Australasian Society of Oral Medicine and Toxicology ASOMAT submission to Amalgam Review Working Party (incorporating response to a review of ASOMAT’s preliminary, Sept. 1997, submission to NHAC ) Date: May 1998 Authored by: President: Dr. Roman Lohyn 8 Floor, 175 Collins Street th Melbourne 3000 Tel: (03) 9650-1660 Fax: (03) 9650-8161 Secretary: Dr. Robert Gammal 102/222 Pitt Street, Sydney 2000 Tel: (02) 9264-5195 Fax: (02) 9283-2230 On behalf of ASOMAT P.O.Box A860, Sydney South, N.S.W. 2000 Tel: (02) 9867-1111 Fax: (02) 9665-5043
Transcript
Australasian Society of Oral Medicine and Toxicology
ASOMAT submission to Amalgam ReviewWorking Party
(incorporating response to a review of ASOMAT’s preliminary, Sept. 1997, submission to NHAC )
Date: May 1998
Authored by:
President: Dr. Roman Lohyn8 Floor, 175 Collins Streetth
ASOMAT would like to note that its original submission was presented in response to a requestfrom NHAC in August 1997. At that time ASOMAT was specifically told not to make it tooextensive or large because NHAC, due to workload, would not have time to read it. ASOMAT’ssuggestion of an overview without great detail was deemed to be appropriate for the purpose at thetime, and that a more extensive submission could be made later. ASOMAT was therefore surprisedto learn that its preliminary submission had been sent for a review by Prof. Moore. ASOMAT wasalso surprised that it was not given the opportunity beforehand to prepare a more throughlydocumented and extensive document for review, which would more accurately reflect the situationas seen by ASOMAT. ASOMAT is committed to cooperation with NHAC/NHMRC in the reviewof this issue and therefore urges that the review process be as transparent as possible in order toobviate any perception of bias. One method to achieve this would be timely consultation andcommunication with parties who have an acknowledged interest in the issue.
As far as Prof. Moore’s review is concerned, ASOMAT notes that Prof. Moore has been publiclyaligned with the Australian Dental Association’s stand on amalgams for some years and hasconsistently been cited by the ADA as supporting their views. ASOMAT was not surprised,therefore, by the tenor of Prof. Moore’s evaluation of its submission. ASOMAT offers the followingobservations to assist NHMRC in its objective evaluation of this issue.
Prof. Moore’s comments that the amalgam problem is a diminishing one is correct in only one specific regard. That point is that as fewer amalgams are placed we can expect fewer NEW amalgamrelated problems in the future. As far as existing amalgam bearers are concerned, we can expect, if our present experience is any guide, increasing problems in the future as the heavy metal tissue loadsincrease over time. Amalgam derived mercury related health problems of this exposed group need tobe acknowledged as a valid clinical entity so that affected people can receive appropriate care evenin a situation where amalgams might no longer be in use. In this regard, Health Canada hasdistributed a letter to all dentists in Canada to bring this issue to their attention.
ASOMAT was formed in order to create awareness of research, hitherto ignored, which supports theview that amalgams are not harmless. This was done out of necessity because of the regrettable onesided portrayal and widespread misrepresentation of this issue by the dental associations. It shouldnot be surprising, therefore, that ASOMAT has presented research which presents a view differentto that held by the ADA and Prof. Moore. This does not invalidate the submission but should serveto stimulate a more thorough examination of the issue. It is then up to NHMRC to objectivelyevaluate both sides of the argument, using the same scientific standards for both.
