Sorry those pictures are not allowed on the world wide web.

Jan these people get weary from all the insults!

Joel

This of course is pathetic for a dental newsgroup ......

JOEL

REPLY

Here ya go ,,,,,,,,

The Amalgam Controversy: An Evidence-Based Analysis
Dodes J.E.[1]
JADA 2001; 132:348-356.

Abstract

Background. There are a number of patients and health care
professionals who believe dental amalgam restorations are a factor in
a host of diseases and conditions. They have been influenced by
anecdotal case reports in the medical and dental literature, research
published in the refereed literature and media stories concerning the
alleged dangers of amalgam restorations.

Methods. The author uses an evidence-based approach in analyzing the
data both supporting and condemning the continued use of amalgam
restorations. He reviewed the articles from both peer-reviewed and
non–peer-reviewed sources and evaluated their relevance, research
design and statistical analysis, as well as whether the conclusions
follow from the data.

Conclusions. There are numerous logical and methodological errors in
the antiamalgam literature. The author concludes that the evidence
supporting the safety of amalgam restorations is compelling.

Clinical Implications. Amalgam restorations remain safe and effective.
Dentists should educate patients and other health care professionals
who may be mistakenly concerned about amalgam safety.

****************

From the Pa Dental Law ......

Cross References

  This section cited in 49 Pa. Code §  33.404 (relating to reporting
continuing education credit hours).

§ 33.213. Replacement of dental amalgams—statement of policy.
(a)  Background. The safety of dental amalgams, specifically, whether
the mercury in amalgams causes or contributes to a variety of health
problems, has become a recurring issue in dentistry. The Board has
neither the resources nor the mandate to make or endorse scientific
findings on this issue. It is aware, however, of no conclusive
evidence that the removal of amalgams will cure or ameliorate
disorders other than those associated with confirmed allergic
reactions to mercury. Nonetheless, nonallergic patients may request
replacement of amalgam restorations in the belief, or merely the hope,
that a medical condition will thereby disappear or improve. Dentists
receiving these requests must make ethical and professional decisions
compatible with the best interests of their patients.

(b)  Purpose. Section 4.1(a)(8) and (9) of the act (63 P. S. §
123.1(a)(8) and (9)) authorizes the Board to take disciplinary action
against licensees who engage in unprofessional conduct or commit acts
of negligence, incompetence or malpractice. The replacement of
amalgams may implicate both provisions by, for example, generating
complaints of unnecessary or even harmful treatment. The Board
therefore provides the following guidelines to assist its licensees in
conforming their behavior to the requirements of the act. In a
disciplinary action brought against a dentist for treatment associated
with replacing amalgams, the Board will consider whether these
guidelines were followed.

(c)  Guidelines.

  (1)  The Board recommends that, before replacing amalgams in a
nonallergic patient, the dentist:

    (i)   Explain to the patient the current status of research on
the safety of dental amalgams.

    (ii)   Provide the patient with information on contraindications
and costs associated with removal/replacement of amalgam restorations.

    (iii)   Advise a patient relying on third-party payment to
ascertain whether the insurer will cover removal/replacement
procedures.

    (iv)   Encourage a patient seeking amelioration of a medical
condition to consult with a physician and, as appropriate, secure from
the physician documentation of recommendations made to the patient.

    (v)   Memorialize in writing the disclosures made to the patient
and the patient’s informed consent.

  (2)  The Board recognizes the right and duty of dentists to refuse
to replace amalgam restorations when, in their professional judgment,
this procedure would not be in the best interests of the patient.

Source

  The provisions of this §  33.213 adopted January 18, 1965; amended
September 12, 1975, effective September 13, 1975, 5 Pa.B. 2397;
amended June 23, 1995, effective June 24, 1995, 25 Pa.B. 2492.
Immediately preceding text appears at serial page (151838).

************************************************************

Copyright © 1998-2004 American Dental Association. All rights
reserved.

COSMETIC & RESTORATIVE CARE
The amalgam controversy
An evidence-based analysis

JOHN E. DODES, D.D.S.
A B S T R A C T

Background. There are a number of patients and health care
professionals who believe dental amalgam restorations are a factor in
a host of diseases and conditions. They have been influenced by
anecdotal case reports in the medical and dental literature, research
published in the refereed literature and media stories concerning the
alleged dangers of amalgam restorations.

Methods. The author uses an evidence-based approach in analyzing the
data both supporting and condemning the continued use of amalgam
restorations. He reviewed the articles from both peer-reviewed and
non–peer-reviewed sources and evaluated their relevance, research
design and statistical analysis, as well as whether the conclusions
follow from the data.

Conclusions. There are numerous logical and methodological errors in
the antiamalgam literature. The author concludes that the evidence
supporting the safety of amalgam restorations is compelling.

Clinical Implications. Amalgam restorations remain safe and effective.
Dentists should educate patients and other health care professionals
who may be mistakenly concerned about amalgam safety.

Evidence-based care, or EBC, is the name of a clinical decision-making
paradigm first described in 1993.1 To provide EBC, clinicians must
develop appropriate skills to evaluate research literature and
clinical data. These skills require an understanding of the rules of
evidence (box, “Evidence-Based Approach Rules of Evidence for
Evaluating Reports of Treatment Efficacy”) and the realization of the
limitations of clinical experience. The skill of critically evaluating
research literature and clinical data is barely touched on in dental
school. Enid Neidle, former director of the ADA Council on Scientific
Affairs, commented that dental education is too authoritarian, leaving
many students “susceptible to the experiences of others” and willing
to accept the views of an authority figure without demanding to know
the science supporting those views.2
EVIDENCE-BASED APPROACH RULES OF EVIDENCE FOR EVALUATING REPORTS OF
TREATMENT EFFICACY.*

Questions to ask when using an evidence-based approach to evaluate
research literature and clinical data:

*

Are the results applicable to a particular patient?
*

Were the study patients randomly and properly assigned?
*

Were all of the patients in the study followed up completely or was
there an excessive dropout rate?
*

Were the study populations analyzed in their randomized groups?
*

How blinded was the study?
*

Except for the experimental intervention, were the groups treated
equally?
*

Was the statistical analysis done properly?
*

Did the authors perform so many statistical tests that a mistaken
“significant” finding was found?
*

Did the article report on the participants’ compliance with the
treatment?
*

Were all the clinically significant outcomes discussed?
*

Were the side effects and negative effects of the treatment reported
and discussed?
*

Do the benefits of the treatment outweigh any potential negative
effects and costs?

