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FDA
PRESENTATION: AN EVALUATION OF DENTAL AMALGAM MERCURY RELEASE
AND CORRESPONDING TOXICOLOGY CONCERNS
By
Boyd E. Haley, Ph.D., Professor, Department of Chemistry, University of
Kentucky 7 September 2006
A
simple computer search of the literature confirms that mercury and
organic mercury are extremely toxic agents and the mere presence of
mercury in the body should be proof of toxicity. It has also
been
clearly shown by many, even the World Health Organization, that
amalgams are the major contributor to human body burden. The
EPA
and National Academy of Sciences (NAS) report that 8 to 10% of American
women have such high mercury body burdens that put to elevated risk for
neurodevelopmental disorders any child they would give birth
to.
The Center for Disease Control states that 1 in 6 American children
have a neurodevelopmental problem. SO THE PROBLEM OR ISSUE IS
NOT
WHETHER OR NOT AMALGAMS AND THE MERCURY THEY DELIVER IS A HEALTH RISK,
THIS IS AN OBVIOUS FACT ACCORDING TO THE EPA AND NAS. THE
REAL
PROBLEM IS HOW DO WE CONVINCE THE CONTROLLING BUREAUCRATIC AGENCY, THE
FDA, TO ADMIT THAT THEY HAVE BEEN WRONG FOR MANY YEARS IN NOT
EVALUATING THE MERCURY RELEASE FROM DENTAL AMALGAMS. One
has to ask the simple question “Why are producers of amalgam products
not required to produce data in the packages that describe the amount
of mercury vapor that escapes daily from an amalgam of known weight and
surface area under conditions that mimic the mouth with regards to
temperature, pH and brushing?” In my opinion, the reason they
don’t is well known since to do so would quickly establish their
amalgam products as dangerous to human health. A recent study
on
the levels of mercury in autopsy tissues and existing dental amalgams
clearly states “Mercury levels were significantly higher in brain
tissues compared with thyroid and kidney tissues in subjects with more
than 12 occlusal amalgam fillings (all P<0.01) but not in
subjects
with 3 or less occlusal amalgams (all P > 0.07.”36
The
recent
(prepared August 2006) FDA staff white paper39 on the evaluation of
dental amalgam safety is almost totally based on a fatal
flaw.
This flaw is the old, widely used perception that mercury exposure can
be evaluated by measuring urine mercury levels. This concept
has
been used consistently by leading toxicologists for many years
primarily, in my opinion, because it was easiest to do. But,
it
also gave misleading information. Consider the data published
by
many authors in this area. Routinely you see shotgun patterns
when plotting number of amalgam fillings versus blood, urine, hair, or
body tissues level of mercury. This immediately tells one
that
there is not a linearity, or direct correlation, between the two
factors being plotted and that other factors that need consideration
must be identified. In my opinion, these factors are genetic
susceptibility to mercury retention toxicity, exposure to compounds
with synergistic toxicities, use of antibiotics, etc. as elaborated on
below. Also, reports
confirm that the ratio of fecal to urine excretion is 12 to1.
This proves that the vast majority of excreted mercury leaves through
the bilary transport system of the liver via the fecal route as the
mercury-glutathione complex. Urine mercury therefore
represents a
minor excretory route of less than 8% of mercury being
excreted.