Prof. Moore’s assertion that ASOMAT’s submission was based almost entirely on the work ofRichardson is a regrettable misrepresentation, and completely untrue. The submission was based onthe references supplied, references which Prof. Moore apparently did not read. Not having readthem, of course, he was unable to recognise their connection to the ASOMAT submission. Prof.Moore’s opinion that there is not much science in the ASOMAT submission is surprising. ASOMATprovided approximately 80 references with its original submission so Prof. Moore’s characterisationof the ASOMAT submission is incongruent with the reality of the document. Prof. Moore maydisagree with ASOMAT’s assessment of the cited research, hopefully only after reading it first, buthe cannot characterise it as ‘not much science’. It can be judged as good science or bad science butnot as ‘no science’. ASOMAT is confident that if Prof. Moore had looked at the references he wouldhave acknowledged their relevance and contribution to the overall understanding of this issue.
Prof. Moore has provided very few references himself, quoting only Eley’s work which criticised Dr.Richardson’s risk assessment study for Health Canada. It is ASOMAT’s impression that Prof. Moore
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has not read Dr. Richardson’s study and that he is not completely familiar with its background.ASOMAT is surprised that Prof. Moore has accepted at face value the reported criticisms of Dr.Richardson’s work without carrying out a more detailed assessment of both.
It needs to be pointed out that Dr. Eley is a dentist from the Periodontal Department of the King’sCollege School of Medicine and Dentistry in London. He has, to the best of ASOMAT’s knowledge,no formal background in toxicology or risk assessment. His criticism of Dr. Richardson containserrors of fact as well as evidence of a lack of understanding of the subject, and was published not ina peer reviewed journal appropriate for the subject, but in the journal of the British DentalAssociation. Just as one would not expect an article on the mechanical performance of dental fillingsin a risk assessment journal, one would not, by the same token, expect any article detailing criticismof a major risk assessment study to be in a dental journal. It should be more appropriately submittedto a relevant journal, where knowledgeable and experienced reviewers can assess the merits of thecriticism, not to one whose reviewers have no understanding of the subject, or a vested interest inunfounded criticism.
Dr. Richardson, on the other hand, is a specialist in this area who used standard accepted techniquesand whose paper, the conclusions of which, incidentally, were validated by other researchers, waspeer reviewed by 16 other people before being submitted to Health Canada and by a further threeanonymous peer reviewers before being published, a total of 19 experts who found his approach andmethodology to be appropriate. ASOMAT is perplexed by Prof. Moore’s willingness to dismiss Dr.Richardson’s work so readily on the assessment of someone with no demonstrated expertise in thefield. ASOMAT requested, and has included in this submission, (Appendix 10) a letter from Dr.Richardson responding to Eley’s criticism of his research. This will, hopefully, be helpful toNHMRC in determining the credibility of Dr. Richardson’s work.
In his communication with ASOMAT, Dr. Richardson also stated that he would be willing tocollaborate with Prof. Moore in helping to establish appropriate TDI levels for mercury exposurefrom dental amalgams. He would also be willing to confer with NHMRC during a planned trip toAustralia in September 1998. ASOMAT respectfully encourages NHMRC to take advantage of Dr.Richardson’s willingness to assist in this matter.
It is correct that neither Germany nor Sweden have banned amalgam fillings with the one exceptionbeing the banning of one specific form of amalgam. The overall situation in Europe is that the German and Norwegian Health Departments have issued directives that dentists not use amalgamsin pregnant women or in children. This is advice which ASOMAT believes is accurate but NHMRCshould confirm this independently. ASOMAT is also reliably informed that the Swedish SocialServices Department recently announced that reimbursement for amalgam fillings will cease by theyear 2000. This is not a department of the Swedish Government concerned with environmentalaspects but with the health care of the community. NHMRC should confirm this independently aswell.
There is some truth in Prof. Moore’s comment about reductions in mercury use being forenvironmental reasons. Indeed one of NHMRC guidelines state ‘salvage all amalgam scrap andstore in a tightly closed container. Storage under water offers no protection’. Further, the AmericanDental Association (JADA 105: pp930 1982) recommended that amalgam scraps be stored underphotographic fixer solution in a tightly closed container. In light of such warnings it would seemthat the only safe place to store this material is in teeth. Nevertheless, ASOMAT applauds efforts toreduce mercury in the environment and is comforted by reassurances that authorities would neveruse such statements as a convenient rationale for avoiding a full and frank discussion of the dangersof mercury toxicity from dental amalgams.
