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| A hundred and fifty years of misuse of mercury and dental amalgam |
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| — still a lesson to learn |
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| by Mats Hanson |
| (på svenska) |
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MERCURY HAS LONG BEEN USED as a medicine to treat various diseases, such as syphilis and typhoid fever, or parasites. Certainly a treatment with such a "powerful" medicine impressed patients, and when poisoning symptoms appeared they could always be blamed on worsening of the original disease. The use of mercury in medicine repeatedly led to controversies because of toxic effects which often were very difficult to differentiate from the symptoms of the disease for which the metal was administered.
One of the first careful descriptions of the symptoms of mercury poisoning was an attempt to resolve the question of whether mercury poisoning produced symptoms distinctly different from those of syphilis for which mercury was the preferred treatment (Kussmaul, 1861). Exposures in the studied mirror factories were generally high, but already Kussmaul noted that sensitivity towards this metal was highly individual and unpredictable. Kussmaul's book is still highly readable and also contains a long section on the history of mercury and its uses and misuses. From this source you get the information that the name "quack" for a person without formal medical education, but who is practicing medicine, originates from "Quecksalber", someone who is using mercury ointments to treat diseases. Since also regular medicine extensively used mercury for the same purposes, the professions of medicine and dentistry have come up with other strange explanations for the origin of the word.
” ... a dissolution of the tooth will occur ... Amalgam destroys the teeth.”
In the USA, the use of mercury as a universal medicine for almost any disease made large parts of the population turn their backs on established medicine from the middle of the 1800s (Risse, 1973). The worst medical poison use was gradually abandoned. But not in dentistry. Both the American Medical Association and the Americal Dental Association were founded to defend the use of mercury, the former for calomel (mercurous chloride) and the latter for amalgam. Apparently we have a very similar development today; people turn to alternative care and health foods and the establishment defending current practice and denying risks.
From society's point of view, the amalgam question hardly contributes to increased confidence in authorities, health care and researchers. Almost every person in Sweden knows that mercury is poisonous and that it is part of amalgam. It is an absolutely absurd state of affairs when mercury is considered toxic everywhere except in the mouth, when toothpaste, which binds mercury from amalgam and supposedly makes it harmless, is sold in pharmacies only, when patients are not allowed to take their extracted teeth filled with amalgam home from the dentist, with the argument that it is environmentally hazardous waste, when filters are installed in crematoria etc.
 Amalgam is the main source of mercury exposure in the western world. However, experts from the Swedish National Board of Health and Welfare (Socialstyrelsen) have first stated that no systematic release of mercury from amalgam has ever been observed, and when this was proven false, they claimed that the amounts were far less than is obtained from food, which is also false. It is astounding that mercury researchers did not detect this fact. If they did notice, but abstained from whistle-blowing, questions of morality and ethics arise. People with amalgam are exposed to from tens to several hundreds of micrograms of mercury per day. In several respects this exposure is special, and data and limit values from other types of exposure are just not applicable.
The limit values for industry cannot be used when the whole population is exposed. The limit values for Hg (from here on mercury will frequently be referred to by its chemical abbreviation, Hg) are largely based on conditions in the chloralkali industry (producing chlorine and sodium hydroxide with the help of mercury electrodes), where chiefly male workers are employed. At least half of those exposed to mercury from amalgam are women. Mercury reacts with chlorine. Realistic animal experiments by Viola and Cassano (1968) clearly show that the presence of chlorine in such factories reduces the total uptake of mercury by half (kidney contents) and that the content in the brain is only one tenth compared to mercury alone. Precipitated calomel could be swept up from the floor in chloralkali factories. When rats were exposed to both gases together, the mixture was strikingly less toxic than the exposure to mercury alone. The Hg-only rats had severe neurological symptoms and the mercury+chlorine-rats mild gastrointestinal disorder. The reaction between mercury and chlorine gas has been known at least since the turn of the century. Amalgam fillings in cavities will have their hidden surfaces exposed to other conditions than the visible surfaces (oxygen pressure, acidity, ionic composition etc.). The variable conditions will promote corosion and metal release. In addition there will be a constant abrasion of the fillings. The metal release in the form of ions will generate a current according to Faraday's law. It should be pointed out that the magnitudes of the oral currents are in the same range as those induced in the tissues of a human directly standing under a high-voltage transmission line. Possible health effects of such exposures are disputed. More certain effects of the oral currents are transport of metal ions from corroding fillings into surrounding tissues, since positive metal ions will follow the direction of the current (Wranglén & Berendson, 1983).