Also, urine mercury is a measure of exactly that, mercury being
excreted by the kidney---not total mercury exposure. Yet, the
FDA
white paper evaluated most of the research documents based on urine
mercury levels that, in my opinion, has been proven to be very
misleading. Even the ATSDR 1999 and 2005 reports creating an
MRL
(minimum risk levels) and the current EPA RfC (reference concentration)
appear to based mostly on reports using urine mercury levels as a
measure of toxic exposure. Even the data in the recent JAMA
articles on the children’s amalgam trial show that urine mercury levels
are not an evaluation of dental amalgam mercury exposure (see below) as
the children appear to lose the ability to excrete mercury in the urine
with increased time of mercury exposure29. That is, even with
increased amalgams the children’s urinary mercury levels dropped after
two years exposure to 7 years exposure by almost the entire increase
that was affected by placement of amalgams within the first two
years. This indicates that the children are now retaining
this
mercury. Does
the above make sense? Consider another research project
evaluated
by the FDA staff, that of Vamnes et al.38. This study
described
the initial blood mercury levels and the effect of chelation with DMPS
on blood mercury levels of four cohort groups: Group1, 19 controls who
never had amalgams; Group 2, 21 healthy persons with 43
existing
amalgam surfaces; Group 3, 20 persons claiming self-reported symptoms
with 37.5 surfaces; and Groups 4, 20 persons with amalgams removed
(approximately 48 surfaces) 31.5 months earlier. The blood Hg
levels were about 2.5, 5.0, 5.0, and 4.0 mcgs for the groups,
respectively. The FDA white paper gave this evaluation “The
data
show that there is not difference in Hg blood levels in subjects with
and without self-reported symptoms thought to be caused by amalgams and
that chelation by DMPS is short-lived and has minimal impact on blood
Hg levels.” DMPS created a brief 24-30% drop in blood mercury
that returned to pre-chelation levels within 2 hours. In my
opinion, both (1) the rapid return of the chelated blood to
pre-chelation levels and (2) the high blood Hg levels of those with
amalgams removed when compared to the low levels in those who have
never had amalgams demonstrate that amalgams contribute to a long-term,
high mercury body burden that maintains a steady blood Hg level years
after they are removed. It is the amalgam induced body burden
of
mercury, not the blood or urine levels that cause toxic effects and
this fact was not considered by the FDA white paper. In
the summary statement the FDA white paper stated “Chelation of Hg
decreased blood and urine levels by 30% but for only a short time after
which levels rapidly (within 2 hours) return to pre-chelation
levels. Removal of a substantial number of amalgam
restorations
does not result in a large decrease in blood Hg levels, even 2-3 years
after removal.” With this they appear to assume that
mercury’s
toxic effect can be measured by blood and urine levels, and this is
obviously not true, but it is the erroneous spin that all of the
pro-amalgam supporters place on such data. This is done to
avoid
facing the fact that it is mercury body burden, not urine or blood
levels that correlate with toxicity. Retention of mercury by
the
body has to decrease the level in the blood and urine so the reverse is
true for those exposed, low blood and urine levels identify the
individuals who are not effectively excreting mercury from their
body. This ineffectiveness can be caused by genetic
susceptibility, diet, antibiotics and exposure to other toxic materials. However,
the case against mercury levels produced by amalgams in the human body
as being safe is growing. In Alzheimer’s disease (AD) the
aberrant biochemical events and the pathological hallmarks are well
described. So is the research that shows that mercury, and
only
mercury, will produce the aberrant biochemistry and produce most of the
pathological hallmarks in appropriate test systems12, 13, 28 and
references therein. Also, a recent study has indicated that
the
increase in brain amyloid protein is due to an aberrant brain heme
level and the heme synthetic pathway is one known to be extremely
sensitive to mercury33. In spite of all this molecular level
data
the Alzheimer’s Association of America supports the ADA in its plan to
continue exposing Americans, some of whom are destined to become
demented with AD, to a 40 to 60 year exposure to mercury from dental
amalgams. It seems logical to me that this exposure, even if
you
don’t want to think it causal for AD, would certainly exacerbate the
rate of biochemical breakdown of the human brain of those who later
suffer from AD type dementia.
It
is also well known that the genetic inheritance of the APO-E4 form of
apolipoprotein-E greatly increases the risk of early onset AD whereas
inheritance of the APO-E2 form appears to be protective against
AD. Both of these forms appear to do their biological
functions
adequately, and one of these functions is to remove oxidized
cholesterol from the brain, into the cerebrospinal fluid, across the
blood brain barrier and into the blood for removal by the
liver.