* Source: Guyatt and colleagues.1,3

I attempt to follow the evidence-based approach rules in evaluating
data on the possible dangers of amalgam restorations.

To apply an evidence-based approach to the dental amalgam controversy
requires studying articles on the subject that have been published in
peer-reviewed and non–peer-reviewed publications and evaluating them
as to their relevance, research design and statistical analysis, as
well as to whether the conclusions follow from the data.1,3,4

In this article, I attempt to follow the evidence-based approach rules
in the evaluating data on the possible dangers of amalgam
restorations.
HISTORY OF DENTAL AMALGAM

The history of dental amalgam restorations containing mercury is a
long one. Tin-mercury dental restorations are reported to have been
used in China in A.D. 600.5 Silver-mercury restorations were
introduced to the Western world in France in the 1830s. In the 1850s,
American dentists who used amalgam were threatened with malpractice
actions by dentists who did not. This became known as the “amalgam
wars.” In 1896, Dr. G.V. Black published a detailed scientific report
advocating the use of amalgam,6 but it still took many years for Dr.
Black’s conclusions to be universally accepted by the dental
profession.

In 1926, Alfred Stock, Ph.D., a German chemist, published an article
condemning amalgam restorations.7 Dr. Stock had been exposed to high
mercury levels while working in his chemical laboratory. He recognized
the danger posed by the type of amalgam that was in use at that time;
a tablet had to be heated in a spoon until the beads of mercury
appeared, and then it was transferred to a mortar and pestle for
trituration.

This procedure produced a significant release of mercury vapor. Dr.
Stock’s concerns led to a commission’s being established to
investigate his allegations. In 1930, the commission issued a report
that validated the safety of the newer dental amalgam formulation,
which no longer required heating and rapidly was replacing the older
formulations.8

In the 1970s, Dr. Hal Huggins began promoting the theory that amalgam
restorations caused a wide variety of diseases. In 1985, he published
a book that detailed his beliefs about mercury toxicity.9 Dr. Huggins
contends that amalgam restorations release enough mercury to cause
neurological, cardiovascular, immunological, collagen, emotional and
allergic diseases and disorders. The resulting conditions are said to
include multiple sclerosis, depression, high or low blood pressure,
tachycardia, arthritis, lupus, scleroderma, leukemia, Hodgkin’s
disease, mononucleosis, fatigue, and Crohn’s disease, ulcers and other
digestive problems. Dr. Huggins has attracted many followers, and his
writings and media appearances have led some dentists to question the
safety of amalgam restorations.

A 1995 survey reported that 8.7 percent of dentists wanted to ban
amalgam use and that 14.3 percent were undecided about its safety.10
Much of the opposition to amalgam has been fueled by the media,
particularly the “60 Minutes” segment that was broadcast in 1990.11
Physicians with large public audiences, such as Robert Atkins, M.D.,
and Andrew Weil, M.D., also have warned the public about the potential
danger of amalgam restorations. Both Drs. Atkins and Weil have written
best-selling books on health. Dr. Atkins hosts a nationally syndicated
radio program, and Dr. Weil has hosted various programs about holistic
health on public television.

Most lay people and many dentists are unfamiliar with the
peer-reviewed dental literature and, therefore, are more easily
convinced by media stories that amalgam is dangerous. The problem is
so serious that the American Council on Science and Health, a consumer
education and advocacy group, has determined that the allegations
against amalgam restorations constitute one of the “greatest unfounded
health scares of recent times.”12
MERCURY AND ITS COMPOUNDS

Mercury and its compounds are everywhere in our environment. Between
2,700 and 6,000 tons of mercury are released annually from the oceans
and the Earth’s crust into the atmosphere.13 Another 2,000 to 3,000
tons are released from human activities, primarily burning household
and industrial waste and, especially, from burning fossil fuels such
as coal.13 Hippocrates was aware of mercury’s toxicity.14 Yet mercury
still has a long history of use in medicaments; for example, calomel
(mercurous chloride) was used well into the 20th century for the
treatment of syphilis. Inorganic mercury still is used widely in
electrical applications, chlorine production and dental restorations.

In 1969, a report written by a committee of international toxicology
experts classified mercury and its compounds according to their order
of decreasing toxicity: methyl and ethyl mercury compounds
(organomercury), mercury vapor (elemental mercury), inorganic salts
and a number of additional organic forms such as phenyl mercury
salts.15

Methyl Mercury. Certain bacteria present in seawater are capable of
transforming elemental mercury into methyl mercury. It then
concentrates in the tissues of fish and other sea creatures and moves
up the food chain, which includes seafood-consuming humans. For
example, industrial waste containing high concentrations of elemental
mercury was released into the waters around Minamata, Japan, for many
years. Fish from these waters were contaminated with methyl mercury
and were responsible for both acute poisonings that resulted in death
and chronic poisonings that resulted in central nervous system
disturbances now known as Mina-mata disease. There also was a
teratogenic effect called congenital Minamata disease.16 It is
estimated that the minimum dose needed to develop symptoms of Minamata
disease was 5 milligrams per day of methyl mercury.17