ASOMAT generally agrees with Prof. Moore’s comment that dentists and dental staff are at riskand has presented a range of studies showing health problems in this group. Whether they are moreor less at risk than the ‘caries-challenged’ patient has not yet been proved.
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ASOMAT has noted the abstracts supplied by Prof. Moore and is disappointed that a broaderselection was not chosen. Almost all the abstracts appear to support the pro-amalgam view and, assuch, do not reflect the reality of the wide divergence of views present in the literature. ASOMAT has taken the liberty of enclosing its own selection of abstracts for NHMRC consideration.ASOMAT acknowledges they reflect the anti-amalgam view, but it seems that this is necessary inorder to achieve some balance. NHMRC will, in due course, decide the worth of these various articles andabstracts but if it is not even aware of their existence in the first place then a considered decision isimpossible.
Prof. Moore mentions the contaminated sites group investigation. ASOMAT has not seen thismonograph but assumes it deals with mercury in the soil. If this assumption is correct, thenASOMAT would draw NHMRC’s attention to the fact that this monograph would most likely bedealing with ionic mercury which is the most common form in soil. If this is true then the monographis of limited relevance here because the pharmacokinetic and toxicological characteristics of ionicand vapour forms of mercury are different.
A comprehensive review will obviously incur some costs. Any decision to proceed with such areview must consider the possible benefits to be gained in undertaking such a review, as opposed tothe costs. ASOMAT contends that there is a significant underlying reservoir of ill health, poorlydefined and inaccurately diagnosed where a major factor is mercury exposure from dental amalgams.The extent of this is unknown but a small clue is evident in a 1992 study carried out by the Social InsuranceOffice of Stockholm County. Results showed that the incidence of sick leave by amalgam affectedpatients in Sweden fell by 50% in the two years after amalgam fillings were removed. If only a minute fraction of health costs in Australia were attributable to mercury exposure from amalgams, and appropriate corrective and preventive measures were instituted, the savings would justify thecost of a review countless times over. More importantly NHMRC needs to consider the costs offailure to prevent mercury contamination of the Australian populace. To cite just one example,research presented by ASOMAT in the following formal response shows neurological damage bymercury in young children at levels previously considered safe. The societal costs associated withsuch interference with our children’s potential is enormous. In this particular issue it is notappropriate to wait until irrefutable evidence exists. Many times judgements need to be made wherecomplete certainty about every single aspect of a problem does not exist. This is one such time.ASOMAT believes that NHMRC’s responsibility is to err on the side of caution particularly whenthe consequences of not doing so have the potential for irreversible damage.
ASOMAT believes that in the light of recent research, detailed in the following sections, the currentevidence clearly raises serious concerns regarding the safety of dental amalgam. As such ASOMATbelieves that a full review of the current literature with a view to formulating a new policy andestablishing TDI levels of mercury from dental amalgams is not only justified but necessary.
Roman LohynPresident ASOMAT
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Response to Prof. Moore’s review of ASOMAT’s preliminary submission
to NHAC in September 1997
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ASOMAT SUBMISSION 1: Dental amalgam is NOT a true alloy. It is made up of 50%mercury, which is NOT locked into a set filling but escapes continuously during the entire life ofthe filling in the form of vapour, ions and abraded particles. This release is stimulated bychewing, brushing and hot fluids. One study reported that levels of mercury vapour in the mouthwere 54 times higher in the mouth of a patient with amalgams after chewing, than levels in themouth of a patient without amalgams after chewing.
Professor Moore: No disagreement. However, there is an implicit assumption thatpresence is equivalent to absorption and thereafter that absorption is equivalentto retention. This is untrue. One has to also consider clearance as part of theoverall assessment of bioavailability, which is invariably less than 100%-oftenvery much less!
