tests done so far, the children were meeting the usual developmental milestones." According to Clarkson, the Seychelle results show that the predictions from Iraq, based on the estimates of adverse effects at 10-20 ppm exposure, are not true. Says Clarkson, "That's interesting, but not too surprising. Bear in mind that [the Iraq] numbers had a lot of uncertainty in them. They could have been as high as 70 ppm. What we're looking at right now is the exposure of the mother during pregnancy and the delayed effects on the child. . . . Suppose the child's brain was somehow damaged during pregnancy; it might be several years before you'd see the results of that. That's why we plan to follow the children until they're six to seven years old or more."

Philip Davidson, a University of Rochester psychologist and Clarkson's colleague on the Seychelles study, also presented additional analysis of the relationship of maternal mercury levels to activity scores in infants at 29 months of age. The original finding, reported in the Winter 1995-1996 issue of Neurotoxicology, showed a correlation between decreasing activity scores and increasing maternal mercury levels. A further analysis revealed that decreased activity was primarily associated with male children of mothers having lower scores on a test of maternal intelligence. Says Clarkson, "We do not know how to interpret a decreased activity level. In studies of childhood exposure to lead, increased activity (hyperactivity) was interpreted as an adverse effect of lead." Clarkson stressed that these findings are preliminary and their health significance is not known. Furthermore, these effects were observed in a population of children where all other tests indicated no problems in development.

As Clarkson's study was unfolding, a second, complementary study of a fish-eating population, led by Philippe Grandjean from Odense University in Denmark, was beginning in the Faroe Islands, located between Scotland and Iceland in the North Atlantic. Because the study results have not yet been published, Grandjean declined to talk about the findings. However, regarding a pilot study of 917 children who were examined at 7 years of age, Grandjean said, "We did see indications of neuropsychological dysfunction associated with increasing methylmercury exposure levels." Also, in a paper presented at the September 1994 National Forum on Mercury in Fish, Roberta White, a neurologist at the Boston University School of Medicine and an investigator with the Faroe Island study, wrote that the preliminary results from the first year of data collection show there is a relationship between maternal intake of seafood during pregnancy and central nervous system function in children 7 years later.

Mercury Timeline


EPA Standards

In the early 1990s, the EPA had begun to prepare its own mercury study for Congress as mandated by the 1990 Clean Air Act. This report included the EPA's own assessment of an acceptable level of methylmercury in fish. Because the report was not completed by the original due date of 15 December 1993, the EPA was sued by the Sierra Club and the Natural Resources Defense Council. Although the agency was granted a one-year extension until 15 December 1994, it decided not to submit its by-then completed report. The environmental groups sued again. The EPA lost and was ordered to submit its report by 15 April 1995. It has since delayed the report yet again and, as of May 1996, was in negotiations to extend the deadline.

Ostensibly, the EPA witheld its report due to the impending arrival of the Seychelles Islands data. "The decision was made to hold the report in anticipation of data," Mahaffey said. Another key factor in the delay, though, was the widespread criticism the agency received in calling for a much stricter standard for the allowable level of methylmercury in fish--.01 micrograms per kilogram (microg/kg) of bodyweight per day. (One part per million is equivalent to 1microg/g). It is a number that the EPA says reflects its broader mandate--one that includes not only public health, but clean water and air, and the protection of fish-eating wildlife (primarily birds), who are also feeling the effects of methylmercury.

"This is really a document about the airborne sources of mercury and their impact," says Mahaffey. Besides air, the EPA is also responsible for regulating the chemical contamination of water under the Federal Water Pollution Control Act. To determine the appropriate health criteria for an allowable concentration of mercury in water, the EPA looks at human consumption of fish--again, because fish is the primary route of methylmercury exposure to humans. "What's critical to understanding our number, which we refer to as a reference dose, is that it represents a quantity of methylmercury that virtually anyone could consume over a long period of time without any adverse health effects," says Mahaffey. The EPA based its reference dose on levels that would be safe for fetuses and women of child-bearing age. That meant using the Iraqi results in their calculations, because according to Mahaffey, it was the best available data at the time. "There are various ethnic groups--people of southeast Asian descent, for example, and Native Americans--that consume more fish than the general U.S. population," says Mahaffey. "Our focus includes the average person by identifying those who would be more highly exposed. We believe if the more highly exposed people are safe then the average person will be safe too."

