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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.
| Fact box: Mercury |
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Mercury, with the chemical symbol Hg
(from Greek "Hydrargyros"), is the only metal adopting liquid form in
room temperature. Mercury appears in seven natural isotopic forms. The
metal is extracted from the mineral cinnabar, mercuric sulfide, in
former times used also for paint. Mercury can easily form alloys
(amalgams) with other metals, thus making them, so to speak, dissolve
into each other, without however forming a regular chemical compound.
There is organic mercury (compounds with carbon) and inorganic mercury
(compounds without carbon, and also pure mercury in atomic or ionic
form).
Among organic compounds are, for instance, methyl mercury (the real name should actually be dimethyl mercury), (CH3)2Hg, easily formed in the intestines when enzymes help methyl groups (CH3)
attach to mercury ions. According to some researchers, this process
may take place also in the oral cavity, where bacteria supposedly will
help metylate mercury leaking from amalgam fillings. Methyl mercury in
turn will easily attach to free SH-groups (sulfhydryl groups, containing
hydrogen and sulfur), which might affect enzymatic functions of the
body, energy production of the cell, detox capacity of the liver etc.
Phenyl mercury(II)hydroxide , (C6H5)Hg(OH) is used
as a preservative in, for instance, cosmetics. The use in vaccines
of thiomersal or sodium ethylmercuric thiosalicylate, (C6)SHgCH2CH3(COONa), which contains mercury, is today heavily debated.
Among inorganic compounds are, for instance, mercury(II)sulfide, HgS, cinnabar, mercury(II)nitrate, Hg(NO3)2, in olden days used in hat manufacturing (poisoned hatters were then considered "mad"), mercury(I)chloride, calomel, Hg2Cl2, which was administered for syphilis. Mercury(II)chloride, sublimate, HgCl2,
was earlier a component in batteries (it is not that common nowadays)
and also used in medicine. Mercury(II)oxide, HgO, was also used in
batteries.
Organic compounds, as well as pure metal mercury, is absorbed in the
gastric tract only to a maximum of 10 percent. Mercury vapor, on the
other hand (which is very easily formed over, for instance, spilt
mercury), is absorbed by the body to appr. 80 percent when inhaled. The
part of it that adopts ionic form might also become methylated into the
most toxic form, methyl mercury.
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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).
| Fact box: Faraday's law |
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Faraday's
electrolytic law shows the relation between electric current and the
electrolyte's atomic properties and the duration of exposure. Thus
I=m*F*z/A*t
where I = current, m = mass, F = Faraday's constant (6.478 C/l), z = valence, A = atomic weight, and t = time.
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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.
| Table 1: Evaporation of mercury |
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Hg-vapor pressure over amalgam (Brecht-Bergen, 1933):
| Ag/Sn/Hg | alloy with | 45 % Hg: | 10.7 % | compared to pure Hg |
| Ag/Sn/Hg | alloy with | 54 % Hg: | 25.7 % | compared to pure Hg |
| Sn/Hg | alloy with | 30 % Hg: | 54.7 % | compared to pure Hg |
(Ag=silver; Sn=tin; Hg=mercury)
Evaporation is proportional to the vapor pressure but will also be
influenced by, for instance, the flow of air over the surface.
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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).
| Table 2: Absorption of mercury in the oral mucosa |
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| Inj. amount (ng) | Remaining Hg after 1, 2, 3 min. |
| 1 | 2 | 3 |
|
| 32 | 14 | 8 | 5 |
| 42 | 21 | 13 | 10 |
| 79 | 34 | 31 | 22 |
| 120 | — | — | 39 |
|
| n= | 3 | 3 | 4 |
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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.
| Fact box: Immunology 1 - The basics |
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The human immune system consists of several kinds of white blood cells and proteins (antibodies or immunoglobulines).
The white blood cells are chiefly lymfocytes (the human body contains around 1012
lymfocytes which amounts to appr. 0.5 kg), but also e.g. monocytes and
granulocytes. Monocytes and some of the granulocytes are capable of
consuming (phagocytizing) viruses and bacteria. Granulocytes are also
involved in allergic reactions, due to their content of histamine.
There are two main types of lymfocytes, B-cells and T-cells.
B-cells produce antibodies, large Y-shaped proteins that attach foreign
substances (antigens), thus presenting them to the rest of the immune
system as something that should be broken down. B-cells are highly
specialized and can only produce antibodies for one kind of antigen.
B-cells can only work in bodily fluids, but T-cells can fight viruses or
bacteria also within cells. T-cells are are of two kinds, T-killer cells (also called T8-cells or cytotoxic T-cells) and T-helper cells (also called T4-cells). T-suppressor cells are sometimes mentioned as yet another kind, supposedly affecting the tolerance against a certain antigen.
The T-killer lymfocytes kill the whole cell that has been infected. Both
B-cells and T-killer cells are assisted by the second kind of
T-lymfocyte, the T-helper cells, which tell the immune system which
B-cells or T-killer cells that need to be activated. In AIDS, for
instance, such helper cells are infected, so the rest of the system can
no longer work against either the HIV-virus nor any other pathogen.