ASOMAT RESPONSE: Bioavailability is related ONLY to absorption. If a substance is notabsorbed it is not bioavailable. Retention is related to clearance, which can be quick or slow. If asubstance is excreted it is no longer retained, but this does not mean it was bio-unavailable priorto excretion. If a substance is absorbed, causes cellular damage and is then fully excreted, doesProf. Moore contend that the substance is of little biological consequence because it has not beenretained? It is well documented in the literature that mercury is stored in tissues. The concept ofretention toxicity is accepted and research using DMPS has demonstrated this clearly(2,3,4,5,6,7,8,9,10,11,12,13). In 1991 The World Health Organization (WHO) published a reportshowing that the mercury retained in the body from dental amalgam exceeds the combinedamount from all other environmental sources, including seafood (14). Prof. Moore’s inferencethat mercury is not very bioavailable is not supported by the scientific literature. This is discussedfurther in following points.
Professor Moore’s comments do not refute ASOMAT’s statement.
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ASOMAT SUBMISSION 2: The absorption rate of inhaled mercury vapour is extremely high,approximately 80% of the inhaled dose, reaching the brain tissue within one blood circulationcycle.
Professor Moore: No disagreement - it is unclear however, how organic mercurywould be synthesised.
ASOMAT RESPONSE: The relevance of Prof. Moore’s observation about organic mercury isunclear. ASOMAT’s submission mentioned only mercury vapour, a form of inorganic mercury,not organic mercury. Is Prof. Moore inferring that the only significance of mercury vapour is thatit can be synthesised into organic mercury, or that only organic mercury is toxic and not mercuryvapour? If so, then this inference is clearly in error and is contradicted by his ownacknowledgment of mercury vapour’s toxicity when he responds to ASOMAT’s statement #3.
Apart from its effects on neurological tissues, mercury vapour in the oral cavity will rapidly reactwith methyl mercaptan (CH3SH), or by its other name methyl-thiol, producingmethylthiol-mercury (CH3S-Hg-Cl) or di(methylthiol)mercury (CH3S-Hg-SCH3). Methylthiol isproduced in the mouth by anaerobic bacteria in periodontal disease or infected root canal filledteeth. The methylthiol-mercury compounds are extremely cytotoxic, due primarily to theirhydrophobic nature, similar to methyl-mercury and dimethyl mercury. This is simple, irrefutablechemistry and would certainly explain why periodontal disease is a major contributing factor tostroke, cardiovascular disease, low birth weight babies and other diseases (268,269,270, 271, 272,273). In regard to Prof. Moore’s concern about organic mercury it should be noted that, while it isoften asserted by the dental associations that methyl mercury is not an issue in relation to dentalamalgams, the fact is that many studies have demonstrated the methylation of inorganic mercuryto methyl mercury. (15,16,17,18,19,20,21,22,23,25,26,27,28,29).
It should also be noted that elemental mercury and mercury vapour released from dentalamalgam can be methylated in the body to form methyl mercury (98,99,120169,185,192,195, 197,198,
208,213). This form of mercury is readily transported across the placenta, and via the breast milk.
Professor Moore’s comments do not refute ASOMAT’s statement.
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ASOMAT SUBMISSION 3: The extreme toxicity of mercury is well documented. Currentresearch clearly demonstrates that inorganic mercury is just as toxic as organic mercury undervarious physiological conditions.
Professor Moore: Inorganic and organic mercury cause toxicity by the samemechanism, but organic mercury is far more toxic because of the ease with whichit passes through lipoprotein membranes. Hg vapour is also toxic because it isuncharged and also readily passes through cell membranes. It is hard to see how"physiological conditions" will influence the toxicity of the various forms ofmercury.
