Is Dental Amalgam Safe?

Part 1 – Scientifically , there is more than reasonable doubt.

Ross Mackay, BDS

As the controversy over the safety of mercury in dentistry increases, recent scientific evidence is now supporting previously anecdotal claims of amalgam’s toxicity and exposing the long held myth of amalgam’s unquestioned safety.

Mercury-containing filling materials, known as amalgams, have been the mainstay of modern restorative dentistry and even today continue to be the most widely utilised material. Dental amalgam is a mixture of approximately fifty percent mercury with silver, tin, zinc and copper in varying ratios. Historically, mercury has been used in dentistry for a long time. During the Ming Dynasty in China there is evidence that amalgam fillings were placed, but it was not until 1812 that Bell, a British chemist, developed the material as we know it today. Amalgam was introduced to the USA in 1833 and it is easy to understand why it rapidly achieved ubiquity. Amalgam produces durable restorations from an easily manipulated, putty-like mixture. While setting, it allows many minutes of working time to mould and form the filling before solidifying at body temperature. Consequently, amalgam was far superior to the commonly used filling materials of the time such as wood, cement and molten lead and much more economical than gold. Amalgam filling material took dentistry from a cottage industry, servicing the wealthy, to the multi-billion dollar profession we know today.

However, the rise of mercury filling material to almost universal use has not been unopposed. In 1844 in the USA the existing dental association banned the use of amalgam because of the known toxicity of mercury. But its use continued to spread until finally economics and practical necessity won out and a new dental association was formed which supported amalgam use, totally eclipsing the former association and silencing any opposition. In the 1930s a German research chemist, Professor Alfred Stock1, published a series of articles criticising amalgam, but due to the lack of a suitable alternative material and a WW2 bombing raid which destroyed his research laboratory, again the amalgam opposition fell silent.

Over the last decade, with the aid of scientific and technological advances, there has been increasing disquiet about the systemic effects of long-term exposure to the mercury which is released from amalgams and retained in the body. Signs and symptoms arising from long-term low-level exposure to mercury are now called chronic mercury toxicity. Results of recent research have led governments in Sweden, Germany and Austria to legislate to restrict the use of amalgam because of the increasing amount of evidence indicating the toxic effects of this material.

It is an undisputed fact that mercury is a very poisonous substance and it is acknowledged as being the most toxic of the heavy metals. Mercury is a strong protoplasmic poison that penetrates all living cells of the human body and a powerful biological poison with no necessary biological function2. Being a nonpolar lipid-soluble entity it is rapidly absorbed through the lungs, skin and mucous membranes. The basis of mercury’s toxicity is its affinity for sulphur. It binds to sulphydryl groups and so inactivates cell enzymes, thereby interrupting cell metabolism and function. Whether and at what level mercury is poisonous depends on each person’s biological sensitivity and its effect may show in different organs3.

Minimata Bay

Medical literature is replete with reports on the pathological consequences of exposure to mercury. One of the most well known examples is the Minimata bay incident of 1953 in Japan, when a plastics factory polluted the bay which was used by the area’s fishermen. The mercury effluent was converted to methyl mercury by organisms in the water and then passed up the food chain to the fish caught for local consumption. Organic methylmercury is one of the most toxic substances known to man and has been reported to be up to one hundred times more toxic than inorganic or elemental mercury4. Initially, the cats went mad and died. Then the local population experienced a whole range of effects, from rapid death due to acute poisoning, through a variety of neurological symptoms and teratogenic effects in the chronically poisoned group.

In relation to chronic exposure from amalgam fillings it is interesting to note the findings of Professor Takeuchi, who has extensively studied the Minimata incident5, especially in the light of evidence that bacteria in the mouth, stomach and the small and large intestine can methylate mercury. He reported four levels into which patients could be divided, depending on the severity of their symptoms:

  1. The most severe ended with death or permanent disability with associated mental disorders;
  2. Advanced or moderate poisoning showed tremor, disturbances of sensation, ataxia, dysarthria, difficulty in hearing and constriction of the visual field;
  3. Less advanced chronic cases had ataxia, dysarthria, constriction of the visual field, disturbance of eyeball movements and ocular dysmetria;
  4. The mildest cases had mainly unspecific symptoms such as fatigue, impairment of memory, slight mental disorders, headaches, slow movements, numbness and tremor of the lips and fingers.