Another aspect of the corrosion process is that crevice corrosion causes hydrochloric acid generation with a pH of 2-3 (Marek & Hochman, 1974). From the anodic region calcium is released and from the cathodic one phosphate. Since a tooth mainly consists of apatite, calcium phosphate, a dissolution of the tooth will occur. The process has been experimentally demonstrated by Wakai (1936) and by Till et. al. (1978). Amalgam destroys the teeth. Since amalgam contains several metals, Faraday's law has to be used with some caution. However, all metals in amalgam can ionize under oral conditions (Wranglén and Berendson, 1983) and investigations of old fillings reveal a loss of mercury which can reach 560 mg/5-10 years from amalgam-filled molars and premolars, equivalent to 150-300 micrograms/day (Radics et. al., 1970) and 10-20 micrograms/cm2 and day (Pleva, 1989). Mercury has an uncanny ability to penetrate various materials (Trachtenberg, 1974), and a tooth cavity can certainly not retain released metal, as also measurements show (Mocke, 1971). In addition to the dissolution of metals, the mercury in the amalgam fillings will also evaporate. Some will be inhaled, some directly absorbed. There is no risk evaluation for the absorption of Hg in the oral mucosa. High levels have been measured. What are the consequences? Mercury vapour is absorbed in the oral mucosa, regardless of mouth or nose breathing. Already in 1882 the evaporation of mercury from amalgam was demonstrated (Talbot, 1882). Stock (1926) showed that dental amalgam fillings more than three years old generated mercury vapor in the mouth (iodine color test). The placement of a new one considerably increased the vapor emission. The vapor generated from oral amalgam fillings is efficiently absorbed in the lungs. Mercury, evaporating from the fillings after chewing and measured in exhaled air or the oral cavity, can in many persons exceed industrially permissible levels (Svare et al, 1981; Patterson et al, 1985; Vimy, 1985 a,b). The results by Stock led Brecht-Bergen (1933) to measure the Hg-vapor pressure over amalgam.
Measuring the concentration of Hg in exhaled air or in the oral cavity leads to difficulties in calculating how much Hg is actually inhaled. Abraham et al (1984) introduced flushing of the mouth for 15 sec through two tubes between closed lips, measuring the evaporation rate from the fillings. A pre-chewing evaporation during 15 sec of 0.07-0.8 ng/s (nanograms/second) with a mean value of 0.15 ng/s was found. After 3 minutes of chewing, the emission was 0.08-10.8 ng/s with a mean level of 1.27 ng/s. The actual values after chewing might be even higher than those measured by Abraham et. al. (1984), since the vapor levels continue to increase during 30 minutes of chewing (Vimy & Lorscheider, 1985). Measured evaporation rates from amalgam fillings in the oral cavity can thus reach 11 ng/s after chewing (Abraham et. al., 1984). A comparison can be made with known evaporation rates from mercury. Pure Hg emits vapor at 2.5 ng/s*cm2 at room temperature and maximum air flow (1 l/min) (Stock & Heller, 1926). This will correspond to about 6 ng/s*cm2 at oral temperature. The highest values recorded by Abraham et. al., assuming an amalgam surface of 10 cm2 will correspond to the vapor pressures (see table above), measured by Brecht-Bergen (1933). The actual evaporation depends on the vapor pressure, the flow of air over the surfaces, abrasion etc. However, nose versus mouth breathing does not seem to have a central role. Early references (Baader & Holstein, 1933) indicate that the oral mucosa can efficiently absorb mercury, which is not surprising since even the outer skin absorbs both Hg-vapor (Hursh et al, 1989) and mercury from grey ointment, an old cure for e.g. syfilis, containing appr. 30% Hg (Schamberg et al, 1918). To test for a possible absorption, known amounts of mercury vapor (30-120 ng) were injected into the closed oral cavity of an amalgam- and gold-free subject (the author) with no detectable mercury emission from lungs or oral cavity. After 0-3 min., remaining mercury was sucked out and the mouth flushed with 30 ml of Hg-free air in order to be able to correctly measure all unabsorbed mercury. It was not possible to obtain an exact zero-value, but losses in syringe and tubing amounted to 5.5 ng (the number of experiments was 6). Breathing through the nose when mercury was present in the oral cavity gave the same values as holding one's breath, indicating that minimal amounts of Hg were transferred from the closed mouth to the trachea (Hanson & Pleva, 1991).