The second highest concentration of APO-E protein is in the
cerebrospinal fluid. The one definite difference between
APO-E4
and APO-E2 is the presence of two cysteines in the APO-E2 that are
capable of mercury binding and therefore mercury removal from the
central nervous system. APO-E4 differs from APO-E2 in that
these
two cysteines have been genetically replaced by arginines that have no
mercury binding capacity. Therefore, as previously reported,
one
of the most logical explanations of the different protective effects of
the widely accepted, differential risk for AD based on APO-E geneotype
can be explained by the loss of mercury binding capacity in the
cerebrospinal fluid and brain of the proteins expressed by these
genes.12 It is this type of genetic susceptibility that may
be
evident in multiple biochemical pathways that place certain individuals
at risk for mercury exacerbated or causal illnesses (see the comments
on the heme synthesis pathway below). Mercury
exposure to humans comes from various chemical forms such as elemental
vapors, inorganic salts and organic-mercurial such as thimerosal and
phenylmercury acetate. All chemical forms of mercury have been proven
toxic at very low levels. There is no doubt that mercury and
mercury compounds represent the most dangerous form of metal toxicity
since research on exposures show them to cause adverse effects in
animals and humans at the very lowest levels of any metal. Mercury and
mercury containing compounds are listed under California’s Proposition
65 as compounds that need to be evaluated for their level of toxicity
to ensure the safety of the citizens of California. Mercury vapor is
one of the most toxic forms of mercury along with some of the organic
mercury compounds. This is probably due to the efficient
partitioning of vaporous mercury into certain body organs (e.g. Central
Nervous system (CNS), kidney) and into specific cellular organelles
(e.g. the mitochondria) based on mercury vapor’s ability to easily
penetrate cell membranes and the blood brain barrier. In this
manner mercury vapor, Hg0, is quite different from ionic Hg2+ and
Hg1+. For example, air and oral ingestion of mercury vapor
(Hg0)
primarily affect the central nervous system whereas the kidney is the
major organ affected by the cationic forms of mercury (e.g. Hg1+ and
Hg2+).
Attempting to determine a lowest observable affect
level
(LOAEL) or no observable effect level (NOAEL) regarding mercury vapor
exposure is, at best, a complicated procedure as explained by the
analysis of published refereed research articles as presented
below. The fact is, the relative toxicity of mercury and
organic
mercury compounds fluctuate dramatically in the same species of animal
depending on: (1) delivery route (2) the presence of other synergistic
toxic metals (3) different diets34 (4) antibiotic exposure34 (5)
genetic type7 with 8.7 to 13.4% showing sensitivity to a diagnostic
patch test 5 & references therein) and gender28,35 (6) state of
health and (7) age of exposure19. The end point for measuring toxicity
is also critical. That is, if lethality versus loss of
neurological function is the end point then different values for a
minimum daily acceptable limit of exposure will be arrived
at.
Also, when lethality and loss of neurological function are compared to
suppression of the immune system as the end point, an even
lower
minimum acceptable daily exposure would be expected. Based on
the
factors affecting mercury retention/excretion the obvious fact is that
no exposure level can be determined that will predict the retention
rate and subsequent mercury body burden of humans. However,
we now have a reliable measure of physiological toxicity of mercury
exposure that is reflected in the “porphyrin profile”.
Porphyrins
are small molecular weight organic compounds that are produced in a
multi-step pathway and ends in the synthesis of heme.