ASOMAT RESPONSE: The general view in the past has been that organic mercury was themost toxic form of mercury but some researchers now believe that mercury vapour is as toxic asmethyl mercury. Nevertheless, physiological conditions exist which, at the individual level, mayenhance sensitivity to toxic insult, enhance toxic response and enhance absorption tissuedistribution and retention. ASOMAT believes it is self evident, for example, that the‘physiological condition’ of an immune compromised subject is different from that of a healthyuncompromised subject, both of whom could be expected to react totally differently to the samelevel of mercury exposure. This is the reason that Canada Health identified specific populationsubgroups in their recommendations.
The synergistic effects of mercury combined with various other substances is also an area ofsignificant concern which has been under-researched to date. The toxic effects of mercury arefurther enhanced when mercury is in combination with other metals such as zinc and lead.
(See Appendix 1 for further discussion )
Professor Moore’s comments do not refute ASOMAT’s statement.
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ASOMAT SUBMISSION 4: The toxic threshold for mercury vapour has never been found.Even the US Environmental Protection Agency has so stated (30,31,32). The existingoccupational standards are all specifically declared to be estimates only, on the appearance ofCLINICALLY OBSERVABLE SIGNS AND SYMPTOMS. Statements by the dental professionthat the amount of mercury exposure encountered by patients from dental amalgams is too smallto be harmful are contradicted by the scientific literature and are totally indefensible. Dentistsreceive no training at all which would enable them to even look for symptoms relating tomercury toxicity.
Professor Moore: I am not certain about this statement. Magos (1975) wrote inthe British Medical Bulletin that the maximum safe level of exposure toatmospheric Hg vapour is 0.05mg/m on a chronic exposure basis. In the samereport Magos wrote that 0.1- 0.2mg/m Hg (chronic exposure) was sufficient toinduce clinical signs. Clinical signs of Hg vapour exposure are intention tremor,erethism, and occasionally salivation and gingivitis. These signs are reversible ontermination of exposure. How does the level of Hg in a human mouth relate tothese figures?
ASOMAT RESPONSE: Methods of clinical and experimental measurements of mercury’simpact on kidney and neurological function have improved significantly since 1975, to the pointthat it is inappropriate to cite individual studies from that time in order to demonstrate safety atcertain levels. It is particularly inappropriate, given that the consensus at that time had alreadyconcluded there was no level of mercury vapour established where the effects could beconsidered harmless. (The International Committee on MAC Values for Mercury 1969, US EPAdocument on mercury 1973 and 1984, US NIOSH document on mercury 1973). More recentlyWHO endorsed the earlier consensus when its 1991 WHO Criteria 118 publication stated clearlythat for mercury vapour "a specific no-observed-effects level (NOEL) cannot be established",meaning that NO level of mercury vapour that can be considered harmless has been found. WHO also stated "There are at present no suitable indicator media that will reflect concentrationsof inorganic mercury in the critical organs, the brain or kidneys, under different exposuresituations."
Various agencies have set various levels for legislative purposes. For example, in the workplace,the U.S OSHA Maximum Allowable Concentration Mercury Vapour (MAC) is 100 mcg / m3and its Time Weighted Average maximum Mercury Vapour (TWA) is 50 mcg / m3. These arethe Mercury Vapour Exposure Levels for occupationally exposed individuals based on a 40 hourper week exposure. They must have regular medical monitoring and medical records must bekept for 30 years after the end of the exposure. (note that people with amalgam fillings areexposed permanently to mercury vapour for 168 hours per week)
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ASOMAT SUBMISSION 4 continued:
The U.S. Environmental Protection Agency sets another level. The US EPA maximum safe levelfor mercury vapour is only 0.3 mcg /m3. Another US agency, The Agency for Toxic Substancesand Disease Registry, is mandated by the US Government to research, and to set MRL’s(Minimum Risk Levels) for toxic substances. It’s MRL’s for Hg vapour exposure are0.02mcg/m3 for acute exposure, and 0.014 mcg/m3 for chronic exposure. The documentedexposure to mercury vapour from dental amalgams, even in the absence of stimulation, havebeen recorded as up to 200 times higher than the ATSDR levels. (33,34,35,36,37,38,39,40, 41,42 ).Contrast the ATSDR 1994 recommended safe levels of 0.014 mcgms/m3 with Prof. Moore’sapparent endorsement of Magos’s 1975 levels of 0.05mgms/m3 (ie 50 mcgms/m3), some 3,500times greater than current non-dental opinion. See Appendix 2 for further information onATSDR and its processes.