It is the symptoms categorised in group four that we find commonly presenting in patients with chronic mercury toxicity. Amelioration of these symptoms is often brought about by removal of the amalgam fillings while supplementing with nutritional and chelating agents.

Even though official estimates of the extent of the poisoning are relatively low (43 deaths and 68 permanently disabled) there have been reports6 that more than half of the exposed population would have suffered some effect from methyl mercury poisoning. In 1987 Professor Takeuchi wrote7, we still have over two thousand patients of mercury poisoning in Minimata. There are so many unhappy and miserable people, who have had experience with non-effective treatments tried frequently and repeatedly. We have no acknowledged treatment for the disease right now. Mercury remains in the patient’s body, especially the brain, for a long period of time.

Alzheimer’s Disease

Recent research on Alzheimer’s Disease has implicated mercury in a possible role as a causative factor. Ehrmann and colleagues presented their research in a series of articles8, 9, 10 in which they found elevated levels of mercury in the brain tissue of Alzheimer’s patients compared with controls. They stated that mercury was the most important of the imbalances they had studied. They found the largest trace element imbalance was the elevation of mercury levels in the nucleus basalis of Meynert. This area is severely degenerated in Alzheimer’s patients. The researchers postulated four mechanisms, by which mercury had previously been shown to act, which could cause the observed effects:

  • It could effect DNA and RNA levels and protein synthesis, leading to neuronal degeneration and death;
  • Mercury can bind to cell membranes, increasing the membrane permeability, leading to cellular dysfunction;
  • There are decreased levels of selenium and zinc in Alzheimer’s patients, which could be caused by mercury binding to these minerals and so making them unavailable for essential cellular functions;
  • The neurofibrillary tangles found in Alzheimer’s patients could be due to the binding of mercury to the tubulin which is necessary for the correct formation of the neurofibril matrix.

The authors themselves say that the extreme elevation of mercury in the nucleus basalis could relate to the severe degeneration of the nucleus and to the cholinergenic deficit in Alzheimer’s disease.

Tubulin in the cytoskeleton is the ‘rail track’ on which wastes are taken out and nutrients are brought in to the cell. Tubulin synthesis has now been shown to be blocked by mercury compounds11 in rats via an abolished GTP-tubulin interaction similar to that found in Alzheimer’s disease brain samples. Among the mercurials, inorganic mercury ion (Hg++) is one of the most potent inhibitors of microtubule polymerisation, both in vivo and in vitro. In contrast to other heavy metals, the capacity of Hg++ to inhibit microtubule polymerisation cannot be prevented by the addition of EDTA and EGTA, both of which bind Hg++ with great affinity. On the contrary, the addition of these two chelating agents potentiates Hg++ inhibition of tubulin polymerisation12 . EDTA is a common food additive and chelating agent, so some caution may be indicated in its use as a chelating agent for mercury toxicity. Duhr et al. have noted amalgam fillings as a primary potential source of the mercury found in Alzheimer’s victims brains. They also concluded that their results suggest certain complexed forms of Hg++ must be considered as a potential source for the aetiology of Alzheimer’s Disease.

It has been observations and research such as presented above that have led to a much closer scientific scrutiny of the potential for amalgam to be a causative factor in human pathology. For mercury from fillings to be a pathological agent, it must be released from the filling, retained in the body and shown to have pathological effects.

Mercury is released from amalgam fillings

For many years it was thought and taught that mercury was locked into the amalgam alloy and not released, totally ignoring some basic laws of physics and chemistry which contradict this stance. All metals will corrode by oxidation and the universal law of entropy states that everything will break down . When dissimilar metals are placed in an electrolyte, such as amalgam fillings in saliva, an electrolytic cell will be set up, creating corrosion in the anodic areas. This means that ions will go into solution from the anodic or corroding areas. More noble metals such as gold and titanium, which are regularly used in dentistry, will corrode silver and mercury found in amalgam. Amalgam, because it is made up of different metals, is self-corroding in saliva.