Evidently,
different toxic metals and other toxic compounds may inhibit the
porphyrin pathway in different manners ending up with a different
urinary “porphyrin profile”. Mercury toxicity has a unique
“prophyrin profile” that today is not known to be produced by any other
toxin. Recent research on dentists and dental technicians has
shown that 85% of these subjects have a porphyrin profile that is
aberrant from normals and symptomatic of low level mercury
toxicity23,24. In addition, 15% of this 85% have a more
dramatic
aberrancy and this aberrancy corresponds to a polymorphism in the CPOX4
gene25. This data clearly shows both the general toxicity of
amalgam mercury vapor and an enhanced sensitivity of a genetic subset
of the population. To date we do not know the effects of
amalgam
mercury on the porphyrin profiles of children although this work was
supposedly done by the group that did the NIDCR children’s amalgam
trials (see comments on JAMA papers below). What we do know
is
that there is a report that the majority of autistic children have an
aberrant porphyrin profile and that this aberrancy was reversed by
treating these children with a mercury chelator26. This new
information will lead to many parents and their children having
prophyrin profiles done to establish if they have become mercury
toxic. At study concept has been initiated by the IAOMT to
test
the porphyrin profiles on dental patients with varying amounts of
amalgam exposure in a manner similar to the study in references
23-25. The
critical question is the effect of mercury vapor exposure on brain
porphyrins profiles since an aberrancy has been reported in brain heme
that has been associated with the inability to remove beta-amyloid
protein from brain cells33. The effect on urinary porphyrins
is
well known and these porphyrins are primarily from the
kidney. It
should be noted that porphyrins lead to heme and heme is critical for
several biochemical mechanisms. First, heme is the oxygen
carrying cofactor for hemoglobin, second, heme is a critical cofactor
for the P450 class of enzymes that are responsible for detoxifying
organic type of toxins from the body, and, third, heme is a necessary
cofactor for one of the complexes in the electron transport system of
mitochondria. Therefore, mercury inhibition of heme
production
could have a multitude of secondary effects that cause human
illnesses. It has been pointed out to me that autistic
children
are usually of very light complexion, indicating a lack of hemoglobin
or oxygen carrying capacity, which is consistent with their abnormal
porphyrin profiles. In
the FDA white paper the elegant work from the laboratories of
Esheverria and Woods was soundly dismissed, as if the “experts” at the
FDA knew more about this research than the authors and the reviewers of
these manuscripts23, 24, 25. The major criticism was the lack
of
non-dental controls or data on other metals, as if there weren’t data
on the general population in medical literature regarding normal
porphyrin levels and the behavioral measures used {Also, consider the
work of Nataf et al. showing the same porphyrin aberrancies in many
autistic children, who were never exposed in a dental
office!).
In spite of the fact that 85% of the dentists and dental technicians
tested showed mercury related toxicities in both behavior and
physiological parameters, and 15% showed an increased mercury induced
neurological deficits with polymorphism of the CPOX4 gene, the FDA and
ADA still maintain that amalgams do not cause any significant medical
problems because the urine and blood levels do not reflect that these
individuals had reached a level of exposure that was toxic. I
think it would be worthwhile to err on the side of caution and warn the
members of the ADA, practicing dentists, of this concern instead of
ignoring it for very questionable reasons. Again, the FDA/ADA
miss the point that it is the mercury body burden, not the blood or
urine levels that defines toxicity, and even body burden has to take
into account genetic susceptibility parameters. It is my
opinion,
that the FDA/ADA do not have the expertise to second guess the findings
of these researchers and in doing so highlight their inability to give
fair-minded judgment to this elegantly designed and performed research
which was done at a high-ranked research university. It
is obvious that lethality requires a higher level of exposure to
mercury vapor than does neurological or developmental damage when
considering infants in utero. Neurotoxicity or a suppressed immune
system in the parent would be considered dangerous for developing and
maintaining a pregnancy that leads to birth of a healthy child. Many
children may appear normal and have apparently non-toxic levels of
blood and urine mercury and still suffer from extreme mercury
toxicity. For example, young athletes and others who died
from
Idiopathic Dilated Cardiomyopathy (IDCM) have been found to have 22,000
times the mercury in their heart tissue whereas the muscular samples
did not18. This level, 178,400ng/g, would have generally been
lethal to the kidney and CNS cells. In my opinion, the
unexplained, abnormal partitioning of huge levels of mercury into
specific organs in certain individuals essentially renders it