The number is not necessarily just for consumption of fish, Mahaffey says, but for any food that would contain methylmercury. For example, if you had methylmercury-contaminated mushrooms, the number would still be applicable. "[The reference dose] is a factor of ten lower than where we believe any effects from methylmercury would start to occur," says Mahaffey. "But we know there is population-to-population variability, that different people may respond to methylmercury at different levels. So we think that factor of ten is a way of dealing with human variability and its response to mercury."

Impacts and Implications

Comparison of Methylmercury Standards

If adopted, the 0.1 microg/kg bodyweight reference dose could have tremendous implications for both consumers and industry. The differing measurements issued by the FDA and the EPA could be confusing for consumers. Also, they could raise a potentially embarrassing question in consumers' minds--if the EPA feels the need to drop its acceptable mercury intake levels, why hasn't the FDA--and erode public confidence in the judgments of both agencies.

The commercial fishing industry would presumably have to harvest fish that could meet a lower standard than the FDA's current level of 1.0 ppm. This would most likely be difficult to do. "Unlike cattle or chickens," notes the FDA's Bolger, "most fish are raised in the wild--the ocean. So it's virtually impossible to control their diet." Should demand exceed supply, fish could be more expensive or unavailable, thus depriving the consumer of the dietary advantages of fish.

There may also be a potentially huge financial impact upon those industries that emit mercury into the air. "We are of the view that there is a plausible link between these industrial sources and the quantities of methylmercury being found in fish," says Mahaffey. In order to reduce the amounts of methylmercury in fish, then, ultimately the EPA must reduce the amounts of methylmercury being emitted into the air. "Right now, pollution standards are based on existing technology," says EPA scientist Martha Keating. "If standards become risk driven, that's a whole new ballgame." More money would have to be spent by industries for research, and presumably for more expensive controls.

But to what end, asks Leonard Levin, manager for exposure and risk analysis, at the Electrical Power Research Institute, which is funded by a consortium of electric utilities. "Even if every industry that emits mercury were closed down tomorrow, it could be decades before we'd see a reduction in mercury levels in fish," he says. This is because large amounts of mercury have built up in the environment, and emissions continue to be released from natural sources. Mahaffey acknowledges this, but says, "You have to start somewhere." She also believes the followup report by the Seychelles investigators, as well as the early information from the Faroe Islands, provides reinforcement for the EPA's position. "One thing we know about neurobehavioral testing is that the more subtle the effect, the harder it is to identify in younger children," said Mahaffey. "So it's our view that, until the data on older children are available . . . it's premature to assess the study." FDA officials, however, disagree with this conclusion.

The FDA supports an ongoing reevaluation of methylmercury levels, something Bolger says his agency has already been doing. With more data beginning to come out from the Seychelles and the Faroe Islands, Bolger cautions, "It's not the end of the story by a long shot." If both studies show central nervous system damage to children, Levin believes that's only half the research picture. The other half includes determining who's doing the polluting, and how much fish people are actually ingesting. "Right now the EPA is using long-range transport modeling to determine how far mercury carries once it leaves an industrial source," he said. According to Levin, "the EPA itself says these models are not that good. But they haven't had time to fine-tune their models. Part of the reason is they're under time pressure because of the lawsuits to get this information out. Now, with the delay, it would be a good time to do some field studies to validate the modeling they've been using, and then to go back and do source-specific analysis."

And while a lot of studies have been done on fish consumption, all of them, according to Levin, have flaws. "There [are] numbers on what's imported, what's purchased, but nothing solid on what's actually consumed. The EPA has relied on self-reported diaries from people in its fish-consuming surveys. So this is something that's amenable to further study," he said.

In response to all the criticism directed at the EPA report, Mahaffey simply says, "Facts are stubborn things. Methylmercury is a neurotoxin, and it's not going away."

Mark Wheeler



Removing Mercury

The best way to remove mercury pollution from soil may one day be simply to grow plants in it. In a study published in the 16 April 1996 issue of the Proceedings of the National Academy of Sciences, researchers at the University of Georgia announced that they had developed a plant capable of absorbing highly toxic mercury ions from a growth medium and reducing them to less toxic and relatively inert metallic mercury. Once converted to its metallic state, the mercury is transferred into the atmosphere as a vapor.


