Amalgam
is the name of the material that dentists use to place a “silver” filling in a
tooth. It is composed of approximately
57-46% powder containing silver, tin, and copper and sometimes zinc, palladium,
or indium in smaller quantities. This
alloy powder is dissolved in approximately 43-54% elemental liquid mercury
(United States 1993). Amalgam has been
used in the field of dentistry for over 100 years (in varying concentrations). There are approximately 22 million amalgam
fillings placed in the teeth of the English and the Welsh per year. In the United States, there are more than
160 million amalgams placed per year.
It is used in about 75% of all fillings in these countries (Eley
2001). Amalgam is a self-hardening
mixture that once set, must be removed by a high-speed drill. Today, it is mainly used in posterior teeth,
usually on occlusal surfaces, as an economical, long-lasting, and durable
alternative to tooth-colored filling materials such as composites and
porcelain. Amalgam undergoes an initial
degradation to form an oxide layer that seals the tooth-restoration interface
and prevents bacterial leakage that could infect the pulp of the tooth and lead
to its extraction (United States 1993).
Mercury
is toxic because it has an affinity for sulfhydryl groups, the functional
components of many enzymes and hormones; it disrupts most biological systems as
a result (Siblerud 1989). Acute mercury
poisoning is progressive in clinical symptoms.
The patients are initially asymptomatic following the first 1-4 hours
after exposure to high levels of mercury vapor. Abruptly, fever, chills, nausea, and respiratory difficulties
such as coughing, shortness of breath, pain and tightness in the chest
begin. Death within a few days may be
caused by pulmonary edema (Morbidity 1991).
Chronic mercury poisoning results from spills indoors where the mercury
slowly volatizes and the vapor is inhaled constantly. Mercury vapor concentration is likely to be highest closer to the
floor where the mercury seeps into cracks or into the pile of carpets. Symptoms include fine tremors in the
fingers, eyelids and lips; psychopathologic symptoms include depression,
irritability, insomnia, emotional instability and exaggerated response to
stimuli (Morbidity 1991).
In addition,
toxicological syndromes include erythism and acrodynia. Erythism consists of personality changes,
withdrawal, and loss of self-control.
Acrodynia is painful, erythmatous extremities, with anorexia, sweating
and photophobia (Kulig 1998). Numerous
cases of acrodynia occurred in the 1970s when inorganic mercury was added to
teething powders, and it is considered to be a form of childhood mercury
poisoning (Agocs 1990). Mad Hatter
syndrome is a result of brain damage due to mercury poisoning of felt-hat
makers who were regularly exposed to mercuric nitrate during the last
century. They were known as “mad
hatters” because of the emotional problems they suffered from: sudden anger,
hallucinations, delusions, loss of memory, and mania (Siblerud 1989).
Mercury exists
in three forms: elemental (Hg), inorganic (Hg+, Hg2+) and
organic (methyl- and phenyl-) mercury.
Elemental mercury exposure is usually due to occupational mercury vapor
inhalation. It is almost completely
absorbed and oxidized to the inorganic forms.
An example of elemental mercury is mercury vapor found in the air that
we breathe (40-120 ng/day). Inorganic mercury is found in particles of
amalgam and some food and medications.
After reaction with the gastric juices in the gastrointestinal tract, it
is absorbed. It remains in the
inorganic state and is readily excreted in the urine. Inorganic (Hg2+) mercury is found in drinking water
(25 ng/day) and seafood is a primary
dietary source of mercury: 20% is inorganic (Hg2+) and 80% is
organic methylmercury. Organic mercury
comes primarily from food, especially seafood and fish from contaminated water,
and agricultural pesticides and herbicides (United States 1993). The EPA proposes a maximum dose of
methylmercury ingestion of 0.1 ug per
kilogram of body weight per day, five times lower than the Food and Drug
Administration’s (FDA) dose of 0.01 mg/m3 per week (Kulig
1998). It is readily taken up by the
body and is highly toxic. Methylmercury
is converted to inorganic mercury by anaerobic bacteria in the sediments of
marine and freshwaters. It binds to the
edible fish muscle fibers and is slow to be released, resulting in accumulation
up the food chain. It is rapidly
absorbed into the blood stream, with 90% of that found in the red blood
cells. However, 90% of dietary
methylmercury is excreted in the feces after going through an enterohepatic
cycle. The excretion of methylmercury
begins as a secretion in bile. The
methylmercury in the bile is reabsorbed in the intestine until the intestinal
flora converts it to Hg2+, which is readily excreted in the
feces (United States 1993).