The half-life of methyl mercury is about 70 days in adults and
slightly longer in fetuses.18 Approximately 15 percent of the body
burden of methyl mercury is in the brain.18 In 1983, Heintze and
colleagues19 reported the methylation of mercury in vitro by oral
streptococci. Their technique, which has not been replicated, yielded
0.029 mg of methyl mercury per gram of powdered amalgam after 35 days
of a complicated procedure. Although it does not appear possible to
recreate this process in vivo,20 their study often is cited as proof
that mercury is converted to methyl mercury in the human
gastrointestinal tract. A close look at their article, however, shows
that the methyl mercury was intracellular and that the bacteria would
have to be digested before the methyl mercury would be released. If
this did occur, the amount of 0.029 mg/g is a fraction of the minimum
safe level.21 Birke and colleagues22 reported no symptoms of poisoning
with levels of 0.8 mg of methyl mercury per day for five years through
the consumption of contaminated fish.

Mercury and its compounds are everywhere in our environment.

Mercury vapor. Mercury vapor (elemental mercury) is the major source
of concern to dentists and patients. Mercury has a high vapor pressure
(.005 mg of mercury at 37 C), and approximately 75 percent of inhaled
inorganic mercury vapor will be absorbed through the lungs.23
Gastrointestinal absorption is low, with estimates ranging from .01 to
10 percent.24 Absorption also is minimal through the skin, although
the precise level has not been determined.18 Elemental mercury
accumulates in the kidneys and brain and is excreted in the urine,
secreted in bile and exhaled from the lungs.18 On an individual basis,
there is little correlation between sampling of hair, blood and urine
and toxic effects at target organs.18 Elemental mercury’s toxicity
probably is a result of its affinity for sulfydryl groups on proteins,
but the results of studies in vitro do not relate well to conditions
in vivo, in which distribution and accumulation of elemental mercury
ions vary immensely from one type of tissue to another.25 Acute toxic
exposures are rare, and there have been cases of elemental mercury
accidentally being released into the bloodstream, such as when a
rectal thermometer breaks, or when several grams of mercury were
swallowed intentionally,26 without any reported adverse effects from
the mercury. Chronic toxicity leads to a condition called erethism,
characterized by insomnia, irritability, loss of memory, lack of
self-control, timidity, drowsiness, depression and eventual tremors.18
The renal effects lead to proteinuria, and a diagnostic discoloration
of the lens of the eye also may develop.

Both the Occupational Safety and Health Administration27 and the
National Institute for Occupational Safety and Health28 give a
threshold limit value, or TLV, of 50 micrograms per cubic meter of
mercury vapor as a time-weighted average based on constant exposure of
40 hours per week. The World Health Organization, or WHO, has adopted
a recommended limit of 25 µg/m3.29

Clinically significant effects (erethism, intention tremor,
gingivitis) have not been reported below air concentrations of 100 µg
mercury/m3.30 Slowed nerve conduction and short-term memory loss have
been observed in and special instrumental tests for tremor
(preclinical effects) have been conducted on people exposed to mercury
levels below 100 µg Hg/m3.30 But no clinical deficiency in kidney
function has been discovered in this same population. The range of
mercury in urine for populations with no identifiable source of
mercury exposure is up to 20 µg/liter.30 Clarkson and colleagues31
estimate the total daily absorption for all forms of mercury to be 2.3
µg/day, compared with the 5.8 µg/day estimated by the Environmental
Protection Agency, or EPA.32 Two-thirds of this difference in
estimates stems from the EPA’s higher allocation of ingesting
inorganic mercury from nonfish food, while the other one-third comes
from the larger EPA estimate of methyl mercury from fish consumption.
AMALGAM CORROSION

Amalgam corrosion is an oxidation-reduction reaction in which the
metals in the amalgam react with nonmetallic elements in the
environment to produce chemical compounds.33 This is important because
corrosion is a major factor in determining the amount of mercury that
is released into the oral cavity. Amalgam corrosion is influenced by
factors that disrupt the surface layer of the restoration such as
toothbrushing and chewing, which can cause an increase in mercury
release. The mercury released in this fashion can be in two forms:
mercury vapor or mercuric ions. The mercury vapor can be inhaled or
exhaled, depending on the subject’s breathing pattern, while mercuric
ions can pass into the saliva and enter the gastrointestinal tract.24
The corrosion of amalgam restorations is complex cand actually
decreases the baseline release of mercury.24

Corrosion is a major factor in determining the amount of mercury that
is released into the oral cavity.
AMALGAM TOXICITY

A minority of dentists and physicians allege that the amount of
mercury that “leaks” from amalgam restorations is sufficient to be a
factor in developing or directly causing a host of diseases including,
but not limited to, Alzheimer’s disease, multiple sclerosis and immune
system dysfunction.9 This measurable leakage can enter the body
through breathing mercury vapor or swallowing the mercury that
dissolves in the saliva. The oral cavity constantly is wet owing to
the continuous secretion of saliva and the high humidity of exhaled
air. Since the absorption of mercury through the gastrointestinal
tract is minimal, the mercury from amalgam that is swallowed adds very
little to the total body burden of mercury.

Investigators have demonstrated that people with amalgam restorations
have higher oral levels of mercury vapor than do people who do not
have amalgam restorations.34 Yet determining the amount of mercury
released and absorbed from amalgam is difficult and complex. Olsson
and Bergman35 have listed the following factors as variables affecting
the amount of mercury released from amalgam restorations: number of
teeth, number of surfaces, baseline mercury release, magnification
factors such as eating or toothbrushing, eating habits, toothbrushing
habits, oral breathing habits, nose-mouth breathing ratio,
inspiration-expiration ratio, swallowing, inhalation absorption,
ingestion absorption and body weight.

