
The ADA Letter To Dan Burton |
Editors
Note:
This letter was originally sent to Congressman Dan Burton
and published on the ADA website, but has since been removed
from public viewing by the ADA. We publish the letter here
in its entirety under the "fair use" principle of
US copyright law. May
11, 2001
The
Honorable Dan Burton
Chairman
Committee on Government Reform
U.S. House of Representatives
Washington, D.C. 20515
RE:
Autism - Why the Increased Rates? A One Year Update
Dear
Mr. Chairman:
The
American Dental Association (ADA) requests that the Committee
on
Government Reform accept this letter as a statement for
the record for the
committee's hearing on April 25, entitled "Autism --
Why the Increased Rates? A One Year
Update."
During
the hearing, Dr. Boyd E. Haley stated in his testimony that
elementary mercury from dental amalgams could work synergistically
with other
ethyl-mercury sources and have a cumulative toxic affect
on the body. Dr.
Haley postulated that this could be a potential cause of
autism and Alzheimer's disease.
There
is no scientifically valid evidence linking either autism
or
Alzheimer's disease with dental amalgam. And there is no
scientifically valid evidence
demonstrating in vivo transformation of inorganic or mercury
vapor into
organo mercury species in individuals occupationally exposed
to amalgam mercury
vapor. (Chang, S.B. et al., Factors Affecting Blood Mercury
Concentrations
in Practicing Dentists; Journal of Dental Research 1992,
71(1) 66-74).
Based
on currently available scientific evidence, the ADA believes
that
dental amalgam is a safe, affordable and durable material
for all but a handful of
individuals who are allergic to one of its components. It
contains a mixture
of metals such as silver, copper and tin, in addition to
mercury, which
chemically binds these components into a hard, stable and
safe substance.
Dental amalgam has been used for more than 150 years and,
during that time, has established
an extensively reviewed record of safety and effectiveness.
Issued
in late 1997, the FDI World Dental Federation and the World
Health
Organization consensus statement on dental amalgam stated,
"No controlled
studies have been published demonstrating systemic adverse
effects from
amalgam restorations." The document also states that,
aside from rare
instances of local side effects of allergic reactions, "the
small amount of mercury
released from amalgam restorations, especially during placement
and removal, has not
been shown to cause any, adverse health effects."
The
ADA's Council on Scientific Affairs' 1998 report on its
review of the
recent scientific literature on amalgam states: "The
Council concludes that,
based on available scientific information, amalgam continues
to be a safe
and effective restorative material." The Council's
report also states, "There
currently appears to be no justification for discontinuing
the use of dental
amalgam."
In an
article published in the February 1999 issue of the Journal
of the
American Dental Association, researchers report finding
"no significant
association of Alzheimer's disease with the number, surface
area or history
of having dental amalgam restorations" and "no
statistically significant
differences in brain mercury levels between subjects with
Alzheimer's
disease and control subjects."
The
U.S. Public Health Service issued a report in 1993 stating
there is no
health reason not to use amalgam, except in the extremely
rare case of the
patient who is allergic to a component of amalgam. This
supports the
findings of the Food and Drug Administration, the National
Institutes of Health
Technology Assessment Conference and the National Institute
of Dental and
Craniofacial Research, that dental amalgam is a safe and
effective restorative
material.
There
have been several peer reviewed scientific studies concerning
the
safety of dental amalgam. These studies disprove any link
between dental amalgam
and various medical conditions. We have listed some of them
below:
* Dahl
JE, Sundby J, Hensten-Pettersen A, Jacobsen N. " Dental
Workplace
exposure and effect on fertility " Scand J Work Environ
Health 1999
Jun;25(3):285-90.
The study groups consisted of 558 female dental surgeons
(1/3 of whom placed
more than 50 fillings a week) and 450 high school teachers
(control) that
had given birth in Norway to at least 1 living child. The
study comprised data
from a total of 1408 pregnancies. The effects of practicing
dentistry and of
the given workplace exposure on fertility were analyzed
with the discrete
proportional hazard regression method. Conclusions: Occupational
exposures had no clear adverse effects on
fertility among the female dental surgeons studied.
* Schuurs
AH. " Reproductive toxicity of occupational mercury.
A review
of the literature" J. Dent 1999;27(4):249-56. This
paper provides insight into the potential reproductive effects
on
handling dental silver amalgam. Both animals and case reports
and
epidemiological studies were reviewed. Conclusions: The
studies conclude that negative
reproductive effects from exposure to mercury in the dental
office are
unproven. Consequently, given the low amounts of mercury
stemming from
dental amalgam fillings, the population at large are at
even less risk than dental
staff.
* Saxe
SR, Wekstein MW et al. "Alzheimer's disease, dental
amalgam and
mercury", JADA 1999 Feb;130(2):191-9
This study consisted of 68 human subjects with diagnosed
Alzheimer's disease
and 33 control subjects without Alzheimer's to determine
mercury levels in
multiple brain regions at autopsy and to ascertain the subjects'
dental
amalgam status and history. Conclusions: Mercury in dental
amalgam
restorations does not appear to be a neurotoxic factor in
the pathogenesis of this disease.
The authors found that brain mercury levels are not associated
with dental
amalgam, either from existing amalgam restorations or according
to subjects'
dental amalgam restoration history. Furthermore, dental
amalgam restorations,
regardless of number, occlusal surface area or time, do
not relate to brain
mercury level.
* Ahlqwist
M, Bengtsson C et al, "Serum mercury concentration
in
relation to survival, symptoms, and diseases: results from
the prospective
population study of women in Gotherburg, Sweden. Acta Odontol
Scand 1999 June;
57(3):168-74
This prospective population study of women in Gothenburg,
Sweden was started
in 1968-69 and comprised of 1462 women aged 38-60 years
at baseline.
Follow-up studies were conducted in 1974-75, 1980-81 and
1992-93. Conclusions: No
statistically significant correlation was observed between
dental amalgam
and the incidence of diabetes, myocardial infarction, stroke,
or cancer. No
association was established between disease and mercury
on a population
basis in middle-aged and older women.
The
National Institute of Dental and Craniofacial Research is
currently
supporting two very large clinical trials on the health
effects of dental
amalgam. Studies underway for several years each in Portugal
and the
Northeastern United States involve not only direct neurophysiological
measures but also behavioral and cognitive functional assessments.
In addition, the
trials are monitoring the impact of amalgam on immune function,
antibiotic
resistance and renal function. Preliminary findings from
these studies are
consistent with any number of small and large epidemiological
studies
published over the years concerning the health effects of
dental amalgam.
The
ADA supports ongoing research in the development of new
materials that
it hopes will someday prove to be as safe and effective
as dental amalgam.
However, the ADA continues to believe that amalgam is a
valuable, viable and
safe choice for dental patients and concurs with the findings
of the U.S.
Public Health Service that amalgam has "continuing
value in maintaining oral
health."
Sincerely,
Signed
Robert
M. Anderton, D.D.S., J.D., LL.M.
President
RMA:MT:chf
Document
Posted: May 11, 2001
Page Updated: May 11, 2001 |
Dr.
Boyd Haley Rebuts the American Dental Association
Position on Mercury-Amalgam Safety |
|
23
May 2001 The
Honorable Dan Burton
Chairman
Committee on Government Reform
U.S. House of Representatives
Washington, D.C.
RE:
May 11th letter by Robert M. Anderton, D.D.S., J.D., LL.M.
and President of the ADA, challenging my statement to the
Committee on Government Reform looking at the topic, Autism-Why
the Increased Rates? A One Year Update.
Dear
Mr. Chairman:
At the
April 25th meeting of your committee I gave testimony that
the President of the American Dental Association (ADA) takes
exception to in a letter sent to you dated 11 May 2001.
Quoting from that letter the testimony the ADA dislikes
is "that elementary mercury from dental amalgam
could work synergistically with other ethyl-mercury sources
and have a cumulative toxic effect on the body. Dr. Haley
postulated that this could be a potential cause of autism
and Alzheimer's disease." I stand by my statement as
a sensible concern based on published scientific research
regarding synergist toxicities caused by two very toxic
agents, mercury and the organic mercury compound thimerosal.
This concern is elevated since mercury exposure from amalgams
to a pregnant mother concentrates in the fetus and a single
vaccine given to a six-pound newborn is the equivalent of
giving a 180-pound adult 30 vaccinations on the same day.
Include in this the toxic effects of high levels of aluminum
and formaldehyde contained in some vaccines, and the synergist
toxicity could be increased to unknown levels. Further,
it is very well known that infants do not produce significant
levels of bile or have adult renal capacity for several
months after birth. Bilary transport is the major biochemical
route by which mercury is removed from the body, and infants
cannot do this very well. They also do not possess the renal
(kidney) capacity to remove aluminum. Additionally, mercury
is a well-known inhibitor of kidney function. Common sense
indicates that the concern I expressed should be taken seriously
since we do not know how combined toxicities effect humans,
especially in utero. Consider the current epidemic
death on birth of over 500 foals from apparently healthy
mares around Lexington, KY. These deaths were identified
as being due to a low level toxicity delivered by caterpillars
eating poison plants and later, on migration, depositing
their waste products on grass being eaten by the mares.