Prof. Moore’s assertion about reversibility of symptoms is also misleading and incomplete. SeeAppendix 2 for further discussion.
Mercury vapour levels in the human mouth have been recorded in many studies. These studiesindicate that stimulation by chewing or increase in temperature will lead to an elevation of themercury vapour levels. These levels remain elevated for about 90 minutes. Thus, during thecourse of a day, the stimulation of regular chewing and grinding could lead to a permanentlyelevated level of mercury vapour. A recently published study gives an indication of the amountof mercury released from dental amalgam (35). Other studies (40,42,47,48,49,51) indicate levels ashigh as 87mcg/m3, and in some individuals this may go as high as 100mcg/m3 (37). Even a levelof only 10mcg/m3 would be 714 times higher than the ATSDR MRL for chronic inhalationexposure to metallic mercury vapour.
The dangers of complacently accepting ‘guesstimated’ safe levels are starkly demonstrated in arecent study (50) which studied 917 children of approximately 7 years of age. Clinicalexamination and neurophysiological testing did not reveal any clear cut mercury relatedabnormalities, but mercury related neuropsychological dysfunctions were most pronounced in thedomains of language, attention, and memory, and to a lesser extent in visuospatial and motorfunctions. These associations remained after adjustment for covariates, and after exclusion ofchildren with maternal hair mercury concentrations above 10 micrograms (50 nmol/g). Theeffects on brain function associated with prenatal methyl mercury exposure appeared to bewidespread, and early dysfunction was detectable at exposure levels currently considered safe. (emphasis by ASOMAT)
See Appendix 3 for further discussion
Professor Moore’s comments do not refute ASOMAT’s statement.
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ASOMAT SUBMISSION 5: Controlled, broad-scale scientific studies investigating the effectson the health of patients of mercury released from dental amalgam fillings have NEVER beenconducted. The true nature and full extent of effects are therefore unknown.
Professor Moore: Agreed that there are no broad scale scientific investigations ofthe possible health effects of Hg exposure in the oral cavity from amalgam fillings- there are probably no health effects to be concerned about if the abovementioned signs are absent.
ASOMAT RESPONSE: If Prof. Moore’s earlier comments (statement 4) are to be taken at facevalue, then the obvious conclusion is that every dentist should be informed that mercuryexposure MUST be considered a potential factor in every patient presenting with excesssalivation and/or gingivitis (the most common oral problem facing the adult population). It isdisturbing that Prof. Moore has listed only four symptoms of mercury exposure. His opinion,unsupported by any citation from the literature, that if any of these symptoms are absent thenthere is probably no health effect, is a gross oversimplification. His opinion is contradicted byeven a perfunctory review of the scientific literature. To suggest that if intention tremor is notpresent there are no health effects to be concerned about is contrary to the published scientificresearch, the advice published by the dental associations and the advice published by themanufacturers themselves.
Professor Moore’s comments do not refute ASOMAT’s statement.
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ASOMAT SUBMISSION 6: Mercury from amalgam fillings is stored principally in thekidneys, liver and central nervous system. This mercury has also been shown to cross the placenta and collect in foetal tissue. Studies show the level of mercury in liver, kidney and braintissue of deceased foetuses, newborn and young children is proportional to the number ofamalgam fillings in the mother's mouth. One such study concludes that "the elevatedconcentrations of inorganic mercury found in the tissues of people with amalgam filings, derivemainly from these fillings and not from other theoretically possible sources.