These confounding variables have caused large variations in the
estimates of daily mercury release and absorption. Several
researchers36,37,38,39,40 and 41 have arrived at figures higher than
10 µg Hg/m3, but other researchers34,42,43,44,45 and 46 consistently
have reported a much lower dose of mercury of around 1 to 2 µg/day. In
1992, Olsson and Bergman35 arrived at an amount of 1 to 2 µg/day of
mercury uptake for subjects with more than eight amalgam restorations.

Analysis of the data concerning daily mercury release and absorption
leads me to conclude that mathematical errors led to serious
mathematical errors led to serious miscalculations in arriving at the
total amount of mercury vapor exposure. These computational errors led
many investigators to overestimate the amount of mercury that is
released and absorbed during daily life. The International Committee
on Maximum Allowable Concentration of Mercury Compounds gives a TLV of
50 µg/m3 of mercury vapor.18

There also are two levels that are used in determining industrial and
other thresholds for mercury concentrations in the air. One is the
lowest observed adverse effect level, or LOAEL, and the other is the
no observed adverse effect level, or NOAEL. These thresholds are based
on the levels at which adverse effects appear or fail to appear. The
LOAEL is 100 µg/m3 for clinical mercurism and 50 µg/m3 for
nephrotoxicity. Both of these levels relate to constant mercury
exposure during a 40-hour work week. The NOAEL is 25 µg/m3 for WHO
industrial threshold, 5 µg/m3 for the general public threshold, and 1
µg/m3 for children, pregnant women and ill people (the last two levels
relate to continuous mercury exposure).47,48
ESTIMATES OF TOXIC MERCURY LEVELS

Using the lowest established value—the NOAEL for children, pregnant
women and ill people of 1µg Hg/m3—as a safe threshold for continuous
mercury vapor exposure for the general public and assuming a
respiration rate of 22 m3 per day, a safe threshold for mercury vapor
absorption by the lungs is 20 µg/day.29 Eley29 also estimated the safe
level for intestinal absorption of mercury from amalgam by multiplying
the lowest NOAEL figure by a factor of 10 to reflect the low
absorption by the gastrointestinal tract and then another factor of 2
to account for the reduced toxicity of mercuric compounds. This
yielded a safe threshold for gastrointestinal absorption of salivary
mercury of 400 µg/day.
ADVERSE HEALTH CLAIMS

Eggleston49 claimed that the mercury from amalgam reduced lymphocyte
responses, thereby compromising immune function. Mackert and
colleagues50 criticized Eggleston for not blinding his study and not
giving a thorough review of his methodology. Mackert and colleagues50
measured the levels of three major populations of lymphocytes in 37
subjects, 21 who had amalgam restorations and 16 who did not. The
results of this study showed no indication that amalgam affects the
human immune system.

Mercury from amalgam also has been implicated in the development of
Alzheimer’s disease.51 However, two studies on patients with
Alzheimer’s disease and on a population of nuns strongly suggest that
this is not true.52,53 Saxe and colleagues’ study,53 in particular,
was compelling because the participants were Roman Catholic nuns who
were 75 to 102 years old and who had lived together in a relatively
homogeneous environment for many years. The nuns with amalgam
restorations did not score lower than the nuns who did not have
amalgam restorations on eight different tests of cognitive function.53

A number of studies have contrasted the general health of subjects who
had and who did not have amalgam restorations. Mackert and Berg-lund54
concluded that the extremely low dosage of mercury attributable to
amalgam restorations was insufficient to produce any detectable
negative effect on general health. Ahlqwist and colleagues55 conducted
a survey of more than 1,000 Swedish women, asking them about 30
specific symptoms and complaints. The researchers attempted to relate
the answers to the size and number of amalgam restorations but could
find no correlation. Berglund and Molin56 measured the blood and urine
mercury levels of people who had and who did not have complaints about
amalgam toxicity. The researchers found the daily dose of mercury from
the patient’s amalgam restorations was low in both groups and did not
differ significantly between groups. These studies are compelling from
an EBC viewpoint, as dose-response curves exist for all known
environmental toxins, with subjects with more severe symptoms having
higher exposure and higher body levels of the toxin in question.
Indeed, in Ahlqwist and colleagues’ study,55 the women who had amalgam
restorations actually exhibited better general health than did the
women who did not have them. The authors said this probably reflected
a greater concern for health matters among those women who received
routine dental care.

It would seem logical and prudent to search for any evidence of
disease among dentists, as they have been shown to have a much higher
and consistent exposure to mercury vapors than the general public.57
This is because dentists inhale dispersed mercury vapors every time
they place or remove amalgam restorations.58,59 Naleway and
colleagues60 reported findings from onsite screenings at the ADA
annual sessions in 1985 and 1986. Measurements of concentrations of
b2-microglobulin in serum and urine, of creatinine concentration in
serum and of creatinine clearance were used to evaluate kidney
dysfunction. The mean urinary values in the 1985 and 1986 surveys were
5.8 µg Hg/L and 7.6 µg Hg/L, respectively.60 Approximately 10 percent
of the subjects had urinary mercury concentrations higher than 20 µg
Hg/L. No clear relationship was demonstrated between elevated urinary
mercury concentrations and kidney dysfunction.60 The general
population has a mean urinary value of 1 to 3 µg Hg/L.61 Although
urine mercury levels can vary greatly from day to day and person to
person, on a group basis, urine concentrations have been found to show
good correlation with exposure to mercury vapor.62 Dentists have a
much higher mean urinary mercury value and yet exhibit no higher
levels of morbidity or mortality.63

Boyd and colleagues64 claimed that sheep kidney function was damaged
dramatically by mercury from amalgam restorations. EBC analysis
concludes that there was no damage because there was neither a
pathological change in the kidney nor an increase in the blood urea
nitrogen, which ordinarily will increase when there is an impaired
glomerular filtration rate.65 In addition, Sandborgh-Englund and
colleagues66 were unable to confirm Boyd and colleagues’ findings.
Ekstrand and colleagues65 found no effects on various parameters of
kidney function in humans and concluded that sheep may not be
appropriate models for testing the toxic effects of dental restorative
materials.