|
Elemental Hg |
40-120 ng/day |
occupational vapor inhalation, oxidized to inorganic forms |
found in the air we breathe, main form of mercury released
from amalgam fillings |
|
Inorganic Hg+, Hg2+ |
25 ng/day (water) |
absorbed in GI tract, readily excreted in urine |
water, particles of amalgam, food (seafood 20%), some
medications |
|
Organic (methyl-, phenyl-mercury) |
Highly
toxic! max. dose: 0.1 ug/kg
body weight per day |
rapidly absorbed by blood stream, enterohepatic cycle |
Seafood (80%), pesticides, herbicides, accumulation up the
food chain |
Table 1. Comparison of the Three Forms of Mercury
The Environmental
Protection Agency estimates the total daily absorption of all forms of mercury
to be 5.8 ug. The literature ranges in estimates of total
daily absorption of mercury from 2 ug
up to 15 ug. Those who eat more seafood are likely to
have the higher range of mercury intake.
Those with the average of 20-30 tooth surfaces filled with amalgam will
have a daily mercury uptake of up to 10 ug
from the amalgams (United States 1993).
A single filling in a posterior tooth can typically cover 3 or more
surfaces.
Amalgam
corrosion is an oxidation-reduction reaction.
The metals in the amalgam produce chemical compounds upon reaction with
nonmetallic elements in the mouth.
Amalgam corrosion is important because it is one of the factors that
determine how much mercury is released into the mouth from the filling (Dodes
2001).
Mercury is
mainly released from dental amalgam as elemental mercury vapor. The vapor
dissolves in the air or saliva in the mouth and is inhaled or swallowed. Mercury diffuses towards the surface of the
filling where a concentration gradient for mercury exists. This diffusion is influenced by temperature,
which is relatively constant in the mouth over time. Daily activities such as chewing and tooth brushing release the
mercury from the surface of the filling (United States 1993).
Mercuric ions
(Hg2+) are also released from the amalgam through electrochemical
corrosion. Theoretical data suggests
that tin and in some cases, zinc, are the corroding metals, dissolving
first. This leaves mainly the mercury
and silver-rich phases thus increasing further mercury release. When two amalgam fillings come into contact,
electrochemical corrosion of mercury may produce Hg2+ ions. These ions bind to the organic components in
the saliva and are swallowed. Reliable
data on electrochemical corrosion does not exist. In fact, it has been questioned whether it even occurs (United
States 1993).
Dental amalgam
fillings are the largest source of inorganic mercury exposure in the general
population (Sandborgh-Englund 1996).
Elemental mercury constitutes 50% by weight of dental amalgam
fillings. The atoms of mercury diffuse
from the amalgam, through the amalgam oxide layer, through the saliva, and into
the air flowing through the mouth. Each
layer provides protection from the mercury atoms diffusing into the mouth. Abrasions, such as brushing and chewing,
alter the oxide layer and thus increase mercury (Hg2+) release. Both elemental and inorganic mercury are
swallowed and introduced into the gastrointestinal tract where the elemental
mercury is converted to inorganic mercury.
The vapor, after absorption into the blood stream, gets distributed
throughout the body, and is concentrated in the kidney (United States 1993).
Elemental mercury dissolves in lipids and thus readily diffuses across cell
membranes, such as the blood-brain barrier or the placenta. Once in the cell, the elemental mercury is
then oxidized to inorganic (Hg2+) ions by catalase enzymes. These ions cannot readily re-cross the
membranes and this explains the accumulation of mercury in the brain and in
fetal tissues. Neurological effects of
mercury poisoning are probably due to the formation of divalent mercury ion by
oxidation in brain tissue which inhibits the brain’s interactions with enzyme
sulfhydryl groups (United States 1993).