Professor Moore: Mercury vapour rapidly oxides to mercuric ion as soon as itreaches the blood stream. This finds its way mainly to the liver and kidney. Mercuric ion does not readily pass into the CNS. Mercury vapour would have tobe in the blood in fairly high concentration to run the gauntlet of oxidation in theplasma to reach the blood brain barrier intact. Hg in the brain can also passback out into the plasma as well as get in. Mercury that does pass into neuronesin the CNS can react with SH group and interfere with protein synthesis. Thesmaller the neurones the more serious the effect this is. Since the smallestneurones are the granule cells of the cerebellar cortex, they sustain damagefirst-probably leading to the intention tremor in clinically affected individuals - acerebellar dysfunction. Chronic mercury exposure can lead to depositions ofcytoplasmic deposits in neurones such as Purinje cells which histochemically stainpositive for Hg - but these are sequestrated deposits and probably don't interferewith the function of the cells.
ASOMAT RESPONSE: ASOMAT disagrees with Prof. Moore’s comments. Prof. Moore statesthat Mercury vapour would have to be in the blood in very high concentrations to reach the bloodbrain barrier intact but he has also acknowledged in statement #3 that Hg vapour was toxic andthat it readily passed through cell membranes. Even Dr. Peter Sheridan, a frequent spokesman forthe ADA on the amalgam issue, states “The brain is the critical target organ for mercury vapourand methylmercury and is most significant in cases of chronic low level exposure to mercuryvapour” (Sheridan P. ‘Amalgam restorations and mercury toxicity’ Masters thesis SydneyUniversity 1991).
Hg vapour passes into the brain easily because while oxidation is quick, it is not instantaneous.There is time for one blood circulation cycle to deliver Hg into the brain. Once in the brain, Hgoxidises and has more difficulty in passing back out. This accounts for the very long estimatedhalf life of mercury in the brain. With continuing exposure, mercury enters the brain morequickly than it is excreted. This has been clearly shown in autopsy studies where the level ofmercury in the brain tissue was related to the number and size of the amalgam fillings (Seestatement #10). Research (46) has shown differences in Hg vapour accumulation compared withaccumulation from Hg in water. It was found that there was 400ng Hg/g wet tissue weight in rat2+
brain after two weeks exposure to Hg vapour but after having rats drink Hg in their water the2+
researchers could only measure about 200 ng Hg/g wet weight after one year.
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ASOMAT SUBMISSION 6 continued:
This research contradicts Prof. Moore’s uncited assertion about Mercury vapour and itsaccumulation in the brain. Even the Magos study, quoted by Professor Moore, contradicts hisown statements. Magos’s research on the subject showed rapid passage of mercury vapour fromblood into body tissues, especially the brain!
Prof. Moore infers above that Hg passes in and out of brain tissue with equal ease, but instatement #8 he states “Stable organic mercury compounds have long biological half lives aswould be expected of highly lipophilic molecules”. Hg deposits in the brain could be present forthe life span of an individual but would in all probability be sequestrated in secondary lysosomesand be totally harmless”. To suggest that no damage could occur from mercury that enters theCNS is a rather surprising comment. The peer reviewed published literature clearly shows thatneurological damage is one of the most reported effects of long term, low level mercurypoisoning (61,62,63,64,65,66,67). Prof. Moore’s suggestion that Hg reacts with SH groups and interferes with protein synthesis iscorrect. However, it also inhibits sodium/potassium transport, creatine kinase activity, andtubulin polymerization as well as numerous other enzymes leading to more toxic effects.
(See Appendix 4 for further discussion about amalgam derived mercury in the CNS)
Professor Moore’s comments do not refute ASOMAT’s statement.
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ASOMAT SUBMISSION 7: Mercury from dental amalgam will also be transported across thebreast milk of lactating women. In fact it has been demonstrated that breast milk increases thebioavailability of mercury to the newborn. Negative developmental effects have been shown (inanimal models) in relation to these sources and concentrations of mercury.
