(This paper was originally published in the Autumn 1986 edition of the peer
reviewed journal Research Forum by Palmer College of Chiropractic)
A chiropractic perspective on the dental amalgam controversy
Kristopher Keller
Abstract
Dental amalgams, commonly known as silver
fillings, account for 75 percent of all single tooth
restorations. Amalgams are composed of several
metals, most notably mercury, which comprises
about 50 percent of the typical filling by weight.
Several recent studies have revealed that mercury
vapor is released from these fillings under the con-
ditions normally
environment.
present
in
the
oral
The concentration of mercury in the oral air of
some subjects exceeded government established
standards for occupational exposure to mercury
vapor. Other studies indicate that psychological
and behavioral changes can occur in humans at
exposure levels below these government standards.
Genetic, dietary and other factors make individual
sensitivity to mercury unpredictable. Though no
major study has ever attempted to find a link
between amalgams and any specific pathology
resulting from mercury toxicity, the available
evidence raises concerns about its safety.
Key Words: Chiropractic, dental amalgam, dental materials, intra-oral galvanism, mercury,
mercury poisoning, selenium.
Introduction
Amalgam is defined as an alloy of two or more metals, one of which is mercury (Hg). Dental
amalgams, commonly known as "silver fillings," contain mercury, silver, tin and sometimes
copper and zinc. (II First introduced in North America in 1833, dental amalgam is now estimated to
represent 75 percent of all single tooth restorations (fillings)y.J) There are several manufacturers
of amalgam, each with a slightly different formula.(4)
Below are the approximate percentages of the component elements:
Mercury (Hg) 50%
Silver (Ag) 35 %
Tin (Sn) 13%
Copper (Cu) 0-3 %
Zinc (Zn) 0-1%
Liquid elemental mercury (Hg) is added in equal parts by weight to the other ingredients to
produce a mass that is pliable enough to be forced into the prepared cavity. Excess Hg is
squeezed out of the amalgam usually by manual pressure. The filling then cures; ideally it
hardens in about a day. The final mass contains about 45-50% Hg by weighus.6)
Recent research shows that amalgam is not entirely chemically stable after curing. In contrast
to earlier studies, recent evidence suggests that amalgam in the oral environment constantly
releases small quantities of cytotoxic corrosion products and Hg vapor. (4,7,8,9,10) The Hg vapor
levels are greatly increased by mildly abrasive action such as chewing gum and brushing.
Ingestion of hot beverages also increases the vapor release. The elevated vapor release
continues after the removal of the stimulation, gradually tapering off over the next few hours.
The current point of controversy is whether or not the levels released are great enough to be
hazardous to the health of the patient. The American Dental Association and associated
organizations have released statements to the effect that except in rare cases of allergic
hypersensitivity, the levels of release are too low for concern. Recent studies revealing
psychological and teratogenic effects at levels of Hg exposure considered safe by current
standards have caused some professionals to question the validity of those standards.
Biological Indicators of Hg Intoxication
A major problem in verifying or refuting the danger of amalgam is the lack of reliable
biological indicators of Hg intoxication and variations in individual sensitivity to Hg exposure.
(2,13,22,24). There has been little success in finding correlations between blood and urine Hg
levels with clinical signs or symptoms. There is also disagreement about whether urine and
blood levels reflect current exposure or are a delayed expression of exposure over the period of
a year. It is generally agreed that urine and blood levels of Hg are very poor predictors of
intoxication. Individual sensitivity and selective tissue accumulation may cause an
unpredictable response in a patient, while renal damage from Hg exposure will affect the urine
and blood levels. (13,23,24,25) In populations with similar exposure, however, careful studies
have shown some dose/response relationship within narrow ranges of urine and blood Hg.
(18,25,26,27)
Because of its strong affinity for sulfur containing proteins, Hg concentration in the hair is a
fairly good indicator of chronic exposure but is subject to error from environmental
contaminants and some shampoos and hair treatments.(13,28) Hair analysis seems to be the
preferred method of evaluating body burden of Hg, as long as care is taken in collecting and
testing. Hair gives a profile of exposure over several months; this is a sufficient time to gauge
most body tissues' burden because the average half-life of Hg in the body is usually quoted at
58 days. (13,22) Some tissues, most notably the CNS, have much longer half-life for Hg and
therefore care must be taken in evaluation of CNS related disorders by hair sampling.