Summers and colleagues67 reported a significant increase in the
proportion of mercury-resistant bacteria present in the intestines of
six monkeys after amalgam restorations were inserted and removed. They
concluded that amalgam may contribute to the emergence of
drug-resistant bacteria. Edlund and colleagues68 retested this
hypothesis with human subjects. They found that analysis of the cohort
with amalgam restorations gave significant results, but when they
compared these results with the normal variations from a control
group, the results no longer were statistically significant.68

The list of supposed symptoms of amalgam toxicity is so inclusive that
any healthy person would find it hard not to confirm the presence of
at least some of the telltale symptoms.

Allergies to components of amalgam do exist. The allergic reaction to
amalgam may be local or more wide-spread. The skin is the most common
site, and the reaction often is self-limiting and subsides within two
or three weeks even without the removal of the restoration.69 The
percentage of people who are allergic to mercury has been shown to be
less than 1 percent.70
DIAGNOSTIC METHODS

Antiamalgam advocates often use a number of scientifically unsupported
diagnostic methods. One is the electrical reading of restorations that
is done with a device similar to a common volt meter. This device is
purported to provide the data necessary to determine the sequence of
removal of the amalgam restorations.9 Marek71 stated that this device
actually records the “difference between the corrosion rate without
that contact of two materials [the electrical probe and the amalgam]
and with the contact of two materials. It is not the corrosion rate,
and there is no way by simple measurement to determine the corrosion
rate or the release rate of ions from a metal in the mouth.” Marek
further stated that because mercury is a more noble metal than the
other components in amalgam, its long-term dissolution rate in saliva
“is not high enough to be reason for concern.”72

A symptom questionnaire routinely is given to patients by dentists who
believe that amalgam is toxic. It often asks for a general history and
includes specific questions concerning skin problems, nervous
disorders, digestion, blood diseases, cancer, endocrine problems and
emotional problems, as well as feelings of malaise, tiredness,
restlessness, boredom or excitability that occur now or have in the
past.9 The list is so inclusive that any healthy person would find it
hard not to confirm the presence of at least some of the telltale
symptoms. These wide-ranging questionnaires neglect a cardinal rule of
toxicology: the specificity of symptoms to a poison. Forensic
pathologists often depend on a patient’s symptoms to determine what
kinds of diagnostic tests should be performed to arrive at a proper
diagnosis and to begin proper treatment. In the case of amalgam, the
diagnostic symptoms are so varied that it would be impossible to
attribute all these responses to a single toxin.

Dr. Huggins9 recommends using hair analysis to determine the patient’s
calcium, manganese, mercury, zinc and potassium levels. Yet an EBC
analysis of the literature demonstrates that “hair grows very slowly,
so even samples taken close to the scalp may not reflect present
bodily conditions.”73 Moreover, different laborato ries reach
different conclusions about the same hair samples,74 and a normal
range for minerals in the hair has not been established.75 Nor is it
clearly understood how mineral content of the hair relates to mineral
concentration in the blood and tissues. Hair analysis may be of value
in determining if a person was exposed to a toxic element such as
arsenic, chromium or lead. But even then, shampoos and hair dyes can
distort the test results.73

An industrial-grade mercury detector also often is used to diagnose
mercury toxicity. This device multiplies the amount of mercury it
actually measures by a large factor so that the reading will give the
amount of mercury vapor in a cubic meter of air. Normal tidal
volume—the amount of air entering the lungs during one normal
breath—is 0.5 L24 (human inspiratory capacity is 2.8 to 4.3 L), a
volume far less than a cubic meter (1,000 L). As I mentioned
previously, mercury release is inconsistent, and total daily dose is
difficult to determine accurately. Taking a reading after a patient
chews vigorously and then extrapolating this value to represent daily
dose can be frightening to a patient who is unaware of these
methodological complexities.

Some physicians and dentists also use a skin patch test to determine
“mercury allergy” or “hypersensitivity.” The reactions of the skin and
the oral mucosa often are different. It is possible for the skin to be
sensitized but not the oral mucosa, there may be concurrent
sensitization of both skin and mucosa, or the mucosa may be sensitized
but not the skin (a rare occurrence).62 Interpretation of patch test
results is difficult and requires the expertise of specially trained
allergists. And even in cases in which these allergists are consulted,
there are numerous situations that can lead to false positive or false
negative reactions.76 This makes patch testing for mercury allergy
highly subjective and of little value.

Data strongly suggest that mercury levels many times higher than those
associated with a mouth full of amalgam pose no risk of adverse health
effects.
CONCLUSIONS

The cardinal rule of toxicology is that “only the dose makes a
poison.” Mercury can be toxic, for example, when high exposures occur
in occupational settings. In these cases, the severity of response
correlates well with the amount and duration of exposure. The
relationship of dose (number and size of amalgam restorations),
exposure time and symptoms has not been established.77

The call to ban amalgam is unusual among potential environmental
toxins. In the past, a specific disease or condition has been
recognized in a population that has been compared with a symptom-free
population and possible causative agents are sought. The best example
is the methods employed to epidemiologically establish the strong
cause-and-effect nature of smoking and both lung cancer and heart
disease. With amalgam, a wide range of diseases and conditions have
been attributed to it based solely on self-reported improvements in
symptoms when the amalgam restorations were removed. The already
collected data on the morbidity and mortality of dentists who have a
proven higher body burden of mercury than do the general public was
ignored. Today, we also have compelling data from groups with and
without restorations who lived under similar environmental conditions
and these, too, refute the claims of amalgam toxicity.