Toxic fertilizer. Arapidopsis plants expressing the merApe9 transgene are capable of absorbing toxic mercury ions.
Photo: Richard Meagher/U. of Georgia

According to the report, the scientists developed the mercury-eating plant by building a synthetic gene, merApe9, and inserting it into the genome of Arabidopsis, a mustard plant. The merApe9 sequence, which is an adaptation of a bacterial gene, encodes the production of mercuric ion reductase.

The viability of phytoremediation, the process of using plants to remove pollutants from the environment, has been shown for many chemicals. Pesticides, herbicides, explosives, solvents, radioactive cesium and strontium, and other heavy metals such as nickel and lead have all been shown in various studies to be potential candidates for phytoremediation cleanup. "The significance of this study," says Ilya Raskin, a professor of plant biology at Rutgers University, "is that it is the first one published . . . [that] demonstrates the potential of genetic engineering for developing plants" capable of absorbing particular chemicals. According to a paper by Raskin that accompanied the study, this research could lead to the development of "a 'molecular toolbox' of genes useful for phytoremediation of metals."

The study also shows that mercury pollution is particularly suited for cleanup using phytoremediation. With most chemicals, the plants that grow on the contaminated medium accumulate large amounts of the toxic substance into their biomass, which must then be disposed of. According to Raskin, substantial savings are still achieved in these cases because the plant biomass represents around 1000 times less toxic material to be disposed of than the soil in which it was grown. However, because of mercury's volatility, it does not accumulate in the plants. According to the study, metallic mercury vapor was emitted by the plants as they grew; the researchers propose that, outdoors, this vapor would diffuse into the atmosphere, quickly reaching nontoxic levels.

According to Raskin, though, regulatory agencies may not accept the evolution of metallic mercury into the air as a safe remediation strategy. In particular, there is concern that mercury vapor in the air will precipitate into the Earth's waters where it can enter aquatic food chains. Through the process of biomagnification, this mercury can reach toxic levels in the predatory fish that humans consume. According to Richard Meagher, one of the authors of the study, however, the mercury vapor released during a phytoremediation cleanup would be insignificant on a global scale. "The amount of vapor coming out of a site will be 10,000-fold less than EPA [emissions] standards," Meagher said.

However, Raskin stresses that phytoremediation of mercury is still in its infancy, and that much more research is needed. "The next step," he said, "clearly is to introduce these genes into high biomass plants and show that it works on soil." Though some phytoremediation schemes have been field-tested, mercury-removing plants have only been grown on agar under laboratory conditions, Raskin said. In addition, Arabidopsis, a common test plant, does not reduce enough mercury and lacks the field cultivation to make it a practical choice for phytoremediation cleanup. "This study is just one step, but it's a very significant one," he said.

Chris Reuther


The Issue of Amalgams

Mercury contained in dental fillings has been blamed for problems from chronic headaches, dizziness, and gastrointestinal complaints to the growing worldwide resistance to antibiotic drugs. Yet some counter that mercury is a well-known substance that has been safely used in teeth fillings for more than 150 years. Such fillings are actually amalgams, blends of metal that today comprise as much as 50% mercury, 35% silver, 13% tin, 2% copper, and a trace of zinc by weight. The first complaints about amalgams arose soon after their invention in 1812 by British chemist Joseph Bell, who melted down coins and then added mercury to make the first restorative paste: impure metals in the coins allowed the amalgam to expand, often fracturing teeth. Others expressed concern about mercury's possible toxicity.

Over the years the controversy has ebbed and flowed. Concern about possible toxic effects arose again in the 1920s, but soon faded, offset by the fact that amalgams make a relatively hard, stable, and inexpensive filling. And, since large numbers of people weren't obviously becoming ill because of amalgams, their use became more widespread.


Over the last 15 years, the controversy has erupted again. In 1981, researchers at the University of Iowa published a paper entitled The Effect of Dental Amalgams on Mercury Levels in Expired Air in the Journal of Dental Research, which proved that mercury vapor is released from fillings when people chew or brush their teeth. In 1991, Fritz Lorscheider, a physiologist from Canada's University of Calgary, and colleagues published in the American Journal of Physiology the results of a study in which the researchers inserted amalgams into the teeth of sheep, then used radioactive tracers to follow the mercury as it entered the body. They found that the mercury became concentrated in the kidneys, brain, and liver, and that it crosses the placental barrier and enters the fetus. The paper was subsequently strongly criticized for procedural errors by several physiologists, but the authors later replicated their findings in a followup study using monkeys.