The absorbtion is thus considerable, indicating that most of the mercury vapor, generated in the mouth, could be absorbed, also when breathing and chewing takes place with closed mouth and nose breathing. The further fate of the absorbed mercury is unknown. Fredin (1988) placed an inverted cup against the oral mucosa and introduced known amounts of mercury vapor. The result was the same but with a slower absorption because of the smaller Hg-exposed surface (5 cm2). Also the results by Hahn et. al. (1989) on mercury release from amalgam fillings, placed in sheep teeth, show a high concentration of Hg in the gum mucosa (323 ng/g). The major part of the mercury from amalgam is found in feces. One hardly needs any scientific training to understand that decades of swallowed Hg in a finely distributed, probably ionised, form is something completely different from an accident, when metallic mercury is swallowed in large gulps, something which usually (!) does not lead to death or serious poisoning since the surface area is small compared to more finely divided mercury. The metal is heavy and passes rapidly through the intestines. No risk evaluation exists. Swallowed mercury salt is absorbed to 15% (8-24%) in humans. Animal experiments show an absorption of 25-40%, when both uptake and elimination to the intestines are measured. There is no risk evaluation for Hg migrating in through the teeth. The mercury content in saliva is approximately 0.5% methylated (Sellars et al, 1996). Methylmercapto-Hg-Cl and methylmercapto-Hg-tiocyanate, formed by bacteria, is found in the roots of teeth (Haley, 1997). Mercury is not the only metal from amalgam: silver, tin, and copper are also released. From other restoration work: gold, palladium, etc. Interactions? Palladium induces immune reactions against both palladium itself and nickel in animals. Root filling materials are a formidable catalogue of poisons. To place gold in contact with amalgam is definitely incorrect treatment. Any plumber would immediately understand why you should not combine the two. The unsuitability of gold-amalgam belongs to 19th century science and was recognized already in the first evaluation of amalgam from 1844 (Westcott, 1844). The lack of knowledge or will to understand this matter leads to grossly incorrect conclusions when assessing the amalgam load (Ahlqwist et al, 1988). Middle-aged women, for instance, do not have just 0-4 visible amalgam fillings as stated in this report; they have gold crowns and gold bridges placed on top of amalgam, resulting in intense corrosion (Halling et al, 1981). The combination gold-amalgam is malpractice and can not be defended by any scientific argument. New types of amalgam, e.g. non-gamma-2-amalgam, with an increased copper content have been introduced with alleged improved properties. The emission of mercury has not been taken into consideration. This type of amalgam sweats out mercury already at room temperature and emit much more mercury vapour than conventional amalgam (Ferracane et. al., 1995). The non-gamma-2-amalgams are hybrids of copper and silver amalgam and have the poor properties of the copper amalgams with regard to mercury emissions. Easily soluble copper salts are also released. Non-gamma-2-amalgam should be classified as copper amalgam. Copper amalgam was condemned already in the 1920s but was still used in child dentistry well into the 1960s.
"Normal" values of mercury in blood and urine were found in the sheep (mentioned above) with amalgam fillings (Hahn et al, 1989), whereas tissue levels were high. The first reliable measurements of Hg in blood and urine immediately demonstrated that blood values remained low until the exposure was considerable. A small increase was found in urine and much higher levels in feces (Stock & Cucuel, 1934). Amalgam placement causes a transient peak of mercury in urine (Frykholm, 1957; Storlazzi & Elkins, 1941; Schneider, 1977). There are several uncertainties relating to blood and urine Hg-levels as diagnostic tools. Most industrial studies relate these parameters to the percentage of affected workers, not to the severity of symptoms. Low-level exposures to mercury during long periods of time can be completely devastating for the affected individual, as Stock's own case demonstrates (Stock, 1926). The latter's and several other observations during the ages indicate that such "micromercurialism" produce symptoms after a long time. Human experiments with single doses of swallowed radioactive ionic or inhaled elemental mercury show that 1-2 % of the absorbed dose is eliminated in the urine during the week after exposure (Rahola, 1973; Cherian, 1978). The observed peak in mercury excretion after amalgam placement thus corresponds to several hundred micrograms of total absorption. The direct demonstration of Hg/amalgam distribution in sheep confirms the low urinary excretion and that the fecal route is likely to be quantitatively more important but very difficult to differentiate from abraded and swallowed amalgam.
Older type of amalgam scale (to the left) and flat pliers for condensation. It is still not unusual that dental care personnel work directly with amalgam, without a fume cupboard or even rubber gloves when pressing out excessive mercury from the amalgam, which is frequently done either entirely by hand or with the help of a pair of flat pliers.