With amalgams the level of exposure can be tested directly by analysis of Hg concentration of
air in the mouth. Several machines developed primarily for industry are available to do this; the
best for this purpose is known as the Jerome Mercury Vapor Analyzer. (13) Some question
exists as to the significance of oral vapor levels if the subject normally breathes through the
nose.
At present the diagnosis of Hg poisoning must be made primarily on the basis of physical
examination and history of exposure with secondary emphasis on laboratory tests. (24)
Factors of Exposure
The major route of entry for Hg vapor is through the lungs. Seventy to 100 percent of
the Hg vapor that is inhaled is retained in the lungs. (11,22) The Hg then diffuses into the
capillaries, 50 percent binding to the plasma proteins and 50 percent to the hemoglobin
in the RBC's. The Hg is then quickly carried to the CNS and other tissues of the body
via the blood circulation. (17)
Elemental Hg is much less toxic when swallowed than inhaled because very little
absorption of elemental Hg takes place in the GI tract. For this reason, Hg that is
swallowed during placement and removal of amalgam is not considered a hazard. (22)
The elevated vapor levels present during these procedures is potentially a risk to both
doctor and patient. (37)
Although the primary route of entry is most likely the lungs, several other routes of
entry for amalgam generated Hg have been proposed. The direct absorption into oral
mucosa does occur but seems to remain fairly localized. (20) Hg is known to penetrate
into the dental pulp one to seven days after placement of the amalgam. (11) Ingalls has
suggested th.at Hg may enter the nerves in the tooth and be transported via axoplasmic
flow directly to the brain. (30) Similarly, Nylander has proposed that Hg vapor may be
absorbed into the olfactory nerves and then transported by axoplasmic flow to the brain.
(31) Autopsy studies by Nilner, et al, however, found no consistent correlation between
Hg concentrations in alveolar nerve tissue and the presence of amalgam fillings. (47)
Symptoms displayed seem to be dependent at least in part on two factors: 1) The
ability of the kidneys to eliminate Hg from the body and 2) The rate of retention and
elimination of various organs. At low levels of exposure the kidneys seem able to
eliminate Hg readily with little sign of renal damage. (12) At these low levels, however,
certain systems are known to retain Hg and build up considerable concentrations. The
blood brain barrier and placenta are permeable to Hg. Once inside the CNS and fetus, Hg
is rapidly oxidized to a less permeating form. Hg is thereby trapped in these tissues and
builds up to levels far above that indicated by the blood levels. (17,22) This would be
consistent with the findings of CNS and embryological disorders found at low exposure
levels. (8,25,26,28)
At higher levels of acute exposure or chronic exposure to lower levels, the kidneys
begin to lose the ability to excrete Hg. The exact mechanism is not understood. It may
have some relationship to findings that Hg accumulates in the distal and convoluted
tubules. (17) Therefore, while blood and tissue levels increase, urine samples actually
show a lower Hg
concentration. Patients exhibiting signs of Hg poisoning may actually have little or no
Hg in the urine.(13,23,24) Psychomotor changes are common; other systemic manifestations
may be present as well, such as anorexia, chest pains, insomnia and bleeding gums. (22)
Heavy exposure most likely will manifest first in bronchial damage and
pneumonitis.(22,23) Severe renal damage with nephrotic syndrome is likely, with the
pattern of urinary Hg reversing again and extremely high levels of Hg being excreted.
Even at these high levels there is very little correlation between signs and symptoms of
intoxication and urine Hg concentration. (27) Severe CNS damage with serious
psychomotor and psychological dysfunctioning will occur. The prognosis at this stage is
poor with death possible.
Individual response and individual organ or system dysfunction may vary greatly from
the norm for a variety of known and unknown reasons.
Factors of Individual Sensitivity
The body has several methods of dealing with toxic substances. It may try to change
them chemically or it may attempt to eliminate them by some excretory process. It may
attempt to isolate the toxin and store it. Most likely a combination of the above will be
employed. Occasionally the methods will backfire and a more toxic substance will be
produced or the stored chemical will be of such a quantity that it will re-enter the system
or damage the tissue.
Hg is excreted in other ways besides the urine. It is excreted in the bile, feces, sweat,
saliva, hair and nails, and vapor in the breath. (11,24) Urine is by far the most important route
of excretion for elemental or inorganic forms of Hg.