The point being it is the infant in utero that suffered
most on exposure to low level, toxins, not the mother. Combined
mercury toxicities can be devastating as I reference below
and in the many references available on the www.altcorp.com
website. What is needed is research by non-biased scientists
to clarify this, something our FDA and NIDCR have refused
to do. As the American public find out what has happened
regarding this issue, they will be quite angry. This is
a biomedical science issue that should have been resolved
a long time ago by the responsible federal agencies.
Below
I present detailed and referenced information supporting
my case and respond to various statements made by the ADA
President that I believe to be misleading and sometimes
flagrantly wrong. The ADA seems to think it has the right
to select which research it believes and to trash that research
that says it is wrong, even though the latter represents
the bulk of published research. To address the issues raised
by the ADA President in his letter I will go in sequential
order of the comments made in the letter placing the ADA
comments in italics and providing scientific references
for my conclusions.
"There
is no scientifically valid evidence linking either autism
or Alzheimer's disease with dental amalgam". First,
mercury is a well-known, potent neurotoxicant, and common
sense would lead to the conclusion that severe neurotoxins
would exacerbate all neurological disorders, including Parkinson's,
ALS, MS, autism and AD. Several research papers in refereed,
high quality journals and scientific publications have shown
that mercury inhibits the same enzymes in normal brain tissues
as are inhibited in AD brain samples (1a-c, 2, 3). AD is
pathologically confirmed post-mortem by the appearance of
neuro-fibillary tangles (NFTs) and amyloid plaques in brain
tissue. Published research, within the past year, has shown
that exposure of neurons in culture to sub-lethal doses
of mercury (much less than is observed in human brain tissue)
causes the formation of NFTs (4), the increased secretion
of amyloid protein and the hyper-phosphorylation of a protein
called Tau (5). All three of these mercury-induced aberrances
are regularly identified as the major diagnostic markers
for AD. In the manuscript published in the J. of Neurochemistry
(5) the authors state "These results indicate that
mercury may play a role in the patho-physiological mechanisms
of AD." In most of these experiments, mercury and only
mercury among the several toxic heavy metals tested, caused
the AD related responses reported. Many medically trained
individuals would agree that if something causes the appearance
of the pathological hallmarks confirming the disease then
it likely causes the disease. I at least have limited my
claims to exacerbation of these diseases to err on the side
of caution.
Further,
consider this about AD. A study of 500 sets of identical
twins from World War II era lead to the conclusion that
sporadic AD which represents 90% of the cases was not a
directly inherited disease. In many cases one twin would
get AD and the other would not. Genetic susceptibility is
involved, but a toxic exposure is required (e.g., if you
are genetically susceptible to being an alcoholic you still
need to be exposed to alcohol to become one). The work by
Rose's group at Johns Hopkins University implicates APO-E
genotype as a "risk" factor with APO-E2 being
protective and APO-E4 being a major risk factor. APO-E2
has the ability to protect the brain from mercury by having
two additional thiol-groups to bind mercury appearing in
the cerebrospinal fluid whereas APO-E4 does not have this
additional capability (1). This may explain the proven genetic
susceptibility to AD of the APO-E4 carriers.
NIH
has spent hundreds of millions of dollars to find a causal
factor for AD. Yet, no virus, yeast or bacteria has been
identified so the cause remains unknown to general science.
The rate of AD per 1,000 population is nearly the same in
California, Michigan, Maine, North Carolina, Florida, Texas,
etc. It is not significantly different for rural versus
urban individuals, or factory workers versus those with
outside jobs. So the primary toxicant that may be involved
is most likely not environmental. Therefore, it must be
a very personal toxicant, like what you put in your mouth.
Since we place grams of a neurotoxic metal, mercury, in
our mouths in the form of dental amalgam this makes it a
good suspect for the exacerbation of AD---not that all would
be affected, just those that are genetically susceptible,
or those who become ill enough to fall prey to the toxicity,
or those that are also exposed to another synergistic toxin
(see below).
The
one fact that ties mercury into a major suspect for AD is
the fact that most of the proteins/enzymes that are inhibited
in AD brain are thiol-sensitive enzymes. Mercury is one
of the most potent chemical inhibitors of thiol-sensitive
enzymes and mercury vapor easily penetrates into the central
nervous system (2). Mercury is not the only toxicant to
inhibit thiol-sensitive enzymes. Thimerosal and lead will
do this also as well as reactive oxygen compounds created
in oxidative stress and many other industrial compounds.
However, mercury has been reported to be significantly elevated
in AD brain (14a,b, 15). Mercury is in many mouths being
emitted from dental amalgam and absolutely would exacerbate
the clinical condition identified as AD. Therefore, mercury
should be considered as a causal contributor since mercury
can produce the two pathological hallmarks of the disease
and inhibits the same thiol-sensitive enzymes that are dramatically
inhibited in AD brain.
It is
documented by a 1991 World Health Organization report that
dental amalgams constitute the major human exposure to mercury.
Grams of mercury are in the mouths of individuals with several
amalgam fillings. Further, the level of blood and urine
mercury positively correlates with the number of amalgam
fillings. This was confirmed by a recently published NIH
funded study (6). Therefore, I fail to see the ADA's viewpoint
that there is no scientifically valid evidence linking mercury
from amalgams to exacerbating AD, especially since mercury
produces the diagnostic hallmarks of AD (4,5). The ADA hides
behind the fact that there has not been an epidemiological
study to attempt to correlate mercury exposure and AD. However,
absence of proof is not proof of absence. This also begs
the question why the ADA, the FDA and the National Institutes
of Dental Craniofacial Research (NIDCR) have not pushed
for such a study? These agencies know this would be immensely
expensive and only the U.S. government could afford to support
any reliable long-term study. Yet, these same responsible
agencies have failed to confirm as safe the placing into
the mouth of Americans grams of the most toxic heavy metal
Americans are exposed to. The dental branch of the FDA has
steadfastly refused to investigate the toxic potential of
dental amalgam.
Look
at the references in the ADA letter! Even they must quote
Scandinavian literature to support their contentions of
safety, and even then they have to reference papers on fertility
instead of neurotoxicity! Where is the ADA, FDA and NIDCR
supported U.S. research in this area? Go to the NIH web-sites
and look for research on the safety of mercury from amalgams,
or try to find an NIH study concerning possible mercury
involvement in any common neurological diseases. NIH does
support research on methyl-mercury, as we seem to like beating
up on the fishing industry whilst leaving the dental industry
alone. However, according to the NIH study about 90% of
the mercury in our bodies is elemental mercury, not methyl-mercury,
showing the exposure is more likely from dental amalgams
rather than fish (6). Support at NIH has been very sparse
for investigating the relationship of elemental mercury
exposure to neurological diseases.
"And
there is no scientifically valid evidence demonstrating
in vivo transformation of inorganic mercury into
organo mercury species in individuals occupationally exposed
to amalgam mercury vapor". There was a paper
published entitled "Methylation of Mercury from Dental
Amalgam and Mercuric Chloride by Oral Streptococci in vitro"
(19). This strongly indicates that "organo mercury
species" are indeed capable of being made in the human
body and may explain the appearance of methyl-mercury in
the blood and urine of individuals who don't eat seafood.
Further,
periodontal disease is considered one of the major risk
factors for stroke, heart and cardiovascular disease and
late onset, insulin independent diabetes. Many studies of
the toxicants produced in periodontal disease have identified
hydrogen sulfide (H2S) and methane-thiol (CH3SH) as major
toxic products of infective anerobic bacteria in the mouth
metabolizing the amino acids cysteine and methionine, respectively.
These volatile thiol-compounds are what cause bad-breath!
Methane-thiol (CH3SH) would react immediately and spontaneously
in the mouth with amalgam generated mercury cation to produce
the following two compounds, CH3S-HgCl and CH3S-Hg-SCH3,
which are organo-mercurial compounds (check this out with
any competent chemist). They are also very similar in structure
to methyl-mercury (CH3-HgCl) and dimethyl-mercury (CH3-Hg-CH3),
the latter which caused the highly publicized death of a
University of Dartmouth chemistry professor 10 months after
she spilled two drops on her gloved hand. We have synthesized
CH3S-HgCl and CH3-Hg-CH3 in my laboratory and tested their
toxicity in comparison to Hg2+. As expected, they were both
more toxic than Hg2+ and this data is available on the www.altcorp.com
web-site. Therefore, the ADA President is badly misinformed
on this issue. Additionally, I am amazed that the researchers
at the ADA and NIDCR did not previously report on this obvious
chemistry as I would imagine this is the kind of topic they
should be addressing.
"Based
on currently available scientific evidence, the ADA believes
that dental amalgam is a safe, affordable and durable
material for all but a handful of individuals who are
allergic to one of its components. It contains a mixture
of metals such as silver, copper and tin, in addition
to mercury, which chemically binds these components into
a hard, stable and safe substance." This is
a totally wrong statement unless you underline the "ADA
believes" and define how big is a "handful
of individuals". Sensible people want "believes"
replaced with "knows" and a "handful"
replaced with a "hard number". Amalgams emit dangerous
levels of mercury and the ADA absolutely refuses to accept
this fact or even to study the possibility. Otherwise, the
ADA administrators seem to be unable to separate fact from
fiction. Consider, if they wanted to destroy my argument
on amalgam toxicity they would reference several solid,
refereed publication showing that mercury is not emitted
from dental amalgams---but they cannot do this with even
one article. They always state the "estimate"
is that a very, very, very small amount. Competent, well-informed
researchers don't use the evasive language used in the ADA
President's letter. They would state the amount is so many
micrograms mercury released per centimeter squared amalgam
surface area and a "handful of individuals" would
be a percentage of our population! Lets look at the published
literature.
