Testimony Before the House Government Reform Committee by Boyd Haley, Ph.D.
November 14, 2002


The major contributor to mercury body burden of American Citizens comes from dental amalgam (1). This belies the propensity of many spokespersons in organized dentistry to compare the safety of mercury in amalgams to sodium in table salt and hydrogen in water. Checking with any university level department of chemistry would immediately elucidate the chemical ridiculousness of their opinions on this issue. Amalgams leak vaporous mercury constantly into the oral cavity and this ends up in the cells of the body causing damage.

Organized dentistry is filled with statements that vastly underestimate the amount of mercury released from dental amalgams. Note the term "underestimate" as they rarely give values obtained by direct, scientific measurements using acceptable chemical protocols. The most widely accepted and taught "estimated" claim by a dental authority is from a manuscript that states it would take 450 to 530 amalgam surfaces to produce 30 micrograms mercury/g creatinine of urine mercury per day (roughly estimated as 0.067 to 0.057 mg/day/surface) (15). This claim has failed numerous scientific examinations, does not remotely explain the microgram level of mercury found in urine and feces in amalgam bearers, yet is taught as fact in many of our nations dental schools.

The absolute truth could be arrived at by the simple process of making numerous, identically sized copies of today's utilized amalgams of know weight and surface area, outside of the mouth. These could be sent to appropriate unbiased laboratories for the determination of the amount of mercury vapor release from these amalgams under controlled conditions. This is simple to do and would resolve the issue of how much mercury would one minimally expect to be exposed to from an amalgam filling. I find it hard to believe that organized dentistry has not done this and knows the answer, it is the first thing a logical scientist would do. When this was done by my students using a popular amalgam material the amounts released were 7.54 mg/cm2/day when undisturbed and increased to 45.49 mg/cm2/day when brushed twice for 30 seconds using a medium bristle toothbrush. However, all that is released by organized dentistry is based on "estimates" that are fraught with vague interpretation and exaggerations. Whom to believe, organized dentistry or those opposed to amalgams, is a reasonable question. I recommend to this committee that it commission a simple study to scientifically measure the release of mercury from dental amalgams by a competent, independent set of laboratories. This testing should measure the release at body temperature, with and without appropriate abrasion to replicate chewing and tooth brushing. Starting with hard, scientific truths is a good way to resolve such disagreements.

A July 2000 report from a National Academy of Sciences study states that 60,000 children are born at risk for adverse neuro-developmental effects each year due to their mothers' exposure to methyl-mercury. A Center for Disease Control and Prevention study in March 2001 (in Morbidity and Mortality Weekly Report) indicates that about 10% of American women of child-bearing age are at risk for having a baby born with neurological problems due to in utero mercury exposure (statistically representing about 375,000 babies/year). The fact that amalgams are most likely the major contributor to the mercury levels in American citizens should be clearly presented to the public. Yet all the American public hears is concerns about mercury in fish.

Mercury in the oral cavity is capable of creating a class of more toxic organic-mercurials. It is well known that oral and intestinal bacteria can methylate mercury to methyl-mercury increasing its uptake by fetal tissues (2,3,4). Further, it is obvious that one of the major neurotoxins produced during gingivitis and periodontal disease, methylthiol (CH3SH), reacts immediately with Hg2+ creating a new class of toxic, organic mercury-thiol compounds, (CH3-S-HgCl and CH3S-Hg-S-CH3), that are extremely dangerous. These compounds would behave similarly to methyl-mercury (CH3HgCl) in that they would easily pass the gastrointestinal and blood-brain barriers. Such compounds formed in the mother's mouth may be the major cause of periodontal disease being the major risk factor for pre-term low birth weight babies.

It has been shown that mercury from amalgams placed in rats distribute to fetal tissues (6). In a comparable human study it was shown that mercury levels in mothers fluids versus that found in similar fetal materials showed increased levels in fetal materials (meconium and cord blood) that correlated with maternal and infant risk factors (7). This additionally adds to the danger of mercury from dental amalgams to babies, pregnant mothers and small children as well as adults. The well-known toxicity of mercury to kidneys makes this especially important to those patients with renal difficulties requiring kidney dialysis.