With the advent of meters capable of measuring levels of mercury in intra-oral air, research has been done establishing that mercury is constantly released from amalgam fillings in pharmacologically significant quantities14,15,16. Mercury release comes from mechanical wear, dissolution, corrosion and vaporisation. Factors which increase the level of mercury released are frictional and compressive forces such as mastication,14,15,17,18 increase in temperature and even tooth brushing16. Vimy and Lorscheider demonstrated that during continuous chewing the mercury release accelerates, rising to a plateau in ten minutes. After cessation of chewing the mercury continues to be released at a declining rate, returning to the pre-chewing level at around ninety minutes18. The pre-chewing level and chewing level of mercury in intra oral air correlate significantly with the number and size of amalgam restorations.15,18 It has also been shown that human plasma mercury levels correlate with the number and total occlusal area of the amalgams present in the mouth.19,20

In 1991 the World Health Organisation (WHO) issued a document21 on environmental mercury exposure stating that the largest estimated intake and retention of mercury and mercury compounds in the general population, not occupationally exposed, is from dental amalgams. They estimated that between 3.8 µg -21 µg/day was the level to which people were exposed from amalgams and between 3 µg – 17 µg/day was retained in the body. From their data it can be extrapolated that exposure to mercury from amalgam fillings can be up to nine times the exposure from all other sources such as fish and air pollution. The WHO document also states that a specific no-effect level cannot be established, which means there is no level of exposure to mercury vapour which can be considered harmless.

At present the consensus of opinion on the average daily absorbed dose of mercury from amalgam is approximately 10 µg. However, Gross and Harrison22, in an electro-chemical study of amalgam corrosion, calculated that an average amalgam filling released 15 µg per day as vapour and particulate material. Consequently, a person with ten average fillings (a number of fillings commonly seen in adults) would be exposed to 150 µg per day, which is far in excess of previous estimations.

Mercury from fillings is retained in the body

The toxicity of mercury is enhanced because it is so readily absorbed, with around 90% to 100% of mercury vapour being absorbed through the lungs. Mercury can also be absorbed through the oral mucosa. The more toxic methyl mercury is not absorbed well in the lungs but is readily absorbed in the gastro-intestinal tract. In autopsy studies, a positive correlation has been demonstrated between the number of occlusal surfaces of dental amalgam and the mercury levels in the brain23. Nylander et al. have shown a two-fold difference in brain mercury concentration and a ten-fold difference in kidney mercury levels between individuals without, compared to those with, aged dental amalgams, respectively24. It has also been found that the daily dose of mercury received from dental amalgam can predict the tissue levels found in human autopsy studies25. In a recent experiment using the chelating drug DMPS, researchers found that following chelation drug challenge, mercury urine levels were higher in subjects with amalgams than those without amalgams. Also, two thirds of the excreted mercury originated from the dental amalgam and the amounts of mercury excreted correlated with the total amalgam occlusal surface area26.

In order to be sure the mercury from dental fillings is retained once it has been absorbed into the body, mercury with a radioactive tracer was used in fillings placed into pregnant sheep. Within two days of placing the fillings, mercury was found in maternal blood, foetal blood and the amniotic fluid. Measurements over a period of time in the ewes showed the kidney to have the largest concentration of mercury then followed by the liver, but virtually all organs in the body showed a build-up of the radioactive mercury. Significant amounts of mercury were found in the urine and faeces also. It should be noted here that the major route of mercury excretion from the body is via the bile through the faeces. The foetuses showed virtually the same pattern (except the liver had the highest recorded level) after just thirty days of exposure to mercury from the fillings placed in the mother27. A similar study in non-pregnant sheep, using whole body image scan as well as tissue scintillation analysis, confirmed that by thirty days following amalgam placement mercury had rapidly located in the kidney and liver. Other major sites of mercury deposition were the oral tissues, jaw bone, lungs and gastro-intestinal tract28.