It is possible that some of the elemental Hg is converted to the more toxic methyl or
organic form in the body. Bacteria native to the human oral environment are known to be
able to methylate Hg, or methylation may take place within the body itself. (12,23) But,
based on the relative amounts of methylated Hg found in exposed individuals, it seems that
inorganic HG is either methylated in small quantities or it is eliminated rapidly from the
body.(9) Autopsies on retired workers from an Hg mine were found to have enormous
quantities of inorganic Hg in thyroid, pituitary, kidney, brain and lung tissue, but levels
of methyl Hg were just slightly above control subjects. (34)
The same study of miners revealed what is thought to be a major detoxification tool
for Hg. A near equimolar concentration of Selenuim (Se) to that of Hg was found in the
tissues tested. (34) This same ratio has been discovered for ocean fish such as tuna.
Fresh and saltwater fish taken from Hg polluted waters do not seem to be able to
maintain this balance and exhibit elevated Hg/Se ratios.(35) Dietary Se has been found to
protect laboratory: animals from high levels of Hg exposure. Se does not reduce the
quantity of Hg retained in the body, in fact Se may actually cause increased retention in
the brain and kidneys while reducing the toxicity. Se itself is a very toxic mineral and its
toxicity is reduced by the presence of Hg. The Se-Hg connection may explain why
people who consume large amounts of seafood have been found to have high
concentrations of Hg in their blood with apparently no ill effects. It has been found that
some species of fish have high enough amounts of Se to act as protection against Hg
from other sources. (36)
Se poisoning was once thought to be a major health hazard, but more recent studies
have shown that Se deficiency in the diet may be a more common occurrence. (36) Many
agricultural soils are deficient in Se and a diet dependent on those foods could
conceivably lead to greater sensitivity to Hg poisoning. (44)
Vitamin E plays a major role in detoxifying Hg in the body. It is thought to act as an
anti-oxidant or radical scavenger and in some way assists Se.(35,36) Other dietary factors
may also have an impact on Hg toxicity. There is some evidence that sulfur containing
amino acids may have an effect on reducing toxicity. (35) Vitamin C is sometimes
recommended as reducing. the effects of Hg hypersensitivity. (5)
Conversely, lead (Pb) is known to increase the toxic effects of Hg and vice versa.
Therefore, sub-acute doses of both of these minerals could result in acute reactions. (28)
Hypersensitivity Versus Toxicity
Hypersensitivity to Hg from dental amalgam exposure is well documented. (11,12) The
most common form of reaction is contact dermatitis. Hg is thought to act as a hapten,
combining with oral mucosa proteins to produce an antigen to which the body responds
in a cell mediated antibody reaction. (13) Mobacken et al found a high correlation
between the presence of oral lichen planus lesions and amalgam restorations. In 64 of
the 67 cases studied, the lesion was in direct contact with an amalgam filling. (14) The
documented cases of hypersensitivity to amalgam almost always follows a previous exposure to Hg. Most of these reactions are self limiting and usually require only palatal
care. But, some cases are cleared up only with the removal of the amalgam. (11)
Systemic hypersensitivity to amalgam is also well documented. (15) This most often
takes the form of diffuse erythema or dermatitis. Other signs and symptoms of
hypersensitivity to amalgam that are reported are given in Table 1. The use of skin patch
tests for determination of potential allergic reaction has been discouraged because of poor
accuracy and the possibility of the test itself sensitizing the patient to further Hg
exposure. (13,16)
Actual toxicity from Hg is often difficult to diagnose even at relatively high levels of
exposure because of individual variability in sensitivity and the non-specific clinical
picture, as listed in Table 2. The toxicity of Hg is in its ability to bind to enzymes,
especially those with -SH groups at the active site, thereby altering or blocking their
actions. Hgis known to stimulate and then completely block acetycholine release from
neurons, (17,18) block progesterone binding sites, (19) reduce synthesis of collagen by
fibroblasts and epithelial cells, (11,20) and reduce RNA concentrations in the hypothalamus. (21) Hg also binds to hemoglobin and plasma proteins very rapidly. (11)
Study of the Hg toxicity syndrome known as acrodynia (Table 5) shows that a
mechanism of hypersensitivity exists which can exhibit the signs and symptoms of acute
Hg poisoning at very low exposure levels. (24,32,33) This is in contrast to the
dermatological presentation of antigen-antibody hypersensitivity. One mechanism for
variations in individual sensitivity is suggested by the Se/Hg detoxification interaction.