impossible to identify a blood or urine level of mercury that is safe
for all. Further, recent research has shown that mercury and
ethylmercury have the ability to inhibit the first step (phagocytosis)
in the innate and acquired immune response of humans at low nanomolar
levels31. This clearly shows that mercury exposures quite
below
the average exposure can cause disruption of the immune system at all
ages. For an accurate
determination of a LOEL or NOEL for injury causing mercury exposure it
is clear that using data from one strain of a genetically inbred rat or
mouse strain could result in a very inaccurate answer. Humans
are
not genetically inbred and their diets differ dramatically and some are
on medications that would enhance the toxicity of all mercury
compounds. Further more, it has been established in the
literature that different strains of mice and rats give different
sensitivities to mercury and that there can be dramatic differences in
sensitivity to specific toxicants between species such as rats and
humans. Therefore, basing safety on animal data is very
misleading. One cannot measure accurately the effects of
mercury
exposure on the IQ of an individual exposed at birth since we do not
know what it would have been without exposure---and a toxicity induced
decrease in IQ, if the individual is not severely compromised, is
difficult to establish. Recent
reports in JAMA have come to the conclusion that amalgams are safe for
use in children29, 30. However, there are numerous flaws with
these studies that do not warrant such a conclusion and the papers
themselves have been highly criticized both on ethical and scientific
grounds by myself and other
scientists.(seehttp://web.mac.com/iaomt/iweb/iaomt_news/).
First
and foremost, these JAMA reported studies excluded all children with
neurological problems (maybe caused by in utero mercury exposure from
the birth mother’s amalams20) from the studies, and there are 1 in 6
children in the USA with neurological illnesses according to the
CDC. So while a neurological healthy child may not respond to
mercury toxic exposures as rapidly as a neurologically unhealthy child
it seems untenable to call amalgams safe for general use in children
which the authors did inaccurately conclude. Second,
the data presented in these JAMA reported studies regarding urinary
excretion of mercury (ref. 27, figure 2, pg 1788, see below) showed
clearly that urinary mercury increased in the first two years of
amalgam exposure then dropped over 40% in the next five years to where
the error bars of amalgam bearers and composite bearers overlapped,
indicating no significant difference in urinary mercury excretion
between the two groups. In fact, the total increase caused by
amalgam placement was lost by year 7. The rationale for this
amazing data was not discussed in the published manuscripts as the
authors appeared to consider urinary mercury as a “measure of exposure”
and were content with a decreased excretion as being explained by a
decreased release of mercury from the amalgams as they aged.
However, mercury does not stop emitting from amalgams after two years
and these children also received new amalgams after year two through
year six. What the authors did not consider was that the
decreased urinary mercury levels were a measure of “a decreased ability
to excrete mercury” via the kidney. The most straight-forward
explanation for this data is that after two years exposure to mercury
vapor from amalgams the children are losing their ability to excrete
mercury through the kidneys. This explanation is consistent
with
amalgam exposure affecting the kidney porphyrin synthetic pathway and
causing additional metabolic problems. This data, data from
the
articles that conclude dental amalgams are safe for all children,
actually proves that basing any safety of dental amalgams on single day
a year urinary mercury levels is totally invalid. Thirdly,
according to most reports that have directly studied the issue, a very
high percentage of mercury is excreted not by the urinary route but by
the fecal route. One study found that the ratio was 12 to 1
with
the fecal excretion being over 90% of the total.37 Therefore,
using a single, yearly spot urine analysis to account for mercury
exposure appears to be a scientifically unacceptable procedure to
evaluate the mercury exposure of these children based on the fact that
urine most likely is a minor excretory route. Fourthly,
why weren’t the porphyrin profiles of these study children evaluated
rapidly and reported? One would be surprised if they remained
normal in light of the reported effects on the porphyrin profiles of
dentists and dental hygienist exposed to mercury vapor that has been in
the literature for some time now.23-25 In fact, the
behavior of the authors of these papers is symptomatic of developing a
study that will show no significant differences while avoiding any
experiments that have been shown to react more rapidly and more
sensitively to mercury toxicity. Mercury
based LOELs and NOELs from non-human data have another
short-coming. For example, it has been known for some time
that
the relative toxicity of mercury containing compounds appears to be
dramatically affected by the presence of other compounds and heavy
metals that synergistically enhance the toxicity of mercury.