This study was condemned on the basis that sheep were not an appropriate model for human comparison, so the work was replicated on monkeys who have a similar diet, feeding regimen and dentition to humans. The results of the monkey study confirmed the findings in the sheep experiments29. Another investigation into mercury levels in monkey organs showed the kidney continuing to accumulate amalgam mercury for as long as one year after placement of the fillings30.

Vimy and co-workers also looked at two groups of pregnant ewes; one group with radioactive mercury containing fillings and the other as a control group with no fillings. Once the ewes gave birth, some of the lambs from the control ewes were breast fed by ewes with fillings. After just thirty days these lambs surrogately fed by the ewes with fillings had the same mercury levels as the lambs born from and fed by these ewes.

Following a methyl mercury poisoning incident in Iraq, researchers found that the infants’ blood levels were higher than their mothers’ during the first four months after birth. Their results indicate that methyl mercury passes readily from mother to foetus and that neonatal blood levels are maintained through ingestion of mercury in mothers’ milk31. The Iraqi research also found children were more susceptible to mercury than their mothers and that sometimes effects such as learning and motor disorders only became obvious as the child matured.

Clearly, performing restorative dentistry involving amalgam on pregnant females should be looked at very seriously. On the basis of current research, Sweden has now banned the use of amalgam fillings in pregnant women.

Pathophysiological effects of dental amalgam

The research is now conclusive that mercury comes out of amalgams and is distributed and absorbed into tissue. It is also accepted that mercury is a toxic substance. But are the levels recorded coming off fillings able to produce pathology? Does the actual mercury from the fillings produce any pathological effects?

Are the mercury exposure levels quoted by sources like the WHO (3.8 µg – 21 µg) or Gross and Harrison (150 µg) able to produce toxic effects? It has been reported that 0.5 µg/l mercury chloride was shown to affect a 50% inhibition of the neurotransmitter glutamate transport, while chlorides of other heavy metals showed no inhibition at concentrations twenty times greater32. Severe symptoms have been reported in children under five with urine mercury levels as low as 6.3 µg/l33. Professor Skare in Sweden found faecal excretion levels of mercury to be twenty times that of urine levels. A person with an average number of fillings was predicted to show a faecal excretion rate of 60 µg of mercury daily, thereby exceeding the WHO maximum allowable intake of 45 µg daily34.

Renal function has been found to be impaired following the placement of amalgam fillings in sheep. Thirty days after placing fillings the inulin clearance rate (a test used to measure glomerular filtration rate) was reduced by 50%. A control group using a non mercury glass ionomer filling material showed no effect on the glomerular filtration rate35. The reduced inulin clearance was still present after sixty days. There was an increase in urinary sodium noticed in the sheep, leading to a negative sodium balance in the animals. It is significant to note here that 70% of sodium is reabsorbed in the proximal tubule of the kidney, which is also the primary site of inorganic mercury accumulation36,37. A decrease in urinary albumin was also noticed and was due to either reduced renal blood flow or impaired glomerular filtration35. Human studies have produced similar results by showing a significant increase in urinary albumin levels one year following removal of all amalgam fillings20. With a kidney biological half life of mercury of approximately 70 days, it takes 5 half lives (350 days) to remove sufficient mercury from the kidney to restore normal renal function and thereby increase albumin excretion back to normal levels. In summary, placing dental amalgams impairs kidney physiology and removal of amalgams in humans restores kidney function38.

Antibiotic resistance has also been linked to mercury39. It was found that humans who have a high prevalence of mercury resistance in their intestinal bacteria, were significantly more likely to also have bacterial resistant to two or more antibiotics. In the study with monkeys, many of the common mouth and intestinal bacteria became resistant to mercury within two weeks of placing amalgam fillings. Even though the monkeys had not been exposed to antibiotics, nearly all of the mercury resistant strains of bacteria were also resistant to one or more antibiotics. Up to 50% of the multi resistant bacteria could transfer their resistant genes to an antibiotic- sensitive strain, indicating that the mercury- and antibiotic-resistant genes were carried on movable genetic agents called plasmids. In some of the monkeys the amalgam fillings were replaced after two months with non-mercury-containing composite resin fillings. The proportion of mercury and antibiotic resistant bacteria then declined in several of the bacterial populations during the subsequent two months. It is accepted that the main route for the excretion of mercury is via the gastro-intestinal tract in levels up to 300 µg per gram of faeces and it is also accepted that amalgam is the main source of exposure to mercury21. Consequently, it is likely that dental amalgam mercury is a selective agent which increases the prevalence of plasmid-associated mercury and antibiotic resistances in the oral and intestinal bacteria of humans.