The actual biochemical relationship is poorly understood, but the ability to use the
mechanism has been shown in rats to be a sex linked characteristic. (36) This indicates
the possibility of genetic variations in Hg sensitivity. As stated earlier, dietary variations
in Se consumption can affect Hg sensitivity. This is an area that has received
considerable attention in animal research, but little in the way of human studies. (35,36)
There are examples in the literature of case studies that seem to be non-allergic
hypersensitivity reactions to amalgam derived Hg. (5)
Table 1
Symptoms of Allergic Hypersensitivity to Amalgam Fillings
(2,12,13)
Absence of lingual papillae
Dermatitis of extremities,
eyes, lips and gingiva
Dry mouth
Eczema
Edema
Erythema
Fever
Hives
Loss of taste
Malaise
Polyps
Stomatatis
Swelling of lips,
tongue and oral mucosa
Table 2
Signs and Symptoms of Mercurial Poisoning
(2,10,22,23,24,43)
Psychological
Anxiety
Apprehension
Decreased mental ability
Depression
Easy embarrassment
Insomnia
Irritability
Lack of concentration
Loss of memory Loss of sex drive
Temper
Tiredness
Personality changes
Psychic disturbances
Shyness
Other PNS and CNS Related Dysfunctions
ALS type syndrome
Amblyopia
Anorexia Paresthesia
Anosmia
Ataxia Polyneuropathy
Cardiac arrythmia
Excessive salivation
Dizziness
Headaches
Increased deep tendon
reflex
Muscular weakness
Peripheral neuritis
Profuse sweating
Tremors of hands, lips,tongue and feet
Kidney Related Disorders
Anemia
Albuminuria
Anuria
Nephrotic syndrome
Oliguria Proteinuria
Renal damage
Thirst - Excessive
GI Tract and Other Signs and Symptoms
Abdominal Cramps
Acrodynia
Blue line on gums around tooth
Colitis
Dermatltus Rhinitis
Diarrhea Sialorrhea
Erythema Stomatitis
Gingivitis
Mercurilentis (Hg deposits on lens of eyes)
Metallic taste
Mucocutaneous lymph node syndrome (Kawasaki's Disease)
Weight loss
Heavy Exposure to Hg Vapor
Bronchitis
Chest Pain
Chills
Cough
Dyspnea
Fever
Hematuria
Hemoptysis
Interstitial pneumonitis
Nausea
Shock
Vomiting
Table 3
Signs and symptoms of Mercurial Toxicity Reported From Occupational Exposure In Dentists and Dental Assistants
(12)
Anorexia
Burning tongue
Death
Decreased reflexes Depression
Diarrhea
Digestive disturbances Emotional instability Erethism
EX<4essive salivation Fatigue
Fever
Fine motor control loss Gingivitis
Headache
Hopeless feeling
Insomnia
Irritability
Malaise
Memory loss
Metallic taste
Mercurilentis
Nasal secretion Increase
Nausea
Nephrotic syndrome
Red palms
Shyness
Sore mouth
Stomatitis
Tremors
Visual disturbances
Including focusing Weakness
Table 4
Signs Associated With Acrodynia
(1,32,46)
Bruxism
Digestive disturbances
Erythema of cheeks and nose Irritability
Lesions of skin on hands and feet
Muscle weakness
Perspiration
Photophobia
Polyarthritis
Profuse salivation
Swelling of extremities
Vomiting
Table 5
Signs and Symptoms Ascribed In Anecdotal Reports to Hg Poisoning in Patients with Amalgams
(5)
Acne
Bradycardia
Depressed WBC count
Difficulty breathing
Elevated WBC count
Emotional instability
Erythema
Excessive shyness
Gall bladder dysfunction
Hallucinations
Lack of energy
Uver dysfunction
Painful menstruation
Severe chest pains
Subnormal body temperature
Tachycardia
Thyroid dysfunction
Weight loss
Toxicity From Amalgam and Equivalent Exposure levels
Dentists and dental assistants are known to be at risk of Hg poisoning. (Table 3) Ten to
twenty-five percent of dental offices have been found to exceed acceptable levels of Hg
vapor in the air. (20) Cases of Hg poisoning of dentists and assistants are well
documented. (2,12) Periodic studies of urine Hg levels in dentists in the U.S. show that
approximately 1.3% have levels in excess of those known to cause physiological changes. Dental
students are found to have significant increases in allergic sensitivity to Hg as they progress
through school. (37,44)
Nylander found increased levels of Hg in the pituitary glands of cadavers of dentists
compared to controls with no known Hg exposure. (31) ln one case the amount of Hg in
the pituitary gland of a dentist was 60 times that of a control with no known exposure. A
study in Sweden found that the rate of glioblastomas for dentists and assistants was
about twice that of the general population. The study did not prove a relationship