Few measurements of fecal mercury levels have been made. Tompsett & Smith (1959) found levels of 50-180 micrograms/day, not considering amalgam fillings as a source. A recent study (Engqvist et. al., 1998) demonstrated that mercury in feces, derived from amalgam, was dissolved to about 70% and the rest was in the form of unchanged, abraded amalgam particles. Only one controlled study (in mice) has assessed blood Hg levels in relation to various levels in inhaled air (Eide & Syversen, 1982). Blood Hg was found to relate exponentially to the exposure level. If the situation is similar in humans, blood Hg levels can be expected to show moderate changes within a broad range of exposures. The degree of mercury exposure from amalgam has apparently been considerably underestimated, based on inadequate measurements. A simple consideration of the amount of mercury in the teeth, compared to the daily intake from food, makes it apparent that amalgam should have to be an exceedingly stable alloy in order to not release more mercury than the daily amount ingested with food. With 5 g mercury in the teeth (10 g amalgam), the fillings should last 4,500 years if they do not release more than 3 micrograms of mercury/day, the approximate amount in food for most persons not eating too much fish. Amalgam fillings seldom last for more than 10 years, although some will remain in the teeth for 2-3 decades. In adults from 13 to 74% of the fillings survived for 10 years, according to one study (Meeuwissen, 1985), and others have reported that 50% were replaced within 5 years and an average life span of 4-8 years (Boyd & Richardson, 1985). In 6 year old children the median survival time for occlusal amalgam fillings was 2 years and 2 months (Walls et al, 1985).
Inorganic mercury has insidious effects, not readily recognized unless one is aware of the exposure and the symptoms of chronic mercury exposure. Stock (1926), himself a victim of chronic mercury poisoning, pointed out that the depressing effects of mercury vapor on the thought processes, makes it even more difficult to determine what causes the deterioration of health. "It was as if my stay in Germany made me more stupid", according to a visiting chemist at Stock's laboratories. There is also a lack of communication between dentistry and medicine: "The dentists are seldom in a position to recognize general effects of amalgam fillings or even learn about them. When the patients suffer from nervousness, intellectual exhaustion, catarrhs etc. they do not go to the dentist whom they also usually do not tell about their problems since they are prevented from talking during the treatment. The family physicians, nerve specialists, laryngologists, internists are the ones they discuss these problems with." (Stock, 1926) The physician in turn is completely unaware of any dental treatments, does not suspect mercury from amalgam, has limited knowledge of poisoning symptoms and also hesitates to interfere in the domains of another profession. It is thus not surprising that reports of mercury poisoning from amalgam are relatively rare in the medical literature. However, they do exist and today there are also numerous descriptions, in the daily press and magazines, of changes in health, caused by amalgam removal. There are many descriptions of the symptomatology of chronic inorganic mercury poisoning. Biochemists have also provided many studies on the cellular and molecular effects of mercury, which together provide sufficient explanations for the many symptoms observed in clinical practice. Some of them appear to be mediated by the immune system. Recently, the immunotoxic effects of mercury has attracted considerable attention and today inorganic mercury is the best studied substance with the ability to cause autoimmune disease. Immune reactions were also considered to be the factor which caused acrodynia in children after calomel (mercurous chloride) exposure. Acrodynia is probably the best studied form of mercury poisoning, or "idiosyncrasy", and the very long time from its first recognition (1828) to the establishment of its mercury etiology (1945), indicates the devious nature of mercury intoxications (more on acrodynia further on). However, even more surprising is that the very possibility of mercury poisoning has to be repeatedly rediscovered, and the very short memory among medical doctors after the acrodynia epidemic.
Mercury poisoning from amalgam fillings have been described several times. Stock (1926) relates cases with devastating psychic effects and also aggravated symptoms when fillings were drilled out without protective suction. Further cases were reported by Stock (1928). Fleischmann (1928) reported that conditions for poisoning were present in carriers of copper amalgam fillings (as judged from the Hg-values in urine and feces), whereas no conclusion could be reached for silver amalgam. Fleischmann, director of the mercury clinic at the Berlin Charité, however, found that the disappearance of symptoms after removal of silver amalgam indicated that poisoning could occur. Harndt, dentist at the clinic, considered patients with gold in contact with amalgam as cases where the enhanced corrosion clearly could cause Hg-poisoning (Harndt, 1930). Additional case-reports have been published by Wesselhaeft (1896), Hyams (1933), Steffensen (1934), Lain & Caughron (1936), Struntz (1956), Schwarzkopf (1959), Rost (1976), Till (1984), Zamm (1986), Pleva (1983) and several others. Taskinen et al (1989) followed a patient who had fillings ground to a bar to support a bridge and 11 more fillings had about 1 mm ground away to improve occlusion. In addition, 3 fillings were replaced during the following session. After a week the patient developed stomatitis, sore throat, rancid taste, loss of the sense of smell, dizziness and headache and later pains in the thorax, fever, elevated sedimentation rate, weakened sense of touch in her left hand and fingers, and cold sensitiveness in fingers, weakened hand grip, cramps in her left foot and loss of sense of touch. The patient felt unwell, lost 9 kg of weight and became anxious and depressed. The fillings were removed with extreme caution. The authors consider the symptoms as corresponding to those of micromercurialism. The experience among members of the Swedish Association of Dental Mercury Patients (Tandvårdsskadeförbundet) is that these types of dental treatments are not at all rare and many persons, because of sensibilization and other factors, react with very similar symptoms to lesser dental treatments. Anorexia hydrargyria has been described in a 15 year old girl who developed head and joint