Data strongly suggest that mercury levels many times higher than those
associated with a mouth full of amalgam pose no risk of adverse health
effects. There is evidence that the body’s mercury burden is highest
immediately after placement or removal of amalgam restorations.29 This
information casts a critical light on those dentists, physicians and
patients who have claimed improvement of symptoms immediately after
amalgam removal.

EBC requires an “acceptance of an uncharacteristically high level of
uncertainty concerning the impact of one’s clinical interventions.”78
In contrast to this, Dr.Huggins has proposed that “in order for
mercury to be a problem, order for mercury to be a problem, it would
have to … demonstrate remission of the symptoms on amalgam removal.”9
Thus, he and those who are similarly opposed to amalgam base their
conclusions on clinical judgments of symptom improvement. In EBC, the
following are seen as potentially leading to incorrect conclusions
about treatment efficacy when one relies on clinical observation:

*

placebo effects of treatment;
*

statistical regression toward the mean;
*

spontaneous remission;
*

natural variability of signs and symptoms;
*

failure to consider treatment dropout;
*

bias in self-reports of symptom remission.79

The logical and methodological errors of the leading opponents of
amalgam restorations are clearly evident when analyzed using the EBC
paradigm.

In 1993, James Mason, M.D., the Assistant Secretary for Health,
reaffirmed the U.S. Public Health Service’s position that “there are
no data to compel a change in the current use of dental amalgam.”80

This review supports Dr. Mason’s conclusion, and I propose that EBC be
used by clinicians as a way to more accurately evaluate health care
interventions.
Dr. Dodes is in private practice, 8639 Wood-haven Blvd., Wood-haven,
N.Y. 11421, e-mail “johndodes@aol.com”. Address reprint requests to
Dr. Dodes.

The author would like to thank Dr. Wilmer Eames for his friendship and
encouragement.

1.

Guyatt GH, Rennie D. User’s guides to the medical literature. JAMA
1993;270(17):2096-7.
2.

Neidle EA. On the brink: will dental education be ready for the
future? J Dent Educ 1990;54(9):564-6.
3.

Guyatt GH, Sackett DL, Cook DJ. Users’ guides to the medical
literature, II: how to use an article about therapy or prevention,
A—are the results of the study valid? JAMA 1993;270(21):2598-601.
4.

Guyatt GH, Sackett DL, Cook DJ. Users’ guides to the medical
literature, II: how to use an article about therapy or prevention,
B—what were the results and will they help me in caring for my
patients? Evidence-Based Medicine Working Group. JAMA
1994;271(1):59-63.
5.

DeMaar FE. Historically, when and by whom was silver amalgam
introduced? Sci Educ Bull 1972;5(1):23-6.
6.

Black GV. The physical properties of the silver-tin amalgams. Dent
Cosmos 1896;38:965-92.
7.

Stock A. Die gefahrlichkeit des quecksilberdampfes und der amalgame
[Danger from mercury and from amalgam fillings]. Med Klin
1926;22:1209-12, 1250-2.
8.

Harndt E. Ergebnisse klinischer untersuchungen zur losung der
amalgam-quecksilberfrage [Clinical examination results of research on
the amalgam-mercury question]. Deutsche Zahnarztliche Wochenschrift
1930;33:564-75.
9.

Huggins HA, Huggins SA. It’s all in your head: Diseases caused by
silver-mercury restorations. Solona Beach, Calif.: APW; 1985.
10.

Product Use Survey, 1995. Clin Res Associates Newsletter.
1995;19(10):4.
11.

Safer M. Is there poison in your mouth [television broadcast]. “60
Minutes.” CBS television. Dec. 16, 1990.
12.

Lieberman AJ, Kwon SC. Facts versus fears: A review of the greatest
unfounded health scares of recent times. 3rd ed. New York: American
Council on Science and Health; 1998.
13.

Foulke JE. Mercury in fish: cause for concern? FDA Consumer
1994;Sept:6-9.
14.

Goldwater LJ. From Hippocrates to Ramazini: early history of
industrial medicine. Ann Med Hist 1936;8:27-35.
15.

Berlin MH, Clarkson TW, Friberg LT, et al. Maximum allowable
concentrations of mercury compounds: report of an international
committee. Arch Environ Health 1969;19:891-905.
16.

Kurland LT, Faro SN, Siedler H. Minamata disease. The outbreak of a
neurological disorder in Minamata, Japan, and its relationship to the
ingestion of seafood contaminated by mercuric compounds. World
Neurology 1960;1:370-95.
17.

Tsubaki T, Irukayama K. Minamata disease: Methylmercury poisoning in
Minamata and Niigata, Japan. New York: Elsevier Scientific Publishing;
1977.
18.

Newman S. Mercury toxicity. In: Workshop on Biocompatibility of Metals
in Dentistry, Chicago, July 11-13, 1984. Chicago: American Dental
Association; 1984:96-8.
19.

Heintze U, Edwardsson S, Derand T, Birkhed D. Methylation of mercury
from dental amalgam and mercuric chloride by oral streptococci in
vitro. Scand J Dent Res 1983;91(2):150-2.
20.

Eley BM, Cox SW. Mercury poisoning from dental amalgam: an evaluation
of the evidence. J Dent 1988;16(2):90-5.
21.

Rupp NW. Clinical experiences of biocompatibility of metals in
dentistry: biological aspects. In: Workshop on Biocompatibility of
Metals in Dentistry, Chicago, July 11-13, 1984. Chicago: American
Dental Association; 1984:265-88.
22.

Birke G, Johnels AG, Plantin LO, Sjostrand B, Westermark T. Mercury
poisoning through eating fish? Lakartidningen 1967;64:3628-54.
23.