specifically with Hg, but only with some factor associated with the dental profession,
such as amalgam, chloroform, or radiography. (38)
Research on Hg toxicity from amalgams in dental patients is in its infancy. Direct
relationship between amalgam and pathologies has not been proven, but available
evidence shows that subjects with amalgams have associated increases in Hg in body
tissues. Nylander found that cadavers of patients with amalgam fillings had
concentrations of Hg in their pituitary glands as high as 19 times that found in non Hg
exposed controls. (31) Friberg, et al, indicated that cadavers with an average number of
amalgams had about three times as much Hg in their brains as did those tested without
amalgams.(9)
Because there have been no studies done to determine if there is a significant increase
in pathologies in subjects with amalgams, we must look at the possibilities suggested by
exposure levels in the same range as those produced by amalgams. Recommended
maximum exposure levels for occupational exposure, eight hours/day and five
days/week, have been established by the National Institute for Occupational Safety and
Health (NIOSJ-i) and the World Health Organization (WHO). (10,48) The NIOSH level is
set at 50 Ng Hg/L air, the WHO level is set at 25 Ng Hg/L air. The WHO standard, when
adjusted for 24 hours/day, seven days/week exposure, is equal to 7.7 Ng Hg/L air.
Several studies have shown Hg vapor levels in excess of these limits in the oral air of
people with amalgam fillings. Mechanical stimulation significantly increases the levels
of Hg vapor produced so most studies are run before and after some. mechanical
stimulation such as brushing teeth or chewing gum for 10 minutes. Ou, et al, found levels
as high as 12.7 Ng/L before brushing and 62.0 after brushing.nol Svare, et al, found
levels as high as 85.5 Ng/L after chewing gum for 10 minutes.(10) Higher concentration
levels are present during installation and removal of amalgams. In some cases removal of
amalgams can produce levels in excess of those established as maximum permissible for
any exposure period. (37)
Research on workers exposed to Hg vapor found a correlation between changes in
short term memory and urine Hg concentration at very low levels of urine Hg. (25) The
average levels tested were above those associated with amalgam exposure, but some
subjects in the test had urine Hg in the same range as found in amalgam studies. Two
interesting side notes from this study are: 1) Workers with the longest exposure (i.e. the
oldest workers) were among those with the lowest urine Hg levels and were eliminated
from the test group; 2) One method of evaluating memory deficiency that is commonly
used in this type of testing was found to be too inaccurate to reveal a significant
correlation. (25)
Several specific maladies have been noted to occur in association with extremely low
levels of Hg exposure. A significant correlation was found between increased stillbirths
and malformed infants and prenatal blood concentrations of Hg similar to those found in
relation to amalgams. (8) Similarly, a Danish study found that women exposed to Hg
in the workplace had a higher incidence of infertility.(26)
A study of school children in Wyoming found a significant correlation between
emotional disturbance and increased Hg exposure as indicated by hair analysis. The
levels of Hg in the hair of both control and disturbed children were far below the level
considered toxic and well within normal limits stated in the literature.(13,24,28) No source
of Hg exposure was postulated.
Studies in the Russian literature report that rats and rabbits exposed for several
months to Hg vapor levels equivalent to those produced by amalgams showed
pathological changes in the CNS, the thyroid and adrenal glands, the heart, and the
liver.(22) How the sensitivity of these laboratory animals compares to that of humans is
not clear.
Galvanism
Amalgam and other metallic dental materials are known to produce small amounts of
electric current. Metals in contact with saliva make up an electrochemical cell.(40) The
chemical reactions that have been suggested to produce the current include some in
which salts and ions of the metals involved are released into the oral environment.