ache, vertigo, loss of memory, tiredness, disturbed sleep and loss of hair. Lack of appetite led to loss of weight and symptoms of anorexia nervosa. There were, however, no psychic problems. The patient had an amalgam-glittering mouth with 10 amalgam fillings. She had at an early school age received 6-8 fillings without problems. In 1986 they were all replaced with new ones, and a few entirely new fillings were also placed. The deep fillings were isolated by cavity liner but not the superficial ones. The girl was treated with dimercaptopropane sulfonate (DMPS), a mercury-binding drug, and the fillings removed which brought about complete recovery. Current evaluation of the toxicity of amalgam fillings by the dental authorities has hardly considered diffusion of mercury through the pulp, the number and quality of the fillings and the toxicity of amalgam for pregnant women, children and adolescents (Dörffer, 1989). The common pathology of mercury intoxication can be readily found in many medical papers and textbooks (e.g. Baader & Holstein, 1933). However, many case reports and the acrodynia epidemic during the 19th and 20th centuries caused mainly by calomel-containing drugs against intestinal parasites and by teething powders, indicate that immunological reactions are involved in some individuals. Autopsied acrodynia children showed widespread destruction of the brain and the proposed sequence was an initial attack on blood-brain/nerve endothelial cells, with a secondary immune reaction to brain components. Recent research supports such a mechanism, since also small amounts of mercury will cause a long-lasting impairment of the blood-brain barrier (Chang & Hartmann, 1972).
There are few descriptions in scientific literature of what it feels like to have chronic mercury poisoning. Stock's paper from 1926 (a) is a classic and gives a vivid description of the affected person's miserable situation. He emphazises the psychic effects which were especially troublesome for a person with an intellectual work. In addition to a number of somatic symptoms, Stock mentions: "Intellectual exhaustion and depression, lack of energy and ability for work, especially intellectual work, increased need for sleep ... most severe for a person with intellectual work was the loss of memory ... Especially the ability to calculate, to do mathematical thinking, also to play chess, was severely affected. The depressed ability to remember and the difficulties in calculating seem to be a special sign of insidious mercury vapor poisoning. The intellectual capacity was also in other ways depressed although not as severely as memory. In addition there was psychic depression, a painful inner unrest, with time also causing disturbed sleep. By nature fond of company and full of enjoyment of life, I withdrew in misery into myself, avoided public relations, people and social contacts, lost the love for art and nature. Humor rusted in. Difficulties which I earlier had managed with ease (and today again can manage with ease) appeared insurmountable. The scientific work required considerable efforts. I forced myself into my laboratory but could not produce anything of value despite all efforts. My thoughts were heavy and pedantic. I had to give up participating in matters which were not of immediate importance. The lectures, previously something I liked, became tormenting. The preparation of a lecture, the writing of a paper, even a simple letter, required immense efforts in handling the contents and language. Not seldom it happened that I wrote words wrongly or forgot letters. To be aware of these shortcomings, not to know their cause, to know no way of getting rid of them, to expect further deterioration - that was not nice!"
Stock (1936) describes the slow development of mercury hypersensitivity, resulting in adverse reactions to levels of Hg vapor which do not at all affect other people and also not the affected person earlier. This sensibilization does occur both in heavy industrial exposures, described by Baader & Holstein (1933) and in the "lighter" poisoning which Stock described (1926). "To provoke a first reaction to mercury vapor, a stronger and longer exposure is needed than if one has already been affected. Then symptoms can appear within an hour after exposure to much lower levels. If further exposure is avoided, the sensitivity disappears slowly, more so if the poisoning has been severe and prolonged. This can take years." (Stock 1936) Three dental cases (dentists) were described by Smith (1978). The first dentist had hand tremor, impaired motor control, indifference towards family and friends and some visual disturbance. They experienced irritability, critical excitability, fearfulness, restlessness, melancholy, depression, weakness, timidity (one case), fatigue (two cases) indecisiveness (one case) and headache (two cases). An ophthalmologist found deposits on the lenses of one of the patients, suggesting heavy metal poisoning. The urine in one of the cases was found to contain more than 300 micrograms of mercury per liter. The two other cases were similar. The dentists stressed the fact that the mental effects of mercury poisoning were most distressing and frightening. Each was so deeply affected by the feeling of hopelessness, depression and futility that they urged the physician (Smith) to bring the cases to the attention of the medical profession. The paper ends with the words: "the medical profession must be on the alert for the appearance of mercury poisoning." This is also the theme of a paper in Comprehensive Psychiatry (Ross et al., 1977): "Need for alertness to neuropsychiatric manifestations of mercury poisoning." Nine persons, laboratory staff at a hospital, had the same symptoms as described earlier. The authors stress "that the presence of several of these symptoms and signs should alert the diagnostician to take a careful occupational history and to obtain laboratory measurements of mercury in the urine or hair before coming to a final diagnosis which might be a low grade inorganic mercury intoxication." The most common form of exposure to inorganic mercury is by inhalation of vapor. There is general agreement that this leads to a slowly developing and insidious poisoning, which primarily gives psychic effects and is very difficult to recognize until more objective symptoms appear. There are numerous more or less extensive descriptions. The one below by Baader is a moderately long one. Others have noted additional symptoms or more rare effects (Baader, 1933, 1961; Stock 1926, 1936; Moeschlin, 1980; Poulsson 1949; Oettingen 1958; Burgener & Burgener, 1952; Schulz 1907; Kussmaul, 1861).