The
rate of release of mercury vapor from amalgam fillings is dependent on many
factors and is thus hard to quantitatively determine (Sandborgh-Englund
1996). A person with a mouthful of old
amalgams and a habit of grinding their teeth at night will have much more
mercury vapor released than someone with very few amalgams and who does not
chew gum.
Placing
and removing amalgam fillings releases a large amount of mercury vapor into the
mouth and is associated with high peaks of mercury in the blood and urine. The kidneys and the central nervous system
are the organs that are most critically affected upon exposure to inorganic
mercury (Sandborgh-Englund 1996). In
the short term, within 48 hours after amalgam removal according to
Sandborgh-Englund (1996), the mercury is widely distributed throughout the
body. However, in the long term,
approximately 2 months according to Sandborgh-Englund (1996), the mercury is
measurable only in the kidneys. The
kidney has the ability to complex with metallo-thionine and selenium which
protects the kidney from damage by greatly reducing the toxicity of
mercury. Thus, the kidney is the main
organ that retains inorganic mercury (Eley 1993). In a study conducted by Boyd et al. (1991), sheep were given
occlusal amalgam dental fillings.
Occlusal surfaces are the stress-bearing surfaces of the teeth and thus
get the wear-and-tear of everyday chewing and grinding. After placement of the fillings, the sheep
displayed a drastic drop in kidney function. This would lead one to draw the
logical conclusion that the mercury in the dental amalgam fillings is harmful
to, in this case, a sheep’s body (Sandborgh-Englund 1996). However, these results have been harshly
challenged for several reasons. The
amalgam placed in the sheep’s teeth contained far more mercury than a dentist
would use. If there is an excess of
mercury it can’t bind properly to the other metals in the amalgam causing an
increased release of mercury. Also,
improperly constituted fillings wear down easily. With sheep being cud-chewers, they grind their teeth round the
clock and would wear down these “soft” fillings faster thus ingesting large
quantities of mercury. Also, the
fillings were placed with poor technique and they put in all twelve fillings at
one time, this is not done in dental practices. The type of kidney damage that Boyd et al. (1991) reported was
not the type that mercury toxicity is known to cause (Baratz 1991). They measured renal toxicity by the glomerular
filtration rate. A reduction in the
glomerular filtration rate should raise blood urea levels. However, in the Boyd et al. (1991)
experiment, the blood urea levels were lowered. And according to Sandborgh-Englund (1996), no evidence of renal
toxicity was found in human subjects after amalgam removal. Boyd et al. did not expose sheep to mercury
alone to prove that the mercury was causing the kidney failure (Baratz 1991).
In
the study conducted by Sandborgh-Englund (1996), seven females and three males
from 30-52 years of age with approximately 13-34 surfaces of amalgam fillings
that were older than ten years, had all their amalgam fillings removed and
replaced with alternative treatments.
They excluded fish from their diets for over a month prior to the study.
Blood and
urine samples were obtained one week prior and one, two and sixty days after
the amalgams were removed. They
analyzed the mercury in whole blood, plasma, and urine. Immediately after amalgam removal, there was
a slight rise in mercury concentration in the plasma, blood, and urine. After two months, these levels decreased to
half of the amounts recorded before the amalgams were removed. No signs of kidney dysfunction were detected
(Sandborgh-Englund 1996). Basically,
there were no changes in any of the measured parameters of the study. This means that there is not a correlation
between elevated mercury levels and renal toxicity due to amalgam
fillings.
Immediately
following amalgam removal, there is a significant increase in mercury levels in
the body followed by an exponential decline.
Inorganic mercury is distributed in a 1:2 red blood cell to plasma ratio
while the organic mercury is sequestered in the red blood cells
(Sandborgh-Englund 1996).
In those with
amalgam fillings, the concentration of mercury in their organs as compared to
the organs of those without amalgam fillings is 2-3 times higher in brain
tissue and nine times higher in the kidneys (United States 1993). There is a
direct correlation between the number of amalgams and higher mercury levels in
the body, and approximately 87.5 ug/m3
mercury is released during chewing.