Studies that have tried to correlate the amount of galvanic action with saliva Hg
concentrations have found very little relationship. Saliva Hg concentrations are found to
be more closely related to blood Hg concentrations. The relationship between galvanism
and oral Hg vapor levels has not been studied. (41)
The greatest flow of current will be between fillings with large differences in
electrical potentials. This current flow is known to be responsible for increased rate of
corrosion in amalgams, but controversy exists as to whether these currents are
responsible for certain types of oral lesions.(29,42,44) Amalgams are found to have
potentials in the range of +50mv to -500mv. Gold fillings and others are found to have
potentials from + 100mv to -200mv.(39) Contact between amalgam and any other type
of material increases the likelihood of current flow because of the different potential
ranges. Other factors affect the rate of current such as contact surface area and internal
resistance of the amalgam.(29) Currents between amalgams have been measured as high
as 100 ua.(42,45)
Discussion
The NIOSH and WHO recommended maximum exposure levels are based, for the
most part, on studies of physiological changes in workers exposed to Hg vapor in an
industrial setting. The populations used to determine safe levels of exposure have been
those populations who have had heavy exposure in industry for years and were still
capable of performing their jobs. (22) The question comes to mind of how many others
were forced to leave these jobs because of Hg related health problems and thus were left
out of the studies. It is possible that the levels being accepted as safe are skewed toward
the higher end of the scale by a hypertolerant test population. Additionally, are we to
accept physiological effects as the criterion of intoxication? Psychological and
embryological changes are known to occur at very low exposure levels. These should
also be considered when establishing permissible exposure levels.
Several aspects of Hg poisoning could be considered to be chiropractic related. The
CNS effects of Hg poisoning are obviously of interest. (17,18) Degenerative joint disease
and skeletal disorders may also have Hg connection. Hg is known to block collagen
synthesis by fibroblasts and epithelial cells. (11,22) One aspect of acrondynia is
polyarthritis and muscle weakness. The effects of galvanism may also have significance
chiropractically. What effect might electrical potentials of 400mv or more have on the
nerves in the tooth pulp that are in contact with the amalgam? What effect on reflex
mechanisms would stimulation of these nerves have? A dramatic demonstration of
galvanic action can be performed by biting down on a piece of aluminum foil between
two amalgams. The same neuronal pathways are being stimulated or at least potentiated
every time those same teeth are in close proximity. Is there a possibility of reflex
muscle contraction in the head and neck in response to this micro-stimulation? Could
this lead to excessive fixation and reduced function in the cervical region?
Several epidemiological studies in the U. S. have found statistical and geographical
correlations between amalgam fillings and the incidence of multiple sclerosis (MS). (30)
These relationships do not prove a cause and effect, of course. The ability of Hg from
amalgam to accumulate in the CNS and its ability to cause antigen-antibody reactions do
lend some credibility to the theory. Additionally, the resemblance between chronic Hg
poisoning and amyotrophic lateral sclerosis (ALS), a syndrome similar to MS, is often
mentioned in the literature.(24)
The question for chiropractic seems to be how this fits into our scope of practice.
Some dentists have been accused of practicing medicine for suggesting that patients with
suspected Hg toxicity have their amalgams replaced. Would it be practicing medicine for
a chiropractor to refer a patient with suspected Hg poisoning to a dentist for evaluation?
The duty
of a primary health care provider is to do what is in the best interest of the patient. The
evidence in no way suggests that everyone with amalgam fillings should have them
replaced, yet there is enough evidence to make one suspect that it could help some
people. Certainly the evidence is strong enough to make one very cautious about the
installation of new amalgam especially in children who would then face a life-long
exposure to a known toxin.
Until recently there were no acceptable substitutes for amalgam other than expensive
gold fillings. In the last year, several new posterior composites have been at least
provisionally approved. Composites have been in use for about 20 years as cosmetically
acceptable materials for front, low-load bearing teeth. The composites, a combination of
synthetic resin and powdered silica or quartz, closely match the appearance of natural
teeth and improvements in the technology have made them nearly as durable as
amalgam. Though they are more difficult to install the overall cost of restoration with
composites is not much different than with amalgam.
Aside from the hypersensitive patient there is no conclusive proof yet that amalgam is
hazardous when used judiciously. But does it make sense to knowingly add to the body's
burden of a toxic chemical? For this reason it is questioned in theliterature whether
amalgam would ever pass FDA approval if introduced as a new material today. (6) It is
the author's desire that increased public and professional awareness of the questions
surrounding the use of amalgam will stimulate further research into their possible toxic
effects especially in the areas of emotional and behavioral disorders and infertility.