It seems that most symptoms could be caused by effects on the nervous system, together with endocrine disturbances and local effects where the metal enters and leaves the body. In addition to the general symptoms of mercury poisoning, there are numerous reports on individual cases of less common forms. Some caution is required, since sometimes these are cases where mercury has been administered to treat various diseases. This has been recognized as a problem since the early days of syphilis treatment (Kussmaul, 1861). The types of symptoms depend on the mercury compound and the mode of administration. An ALS-like syndrome has been reported after exposure to ethylmercury (Kantarjian, 1961), mercury vapor (Adams et al, 1983) and inhaled mercuric oxide (Barber, 1978). Other forms have been called neurasthenia mercurialis, epilepsia mercurialis, dementia mercurialis, schizophrenia mercurialis and various forms of paralysis, affecting different parts of the nervous system: polyradi-culoneuritis, Guillain-Barré and also multiple sclerosis (Kussmaul, 1861, Zangger, 1930, Baader & Holstein, 1933). If the mercury exposure is recognized and interrupted, most cases recover, sometimes slowly but often surprisingly rapidly. In the late 1940s, when the mercury etiology of acrodynia was clarified, also the possibility of MS as an adult form of acrodynia was considered. No general and widespead source of mercury was then regognized. However, in 1966 Baasch, a Swiss neurologist, recognized the possibility of amalgam fillings as being such a source. He concluded that a mercury/amalgam etiology could explain the known facts about MS. Additional protective or aggravating factors in the environment could play a role. Lead was also considered as a possible contributing factor because of its widespread occurrence, known demyelinating activity and some reports on MS after lead exposure. Today we have another significant factor, not recognized by Baasch: selenium (which is protective against mercury). Both MS and a high DMF index (diseased, missing and filled teeth) correlate well with low selenium levels as do a number of other diseases. Baasch noted the presence or absence of amalgam fillings in 500 consecutive MS patients in Zürich. All except one or possibly two had amalgam fillings. However, amalgam fillings are common and this proved nothing. On the other hand there are also other sources of mercury. For instance, a prolonged stay in a house where a barometer had been broken is known to have caused acrodynia (Gädeke, 1962), and in another case the mercury source was sublimate-impregnated wood which was used to heat the house (Gädeke, 1966). The latter case was only recognized as mercury-related because the author recognized the symptoms from the first, more obvious exposure. Other sources are broken thermometers or fluorescent lights, old mercury mirrors, wall paint etc. Three cases were described by Baasch. Two of these had their amalgam fillings removed and they improved. Nothing was done to the third one, a completely paralyzed patient, whose case is described, however, since the disease started a few months after she had her first amalgam fillings, 19 years old, and then had a very rapid progression. She had, 8 years old, been treated with mercury for congenital syphilis. Mercury in mines is usually found in combination with sulfur; as cinnabar, mercuric sulfide. When the ore has been mined, a simple distillation releases the mercury. After various kinds of use, where people become exposed to mercury, when dealing with, for instance, thermometers, paints, amalgam, etc, some mercury will enter the human body and again combine with sulfur, usually in the form of sulfhydryl groups (-SH) in amino acids and proteins (cysteine and methionine). It is quite clear that enough mercury will inactivate any enzyme or process which depends on sulfhydryl groups for its function, e.g. the energy production in the cell.
”Mercury is a radiomimetic metal with the same effects as radiation.”