In the early 1990s, two television newsmagazine programs reported on the mercury controversy--60 Minutes in December 1990 and a similar BBC program, Panorama, in July 1994--and jumpstarted the debate about health concerns yet again. In 1991, the U.S. Public Health Service (PHS) took notice and appointed a committee to study the possible risks of amalgams. The report of their three-year study, entitled Dental Amalgams: A Public Health Service Strategy for Research, Education, and Regulation, published in 1993, found "scant evidence" that people's health was being compromised. The committee did, however, acknowledge that a research program should be designed and implemented to fill the gaps in knowledge about any potential long-term effects of amalgams.

Today, the PHS, the FDA, and the American Dental Association (ADA), among others, stand by the safety of amalgams. So do most dentists--amalgams account for roughly 80% of all tooth restorations. The ADA cites a 1995 study of elderly nuns published in their own Journal of the American Dental Association (not a peer-reviewed journal) that showed no association between long-term use of amalgams and lowered cognitive function. Another study by Danish researchers, published in the January 1996 issue of the European Journal of Oral Sciences also shows no link between mercury vapor released from amalgams and the subjects' self-reported symptoms.

Still, a growing and increasingly vocal number of researchers, many outside the field of dentistry, are questioning the appropriateness of using a toxic substance for dental restoration. Several countries in Europe have, or are considering, a ban on mercury, and Canada is currently reviewing its position on mercury amalgams. "As someone who's studied mercury for 25 years now, it's beyond me why anyone ever thought mercury was a good idea to put in anybody's mouth in large amounts," says Anne Summers, a microbiologist at the University of Georgia. That sentiment is echoed by Lorscheider, who has long been a harsh critic of amalgams: "In the field of medicine, nothing is approved for humans without extensive testing, first in animals and finally in human subjects. Yet we've been sticking this stuff in our mouths for 150 years and nobody's ever looked at it until recently."

Results of a study by NIEHS epidemiolgist Andrew Roland, published in Occupational and Environmental Medicine in 1994, showed a major fertility effect among women exposed to high levels of amalgams. Rowland's team queried a group of dental assistants composed of married women who had wanted to become pregnant within the past four years. He found that women who prepared more than 30 amalgams per week and practiced varying degrees of "poor mercury hygiene" took longer to get pregnant. These women's chances of conceiving during a particular menstrual cycle was only about half that of dental assistants who didn't prepare amalgams. On the other hand, Rowland also found that other women in the study who prepared fewer than 30 amalgams per week turned out to be more fertile than the controls. In response to the results, Rowland makes a call for more research, and a caution about applying the results of an occupational study directly to the consumer.

As part of the body's normal biological process, once elemental mercury (Hg) leeches out of the amalgam and is inhaled or swallowed, enzymes in our cells convert it to mercury ion, which is, says Summers, "very well documented to be neurotoxic, cardiotoxic, and immunotoxic." In a 1993 paper published in Antimicrobial Agents and Chemotherapy, Summers reported a link between mercury and antibiotic resistance. When the mercury ion is eventually sent by the body to the intestines for excretion, it encounters mercury-resistant bacteria. The gene that protects the bacteria from mercury's effects is located on the same DNA fragment as one that also offers resistance to antibiotics. Thus, says Summers, if mercury from amalgams can contribute to development of a population of mercury-resistant bacteria, it may also be developing bacteria that are resistant to antibiotics as well. Summers' work with monkeys showed an eventual resistance to such common antibiotics as penicillin, streptomycin, and tetracycline. Her current work with human subjects has so far substantiated these results.

Between those on both sides of the amalgam issue, every new piece of research is challenged, and every comment contradicted. Even the amounts of mercury being emitted by amalgams are in dispute. According to Lorscheider, mercury vapor is released in amounts of approximately 10 micrograms per day (microg/day). The ADA disputes this figure, saying the preponderance of evidence indicates between 2-4 microg/day. (The allowable OSHA limit for inhaling mercury in the workplace is 50 microg per eight-hour shift.)

The ADA is maintaining its firm support of amalgams, pointing to their 150-year-long safe track record, as well as to the lack of an affordable and tested substitute. "Amalgams are still safe," says Rod Mackert, a professor of dental materials at the Medical College of Georgia and a spokesperson for the ADA. "But the ADA will maintain an open mind about it. If information comes out that indicates otherwise, they would actively pursue it and disseminate to the public."

Mark Wheeler


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Last Update: July 10, 1997

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