References
1. Dorlands Illustrated Medical Dictionary. 26th
Ed. Philadelphia: W. B. Saunders Company,
1985:54.
2. Donovan TE, Handlers JP. A rational'policy on
the use of dental amalgam. CDA Journal 1984;
11:10-2.
3. Department of Biomaterials. Consequences of mercury exposure in dentistry: A
review of the Literature. Florida Dental Journal 1983, Winter; 54(4):17-21.
4. Milleding P, Wennberg A, Hasselgren G. Cytotoxicity of corroded and non-corroded
dental silver amalgams. Scand J Dent Res 1985; 93:76-83.
5. Huggins HA, Mercury - A factor in mental disease? The Journal of Orthomolecular
Psychiatry 1982; 11(1).
.
6. Wolff M, Osborne IW, Hanson AL. Mercury toxicity and dental amalgam.
NeuroToxicology 1983; 4(3):201-204.
7. Ou KHR, Log F, Kroncke A. Zur Quecksilberbnelastung durch Amalgamfullungen.
Dtsch Zahnarztl Z 1984; 39:199-205.
8. Abraham JE, Svare CW, Frank CWo The effects of dental amalgam' restorations on
blood mercury levels. J Dent Res 1984, January; 63(1):71-3.
9. Friberg L, Kullman L, Lind B. K vicksilver i central nervsystemet i relation till
amalgamfyllningar. Lakartidningen 1986; 83(7):519-22.
10. Patterson JE, Weissberg BG, Dennison PI. Mercury in human breath from dental
amalgams. Bull Environ Contam Toxico11985; 34:459-468.
11. Bauer JG, First HA. The toxicity of mercury in dental amalgam. CDA Journal 1982;
Iune:47-60.
12. Bauer IG. Action of mercury in dental exposures to mercury. Operative Dentistry
1985; 10:104-13.
13. Cooley RL, Young JM. Detection and diagnosis of bioincompatibility of mercury.
CDA Journa11984; October: 36-43.
14. Mobacken H, Hersle K, Sloberg K, Thilander H. Oral lichen planus: hypersensitivity
to dental restoration material. Contact Dermatitis 1984; 10:11-5.
15. Nakayama H, Niki F, Shono M, Hada S. Mercury exanthem. Contact Dermatitis
1983; 9:411-7.
16. Mackert JR, Fisher AA. Hypersensitivity to mercury from dental amalgams. Journal
of the American Academy of Dermatology 1985,
May; 12(5):877-80.
17. Placidi GF, Dell'Osso L, Viola PL, Bertelli A. distribution of inhaled mercury (203
Hg) in various organs. Int J Tiss Reac 1983; V(2): 193-200.
18. Cooper GP, Manalis RS. Influence of heavy metals on synaptic transmission: A
review. Neurotoxicology 1983; 4(4):69-84.
19. Greist RE, Coty WA. Binding of the chicken oviduct progesterone receptor to steroid
affinity resins: resistance to elution with mercurial agents. J Steroid Biochem 1984;
21(1):29-34.
20. Payne RW, Bums RA, Davis WJ. The controversy of mercury in amalgam
restorations: review of the literature. ODJ 1984; January:27-8.
21. Lach H, Srebro Z, Dziubek K, Krawczyk S, Szaroma W. The influence of mercury
and lead compounds on the circadian rhythm of cytoplasmic RNA in hypothalamic
neurons of mice. Folia Histochemica Et Cytochemica 1983; 21(3-4) :231-8.
22. World Health Organization. WHO study group on recommended health-based limits
in occupational exposure to heavy metals. World Health Organization, 1980;
Geneva: WHO tecl)nical report series; No. 647.
23. Wyngaarden JB, Smith LH, eds. Cecil Textbook of Medicine. 17th edition.
Philadelphia: W.B. Saunders, 1985:2309-10.
24. Arena JM. Poisoning: Toxicology, Symptoms, Treatments. 4th Edition, Springfield,
IL: Thomas, cl979, pp. 144-9,272.
25. Smith PJ, Langolf GO, Goldberg J. Effects of occupational exposure to mercury on
short term memory. British Journal of Industrial Medicine 1983, November;
40(4):413':9.
26. Rachootin P, Olsen J. The risk of infertility and delayed conception associated with
exposure in the Danish workplace.