Hursh JB, Cherian MG, Clarkson TW, Vostal JJ, Mallie RV. Clearance of
mercury (HG-197, HG-203) vapor inhaled by human subjects. Arch Environ
Health 1976;31(6):302-9.
24.

Eley BM. The future of dental amalgam: a review of the literature,
Part 3—mercury exposure from amalgam restorations in dental patients.
Br Dent J 1997;182(9):333-8.
25.

Joselow MM, Louria DB, Browder AA. Mercurialism: environmental and
occupational aspects. Ann Intern Med 1972;76(1):119-30.
26.

Friberg L. Inorganic mercury: Environmental Health Criteria 118.
Geneva: World Health Organization; 1991.
27.

Occupational Safety and Health Administration. Mercury (aryl and
inorganic compounds). Fed Regist 1989;54(12):2424-16.
28.

National Institute for Occupational Safety and Health. Testimony on
the Occupational Safety and Health Administration’s proposed rule on
air contaminants. Cincinnati: U.S. Department of Health and Human
Services, Public Health Service, Centers for Disease Control.
Subcommittee on Risk Management of the Committee to Coordinate
Environmental Health and Related Programs NIOSH policy statements;
1988.
29.

Eley BM. The future of dental amalgam: a review of the literature,
Part 4—mercury exposure hazards and risk assessment. Br Dent J
1997;182(10):373-81.
30.

U.S. Department of Health and Human Services. Committee to Coordinate
Environmental Health and Related Programs. Subcommittee on Risk
Management. 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. Washington: Department of Health and Human Services;
1993:Appendix III:1. DHHS publication 96-0445.
31.

Clarkson TW, Hursch JB, Sager PR, Syversen TL. Mercury. In: Clarkson
TW, Friberg L, Nordberg GF, Sager PR, eds. Biological monitoring of
toxic metals. New York: Plenum Press; 1988:199-246.
32.

U.S. Environmental Protection Agency, Environmental Criteria and
Assessment Office. Mercury health effects update: Health issue
assessment. Research Triangle Park, N.C.: Office of Health and
Environmental Assessment, Environmental Protection Agency; 1984. EPA
publication 600/8-84-019F.
33.

von Fraunhofer JA, Staheli PJ. Corrosion of dental amalgam. Nature
1972;240(5379):304-6.
34.

Berglund A. Estimation by a 24-hour study of the daily dose of
intra-oral mercury vapor inhaled after release from dental amalgam. J
Dent Res 1990;69(10):1646-51.
35.

Olsson S, Bergman M. Daily dose calculations from measurements of
intra-oral mercury vapor. J Dent Res 1992;71(2):414-23.
36.

Svare CW, Peterson LC, Reinhardt JW, et al. The effect of dental
amalgams on mercury in expired air. J Dent Res 1981;60(9):1668-71.
37.

Abraham JE, Svare CW, Frank CW. The effect of dental amalgam
restorations on blood mercury levels. J Dent Res 1984;63(1):71-3.
38.

Vimy MJ, Lorscheider FL. Intra-oral air mercury released from dental
amalgam. J Dent Res 1985;64(8):1069-71.
39.

Vimy MJ, Lorscheider FL. Serial measurements of intra-oral air
mercury: estimation of daily dose from dental amalgam. J Dent Res
1985;64(8):1072-5.
40.

Vimy MJ, Lorscheider FL. Dental amalgam mercury daily dose estimated
from intra-oral vapor measurements: a predictor of mercury
accumulation in human tissues. J Trace Elem Exp Med 1990;3:111-23.
41.

Hahn LJ, Kloiber R, Vimy MJ, Takahashi Y, Lorscheider FL. Dental
‘silver’ tooth restorations: a source of mercury exposure revealed by
whole-body image scan and tissue analysis. FASEB J 1989;3(14):2641-6.
42.

Olsson S, Bergman M. Letter to the editor. J Dent Res 1985;66:1289.
43.

Mackert JR Jr. Factors affecting estimation of dental amalgam mercury
exposure from measurements of mercury vapor levels in intra-oral and
expired air. J Dent Res 1987;66(12):1775-80.
44.

Berglund A, Pohl L, Olsson S, Bergman M. Determination of the rate of
release of intra-oral mercury vapor from amalgam. J Dent Res
1988;67(9):1235-42.
45.

Olsson S, Berglund A, Pohl L, Bergman M. Model of mercury vapor
transport from amalgam restorations in the oral cavity. J Dent Res
1989;68(3):504-8.
46.

Langworth S, Kohlbeck KG, Akesson A. Mercury exposure from dental
restorations, II: release and absorption. Swed Dent J 1988;
12(1-2):71-2.
47.

Gerstner HB, Huff JE. Clinical toxicology of mercury. J Toxicol
Environ Health 1977;2(3):491-526.
48.

Gerstner HB, Huff JE. Selected case histories and epidemiologic
examples of human mercury poisoning. Clin Toxicol 1977;11(2):131-50.
49.

Eggleston DW. Effect of dental amalgam and nickel alloys on
T-lymphocytes: preliminary report. J Prosthet Dent 1984;51(50):617-23.
50.

Mackert JR Jr., Leffell MS, Wagner DA, Powell BJ. Lymphocyte levels in
subjects with and without amalgam restorations. JADA
1991;122(3):49-53.
51.

Ehmann WD, Markesbery WR, Alauddin M, Hossain TI, Brubaker EH. Brain
trace elements in Alzheimer’s disease. Neurotoxicology
1986;7(1):195-206.
52.

Fung YK, Meade AG, Rack EP, et al. Mercury determination in nursing
home patients with Alzheimer’s disease. Gen Dent 1996;44(1): 74-8.
53.

Saxe SR, Snowdon DA, Wekstein MW, et al. Dental amalgam and cognitive
function in older women: findings from the nun study. JADA
1995;126(11):1495-501.
54.