First,
careful evaluation of the amount of mercury emitted from
a commonly used dental amalgam in a test tube with 10 ml
of water was presented in an article entitled "Long-term
Dissolution of Mercury from a Non-Mercury-Releasing Amalgam".
This study showed that "the over-all mean release of
mercury was 43.5 ± 3.2 micrograms per cm2/day, and
the amount remained fairly constant during the duration
of the experiments (2 years)" (7). This was without
pressure, heat or galvanism as would have occurred if the
amalgams were in a human mouth. Further, research where
amalgams containing radioactive mercury were placed in sheep
and monkeys, showed the radioactivity collecting in all
body tissues and especially high in the jaw and facial bones.
(8,9). Another publication, from a major U.S. School of
Dentistry, stated that solutions in which amalgams had been
soaked were "severely cytotoxic initially when Zn release
was highest" (13). Zn is a needed element for body
health and is found in very low percentages in dental amalgams
when compared to mercury and why mercury was not mentioned
in the abstract of this publication baffles me. Why would
the statement be true? Because Zn2+ is a synergist that
enhances mercury toxicity! However, does this sound like
amalgams are a safe, stable material? We have repeated similar
amalgam soaking experiments in my laboratory and the results
can be seen at www.altcorp.com. Cadmium (from smoking),
lead, zinc and other heavy metals enhanced mercury toxicity
as expected (this research is currently being prepared for
publication).
The
ADA claim that a zinc oxide layer is formed on the amalgams
that decreases mercury release is true, if you don't use
the teeth. The zinc oxide layer would be easily removed
by slight abrasion such as chewing food or brushing the
teeth. Further, my laboratory has confirmed that solutions
in which amalgams have been soaked can cause the inhibition
of brain proteins that are inhibited by adding mercury chloride,
and these are the same enzymes inhibited in AD brain samples.
Further,
mercury emitting from a dental amalgam can be easily detected
using the same mercury vapor analysis instrument used by
OSHA and the EPA to monitor mercury levels. Anyone who does
not believe mercury is emitted from amalgams should consider
doing the following. Have your local dentist make 10 amalgams
using the same material he/she places in your mouth. Take
these 10 amalgams to your nearest research university's
department of chemistry or toxicology department and have
them determine how much mercury is being emitted. For example,
have them calculate how long it would take a single spill
of hardened amalgam to make a gallon of water too toxic
to pass EPA standards as drinking water. You will then have
an answer from an unbiased, solid group of scientists who
are trained to do such determinations. Also, remember the
level of mercury they measure would not include the increase
that would occur with amalgams in the mouth where chewing,
grinding your teeth, drinking hot liquids and galvanism
greatly increase the release of mercury. Since this approach
can be easily done by anyone don't you think the ADA, FDA
and other amalgam supporters would have this published by
now if the level of mercury released was below the danger
level?
Here
is their attempt. According to an ADA spokesman he has "estimated"
that only 0.08 micrograms of mercury per amalgam per day
is taken into the human body. Applying simple math to this
"estimate" of 0.08 micrograms/ day one would divide
this amount by 8,640 (24 hours/day X 60 minutes/hour X 6
ten second intervals/minute) to determine the amount of
mercury in micrograms available for a ten second mercury
vapor analysis. Consider that somewhere between one-half
to five-sixths of the mercury released would be into the
tooth (that area of the amalgam that exists below the visibly
exposed amalgam surface) and not into the oral air. In addition,
some mercury in the oral air would be rapidly absorbed into
the saliva and oral mucosa (mercury loves hydrophobic cell
membranes) and also not be measured by the mercury analyzer.
Further, as the mercury analyzer pulls mercury containing
oral air into the analysis chamber, mercury free ambient
air rushes into the oral cavity decreasing the mercury concentration.
Taking all of this into account you can calculate that most
mercury analyzers could not detect this "estimated"
0.08 micrograms/day level of mercury even if you had several
amalgams. However, the fact is that it is quite easy to
detect mercury emitting from one amalgam using these analyzers.
Therefore, the "estimate" by this ADA spokesman
is way to low. Also, if you gently rub the amalgam with
a tooth-brush the amount of mercury emitted goes up dramatically.
This is a test anyone can do and demonstrate to any group.
The ADA spokesmen state that the mercury vapor analyzer
is not accurate at determining oral mercury levels and they
are quite correct. However, using this instrument would
greatly underestimate the amount of mercury exiting the
amalgam. The very fact that the mercury analyzer detects
high levels of oral mercury strongly indicates the emitted
amount of mercury is too high to be acceptable.
Mercury
release from dental amalgams is also the reason OSHA has
used this analyzer to make the dentists place unused amalgam
in a sealed container under liquid glycerin. This is done
so that the mercury vapors from the amalgams will not contaminate
the dental office making it an unsafe place to work. This
is also the reason the EPA insists that removed amalgam
filling and extracted teeth containing amalgam material
be picked up and disposed of as toxic waste. Apparently,
the only safe place for amalgams is in the human mouth if
you believe what the ADA believes.
"Amalgams
have been used for 150 years and, during that time, has
established an extensively reviewed record of safety
and effectiveness." First, what other aspect of industry
or medicine is still using the same basic manufactured material
that they used 150 years ago? One has to ask the question
as to what has hindered the progress of development of better
and safer dental materials? Also, consider that in the early
1900s the average life expectancy of most Americans was
about 50 years of age and most of them could not afford
dental fillings. Fifty to sixty years is much less than
the average age of onset of AD. Further, amalgams became
more available to most working class Americans after World
War II, or in the early 1950s. The greatest increase in
the use of amalgam occurred at about this time and these
'baby boomers are the great ongoing amalgam experiment'.
They are now reaching the age where AD appears and have
lived most of their lives carrying amalgam fillings. They
also wonder what is causing their chronic fatigue as the
physicians can find nothing systemically wrong with them.
I would encourage all concerned to contact the health experts
on the rate of increase of AD in the U.S.A. at this time.
Consider the cost it will place on the taxpayer and how
much we would save if we could even remove the exacerbation
factors that might speed up the onset of AD. I must point
out that the "extensively reviewed record of safety"
mentioned in the ADA letter was mostly done by dentists
and committees dominated by ADA dentists. Also, much of
the "safety opinion" was developed long before
words like Alzheimer's disease and chronic fatigue were
commonplace. Further, these were "reviews" and
not carefully documented studies based on scientific experimentation
and done by unqualified dentists, not medical scientists.
Dentists are not trained to do basic research, nor are they
trained in toxicology. Furthermore, the ADA does have a
vested interest in keeping amalgam use legitimate. The ADA
was founded on using amalgam technology and participated
in patenting and licensing amalgam technology. One has to
question why there has not been a general outcry by the
bulk of well-meaning dentists and their patients and this
question should be addressed. The International Association
of Oral Medicine and Toxicology, started by American &
Canadian dentists, does adamantly disagree with the ADA
on the issue of safety of dental amalgams and this organization
has the mantra of "Show me your science" with
regards to all dental issues.
The
ADA, through state dental boards stacked with ADA members,
has instigated a "gag order" preventing dentists
from even mentioning to their patients that amalgams are
50% mercury. Dentists cannot state that mercury is neurotoxic
and emits from amalgams and that the dental patient should
consider this as they select the tooth filling material
they want used. If a dentist informs a patient of these
very truthful facts he will be consider not to be practicing
good dentistry and his license will be in jeopardy. Attacking
a person's freedom of speech because he is telling the truth
and causing serious questions to be asked about the protocols
pushed by a bureaucracy (the ADA) makes me seriously question
the commitment the ADA has for the health of the American
people. The negative stand taken by many state dental boards
against even informing the patients about the mercury content
of amalgams and the other filling choices they have does
not speak well for the organized dental profession. What
medical group would give a treatment to a patient without
telling them of the risks involved?
"Issued
late in 1997, the FDI World Dental Federation and the World
Health Organization consensus statement on dental amalgam
stated "No controlled studies have been published
demonstrating systemic adverse effects from amalgam restorations.""
My first comment would be to question "who staffed
these committees and what percentage were connected to the
ADA though the NIDCR or the FDA dental materials branch
or other relationships?" We appear to have the foxes
guarding the henhouse! Then I would again point out that
"absence of proof is not proof of absence". I
would then ask 'have any controlled studies been done and
if not, why not?' If the ADA dentists insist on placing
amalgams in the mouth, are they not required to show it
is safe, not the other way around? Should not the ADA and
others concerned push to require the FDA to prove amalgams
are safe instead of totally ducking this issue. Go to the
FDA dental materials web-site and try to find any evaluation
of amalgam safety---you will not succeed. The dental branch
of the FDA refuses to do a safety study on amalgams and
this is shame on our government.
"the
small amount of mercury released from amalgam restorations,
especially during placement and removal, has not been
shown to cause anyadverse effects." This increase in
mercury exposure has also not been shown to be safe by proving
it does not cause any adverse effects! Are we to believe
this elevated exposure to a toxic metal is good for us?