Journal of Occupational Medicine 1983, May; 25(5):394-402.
27. Roels H, Lauwerys R, Buchet JP, Bernard A, Barthels A, Oversteyns M, Gaussin J.
Comparison of renal function and psychomotor performance in workers exposed to
elemental mercury. Int Arch Occup Environ Health 1982; 50:77-93.
28. Marlowe M, Errera J, Stellern L Beck D. Lead and mercury levels in emotionally
disturbed children. Journal of Orthomolecular Psychiatry; Vol. 12, No.4, 1983.
29. Nilner K. Studies of electrochemical action in the oral cavity. Swedish Dental
Journal Supplement 9, 1981.
30. Ingalls TH. Epidemiology, etiology, and prevention of multiple sclerosis. The
American Jour
nal of Forensic Medicine and Pathology 1983, . March; 4(1):55-61.
31. Nylander M. Mercury in pituitary glands of dentists. The Lancet, 1986, February;
22:442.
32. Thomas CL, ed. Tabers Cyclopedic MedicalDictionary. 12th edition Philadelphia; F
.A.Davis Company 1977.
33. Arena JM. Poisoning: Toxicology, Symptoms,Treatments. 4th edition Springfield, IL.
Thomascl979 p.608.
34. Kosta L, Byrne AR, Zalenko V. Correlation between selenium and mercury in man
following exposure to inorganic
mercury. Nature 1975,March 20; 254:238.
35. Ganther HE. Interactions of vitamin E and selenium with mercury and silver. Annals
New York Academy of Acience. 1980; Vol. 355.
36. Frost DV. Selenium and vitamin E as antidotes to mercury toxicity. International
Conference on Mercury Hazards in Dental Practice; 1981.
37. Naleway, Sakaguchi, Mitchell, Muller, Ayer, Hefferren. Urinary mercury levels in
U.S. dentists, 1975-1983: Review of health assessment. JADA 1985, July; 111:3742.
38. Ahlbom A, Norell S, Rodvall Y, Nylander M. Dentists, dental nurses, and brain
tumors. British Medical Journal 1986, March 8; 292-662.
39. Bergman M, Ginstrup 0, Nillson B. Potentials of and currents between dental
metallic restorations. Scand J Dent Res 1982; 90:404-8. '
40. Lundmark L, Johansson B, Stenman E, Bergman M. Convenient instrument for oral
galvanism measurement. Scand J Dent Res 1982;
90:468-71.
41. Nilner K, Glantz P. The prevalence of copper-,silver-, tin-, mercury- and zinc-ions in
human saliva.
Swed Dent J 1982; 6:71-7.
42. Holland RI. Galvanic currents between gold and
amalgam. Scand J Dent Res 1980; 88:269-72.
43. Block JB. The signs and symptoms of chemical
exposure. Springfield, IL: Thomas, c1980.
44. Passwaer RA. Selenium as Food & Medicine.
Keats Publishing, c1980.
45. Ayres S. Amalgam and gold dental fillings:
Reaction from electrogalvanic current. Journal
of the American Academy of Dermatology
. (14(2) Part 1, Feb 1986.
46. Berkow R, ed. The Merck Manual. 14th edition.
Merck Sharp & Dome Research Laboratories
1982.
47. Nilner K, Akerman S, Klinge B. Effect of dental amalgam restorations on the
mercury content of nerve tissues. ACTA Odontol Scand 1985; 43:303-7.
48. Criteria for a recommended standard occupational exposure to inorganic mercury
U.S. Department of Health, Education,
and Welfare Public Health Service. National Institute for Occupational Safety and
Health 1973.
Acknowledgements
My deepest gratitude to the many friends and associates who have supported and
encouraged me in my labors. Unfortunately, there are too many to name individually;
you know who you are.
Special thanks to the staffs of the Palmer Health Sciences Library and Palmer
Research department for their expertise and professionalism.
Thanks to Susanne Olgaard and Dennis Miller for their translations. Thanks also to my
advisors on this project, Dr. Saroja Reddy, Dr. Moin Ansari and Dr. Louis Freedman, for
their patience and gentle criticism. Last but not least, thanks to Dr. Larry Sigulinsky for
his artwork. .
(Kristopher Keller is a tenth quarter student at Palmer College of Chiropractic, 1000
Brady Street, Davenport, Iowa 52803. Correspondence or requests for reprints should be
addressed to him at the college.)