Newer fillings release four times as much mercury after chewing and
one-week old fillings show 17-times more mercury released after chewing. The chewing surface of a five-year old
amalgam has lost almost half of its mercury, whereas a 20-year old amalgam had
lost almost all of its mercury (Siblerud 1989). In a study conducted by R. L. Siblerud (1994), he speculates that
mercury may be an etiological factor in depression, excessive anger and
anxiety, fatigue and insomnia. This may
be due to mercury’s interaction with neurotransmitters such as acetylcholine,
in the brain. Also, a small proportion
of the population may have an allergy to the mercury in amalgams, but this is
exceedingly rare (United States 1993).
Despite the
negative data implicating mercury as the culprit for many diseases and
problems, there is no scientific data proving this. In the few scientific experiments that exist, many were flawed in
their experimental procedures. Also,
many of these experiments discuss total blood mercury content. However, they blur the distinction between
inorganic mercury from amalgams and organic mercury from fish consumption,
skewing the results. The United States
Department of Health and Human Services dental amalgam report (1993) says that
there is not enough evidence to prove that the health of those receiving
amalgams is in jeopardy, nor is there enough evidence that removing any
existing amalgam fillings would have a beneficial effect on health. In fact, the removal process itself causes
additional exposure to mercury. The
amount of mercury released from amalgam fillings is insignificant compared to
the total daily intake of mercury.
Mackert (1991) says that the daily intake of mercury from amalgams is
1.2 ug, compared to the total daily intake of mercury between
10-20 ug. In addition, there have been many anecdotal reports of people
being miraculously cured of their diseases, from multiple sclerosis to
depression, immediately upon removal of all their amalgam fillings. However, the removal process exposes the
patient to more mercury than putting in a filling or leaving it alone does
(Baratz 1991) and mercury levels have been proven to be highest after removal
of amalgams (Sandborgh-Englund 1996).
This shows that there is no basis for these “overnight cures.”
Dentists have
a higher mean urinary mercury value but they do not exhibit any higher levels
of mortality or morbidity (Dodes 2001).
Data strongly suggest that higher mercury levels associated with a mouth
full of amalgam do not pose any adverse health effects (Dodes 2001). The weight of the published evidence
indicates that the level of mercury absorbed from dental amalgam fillings
contributes insignificantly to the total daily dose of mercury. No adverse health effects can be attributed
to the mercury in dental amalgams (Mackert 1991).
Agocs, Mary M, R.A.
Etzel, R.G. Parrish, D.C. Paschal, P.R. Campagna, D.S.
Cohen, E.M. Kilbourne, and J.L.
Hesse. Mercury exposure from interior
Latex paint. The
New England Journal of Medicine 323: 1096-1100, 1990.
Baratz, Robert. Heavy metal. (dental fillings). Harvard
Health Letter 16:4-5,
Mercury from dental “silver” tooth fillings impairs sheep
kidney function.
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Journal of Physiology 261, 1991.
Journal of the
American Dental Association 132:348-356,
2001.
mercury from dental amalgam: a review of recent
findings. British Dental
Journal 175:161-168, 1993.
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Dental
Association 122:54-61, 1991.
Morbidity and
Mortality Weekly Report. Acute, chronic
poisoning, residential
exposures to elemental
mercury—Michigan, 1989-1990. Journal of the
American Medical Association 266:196-197, 1991.
evidence of renal toxicity from
amalgam fillings. American Journal of
Physiology 271:R941-R945, 1996.
Siblerud, Robert L,
J. Motl and E. Kienholz. Psychometric
evidence that mercury
from
silver dental fillings may be an etiological factor in depression,
excessive
anger, and anxiety. Psychological Reports 74:67-80, 1994.
Siblerud, Robert
L. The relationship between mercury
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and mental health. American
Journal of Psychotherapy 43:575-587,1989.
United States. Department of Health and Human Services.
Committee to
Coordinate Environmental Health and
Related Programs. Risk
Management Subcommittee. Dental amalgam: a scientific review
and recommended Public Health
Service strategy for research, education,
and regulation: final report of the
Subcommittee on Risk Management of
the Committee to Coordinate
Environmental Health and Related
Programs, Public Health
Service. The Service [Washington, DC], 1993.
Copyright © 2002 Gail Garrett and Koni Stone
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