If one were in a building that caused the rise in blood/urine
mercury that appears after dental amalgam removal, then
OSHA would shut the building down. In fact, no study by
the ADA or NIDCR has been completed that specifically and
accurately addresses this issue. Yet, the ADA leads us to
believe that additional exposure to toxic mercury from these
procedures is not dangerous to our health. Mercury toxicity
is a retention toxicity that builds up during years of exposure.
The toxicity of a singular level of mercury is greatly increased
by current or subsequent, low exposures to lead or other
toxic heavy metals (12). Therefore, the damage caused by
amalgams could occur years after initial placement and at
mercury levels now deemed safe by the ADA.
Our
ability to protect ourselves from the toxic damage caused
by exposure to mercury depends on the level of protective
natural biochemical compounds (e.g. glutathione, metallothionine)
in our cells and the levels of these protecting agents is
dependent upon our health and age. If we become ill, or
as we age, the cellular levels of glutathione drop and our
protection against the toxic effects of mercury decreases
and damage will be done. This is strongly supported by numerous
studies where rodents have been chemically treated to decrease
their cellular levels of protective glutathione and then
treated with mercury, always with dramatic injurious effects
when compared to controls. Therefore, published science
indicates that mercury toxicity is much more pronounced
in infants, the very old and the very ill.
A recent
NIH study on 1127 military men showed the major contributor
to human mercury body burden was dental amalgams. The amount
of mercury in the urine increased about 4.5 fold in soldiers
with the average number of amalgams versus the controls
with no amalgams. In extreme cases it was over 8 fold higher.
Since the total mercury included that from diet and industrial
pollution are we to expect that this 4.5 to 8 fold average
increase in mercury is not detrimental to our health? Does
this indicate that amalgams are a "safe and effective
restorative material"? Is the public and Congress
expected to be so naïve as to believe that increased
exposure above environmental exposure levels is not damaging?
Then why are pregnant mothers told to limit seafood intake
when mercury exposure from amalgams is much greater? Then
why is the EPA pushing regulations to force the chloro-alkali
plants and fossil fuel plants to clean up their mercury
contributions to our environment? Obviously, from this study
most of the human exposure to mercury is from dental amalgams,
not fossil fuel plants. Yet, the FDA lets the dental profession
continue to expose American citizens to even greater amounts
of mercury. They do this by refusing to test amalgam fillings
as a source of mercury exposure. Also, remember that the
amalgam using ADA dentists are a major contributor to mercury
in our water and air through mercury leaving the dental
offices, and even when we are cremated.
"The
ADA's Council on Scientific Affairs 1998 report on its review
of the recent scientific literature on amalgam states:
"The Council concludes that, based on available scientific
information, amalgam continues to be a safe and effective
restorative material." and "There currently
appears to be no justification for discontinuing the use
of dental amalgam." What would you expect an ADA
Council to say? The ADA, as evidenced in the current letter
by the President of the ADA, only quotes and considers valid
the published research that supports their desire to continue
placing mercury containing amalgam fillings in American
citizens. When were dentists trained to evaluate neurological
and toxicological data and manuscripts? What is needed is
an international conference where both the pro- and anti-amalgam
researchers show up and present their data in front of a
world-class scientific committee. I would challenge the
ADA to line up their scientists and supporters to participate
in such a conference. This could be held in Washington,
D.C. so the FDA officials could easily attend. Perhaps we
could persuade the FDA to sponsor such a conference. However,
this is unlikely since a recent written request to have
a conference to evaluate the safety of amalgams was rejected
in a letter from the FDA and signed by three FDA/ADA dentists
who presented the ADA line on this issue. Doesn't it seem
a bit fraudulent to have FDA/ADA dentists deciding on whether
or not a safety study should be done on mercury emitting
amalgams being placed in human mouths with the blessing
of the ADA? This does seem like a conflict in interest that
Congress should address.
"In
an article published in the February 1999 issue of the Journal
of the American Dental Association, researchers report
finding "no significant association of Alzheimer's
disease with the number, surface area or history of having
dental amalgam restorations." This research was
lead by a dentist, Dr. Sax. It was submitted to the J. of
the American Medical Association and rejected. It was then
submitted to the New England Journal of Medicine and rejected.
It was then published in the ADA trade journal, JADA, that
is not a refereed, scientific journal. JADA is loaded with
commercial advertisements for dental products. They even
called a "press conference" announcing the release
of this article! Calling a press conference for a twice-rejected
publication that is to appear in a trade journal is playing
politics with science at its worst! At this press conference
two of the authors made unbelievable statements that were
not supported by any of the data in the article and conflicted
with numerous major scientific reports, including the 1998
NIH study (6). Some of these were high-lighted in the side-bars
of the ADA publication. I would suggest that those concerned
with this article visit Medline and look at the publication
records of the two individuals who made these statements.
Also, look at the three earlier excellent publications in
refereed journals by some of the other authors showing significant
mercury levels in the brains of AD subjects compared to
controls (14a,b, 15). However, put a dentist in charge of
the project and the data gets reversed!
Apply
some common sense. The ancillary comments by some of the
authors and the results of the JADA publication are in total
disagreement with the vast majority of research published
that looks at elevated mercury levels in subjects with amalgam
fillings. For example, the NIH study on military men discussed
above showed a very significant elevation of mercury in
the blood that correlated with number of dental amalgams
(6). Another recent publication demonstrated elevated mercury
in the blood of living AD patients in comparison to age-matched
controls (10). These studies clearly show that there should
be increased mercury in your blood if you have amalgams
and especially if you have AD and amalgams (6,10). Does
not the brain have blood in it? This makes it a total mystery
as to how could the authors of the JADA article not find
elevated brain mercury levels in patient with existing amalgams
and/or AD. Even cadavers have brain mercury levels that
correlate with the number of amalgam fillings they had on
death.
Further,
if you are addressing the contribution of amalgams to brain
mercury and AD wouldn't it be important to divide the AD
and control subjects into those with and without existing
amalgams on death? In the JADA article this was not done
and represents a major research flaw! That this was not
done also arouses suspicion. I participated in submitting
a letter pointing out this flaw to editors of JADA but they
refused to acknowledge the letter and did not publish our
comments. It is my opinion that the entire situation around
this singular supportive publication of the ADA position
on amalgams, brain mercury levels and AD represents a weak
attempt at controlling the mind-set of well-meaning dentists,
scientists, physicians and medical research administrators.
It definitely impedes honest scientific debate. It also
explains the cavalier attitude of the ADA and NIDCR about
elemental mercury exposure and toxicity when compared to
the more serious approaches taken by the EPA and OSHA.
With
regards to the JADA article summary that "no statistically
significant differences in brain mercury levels between
subjects with Alzheimer's disease and control subjects."
Here I must quote Mark Twain on honesty, "There are
liars, damned liars and statisticians." Comparing the
level of mercury in the AD versus control alone using straight-forward
statistics previously showed a significant difference on
mercury levels in AD versus control subjects (14a,b, 15).
However, there are anomalies, confounders and other factors
that can be considered in this situation, especially if
you don't like the initial results. This allows one to invoke
a Bon-Feroni statistical manipulation. With Bon-Feroni you
include the comparison of one pair of data (that may be
statistically significantly different taken alone, e.g.
mercury levels in the brains of AD versus control subjects)
with several other pairs of data rendering the difference
statistically insignificant. One known weakness of the Bon-Feroni
treatment of several coupled pairs of comparisons is that
one very likely will miss a single comparison that is significantly
different, and clever people know this. It is my opinion
that application of the Bon-Feroni manipulation is what
happened in this JADA study that reversed the previous significance
of the mercury levels in AD versus control brain previously
reported. Research previously reported by some of the very
same researchers involved in the JADA study consistently
indicated that mercury levels were higher in AD versus age-matched
control brains (14a,b, 15). Only when an ADA dentist became
involved did the results change to being insignificant.
I think the data used in this JADA article and funded by
NIH needs to be re-evaluated by a different statistician
if we are to ever really know if the mercury levels in the
AD brains differed significantly from controls.
The
letter from the ADA President then lists four publications
as proof of amalgams having no statistically significant
negative effects. Two of these were published in Scandinavian
Journals, another was a review of the literature in a Dental
Journal, and one was the JADA article mentioned above. Sweden
is well known to have lead the world in the restriction
and replacement of dental amalgams with non-mercury containing
materials. Forces are pushing hard to get the use of amalgams
accepted again in Sweden to eliminate this embarrassment
to our ADA. The current situation in Sweden and some other
European countries, Canada and Japan seriously questions
the ADA contention of amalgam safety. What if people in
Sweden become healthier without amalgams?
Additionally,
the studies quoted by the ADA President were epidemiological
studies. These are very complex as many confounders are
included which make finding a statistically significant
difference very difficult. So the results are negative,
nothing found, and not surprising. However, they are in
disagreement with numerous other similar reports and appear
to be hand-selected to support the ADA position. One has
to wonder, since the ADA President seemed to visit Swedish
journals to support the ADA position, how he missed the
research of the Nylander group in Sweden that showed increased
mercury content in brains and kidneys of humans in relationship
to exposure to dental amalgams (17,18). Also, the referenced
studies in the ADA letter did not involve neurotoxicity,
autism or neurological disease---which is the question at
hand. Rather, they addressed fertility, reproduction and
other systemic illnesses. Could not the ADA find references
to focus on neurotoxiological studies? What about the 1989
study that showed elevated levels of mercury in 54 individuals
with Parkinson's disease when compared to 95 matched controls
(16)? Further, one ought to consider who was doing these
touted ADA studies and any vested interest they may have
in the outcome. I am also aware of studies done in the U.S.A.
by major research universities that would disagree with
the conclusions drawn by the ADA on this subject yet these
articles are not considered in the ADA letter.