Youngsters that die of idiopathic dilated cardiomyopathy (IDCM) have 22,000 times more mercury in their heart tissue than comparable controls (8). These are the young athletes that die in high school on exertion during athletic events. It is a critical question why this observation has not received any significant attention from our NIH and AMA. Doesn't any responsible group want to know where this mercury comes from and if it is causal?

Data on the level of mercury in the birth hair of autistic versus normal children shows that a subset of the population, the autistics, are not effective at excreting mercury (5). In normal children the level of mercury in birth hair goes up with increasing amalgams in the birth mother. In contrast, in autistic children there is very little excretion of mercury in their birth hair no matter how many amalgams the birth mother has. Yet, exposing these children to a mercury challenge test to determine toxic exposure to mercury shows that the autistic children have retained higher amounts of toxic heavy metals. These observations demonstrate that autistics represent a sub-set of the population that do not physiologically handle mercury excretion like normal individuals. Autistics are therefore much more susceptible to neurological damage through exposures to mercury. It is important to note that it is the mercury retained in the body's cells that cause toxicity, not that that is found in the urine, hair and feces.

Studies on the toxicity of mercury to mammalian neurons in culture demonstrate that low nanomolar levels can have lethal effects. Experiments using this system have also demonstrated, in agreement with published literature, that many antibiotics, other heavy metals and chemicals increase the toxicity of mercury and thimerosal (ethyl mercury). Additionally, in this same system the female hormone estrogen decreases thimerosal's toxic effects. In contrast, the male hormone testosterone greatly increases the toxicity. This may explain the 4 to 1 ratio of boys to girls that become autistic and the observation that boys represent the vast majority of the severe cases of autism.

Considering the variances in human health, age, sex, genetic diversity and exposures to toxins unknown the universal scientific truth is: "We do not know what the tolerable level of mercury is for each individual as it can vary dramatically from person to person".

It is quite plausible that neuronal impairment, as occurs in autism, would happen in the human infant exposed to mercury compounds unless the mercury was rendered harmless by the body's protective compounds such as glutathione and metallothionine. However, pre-exposing unborn children to mercury from the mother's amalgam would reduce the availability of such protective compounds and exacerbate the toxic effect. The observed toxic nanomolar level is much less (about 100-fold) than the concentration found in the brains of aged patients in many studies. It is important to note that it is not just the level of mercury that determines toxic effects! It is the level of mercury in relation to the level of the body's protective compounds, and these compounds decrease with age, disease, other toxic exposures, oxidative stress and genetic susceptibility.

Autism appears to represents a damage caused by an exposure to ethyl mercury in an infant with a developing nervous system and other organ immaturity that decreases their ability to excrete and decrease the toxicity of mercurials. This is not surprising at it is similar to what happened in the mercury caused diseases acrodynia and Minamata Bay disease.

One has to consider what is the likely danger to an aging population that is chronically exposed to mercury for 40 to 60 years from dental amalgams? The data regarding 'the specific ability' of mercury (a known neurotoxin, found in gram quantities in many American mouths) to cause much of the aberrant biochemistry found in the brain and to produce many of the widely accepted diagnostic hallmarks of Alzheimer's disease (AD) is unquestionable. It is also easy to explain, mercury reacts with the most readily available, thiol-reactive proteins it encounters and inhibits their functions that are necessary for cell function and life. The axon of the nerve cell is very dependent on a protein called tubulin to maintain its structure and function. Tubulin is adversely affected in dramatic fashion by very low concentrations of mercury.

It is only the value and popularity of amalgam material by organized dentistry that keeps mercury from being regarded by medicine as a major exacerbating factor, if not causal, for AD. For example, mercury dramatically inhibits the functions (among others) of the brain proteins tubulin (greatly inhibited and abnormally polymerized in AD brain)(9), creatine kinase (over 90% inhibited in AD brain) (10), and glutamine synthetase (greatly inhibited, extruded into and elevated in the cerebrospinal fluid, blood in AD) (11). The latter enzyme is used in the brain to remove the excito-toxic amino acid, glutamate. If glutamate builds up in brain tissues it would cause neuronal death.