T-lymfocytes are produced in the bone marrow, then, in the thymus gland,
they are "trained" to deal only with foreign substances and not to
react to the body's own proteins or cells. When this function is
disturbed, autoimmune diseases may occur, such as MS.
In their de-activated states, both B-cells and T-cells have a memory
function. Such "memory cells" have a lower threshold of activation than
other cells and mobilize quicker against antigens.
Antibodies, finally, are of five kinds: IgG (also called
gammaglobulin) is the most important and the only type that can permeate
the placenta from mother to foetus. IgA works in secretion; saliva,
phlegm and sweat. IgE works for instance against parasites but is also
involved in allergic reactions. There are also antibodies called IgM,
which resemble IgG, and the IgD type with unknown function.
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| Fact box: Immunology 2 - Reactions to mercury |
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Mercury is known to be immunotoxic. Inhalation or swallowing of mercuric
chloride or methyl mercury in doses relevant to industrial exposures or
intake in food produces the same systemic autoimmune reactions which
have been demonstrated after subcutaneous administration in susceptible
rat strains (Bernaudin et al 1981). Amalgam, placed in the teeth of mice
has the same effect (Hultman et al, 1994).
The autoimmune disease is characterized by antibodies to a variety of
proteins, mainly of endothelial origin (Sapin et al, 1981). Also an
unspecific IgE induction has been noted (Provoust-Danon et al, 1981).
IgE, immunoglobulin E, is typical of allergies. Outbred animals show a
more complicated response (Dieter et al, 1983; Robinson et al, 1984).
The effects on the immune system are thought to be mediated by
interaction between mercury and T-cells, where the helper/suppressor
ratio is altered. A genetically determined unspecific activation of
immunoglobulin-producing B cells is the result (Pelletier et al, 1985).
Long-term exposure of rats and rabbits to low levels of Hg-vapor caused
first a stimulation of the immune response and later a decline with poor
protective activity against bacterial antigens (Trachtenberg, 1974).
Individual response was noted and also the very long time required for
recovery after discontinuation of the exposure. Trachtenberg considers
that immunological changes occur significantly earlier than other signs
of latent toxic effects.
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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!"
| Fact box: Alfred Stock |
|
 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.
Through his work, Stock became poisoned by mercury and tried to warn
other scientists as well as dentists working with dental amalgam. He
wrote about fifty papers about mercury and described his own misery due
to the poisoning in "Die gefährlichkeit des Quecksilberdampfes" (The
danger of mercury vapor) from 1926 (see quotation in the main text
above). Stock mentions Faraday and Pascal as possible fellow-sufferers
of mercury poisoning and concludes:
"Undoubtedly, mercury — the use of which research unfortunately cannot
renounce — has caused severe damage to science, in the past like still
today, by depriving so many researchers of their energy (stamina?).
May this warning of today help people to better consider and avoid the
dangers of this malicious metal."
In "Die Gefährlichkeit des Quecksilberdampfes und der Amalgame" (also from 1926) Stock says:
"Also with us, the true source of our complaints was not detected for
many years, with me not even for two decades, not even by distinguished
physicians. With me they searched for it in an illness of the nose and
subjected it, without success, to bleeding surgery, to burning, to
corroding etc. Some of my coworkers were treated for sinusitis."
Only by coincidence were their eyes later opened, Stock says, and
they realized that the common cause of their ailments was mercury.
This metal is a typical respiratory poison, he writes in "Die chronische
Quecksilber- und Amalgamvergiftung" (1939):
"The intake of mercury vapor by the respiratory organs has an
incomparably more harmful effect than the introduction of the same
amount of mercury through the stomach [... ] If one inhales mercurial
air, then the breathed-out air is almost mercury-free. "
After that Stock mentions appr. twenty symtoms of mercury poisoning, (such as those mentioned in table 3 below), and adds:
"The individual symptoms are not very characteristic, so the patients
and their physicians normally do not consider poisoning or illness at
all, but ascribe the conditions to exhaustion, 'nervousness', old age
etc."
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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).
| Table 3: Symptoms of mercury poisoning |
|
Stomatitis gingivitis
lose teeth
salivation/dry mouth
foul breath
metal taste
diarrhea
nephritis
anemia, relative lymphocytosis
anxious seclusion
uncertainty
shyness
irascibility
labile mood
forgetfulness, memory loss
feeling of intellectual inadequacy
thyroid disturbance
disturbance of sleep
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tremor, jerks, shaky handwriting
intention tremor
difficulty to speak
fatigue
pressure over head, headache
dull pains in limbs and joints
disturbance of blood circulation
increased sweating
irregular heart
pressure over chest
lowered blood pressure
sensory disturb. of skin
irregular menstruation
eye pigmentation
skin changes, eczema |
Common misdiagnoses: neurasthenia, hysteria, schizophrenia
(Baader, E., Quecksilbervergiftung, in “Handbuch der gesamten Arbeitsmedizin”, 1961.)
|
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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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