At the
end of the last publication the quote "Conclusions:
No statistically significant correlation was observed
between dental amalgam and the incidence of diabetes,
myocardial infarction, stroke, or cancer." How
does this relate to an article published in the J. of the
American College of Cardiology where the mercury levels
in the heart tissue of individuals who died from Idiopathic
Dilated Cardiomyopathy (IDCM) contained mercury levels 22,000
times that of individuals who died of other forms of heart
disease? Where did this tremendous amount of mercury come
from? Even a Bon-Feroni manipulation could not make this
difference insignificant! Many who die of IDCM are well-conditioned,
young athletes who drop dead during sporting events---and
they live in locations and in economic environments where
sea-food is not a dietary mainstay. Perhaps the victims
of IDCM are within the ADA Presidents "handful of
individuals who are allergic to one of its components."
"The
National Institute of Dental and Craniofacial Research is
currently supporting two very large clinical trials
on the health effects of dental amalgam. Studies underway
for several years each in Portugal and the Northeastern
United States involve not only direct neurophysiological
measures but also cognitive and functional assessments."
Do we really think that the NIDCR and associated ADA
personnel are going to deliver up a conclusion to American
parents saying "we put a mercury containing toxic material
in your child's mouth that lowered his/her I.Q. and made
him more susceptible to neurological problems in comparison
to the children whom we selected to not get exposed to this
toxic material"? It is my opinion that most bureaucracies
don't have a brain or a heart, but they do have a very strong
survival instinct. Therefore, the results presented from
this study will likely follow previously ADA supported research,
i.e. no significant results.
Since
the NIDCR started this project only 4 years ago one has
to ask why it took so long for them to get involved since
the "amalgam wars" have been going on for scores
of years? Was it the overwhelming amount of modern science
showing mercury from amalgams being a major part of the
daily exposure that forced their hand and they had to develop
a defense? Would I trust the conclusions of this study without
knowing who put it together and who did the statistics?
Not any more than I trust the conclusions of the JADA article
mentioned in the ADA letter that stupendously concludes
that mercury from dental amalgams does not get into the
brain.
As was
proven by the tobacco situation, trying to find any significant
negative effect of one product (amalgams) related to any
disease through epidemiological studies is very difficult
and complex. To do this with mercury would be difficult
because of the synergistic effect two or more toxic metals
or compounds (e.g. cadmium from smoking) may have on the
toxicity of the mercury emitted from amalgams. For example,
one publication showed that combining mercury and lead both
at LD1 levels caused the killing rate to go to 100% or to
an LD100 level (12). An LD1 level is where, due to the low
concentrations, the mercury or the lead alone was not very
toxic alone (i.e., killed less than 1% of rats exposed when
metal were used alone). The 100% killing, when addition
of 1% plus 1% we would expect 2%, represents synergistic
toxicity. Therefore, mixing to non-lethal levels of mercury
plus lead gave an extremely toxic mixture! What this proves
is that one cannot define a "safe level of mercury"
unless you absolutely know what others toxicants the individual
is being exposed to. The combined toxicity of various materials,
such as mercury, thimerosal, lead, aluminum, formaldehyde,
etc., is unknown. The effects various combinations of these
toxicants would have is also not defined except that we
know they would be much worse than any one of the toxicants
alone. So how could the ADA take any exception, based on
intellectual considerations, to my contention that combinations
of thimerosal and mercury could exacerbate the neurological
conditions identified with autism and AD? Autism and AD
have clinical and biological markers that correspond to
those observed in patients with toxic mercury exposure.
Why would the ADA take this position? I personally feel
like I have been in a ten year argument with the town drunk
on this issue. Facts don't count and data is only valid
if it meets the pro-amalgam agenda.
The
ADA was founded on the basis that mercury-containing amalgams
are safe and useful for dental fillings. This may have been
an acceptable position in 1850. However, modern science
has proven that amalgams constantly emit unacceptable levels
of mercury. Especially as the average life span has increased
from 50 to 75-78 years of age where AD and Parkinson's become
prevalent diseases. The ADA can try to verify its position
using selected epidemiological studies. But the bottom line
is that amalgams emit significant levels of neurotoxic mercury
that are injurious to human health and would exacerbate
the medical condition of those individuals with neurological
diseases such as ALS, MS, Parkinson's, autism and AD.
I am
hoping that the ADA sent this letter to your committee and
also placed it on the ADA web-site to indicate that they
are now willing for a wide-open discussion to take place
on the issue of dental amalgams. I, for one, would welcome
a major scientific conference on this issue. The ADA should
feel free to post my letter in response and address any
issue they feel that I am mistaken about. However, in closing
I urge your committee to push forward on the study of the
potential dangers of mercury in our dentistry and medicines.
This includes mercury exposures from amalgams, vaccines
and other medicaments containing thimerosal. The synergistic
effects of mercury with many of the toxicants commonly found
in our environment make the danger unpredictable and possibly
quite severe, especially any mixture containing elemental
mercury, organic mercury and other heavy metal toxicants
such as aluminum.
Sincerely,
Boyd
E. Haley
Professor and Chair
Department of Chemistry
University of Kentucky
REFERENCES:
1. a.
Duhr, E.F., Pendergrass, J. C., Slevin, J.T., and Haley,
B. HgEDTA Complex Inhibits GTP Interactions With The E-Site
of Brain b-Tubulin Toxicology and Applied Pharmacology 122,
273-288 (1993).; b. Pendergrass, J.C. and Haley, B.E. Mercury-EDTA
Complex Specifically Blocks Brain b-Tubulin-GTP Interactions:
Similarity to Observations in Alzheimer"s Disease.
p 98-105 in Status Quo and Perspective of Amalgam and Other
Dental Materials (International Symposium Proceedings ed.
by L. T. Friberg and G. N. Schrauzer) Georg Thieme Verlag,
Stuttgart-New York (1995).; c. Pendergrass, J.C. and Haley,
B.E. Inhibition of Brain Tubulin-Guanosine 5'-Triphosphate
Interactions by Mercury: Similarity to Observations in Alzheimer's
Diseased Brain. In Metal Ions in Biological Systems V34,
pp 461-478. Mercury and Its Effects on Environment and Biology,
Chapter 16. Edited by H. Sigel and A. Sigel. Marcel Dekker,
Inc. 270 Madison Ave., N.Y., N.Y. 10016 (1996).
2. Pendergrass, J. C., Haley, B.E., Vimy, M. J., Winfield,
S.A. and Lorscheider, F.L. Mercury Vapor Inhalation Inhibits
Binding of GTP to Tubulin in Rat Brain: Similarity to a
Molecular Lesion in Alzheimer's Disease Brain. Neurotoxicology
18(2), 315-324 (1997).
3. David, S., Shoemaker, M., and Haley, B. Abnormal Properties
of Creatine kinase in Alzheimer's Diseased Brain: Correlation
of Reduced Enzyme Activity and Active Site Photolabeling
with Aberrant Cytosol-Membrane Partitioning. Molecular Brain
Research 54, 276-287 (1998).
4. Leong, CCW, Syed, N.I., and Lorscheider, F.L. Retrograde
Degeneration of Neurite Membrane Structural Integrity and
Formation of Neurofibillary Tangles at Nerve Growth Cones
Following In Vitro Exposure to Mercury. NeuroReports 12
(4): 733-737, 2001.
5. Olivieri, G., Brack, Ch., Muller-Spahn, F., Stahelin,
H.B., Herrmann, M., Renard, P; Brockhaus, M. and Hock, C.
Mercury Induces Cell Cytotoxicity and Oxidative Stress and
Increases b-amyloid Secretion and Tau Phosphorylation in
SHSY5Y Neuroblastoma Cells. J. Neurochemistry 74, 231-231,
2000.
6. Kingman, A., Albertini, T. and Brown, L.J. Mercury Concentrations
in Urine and Whole-Blood Associated with Amalgam Exposure
in a U.S. Military Population. J. Dental Research 77(3)
461-71, 1998.
7. Chew, C. L., Soh, G., Lee, A. S. and Yeoh, T. S. Long-term
Dissolution of Mercury from a Non-Mercury-Releasing Amalgam.
Clinical Preventive Dentistry 13(3): 5-7, May-June (1991).
8. Hahn, L.J., Kloiber, R., Vimy, M. J., Takahashi, Y. and
Lorscheider, F.L. Dental "Silver" Tooth Fillings:
A Source of Mercury Exposure Revealed by Whole-Body Image
Scan and Tissue Analysis. FASEB J. 3, 2641-2646, 1989.
9. Hahn, L.J., Kloiber, R., Leininger, R.W., Vimy, M. J.,
and Lorscheider, F.L. Whole-body Imaging of the Distribution
of Mercury Released from Dental Filling Into Monkey Tissues.
FASEB F. 4, 3256-3260, 1990.