Mackert JR Jr., Berglund A. Mercury exposure from dental amalgam
restorations: absorbed dose and the potential for adverse health
effects. Crit Rev Oral Biol Med 1997;8(4):410-36.
55.

Ahlqwist M, Bengtsson C, Furunes B, Hollender L, Lapidus L. Number of
amalgam tooth restorations in relation to subjectively experienced
symptoms in a study of Swedish women. Community Dent Oral Epidemiol
1988;16(4):227-31.
56.

Berglund A, Molin M. Mercury vapor release from dental amalgam in
patients with symptoms allegedly caused by amalgam fillings. Eur JOral
Sci 1996;104:56-63.
57.

Eley BM. The future of dental amalgam: a review of the literature,
Part 2—mercury exposure in dental practice. Br Dent J 1997;182(8):
293-7.
58.

Joselow NM, Ruiz R, Goldwater LJ. Absorption and excretion of mercury
in man, XIV: salivary excretion of mercury and its relationship to
blood and urine mercury. Arch Environ Health 1968;17(1):35-8.
59.

Powell LV, Johnson GH, Yashar M, Bales DJ. Mercury vapor release
during insertion and removal of dental amalgam. Oper Dent
1994;19(2):70-4.
60.

Naleway C, Chou HN, Muller T, Dabney J, Roxe D, Siddiqui F. On-site
screening for urinary Hg concentrations and correlation with
glomerular and renal tubular function. J Public Health Dent 1991;
51(1):12-7.
61.

Dentists’ health results analyzed. Average urinary mercury levels
found lower. ADA News. April 15, 1985:10.
62.

Cooley RL. Detection and diagnosis of biocompatibility of metals In:
Workshop on Biocompatibility of Metals in Dentistry, Chicago, July
11-13, 1984. Chicago: American Dental Association; 1984:179-200.
63.

Council on Dental Materials, Instruments and Equipment and Council on
Dental Therapeutics. Safety of dental amalgam. JADA 1983;106:519-20.
64.

Boyd ND, Benediktsson H, Vimy MJ, Hooper DE, Lorscheider FL. Mercury
from dental ‘silver’ tooth restorations impairs sheep kidney function.
Am J Physiol 1991;261:R1010-4.
65.

Ekstrand J, Bjorkman L, Edlund C, Sandborgh-Englund G. Toxicological
aspects on the release and systemic uptake of mercury from dental
amalgam. Eur J Oral Sci 1998;106:678-86.
66.

Sandborgh-Englund G, Ekstrand J, Elinder CG, Johanson G, Skare I.
Kinetics of mercury vapor after inhalation: an experimental study in
man (abstract 380). J Dent Res 1997;76:1142.
67.

Summers AO, Wireman J, Vimy MJ, et al. Mercury released from dental
‘silver’ restorations provokes an increase in mercury- and
antibiotic-resistant bacteria in oral and intestinal floras of
primates. Antimicrob Agents Chemother 1993;37(4):825-34.
68.

Edlund C, Bjorkman L, Ekstrand J, Sandborgh-Englund G, Nord CE.
Resistance of the normal human microflora to mercury and
antimicrobials after exposure to mercury from dental amalgam
restorations. Clin Infect Dis 1996;22(6):944-50.
69.

Veron C, Hildebrand HF, Martin P. Amalgames dentaires et allergie
[Dental amalgams and allergy]. J Biol Buccale 1986;14:83-100.
70.

Bauer JG, First HA. The toxicity of mercury in dental amalgam. CDA J
1982:10(6):47-61.
71.

Marek M. Corrosion, galvanic cell production, and release of metal
ions. In: Workshop on Biocompatibility of Metals in Dentistry,
Chicago, July 11-13, 1984. Chicago: American Dental Association;
1984:134-64.
72.

Marek M. Questions and answers. Workshop on Biocompatibility of Metals
in Dentistry, Chicago, July 11-13, 1984:348-51.
73.

Bershad S. The effects of nutrition on skin and hair. In: Total
nutrition. Herbert V, Subak-Sharpe GJ, eds. New York: St. Martin’s
Press; 1995:620-1.
74.

Barrett S. Commercial hair analysis: science or scam? JAMA
1985;254(8):1941-5.
75.

Herbert V, Barrett S. Vitamins and ‘health’ foods: The great American
hustle. Philadelphia: Stickley; 1981:45-6.
76.

Bandmann HJ, Fregert S. Patch testing. New York: Springer-Verlag;
1975.
77.

Malt UF, Nerdrum P, Oppedal B, Gundersen R, Holte M, Lone J. Physical
and mental problems attributed to dental amalgam restorations: a
descriptive study of 99 self-referred patients compared to 272
controls. Psychosom Med 1997;59(1):32-41.
78.

Marbach JJ, Raphael KG. Treatment of orofacial pain using
evidence-based medicine: the case for intraoral appliances. In:
Campbell JN, ed. Pain 1996: An updated review. Seattle: IASP Press;
1996:413-22.
79.

Raphael K, Marbach JJ. Evidence-based care of musculoskeletal facial
pain: implications for the clinical science of dentistry. JADA
1997;128(1):73-9.
80.

Mason JO. Introductory letter. In: U.S. Department of Health and Human
Services. Committee to Coordinate Environmental Health and Related
Programs. Subcommittee on Risk Management. 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. Washington: Department of
Health and Human Services; 1993. DHHS publication 96-0445.

Dr. Steve gave you good advice - I concur.  Be happy Jan didn't reply, *if*
you bought her advice you would have had several sleepless nights worrying.

carabelli

Nope,  you were right on that one.

Stupid questions always get goofy answers.

--
W_B

wubbabubbazG@RBAGEyahoo.com
Take out the G'RBAGE