For
example, mixing of an LD1 dose of mercury with a 1/20 dilution of an
LD1 of lead produces a mixture with an LD100, not an LD2 or less that
would be expected with additive toxicities1. Since there is
considerable concern about the lead levels in the drinking water in our
nation’s capital it seems the citizens there would be under more toxic
stress than in locations with little or no lead exposure.
This
data strongly implies that synergistic toxicity of mercury with other
readily available toxic metals would dramatically enhance the toxicity
and lower the LOEL and NOEL values. What
we do know from a study entitled “Mercury in Brain Tissue of Infants”
is that the mercury levels in the brain stem of infants from California
had a mean of over 55ng Hg/g wet weight of tissue. This is
roughly 55 micrograms/kg. Assuming a kg of tissue is about 1
liter then the mercury concentration is about 275 nanomolar.
It
has been clearly shown that neurons in culture are destroyed by levels
of mercury much less than 50 nanomolar with no synergistic compounds,
such as lead, aluminum or cadmium, present to enhance mercury
toxicity28. This level of mercury is especially toxic in the
presence of testosterone whereas estradiol affords
protection.
Given the findings of elevated testosterone in the amniotic fluid of
mothers who gave birth to autism spectrum children this has to be a
concern. Consider also
that mercury from different exposures are at the least additive in
their toxicity effects. A report from the National Center for
Health Statistics, Center for Disease Control and Health in 2003 stated
that approximately 8% of women of child-bearing age had concentrations
of mercury higher than the USA EPA’s recommended reference dose, below
which exposures are considered to be without adverse
effects3.
This blood level in women caused more recent concern with data showing
that cord blood was 1.7 times the level of maternal blood indicating
that more than 8% of children being born are being exposed to toxic
levels of mercury from their mother’s blood. These
individuals
would definitely be more at risk during transient mercury exposures
than would the general population and are certainly not comparable to
animals in a pristine environment being exposed to only one mercury
toxicant. Therefore, a 10-fold reduction for mercury in
medicaments, as is common in converting a LOEL into a NOEL, most likely
does not provide the protection factor as it would for exposures to
most non-mercury toxicants that have less defined synergistic
partners. It is
well known that diet plays a major role in the ability of mammals to
excrete mercury2. Studies have shown that three different
diets
fed to adult female mice (high protein synthetic diet; standard rat
chow diet; milk diet) dramatically changed the rate of fecal excretion
of mercury. Mercury was introduced orally as methyl-mercury
(MeHg) and diet caused differential rates of whole body mercury
elimination. The results showed that mice fed a synthetic,
high
protein diet had the lowest tissues levels of mercury whereas those fed
the milk diet retained the highest mercury levels. This was
confirmed by the total percentage of mercury excreted in the feces
after 6 days of 43%, 29% and 11% in the high protein, rat chow and milk
diets, respectively Therefore, diet plays a major role in the fecal
excretion rates of mercury from an organic mercury compound.