10. Hock, C., Drasch, G., Golombowski, S., Muller-Span,
F., Willerhausen-Zonnchen, B., Schwarz, P., Hock, U., Growdon,
J.H., and Nitsch, R.M. Increased Blood Mercury Levels in
Patients with Alzheimer's Disease. J. of Neural Transmission
v105(1) 59-68, 1998.
11. Frustaci, A., Magnavita, N., Chimenti, C., Caldarulo,
M., Sabbioni, E., Pietra, R., Cellini. C., Possati, G. F.
and Maseri, A. Marked Elevation of Myocardial Trace Elements
in Idiopathic Dilated Cardiomyopathy Compared With Secondary
Dysfunction. J. of the American College Cardiology v33(6)
1578-1583, 1999,
12. Schubert, J., Riley, E.J., and Tyler, S.A. Combined
Effects in Toxicology-A Rapid Systemic Testing Procedure:
Cadmium, Mercury and Lead. J. of Toxicology and Environmental
Health v4, 763-776,1978.
13. Wataha, J. C., Nakajima, H., Hanks, C. T., and Okabe,
T. Correlation of Cytotoxicity with Element Release from
Mercury and Gallium-based Dental Alloys in vitro.
Dental Materials 10(5) 298-303, Sept. (1994)
14. a. Ehmann, W., Markesbery, W., and Alauddin, T., Hossain,
E. and Brubaker, E., Brain Trace Elements in Alzheimer's
Disease. Neurotoxicology 7(1) p197-206, 1986. b. Thompson,
C. M., Markesbery, W.R., Ehmann, W.D., Mao, Y-X, and Vance,
D.E. Regional Brain Trace-Element Studies in Alzheimer's
Disease. Neurotoxicology 9, 1-8 (1988).
15. Wenstrup, D., Ehmann, W., and Markesbery, W. Brain Research,
533, 125-131, 1990.
16. Ngim, C.H., Devathasan, G. Epidemiologic Study on the
Assocaiation Between Body Burden Mercury Level and Idiopathic
Parkinson's Disease. Neuroepidemiology, 8, 128-141, 1989.
17. Nylander, M., Friberg, L. and Lind, B. Mercury Concentrations
in the Human Brain and Kidneys in Relation to Exposure from
Dental Amalgam Fillings. Swedish Dentistry J. 11:179-187,
1987.
18. Nylander, M., Friberg, L., Eggleston, D., Bjorkman,
L. Mercury Accumulation in Tissues from Dental Staff and
Controls in Relation to Exposure. Swedish Dental J. 13,
235-243, 1989
19. Heintze, U. Edwardsson, S., Derand, T. and Birkhed,
D. Methylation of Mercury from Dental Amalgam and Mercuric
Chloride by Oral Streptococci in vitro. Scand. J. Dental
Research 91(2) 150-152, 1983. | |
Dr.
Boyd Haley's Curriculum Vitae
CURRICULUM
VITAE BOYD
E. HALEY, Ph.D. Born 22-09-40 Greensburg, Indiana
ADDRESS: Advanced
Science Technology Commercialization Center, ASTeCC
Room A057
University of Kentucky
Lexington, KY 40506-0286
Laboratory: Telephone; (606) 257-2300 ext 246 FAX; (606) 257-3040
Chemistry Office: Telephone; (606) 257-7082
EDUCATION:
Institution Year Degree/Area
Franklin College
1963 B.A./Chemistry-Physics
University of Idaho 1967 M.S./Organic Chemistry
Washington State University 1971 Ph.D./Chemistry-Biochemistry
Yale University Medical Center 1971-74 Postdoctoral Fellow
RESEARCH AND
PROFESSIONAL EXPERIENCE:
1963-1964
Research Scholar, Food and Drug Administration.
1964-1966 U.S. Army Medic
1966-1967 Graduate Student, University of Idaho
1967-1971 Graduate Student, Washington State University
1971-1974 Postdoctoral Scholar, Yale University
1974-1979 Assistant Professor, Department of Biochemistry, University
of Wyoming, Laramie, WY
1979-1981 Associate Professor, Department of Biochemistry, University
of Wyoming, Laramie, WY
1981-1985 Professor, Department of Biochemistry, University of
Wyoming, Laramie, WY
1985-1997 Professor of Medicinal Chemistry, College of Pharmacy,
University of Kentucky, with
joint appointments in Biochemistry & Chemistry
1997-present Chairman & Professor, Department of Chemistry
with joint appointment in College of
Pharmacy
PROFESSIONAL
ORGANIZATIONS, SOCIETIES, HONORS AND RESPONSIBILITIES
1959 President's
Scholarship, Franklin College, Indiana
1962 Chi Beta Phi, Franklin College
1962 James M. Sprague Award - $400 award to outstanding
undergraduate junior majoring in science.
1963 Kennedy Scholar, Food and Drug Administration,
Washington, D.C.
1970 Sigma Xi
1975 Dreyfus Foundation Visiting Researcher, Enzyme Institute
University of Wisconsin
1977 American Society of Biological Chemists
1981 Biophysical Society
1981 Served on NIH Physiological Chemistry Study Section
1981 Research was presented as a "highlight" in NIH
report on
"Cellular and Molecular Basis of Disease Program"
1984 "TOP" Professor Award, University of Wyoming
1982 Served on NIH Physiological Chemistry Study Section
1983 Served on NIH Physiological Chemistry Study Section
1985 Permanent member NIH Biomedical Sciences, Study Section
1991 Honorary Doctorate in Arts & Sciences, Franklin College
1992 Society for Neuroscience
GRANT SUPPORT
1975 - 1978
National Institutes of Health, "Application of Photoaffinity
Nucleotide Analogs", $82,000, Prinicipal Investigator
1975 Research
Coordination Committee, University of Wyoming $1,800
1978 - 1981
National Institutes of Health, "Application of Photoaffinity
Nucleotide Analogs", $183,696, Prinicipal Investigator
1978 - 1981
Eleanor Roosevelt Cancer Institute Grant, $11,400
1979 - 1983
PHS Research Career Development Award, $185,000
1981 - 1986
National Institutes of Health, "Application of Photoaffinity
Nucleotide Analogs", $434,000, Prinicipal Investigator
1982 ASBC
Travel Award to attend 12th IVB Congress, Perth, Australia
1983 - 1984
National Science Foundation, "Melatonin Photoaffinity Probe",
$84,000, Co-Principal Investigator
1983 - 1985
National Institutes of Health, "Epididymal Sperm Nucleotide
Binding proteins", $190,000, Co-Principal Investigator
1985 - 1988
U.S. Army Mycotoxin Photoprobes, $390,000, Co-Principal Investigator
1986 - 1989
NIH, "Forskolin Photoaffinity Probes", $170,000, Co-Principal
Investigator
1986 - 1991
NIH, "Application of Photoaffinity Nucleotide Analogs"
$781,661, Principal Investigator
1989 - 1994
NIH, "Nucleotide-Tubulin Interactions in Alzheimer's Disease",
$405,259, Co-Prinicipal Investigator
1990 - 1996
Lexington Clinic Foundation For Medical Education and Research,
"Inhibition of Neoplastic Cell Proliferation Through Utilization
of Photoactive DNA & RNA Synthesis, $100,000, P.I.
1990 - 1993
Eli Lilly, "Development of a Diagnostic Test for Alzheimer's
Disease, $378,000, P.I.
1995 - 1997
Wallace Research Foundation, "Development of Diagnostic Tests
Using Nucleotide Photoaffinity Probes". $109,000 for two
years.
1997-1998
Wallace Research Foundation, "Development of Diagnostic Tests
Using Nucleotide Photoaffinity Probes". $74,344.
1997-2000
NIH, "Application of Photoaffinity Nucleotide Analogs",
$378,081, P.I.
1997-1998
Isostent, Inc. "Photoattachment of 32P to angioplastic ballon
cathers" $52,000.
Pending NIH,
"Identification of CSF proteins Related to ALS"
NIH, "Photomodification of Antibodies for Diagnostic and
Therapeutic Applications".