A recent study done by Godfrey and Campbell40 used the chelating drug DMPS in urine provocation tests on patients with chronic mercury toxicity. In some patients they were able to equate an improvement in signs and symptoms of chronic mercury toxicity with a decrease in urine mercury levels following DMPS provocation. They looked at four groups of patients:

  • those who had amalgams and were diagnosed as suffering from mercury toxicity;
  • dental personnel;
  • patients who had been diagnosed as suffering from mercury toxicity and then been treated by amalgam removal, mineral supplements and chelation therapy;
  • non-amalgam asymptomatic controls.

Patients who exhibited signs and symptoms of chronic mercury toxicity had an average pre-DMPS urine mercury level of 5.4 µg/litre and following an injection of DMPS this increased to 314.4 µg/l as compared to amalgam free controls whose levels went from 1.8 µg/l to 39.1 µg/l. The authors noted that some patients in group 3 experienced a transitory recurrence of their symptoms following DMPS injection. This was probably due a mobilisation of residual mercury from their tissues. Some patients in group 1 found temporary relief of their symptoms, particular chronic fatigue, following DMPS injection.

Dentists and dental personnel work under conditions which constantly expose them to mercury vapour. Are we being affected by this mercury pollution? Dentists and their assistants are not dying in large numbers from overt mercury poisoning, but the words of Dr. Brooks41 in his article on CNS toxicity of mercury may give us cause for concern and explain some of the following statistical data:

An environmental or occupational exposure to mercury that is of itself insufficient to cause overt CNS toxicity, by diminishing the safety factor for inactivation of glutamate could, nevertheless, accelerate processes of excitotoxic neurodegeneration associated with disease or aging. ‘Silent’ impairment of this kind is suggested by the delayed emergence of neurologic dysfunction following remote occupational exposure to elemental mercury vapour.

It has been found in a study in the USA, that dental assistants who prepare thirty or more amalgam fillings per week have a fertility rate only fifty percent that of matched controls. Joel Butler, a professor of psychology in the USA, found neuropsychological dysfunction present in 90% of dentists tested. In particular:

  • areas of suboptimal function were evident in shifting tasks
  • attention span, ability to concentrate
  • recent memory deficits
  • visual recall, control dyspraxia
  • tremor and perceptual accuracy in judgement.

Psychological problems were concentrated in the areas of irritability, impatience, tension, frustration and conflict. Notably absent was calmness. Observation of data suggests that the longer a dentist practices, the less ability s/he has to pass the entrance exams into dental school.42


Since amalgam came into use over 150 years ago many claims have been made and much anecdotal evidence has been presented concerning the toxicity of dental amalgam and the amelioration of symptoms and diseases following the removal of mercury fillings. Yet little if any good scientific investigation into these claims had been carried out. So to try and explain these observations scientifically and bring their findings to the attention of the profession, researchers throughout the world, over the past decade, have been investigating the potential toxic consequences of implanting mercury alloys into the teeth of human beings.

With no scientific research or ongoing monitoring, amalgam has been declared safe and nontoxic by the dental profession on the basis of the anecdotal evidence that each year more than 100 million amalgam fillings are placed in the United States. And since amalgam has been used for more than 150 years, literally billions of amalgam fillings have been successfully used to restore decayed teeth.43 To date, the research has led to the following facts:

  • dental amalgam is a major source of mercury pollution
  • dental amalgam releases mercury into intra-oral air in significant pharmacological levels
  • dental amalgam mercury is inhaled and swallowed
  • it is distributed to body tissues and amalgam mercury can alter cell function.

Scientifically, there is now reasonable doubt concerning the safety and continued use of mercury in dentistry.


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Part 1 of this article was published in the ACNEM Journal, Vol. 12 No. 2, December 1993