As
expected, diet also affected the excretion rate of mercury from body
tissues. The retention of mercury in the body of a child on a
milk diet would be much higher than for a child not on a milk
diet. Twenty-year-old studies report that suckling animals
absorb
about 50% of Hg2+ versus 5% in non-suckling animals11. Since
the
level of toxicity would likely increase with retention time, especially
if the exposure rate to mercury were consistent over any significant
period of time, then the diet can have a major affect on the calculated
NOELs and minimum acceptable daily levels. Toxicity
is also known to vary with the chemical species of mercury that exists
in the body’s tissues. Diets can change this as it was
observed
that foods ingested played a major role in the mercury chemical species
that existed in the mice given oral doses of MeHg. Hg2+ was the species
found at the highest level in test animals on a synthetic protein diet
(35.3%) and was the lowest in test animals on a milk diet
(6.6%).
It is reasonable to predict that diet changes the conversion of MeHg to
Hg2+ and would likely do so for other organic mercury compounds, such
as ethyl-mercury (Et-Hg), which is released from thimerosal.
Since the toxicity of organic mercury compounds (e.g. MeHg versus EtHg)
which partition similar to mercury vapor has been suggested to be
greater than Hg2+ (inorganic mercury) and toxicity is partially
determined by the rate that the compound is converted to Hg2+ after the
chemical nature of the mercury source has allowed effective
partitioning across the blood brain barrier. Other
studies confirm that the renal uptake and toxicity of circulating
mercury is significantly enhanced in rats by the co-ingestion of the
essential amino acid L-cysteine8 and disease marker homocysteine9.
Elevated blood homocysteine level is a major risk factor for
cardiovascular disease. Therefore, humans with risk for
cardiovascular disease would be more at risk for low level mercury
exposure than others. This would also be true for Alzheimer’s disease
where elevated homocysteine has also been reported.32
Medical
status
is of concern when considering mercury compound toxicity, especially
when bacterial infections are being treated. Treatment of
adult
female mice with widely used antibiotics 7 days prior to MeHg exposure
dramatically influenced mercury retention of tissues from mice
receiving similar organic mercury exposures2. The calculated
whole body mercury elimination half-times from day 1 to day 6 varied
from 34, 10 and 5 days for mice fed a milk diet, mice chow or high
protein diet respectively. A remarkable 6.8 fold increase in
retention half-life existed between a milk diet and high protein diet
that was caused by antibiotic treatment that also changed the gut
microflora. Antibiotic treatment dropped the fecal mercury
excretion to near zero in the high protein and milk diets and to less
than 8% with the mouse chow diet. Therefore, it can be
concluded
that the relative toxicity of mercury and mercury compounds would be
dramatically increased if the test subject were on antibiotics. The
toxicity of mercury vapor is dependent on retention and excretion and
these vectors are dramatically affected by diet and antibiotic
treatment as well as other factors. This makes it
nearly
impossible to define a safe level of exposure for mothers and their
infants in utero. Being exposed minute by minute to mercury
vapor
for years has never been established as safe, but reasonable concerns
have been effectively nullified by the dental organizations giving
their opinions regarding perceived safety. It is incredible that the
responsible US government agencies and the organizations and companies
using dental amalgam have not felt the need to produce such
research. Especially with the obvious severe toxic nature of
mercury vapor and the ease with which the amount of mercury vapor that
would escape from a dental amalgam could be measured. The quality data
is just not available in the literature to evaluate and determine the
level at which mercury vapor is emitted from the various types of
dental amalgam. However, it is my opinion that the reason is
not
because it would be difficult to do, but to do so would place the
manufacturers and users of dental amalgam at risk for major lawsuits
and they would lose their businesses. The
process of placing or removing dental amalgam’s in a pregnant mother
has to increase the exposure of the in utero infant to elevated mercury
vapors as it would dramatically increase the mother’s blood mercury
levels. It is well known that mercury vapor can cross the
placenta, and is even concentrated in the cord blood versus the
mother’s blood. Other studies have shown that mercury
increases
in the birth hair of normal children in response to increasing dental
amalgams in the birth mother20. Other similar studies point
to
aberrant mercury hair levels in children with neurological
problems20,21. There can be little doubt that the exposure of a
pregnant mother to mercury vapor by aggressive dental amalgam treatment
could cause harm to her infant in utero. Finally,
based on the exacerbation of mercury toxicity by variation in human sex
hormone presence, dietary factors, other toxic metals, antibiotic
usage, and genetic susceptibility factors there is no intelligent way
that anyone can say they know that a specific exposure to mercury to an
infant in utero or an aged ill person would not cause a significant
affect on their health.