TEACHING EXPERIENCE
Introductory
Comparative Biochemistry
General Biochemistry
Problems and Topics in Biochemistry
Mercury Toxicity: Chemistry and Biochemistry Involved
Advanced Problems and Topics in Biochemistry
Nucleic Acids and Protein Biosynthesis
Nucleotides in Regulation of Biological Phenomena
Bioenergetics
Medicinal Chemistry
Natural Products and Bio-organics
Graduate level Biochemistry, Protein Chemistry
INVITED LECTURES:
1975 - Sloan
Kettering Memorial Cancer Institute, New York
thru Colorado State University (3)
1979 Albert Einstein University, New York
Hoffman-LaRoche Research Institute, Nutley, New Jersey
University of Colorado Medical School Denver (3)
University of Colorado, Boulder (2)
Yale University Medical School (2)
The Salk Institute, San Diego
University of California, Davis
Stanford University Medical School
University of California, San Diego
University of Washington, Seattle
Washington State University
Kansas State University
1979 Symposium Speaker, ASBC Meeting, Dallas, Texas
1979 Symposium Speaker, New York Academy of Sciences Meeting,
New York
Department of Molecular Biology, National Jewish Hospital, Denver
University of California, Riverside
Workshop Speaker, ICN-UCLA Conference on Adenylyl Cyclase
1982 Symposium Speaker, 1982 FASEB Meeting, New Orleans
1982 Guest Lecturer and Scientist, German Cancer Research Center,
Institute of Cell and Tumor Biology, Heidelberg, West Germany,
May
1982 Centre National De La Recherche Scientifique, Laboratoire
D'Enzymologie, Gif Sur Yvette, France, June
1982 Workshop Speaker, ASBC Meeting in New Orleans (Photoprobe
utilization, sponsored by Schwarz-Mann)
1982 Symposium Speaker, Society for the Study of Reproduction,
Madison
Wisconsin, August
1982 Department of Biochemistry, University of Wisconsin, November
1982 Department of Chemistry, New Mexico State University, November
1982 Department of Chemistry, University of Colorado, December
1983 Institute of Infectious Diseases, U.S. Army Medical Research
Institute, Ft. Detrick, Michigan, January
1983 Department of Biochemistry and Biophysics, Oregon State University
1983 Department of Biochemistry, Texas Health Science Center,
San Antonio, TX
1983 Department of Biochemistry, University of Mississippi Medical
Center
1984 Department of Biochemistry, University of Kentucky, Lexington,
KY
1985 Department of Physiology and Biophysics, Northwestern University
Medical School, Chicago, Illinois
1985 Department of Chemistry, University of Southern California,
Los
Angeles, California
1985 Department of Physiology, University of Illionis at Chicago,
Chicago, Illinois
1985 Department of Biochemistry, Ohio State University, Columbus,
Ohio
1985 Department of Physiology, Yale University Medical School,
New
Haven, Connecticut
1986 Department of Biochemistry, Case Western University, School
of
Medicine, Cleveland, Ohio
1986 Department of Biochemistry, Indiana University, School of
Medicine, Indianapolis, Indiana
1986 Department of Biochemistry, Washington University, School
of
Medicine, St. Louis, Missouri
1987 Division Fermentation Products Research Division, Eli Lilly
Research Laboratories, Indianapolis, Indiana
1987 Department of Chemistry, University of South Florida, Tampa,
Florida
1987 Department of Molecular Biology and Biochemistry, University
of
Wyoming, Laramie, Wyoming
1988 Worcester Foundation, Shrewsbury, Massachusetts
1988 Department of Biochemistry, University of Colorado, Denver,
Colorado
1988 Department of Biochemistry, University of Delaware, Newark,
Delaware
1989 University of California at San Diego
1989 University of California at Los Angeles
1989 Texas College of Osteopathic Medicine, Fort Worth, Texas
1990 Wright State University, Dayton, Ohio
1990 Athena Neurosciences, S. San Francisco, California
1990 Eli Lilly & Co., Indianapolis, Indiana
1990 Connaught Laboratories, Toronto, Canada
1990 University of East Carolina Medical School, Greenville, North
Carolina
1990 Hoffman-LaRoche Research Center, Nutley, New Jersey
1991 Eli Lilly & Co., Indianapolis, Indiana
1991 City University of New York, New York, New York
1991 University of Cincinnati, Cincinnati, Ohio
1991 University of Colorado, Boulder, Colorado
1991 University of Missouri at Kansas, Kansas City, Missouri
1992 Williams College at Williamsburg, Massachusetts
1992 Centre College at Danville, Kentucky
1992 University of Colorado, Boulder, Colorado
1992 Eli Lilly & Co., Indianapolis, Indiana
1992 Merck Laboratories, West Point, Pennsylvania
1993 NIH Rocky Mountain Laboratory, Hamilton, MT
1993 Intern. Acad. Oral & Medical Toxicology, Chicago, IL
1993 Univ. Tenn. at Memphis, Memphis, TN
1993 Penn State University, College Station, PN
1993 University California, Riverside, Riverside, CA
1993 Mayo Clinic, Jacksonville, FL
1993 Washington University, St. Louis, MO
1993 University of Arkansas, Little Rock, AR
1994 European Academy of Science, Otzenhausen, Germany
1994 Intern. Acad. Oral & Medical Toxicology, London, England.
1994 Great Lakes College for Advancement of Medicine, Cincinnati,
OH
1995 American College for the Advancement of Medicine, Colorado
Springs, CO.
1995 Pfizer Pharmaceuticals, Groton, CN
1995 Ohio State University, Dept,. Chemistry, Columbus, OH
1996 Intern. Acad. Oral & Medical Toxicology, Tuscon, AZ
1996 University of Wyoming, Laramie WY
1996 American College for the Advancement of Medicine, Colorado
Springs, CO.
1997 American Academy Biological Dentistry, Carmel, CA March 7-9.
1997 International Academy of Oral and Medical Toxicology, Louisville,
KY March 14-16
1997 Washington State University, Dept. of Chemistry and Biophysics,
Pullman, WA, March 27-30.
1997 American Society of Biochemistry and Molecular Biology, Symposium
talk, August 24-28.
1997 Canadian Academy Oral and Medical Toxicology, Toronto, Canada.
September 19-21.
1997 Capital University of Integrative Medicine, Washington, DC,
October 16-18
1997 American Academy Environmental Medicine, San Diego, CA, October
24-26.
1997 University of Missouri at Kansas City, Dept. Biology &
Biophysics, November 20-22.
SERVICE TO
DEPARTMENT, COLLEGE AND UNIVERSITY:
1975-1979
Faculty Senate
Biological Interdepartmental Seminar Committee
University Grievance Procedure Committee
College of Agriculture Teaching Improvement Committee
College of Agriculture Academic Planning Committee
Faculty Senate Nominating Committee
Division of Biochemistry Undergraduate Teaching Committee
Division of Biochemistry Graduate Program Committee
University Research Coordination Committee
Chairman of the Graduate Committee, Biochemistry Department
1979-1982 College of Agriculture Tenure and Promotion Committee
1979 College of Agriculture Dean Search Committee
1981 Vice-President for Research Search Committee
1981 College of Human Medicine Evaluation Committee
1981-1982 Biomedical Research Funding Committee
1982 Chairman, Department of Zoology and Physiology Review Committee
1986 Research Committee College of Medicine
Ad Hoc Committee to Review Center on Aging
Ad Hoc Medical Center Research Advisory Committee
Working Group for Biotechnology Center
Center for Pharmaceutical Science and Technology Advisory Committee
College of Pharmacy Graduate Program
College of Pharmacy Research and Seminar
1987 Markey Cancer Center Internal Advisory Committee
College of Medicine Research Committee
Tobacco and Health Advisory Committee
1988 College of Pharmacy BRSG Committee, Tenure and Promotion
1989 Chairman, College of Medicine BRSG Committee
Member, Tobacco & Health Advisory Committee
Member, Markey Cancer Center Advisory Committee
1990 Chairman, College of Medicine BRSG Committee
1991-1992 Member, Intellectual Properties Committee
Member, Search Committee Cancer Center Director
Member, Cancer Center Advisory Committee
Member, Search Committee Diagnostic Radiology Chair
Member, Academic Area Committee, Biological Sciences
1993-1995 Chair, Research and Seminar Committee
Member, Appointment, Tenure and Promotion Committee
1996-1997 Chair, Graduate Program task force, College of Pharmacy
Chair, Physical Plant section, College of Pharmacy self-study
University Chemical Safety Committee
College of Medicine Academic Council
College of Pharmacy Tenure and Promotion Committee
PUBLICATIONS (REFEREED JOURNALS)
1. Haley,
B. and Yount, R. Gamma-fluoradenosine Triphosphate.Synthesis,
Properties and Interaction with Myosin and Heavy Meromyosin. Biochemistry
II, 2863-2871 (1972).
2. Haley,
B., Yount and Hoffman, J. Selective Inhibition of Divalent Metal
Ion Requiring ATPase Activity of Human Red Cell Ghost by an Analog
of ATP. The Physiologist 16, 333-334 (1973).
3. Haley,
B. and Hoffman, J. Interactions of Photo-Affinity ATP Analog with
Cation-Stimulated ATPase Activities of Human Red Cell Ghost. Proc.
Natl. Acad. Sci. 71, 3367-3371 (1974).
4. Staros,
J.V., Haley, B. and Richards, F.M. Human Erythrocytes and Resealed
Ghost: A Comparison of Membrane Topology. J. Biol. Chem. 249,
5004-5007 (1974).
5. Pomerantz,
A., Rudolph, S.A., Haley, B. and Greengard, P. Photoaffinity Labeling
of a Protein Kinase from Bovine Brain with 8-Azido-adenosine-3',
5'-monophosphate. Biochemistry 14, 3852-3857 (1975).
6. Haley,
B. Photoaffinity Labeling of cAMP Binding Sites of Human Red Blood
Cell Membranes. Biochemistry 14, 3852-3857 (1975).
7. Staros,
J.V., Richards, F.M. and Haley, B. Photochemical Labeling of the
Cytoplasmic Surface of the Membranes of Intact Human Erythrocytes.
J. Biol. Chem. 250, 8174-8178 (1975).
8. Malkinson,
A.M., Krueger, B.V., Rudolph, S.A., Casnelli, J.E., Haley, B.
and Greengard, P. Widespread Occurence of a Specific Protein in
Vertebrate Tissues and Regulation by cAMP of its Endogenous Phosphorylation
and Dephosphorylation. Metabolism 24, 331-341 (1975).
9. Haley,
B. Photoaffinity Labeling of Adenosine 3', 5'-Cyclic Monophosphate
Binding Sites. Methods in Enzymology, Jacoby and Wilchek, Editors.