Other studies on neurons in culture have demonstrated that low nanomolar levels of mercury (sub-lethal doses) effect the production of pathological hallmarks of AD. These are greatly decreased glutathione levels, neurofibillary tangles (12), abnormally aggregated tubulin (13), increased hyper-phosphorylation of protein-Tau (14), and increased production of beta-amyloid protein (the constituent of amyloid or senile plaques) (14). In light of these results it seems unreasonable to accept amalgams, the major contributor to mercury body burden, as a safe dental filling. If mercury from amalgams is not causal for AD it, at the very least, would have to be considered a major exacerbating factor.

Addressing the initial issue of concern by the National Academy of Science, the grave concerns expressed about mercury by the OHSA and EPA agencies, and the identification of amalgams as the major contributor to human body burden by the NIH and WHO. Doesn't common sense tell us that it is time to remove the mercury exposure from amalgams from all citizens? If doubt persists in legislative minds then you have the power to have amalgams tested by an unbiased, set of credible laboratories to determine how long it takes a half-gram amalgam to make a gallon of water unsafe to drink by OHSA and/or EPA standards. It is common to find blood or urine mercury levels in the 2 to 30 micrograms per liter level. In my department sewage water must be many folds lower at 0.5 micrograms per liter of water to meet EPA standards. I agree with this EPA standard as I don't want to see our lakes and tributaries polluted by a build up of retained mercury. However, it begs the question why we don't hold medicine and dentistry to a similar, reasonable standard with regards to pollution of our citizen's bodily fluids.

1. Kingman, A., Albertini, T. and Brown, L.J., Mercury Concentrations in Urine and Whole Blood Associated with Amalgam Exposure in a US Military Population. J. of Dental Research, 1998 V77(3) p461,.
2. Heintze et al., Methylation of Mercury from Dental Amalgam and HgCl2 by Oral Streptococci. Scandinavia J. Dental Research, 1983, V91: p150.
3. Rowland, Grasso and Davies, The Methylation of Mercuric Chloride by Human Intestinal Bacteria., Experientia. Basel 1975, V31, p1064.
4. Leistevuo, J. Leistevuo, T. Helenius, H. Pyy, L. Osterblad, M. Huovinen, P, Tenovuo, J., Dental Amalgam Fillings and the Amount of Organic Mercury in Human Saliva. Caries Research 2001, V35(3), p 163.
5. Holmes, A., Blaxill, M., and Haley, B. Reduced Levels of Mercury in First Baby Haircuts of Autistic Children. 2002 submitted International J. Toxicology.
6. Takahashi, Y. et al., Release of Mercury from Dental Amalgam Fillings in Pregnant Rats and Distribution of Mercury in Maternal and Fetal Tissues. Toxicology 2001, V21;163(2-3), p115.
7. Ramirez, G.B., Cruz, M., Pagulayan, O. Osteas, E. and Dalisay, C. Pediatrics, 2000, V106(4), p774.
8. 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 , 1999, V33(6) p1578.
9. 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).
10. David, S., Shoemaker, M., and Haley, B. Abnormal Properties of Creatine kinase in Alzheimer's Disease Brain: Correlation of Reduced Enzyme Activity and Active Site Photolabeling with Aberrant Cytosol-Membrane Partitioning. Molecular Brain Research 54, 276-287 (1998).
11. Gunnersen, D.J. and Haley, B. Detection of Glutamine Synthetase in the Cerebrospinal Fluid of Alzheimer's Diseased Patients: A Potential Diagnostic Biochemical Maker. Proc. Natl. Acad. Sci. USA, 88, 11949-11953 (1992).
12. Leong, CCW, Syed, N.I., and Lorscheider, F.L. Retrograde Degeneration of Neurite Membrane Structural Integrity and Formation of Neruofibillary Tangles at Nerve Growth Cones Following In Vitro Exposure to Mercury. NeuroReports 12 (4):733-737, 2001.
13. Pendergrass, J.C. and Haley, B.E. Mercury-EDTA Complex Specifically Blocks Brain b-Tubulin-GTP Interactions: Similarity to Observations in Alzheimer"s Disease. pp98-105 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).
14. 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 ?-amyloid Secretion and Tau Phosphorylation in SHSY5Y Neuroblastoma Cells. J. Neurochemistry 74, 231-231, 2000.
15. Mackert, Jr. and Bergland, A. Mercury Exposure from Dental Amalgam Fillings: Absorbed Dose and the Potential for Adverse Health Affects. Crit. Rev. Oral Biol. Med., 8(4): 410-436, 1997.