CONCLUSIONS:
First, it is well known that blood, urine and hair mercury levels are
not a good measure of human mercury body burden. It is the
retained mercury that causes neurotoxicity, not the blood or urine
levels. Second, it is well known that genetic susceptibility,
health, sex, diet, use of antibiotics, age, etc. can dramatically
affect the retention of mercury by humans and animals and affect the
toxicity level. Therefore, the exposure to mercury in a group
of
healthy, mid-age, male factory workers is not a good measure of safe
inhalation amounts of mercury for all. In fact, the only
proven
safe level of chronic mercury exposure is no exposure at all.
We know that alcohol is a toxic material and mere presence in the blood
stream or oral air can lead to a conviction. However, the
presence of the more toxic mercury, known to have adverse effects of a
more permanent nature in humans, is not judged by the FDA based on its
mere presence, it is required that studies be done to prove it has
toxic effects in humans--- but only if it comes from dental amalgams or
vaccines. Yet the cost of such studies are such that only the
USA
government agencies such as the FDA or CDC could afford to do such
studies or have the power to insist that the manufacturers of amalgams
do so. However, this is something the FDA and CDC have
steadfastly refused to require. No other compound, drug, etc.
seems to have this special consideration, which is amazing in light of
the known, potent neurotoxicity of mercury vapor.
When agencies such as the EPA and National Academy of Sciences report
that a large percentage of American women have mercury levels which
render susceptibility to neurological damage to any child they would
give birth to, and when the CDC states that 1 in 6 American children
have neurodevelopmental disorders, and when solid laboratory research
shows that the major contributor to human mercury body burden comes
from dental amalgam it seems as if the FDA and CDC are being remiss in
performing their assigned task of protecting the American public from
toxic damage by not eliminating or phasing out the use of dental
amalgam.
The above is especially true when studies on dentists themselves show
that 85% have aberrant porphyrin metabolism caused by mercury exposure
and 15% of this group have a more severe response that is correlated to
a genetic susceptibility. This genetic susceptibility also
seems
to apply to children in the autism spectrum disorders group which has
lead to the recent epidemic of neurological problems in
children.
French researchers have also shown that a high percentage of autistic
children have the same aberrant porphyrin profile as the dentists
exposed to amalgam mercury vapors, and that this aberrancy can be
reversed by chelation of the mercury from their bodies. The
FDA
white paper seems not at all concerned that our dentists and dental
technicians may be suffering from an occupational exposure to mercury,
or is it they are afraid that accepting this fact will be detrimental
to their goal of keeping amalgams as a dental filling material?
No other material has near the number of close mimicking abilities of
mercury with regards to producing the aberrant biochemistry and
producing the known diagnostic hallmarks of Alzheimer’s disease (AD)
than mercury. Many Americans have grams of mercury vapor
releasing amalgams within two inches of their brains and it is
inarguable that this minute by minute exposure for 20 to 50 plus years
would not push those condemned to die with AD into dementia earlier,
and at a great cost to their families and our medical system.
Yet, in spite of all of this knowledge American Dentistry and Medicine
remains silent and in active denial that these modern man diseases,
which first occurred after the dental and medical introduction of the
use of mercury, may be caused or even exacerbate these awful
neurological illnesses for which medicine has no explanation for.
First do no harm, this is one of the major mantras of
medicine.
It seems as if the FDA has chosen to ignore this advice in the past as
certainly there can be no doubt about amalgam’s contribution to human
mercury body burden and the opinion of the EPA and NAS that this
mercury body burden is not healthy and most likely is quite damaging.
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