The free-radical nature of mercury toxicity was anticipated very early. Already at the turn of the century, Schulz (1907) wrote that mercury was in a constant interchange between calomel and sublimate (monovalent and divalent mercury, respectively), promoting oxidation reactions. Such a behavior will also explain why the undoubtedly small amounts, which are absorbed even during massive poisonings, have such pronounced effects on tissue sulfhydryl groups. The sulfur-mercury bond has a short lifetime, despite the theoretically high affinity of Hg for sulfhydryl groups (Rabenstein & Isab, 1982). Clarkson (1972) pointed out that not even in the kidneys will there be enough mercury to occupy more than a fraction of available sulfhydryl groups. Mercury functions as a catalyst in oxidation of sulfhydryl groups. A direct demonstration of enzymatic generation of radicals by HgCl2 (mercuric chloride) was presented by Cantoni et. al. (1984). There was a concomitant formation of DNA single strand breaks, indicating hydroxyl radical formation or something equally reactive. It is likely that some of the mercuric chloride was converted to the mercurous form by enzymes or sulfhydryls and then reoxidized with a concomitant formation of radicals. A free-radical view of mercury toxicology gives a coherent picture of why the metal has such diffuse and widespread effects on the human metabolism. It will also give a clear indication of possible treatments with antioxidants. Hg in low amalgam concentrations in cell and animal experiments produces serious disturbances in basal metabolic processes: Calcium balance (Chavez & Holquin, 1988), microtubuli of the cell skeleton (Pendergrass et al, 1997), free radical production (Cantoni et al, 1984), glutamate balance (Brookes, 1988), immune system (Hultman et al, 1994), etc. Mercury is a radiomimetic metal with the same effects as radiation. A spectrum of pathological effects can be expected and have been seen both in amalgam patients and in other exposures to mercury. With regard to mercury as a cause of specific illnesses, it is safe to conclude that mercury gives mercury poisoning. It is then up to the medical doctors to diagnose correctly. On the other hand, if you have been labeled with a diagnosis which involves certain signs and symtoms, you should absolutely not be exposed to a substance which produces the same symptoms and is likely to affect the same biochemical processes.
How many physicians have heard the story of how medical science eradicated the disease called acrodynia? Very few probably since the discovery and cessation of a major poisoning is hardly anything to be proud of. However, medical science ought to learn an important lesson from a disease which cost numerous children's lives. Acrodynia has obvious relations to the amalgam issue since there are numerous, now-living persons, who developed acrodynia in childhood but recovered. At older age they received amalgam fillings, and their poisoning symptoms quickly reappeared, but now they did not realize their origin. It is quite rewarding to study the publications on acrodynia, since there are careful descriptions from both before and after the mercury etiology was recognized. Even the psychosomatization was not missing. Spitz and Wolf (1946) described under the title "Anaclitic depression" a syndrome among children in a nursery (5-11 months of age). Several of the children died and arrested development was noted in others. The authors considered the illness to be comparable to melancholia in the adult and caused by "withdrawal of the love object". The psychic diagnosis is discussed (and rejected) in a review paper by Leys (1950), where these cases were considered typical of acrodynia.
”How many physicians have heard the story of how medical science eradicated the disease called acrodynia?”
The first appearance, at least in a sufficient number of cases to be recognized as something special, was in a block at Rue d'Orsay in Paris in September 1828. In this house a number of children, and also adults, fell ill. An infectious agent was suspected. The epidemic was described in medical journals and subsequently cases were reported from other places, often isolated cases among children, but sometimes groups of children and also adults were affected. Epidemics from prisons and military camps were reported. The disease spread during the 1800s, and at the end of the century it had expanded to large parts of the world. In England, Australia, the southern USA and other English-speaking countries mainly children below 2 years of age were affected. The peak was at 9 months of age. On the continent the peak was at 2 1/2 years and continued up to 9 years. In England 585 deaths because of acrodynia were officially registered between 1939 and 1948. In the year 1952-53, acrodynia cases constituted 3.6% of all visits to the children's hospital in a British city. In Australia the disease had epidemic forms. The responsible virus was discussed and its mode of transmission from person to person. Epidemics could occur in isolated, rural areas. The cause was unknown. The disease had other names besides acrodynia. Because of the swollen, painful hands and feet with peeling skin and a reddish color, it was called "pink disease". Skin problems in other parts of the body were also common. After physicians who described various features, it was also called Feer's disease, Selter's disease and Swift's disease. More symptom-describing was erythema arthriticum epidemicum, vegetative neurosis of childhood, vegetative encephalitis, erythroderma polyneuritis, throphodermatoneurosis, primary emotional disorder. A physician wrote: "... it is difficult to imagine anything more pathetic than a baby suffering from pink disease with complete apathy and loss of interest in his surroundings." (Southby, R. "Pink disease with clinical approach to possible etiology", Med J. Austr. 