V 46, pp. 339-346 (1976).
10. Owens,
J.R. and Haley, B.E. A Study of Adenosine 3', 5'-Cyclic Monophosphate
Binding Sites of Human Erythrocyte Membranes Using 8-Azido-adenosine-3'-5'
Cyclic Monophosphate. J. Supra. Mole. Structure 5, 91-102 (1976).
11. Skare,
K., Black, J.L., Pancoe, W.L. and Haley, B. Determination of the
Cellular Location of Cyclic Nucleotide Binding Sites Using 8-Azido-adenosine-3',
5'-monophosphate, A Photoaffinity Probe. Arch. Biochem. Biophy.
180, 409-415 (1977).
12. Lau, E.,
Haley, B. and Barden, R. Interactions of a Photoaffinity Analog
of CoA with CoA Enzymes. Biochemistry 16, 2581-2585 (1977).
13. Owens,
J.R. and Haley, B. A Study of Adenosine 3', 5'-Cyclic Nucleotide
Binding Sites of Human Erythrocyte Membranes Using 8-Azido-adenosine
3'-5'-Cyclic Monophosphate. Cell Shape and Surface Architecture:
Progress in Clinical and Biological Research 17, 65-76 (1977)
14. Lau, E.P.,
Haley, B. and Barden, R. The 8-Azidoadenine Analog of S-Benzoyl
(3'-dephospho) Coenzyme A-A Photoaffinity Label for Acyl CoA;
Glycine N-Acyltransferase. Biochem. Biophys. Res. Commun 76, 843-849
(1977).
15. Geahlen,
R.T. and Haley, B. Interactions of a Photoaffinity Analog of GTP
with the Proteins of Microtubules. Proc. Natl. Acad. Sci. 74,
4375-4377 (1977).
16. Owens,
J.R. and Haley, B. Use of Photoaffinity Nucleotide Analogs to
Determine the Mechanism of ATP Regulation of a Membrane Bound,
cAMP Activated Protein Kinase. J. Supra. Mole. Structure 9, 57-68
(1978).
17. Czarnecki,
J., Geahlen, R.T. and Haley, B. Synthesis and Use of Azido Photoaffinity
Analogs of Adenine and Guanine Nucleotides. Methods in Enzymology
56, 642-653 (1979).
18. Marcus,
F. and Haley, B. Inhibition of Fructose 1,6-biphosphatase by the
Photoreactive AMP Analog, 8-Azido-AMP. J. Biol. Chem. 254, 259-261
(1979).
19. Geahlen,
R., Haley, B. and Krebs, E.G. Synthesis and Use of 8-azidoguanosine
3', 5'-cyclic Monophosphate as a Photoaffinity Label for Cyclic
GMP-dependent Protein Kinase. Proc. Natl. Acad. Sci. 76, 2213-2217
(1979).
20. Geahlen,
R. and Haley, B. Use of GTP Photoaffinity Probe to Resolve Aspects
of the Mechanism of Tubulin Polymerization. J. Biol. Chem. 254,
11982-11987 (1979).
21. Haley,
B. Application of Photoaffinity Nucleotide Analogs to Biological
Membrane Research. Selected Aspects of Cancer-Related Protein,
Carbohydrate, Lipid and other Biochemistry, International Cancer
Research Data Bank, p. 87 (1979).
22. Owens,
J. and Haley, B. Mechanism of MgATP Regulation of Membrane Bound
Type I cAMP Activated Protein Kinase. Transmembrane Signaling.
Alan R. Liss, Inc. New York, New York, pp. 149-160 (1979).
23. Forrester,
I.T., P.K. Schoff, B.E. Haley and R.G. Atherton. Determination
of Protein Kinase Activity in Intact Mammalian Sperm. J. of Andrology
1, 70 (1980).
24. Briggs,
F. Norman, Al-Jumaily, Walid and Haley, Boyd. Photoaffinity Labeling
of the (Ca+Mg) ATPase of Skeletal and Cardiac Sarcoplasmic Reticulum
with [32P-]-8-Azido ATP. Cell Calcium 1, 205-215 (1980).
25. Hoyer,
P., Owens, J.R. and Haley, B.E. Use of Nucleotide Photoaffinity
Probes to Elucidate Molecular Mechanisms of Nucleotide Regulated
Phenomena. Annals of New York Academy of Science 346, 280-301
(1980).
26. Takemoto,
D.J., B.E. Haley, J. Hanse, P. Pinbett and L.J. Takemoto. GTPase
from Rod Outer Segments: Characterization by Photoaffinity Labeling
and Tryptic Peptide Mapping. Biochem. Biophys. Res. Commun. 102,
341-347 (1981).
27. Leichtling,
B.H., Coffman, D.S., Yaeger, E.S., Rickenberg, H.V., Al-Jumaily,
W. and Haley, B.E. Occurrence of the Adenylate Cyclase "G-Protein"
in Membranes of Dictyostelium discoidium, Biochem. Biophys. Res.
Commun. 102, 1187-1195 (1981).
28. Schoff,
P.K., Forester, I.T., Haley, B.E. and Atherton, R. A Study of
cAMP Binding Proteins on Intact and Distrupted Sperm Cells Using
8-Azidoadenosine-3', 5'-Cyclic Monophosphate. J. Supra. Molecular
Structure 19, 1-15 (1982).
29. King,
M.M., Carlson, G. and Haley, B.E. Photoaffinity-Labeling of the
Subunit of Phosphorylase Kinase by 8-Azidoadenosine-5'-Triphosphate
and its 2', 3' -Dialdehyde Derivative. J. Biol. Chem. 257, 14058-14065
(1982).
30. Potter,
R. and Haley, B.E. Photoaffinity Labeling of Nucleotide Binding
Sites with 8-Azidopurine Analogs. Meth. Enzymol. 91, 613-633 (1982).
31. Hoyer,
P.B. and Haley, B.E. Utilization of Nucleotide Photoaffinity Probes
to Study Protein-Nucleotide Interactions in Cell Fractions. J.
Cellular Biochemistry, submitted. (1983)
32. Haley,
Boyd. Development and Utilization of 8-Azidopurine Nucleotide
Photoaffinity Probes. Federation Proceedings 42, 2831-2836 (1983).
33. Khatoon,
S., Atherton, R. Al-Jumaily, W. and Haley, B.E. Use of Nucleotide
Photoaffinity Probes to Study Hormone Action. Biology of Reproduction
28, 61-73 (1983).
34. Kaiser,
I.I., Kladianos, D.M., Van Kirk, E.A., and Haley, B.E. Photoaffinity
Labeling of catechol-o-methyltransferase with 8'-Azido-S-adenosylmethionine.
J. Biol. Chem. 258, 1747-1751 (1983).
35. Abraham,
K., Haley, B. and Modak, M. Biochemistry of Terminal Deoxynucleotidyl
Transferase: 8-Azido ATP as A Substrate Binding Site-Directed
Photoaffinity Labeling Prob. Biochemistry 22, 4197-4203 (1983).
36. Haley,
B.E., Ponstingl, H. and Doenges, K.H. Photoaffinity Labeling of
Pure Tubulin Using 8-Azidoguanosine triphosphate at the b-Subunit.
Hoppe-Seylers J. Physiol. Chem. 364, 1137 (1983).
37. Woody,
A.M., Vader, C.R., Woody, R.W. and Haley, B.E. Photoaffinity Labeling
of DNA-dependent RNA polymerase from E. coli with 8-azidoadenosine-5'-triphosphate.
Biochemistry 23, 2843-2848 (1984).
38. Owens,
J.R. and Haley, B.E. Synthesis and Utilization of [5'-32P]-8-Azidoguanosine-3'-phosphate-5'-phosphate:
Photoaffinity Studies on Cytosolic Proteins of E. coli. J. Biol.
Chem. 259, 14843-14848 (1984).
39. Pfister,
K.K. , Haley, B.E. and Witman, G.B. The Photoaffinity Probe 8-azidoadenosine-5'-triphosphate.
Selectivity Labels the Heavy Chain of Chlamydomonas 12S Dynein.
J. Biol. Chem. 259, 8499-8504 (1984).
40. Atherton,
R.W., Khatoon, S., Schoff, P.K. and Haley, B.E. A Study of Rat
Epididymal Sperm Adenosine-3', 5'-monophosphate-dependent Protein
Kinase: Maturation Differences and Cellular Location. Biol. of
Reproduction 32, 155-172 (1985).
41. McMurray,
M.M., Hansen, J.S., Haley, B.E., Takemoto, D.J. and Takemoto,
L.J. Interspecies Conservation of Retinal Guanosine-5'-triphosphatase:
Characterization by Photoaffinity Labeling and Tryptic Peptide
Mapping. Biochemical Journal 225, 227-232 (1985).
42. Khatoon,
S., Haley, B.E. and Atherton, R.W. A Comparative Analysis of cAMP-dependent
Protein Kinase Regulatory Subunits in Sea Urchin and Rat Sperm.
J. Andrology 6, 251-260 (1985).
43. DeBortoli,
M.E., Issa, H.A., Haley, B.E. and Cho-Chung, Y.S. Elevated Levels
of p2l ras Protein in Hormone-Dependent Mammary Carcinomas of
Humans and Rodents. Bioch. Biophys. Res. C | |