2, 1949, 801, quoted in Warkany, 1966.) The children had pains in hands and feet and those were often swollen, damp, sensitive to touch and felt cold. Demyelination, i.e. degeneration of the insulative lipoid sheath surrounding the nerve, was noted in biopsies. There were disturbances of blood circulation and temperature regulation; in severe cases fingers and toes could be lost by gangrene. Blood pressure and levels of the "stress hormone" adrenalin were often high. The victims exhibited extreme muscle weakness; they usually couldn't stand nor walk. Loss of weight, tremor and shaking, cramps and uncontrolled movements, abdominal tenderness and gastrointestinal troubles belonged to the clinical picture. Also conjuctivitis and fever was reported in earlier descriptions. Fever was apparently very common in Germany and Switzerland, where the most common misdiagnosis was scarlet fever. In a considerable number of cases there were salivation, swollen gingiva, loss of teeth and necrosis of the jaws. What caused the disease? Guesses were numerous. Vitamin deficiency, neurosis, endocrine disturbance, adrenal insufficiency, electrolyte imbalance, allergy, hysteria, trikinosis, rye fungus (ergot). The similarity to pellagra (vitamin B3-deficiency) was pointed out several times. There were studies to assess possible contacts with animals; unknown viruses and a variety of microorganisms were suspected. The similarity to arsenic poisoning was noted in 1889. Mercury poisoning and the similarity in symptomatology to effects of mercury treatments with grey ointment was first suggested in 1846 and again in 1922. That year a physician wrote: "For a while I had the idea that it could be a metal poisoning. Several of my patients had been treated with large doses of calomel at the onset of the disease. There were, however, cases where no calomel treatment could be found and this drug could be eliminated." (Zahorsky J. "Three cases of arythredema [Acrodynia] in infants", Med Clin N. Amer, July 1922, 97, quoted in Warkany, 1966.) Why did he think of mercury? The reason was the oral changes: "A symptom which is almost unknown in every disease except poisoning with mercury or phosphorus." In the USA the idea of poisoning also appeared. Bilderback described a number of cases in 1920 and noted that the disease "was more like a low-grade poisoning or a deficiency disease than an infection. The children were, however, well-fed. Low-grade toxemia remained." In 1945 an American physician, Warkany, got the idea to send a urine sample to a laboratory for metal analysis, because of the similarity in symptoms with arsenic and thallium poisonings. The urine contained 360 micrograms Hg per liter and no other metals. Additional measurements demonstrated mercury in most urine samples, however not in all. Careful studies showed mercury exposure in every case, most often from teething powders. Warkany wrote that "its seems rather odd that one could not detect the injurious mercury at the entrance of the alimentary canal, whereas it could be demonstrated at the end of the urinary tract." The onset of disease could be delayed weeks to months after the mercury exposure. There were also cases of typical, acute, poisonings, immediately or after weeks followed by acrodynia (suggesting the involvement of immune reactions). Often the exposure to mercury could be difficult to find. In a series of 40 patients, 19 had been exposed to calomel in teething powders, 6 to mercury in other types of tablets or powders, and 7 to calomel in worm-medicine. Four cases had been exposed to ammoniated mercury for skin treatment and 3 cases had been exposed to mercuric chloride after washing diapers in sublimate solution. Another case had been exposed to mercuric iodide. Broken barometers, sublimate-impregnated wood, paint and recently broken fluorescent lamps had been other sources of exposure. The mercury etiology was doubted, since many children had high mercury levels in urine without showing the symptoms of acrodynia. An estimate indicated that about one child of 500 exposed developed acrodynia. There was never any study if there were any other signs of disease or if mercury-exposed children got other diagnoses, when symptoms were different from those usually connected with pink disease. The sale of calomel powders was forbidden or restricted in several countries, first in Australia. The epidemics quickly disappeared. USA followed, but in England the disease continued since the mercury etiology was slow to be accepted. In USA the FDA had attempted to remove calomel-containing teething powders as early as 1931. In England a court case got the preparations off the market in 1953. Still, sporadic cases are reported from various parts of the world, always in association with mercury exposures. Warkany pointed out that the disease disappeared without any acrodynia foundation, no parent support group, no research money and in silence. "A subtle, complicated, and no doubt molecular disease was eradicated by such a prosaic measure as removing calomel from oldfashioned teething powders and worm medicines," Warkany wrote (1966), and he also said: "There were data on electrolyte changes explaining the symptoms of acrodynia and their alleviation by subtle saline treatments. But these data did not take into account the one electrolyte that mattered, namely mercury."
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Copyright © Mats Hanson, 2003. (Fact boxes interspersed in the main text were written or compiled by the Art Bin editor, except for the one about immunological reactions to mercury, which was written by Mats Hanson. Tables are by Mats Hanson.)
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Alfred Stock (1876-1946), German chemist, appointed professor of inorganic chemistry at the polytechnicum of Breslau in 1909. In 1916 he joined the Kaiser Wilhelm Institute in Berlin and became its director in 1921. Stock was renowned for his experiments with boron, silicon, phosphorus — and mercury. He coined the term ligand for a molecule or ion bound to a central atom in a complex compound. The system of marking oxidation number in synonymous compound names with a Roman numeral, as in iron(III)oxide, was originally also his concept.