Professor Moore: Mercury vapour if it reaches the lactating mammary gland,would be expected to be present in the milk. It is unlikely that tiny amounts ofmercuric ion would so partition into milk under realistic conditions of Hgexposure from amalgam.
ASOMAT RESPONSE: Contrary to Prof. Moore’s unreferenced speculation about whether theabove statement is likely or not, the fact is that in the peer reviewed literature it has been welldocumented for some time now, that mercury from dental amalgams not only enters the breastmilk but that it also crosses the breast and enters the neonate.(68). Several studies have alreadyestablished the transfer of dental amalgam mercury into the tissues of unborn babies, in bothanimals and humans (236). The study on humans by Drasch et al (57) concluded: "Futurediscussion on the pros and cons of dental amalgam should not be limited to adults or childrenwith their own amalgam fillings, but also include foetal exposure. The unrestricted application ofamalgam for dental restorations in women before and during the child bearing age should bereconsidered." Vimy et al.,(89) studied lactating women with aged amalgam fillings and foundthat increased Hg excretion in breast milk correlated with the number of fillings or Hg vapourconcentration levels in the mouth air.
The publication of these studies has already resulted in the issuing of government advisoriesagainst the use of mercury amalgam dental fillings in pregnant females (Germany, Sweden andCanada).
(See Appendix 5 for further discussion)
Professor Moore’s comments do not refute ASOMAT’s statement.
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ASOMAT SUBMISSION 8: The halftime for the elimination of a single dose of mercury isextremely long, certainly at least 30 days for the whole body, and perhaps as long as 10,000 daysfor the brain. Multiple small doses will therefore result in body accumulation.
Professor Moore: Stable organic mercury compounds have long biological halflives as would be expected of highly lipophilic molecules. Hg deposits in the braincould be present for the life span of an individual but would in all probability besequestrated in secondary lysosomes and be totally harmless.
ASOMAT RESPONSE: It is difficult to believe that Professor Moore actually holds the viewthat mercury in the brain is totally harmless. His opinion is totally contradicted most recently bythe Faroe Islands Study (Appendix 3) as well as by a variety of published literature, and even bythe dental manufacturers (65,66,67,64,62,70). The toxicity of this material was tragicallydemonstrated with the recent death of Prof. Karen Wetterhahn, (The Scientist 11 (21) October1997, front page). Prof. Wetterhahn died from exposure to two drops of dimethyl mercury thatpenetrated her latex gloves. She first lost her balance, then her hearing and eyesight, went into acoma and died 10 months after exposure, despite valiant attempts to save her life. Dimethylmercury is less reactive than Hg but is definitely more lethal due to the fact that it concentrates2+
in the central nervous system. In the absence of scientific evidence that sequestered mercury is totally harmless it is appropriateto be guided by the conclusions of peer reviewed research in preference to unsubstantiatedpersonal speculation.
(See Appendix 6 for further discussion.)
Professor Moore’s comments do not refute ASOMAT’s statement.
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ASOMAT SUBMISSION 9: Sheep and monkey studies have confirmed that the mercury fromdental amalgams enters and accumulates in the patient throughout the body, including the brain.
Professor Moore: The level of accumulation of mercury in the body as themercuric ion bound to proteins could increase with time but experience suggeststhat such accumulations associated with Hg exposure from amalgam would berendered harmless by the normal detoxification processes available to the body.
ASOMAT RESPONSE: Professor Moore's statements are again made with no scientificevidence at all to support them, and in fact are again contradicted by published peer reviewedresearch. The experience of those involved in this issue who actually treat patients is in fact theexact opposite of what Prof. Moore asserts. Normal detoxification by glutathione andmetallothionine can remove mercury from the body but the mercury that remains contributes tothe inhibition of a biomolecule that the body needs badly enough not to slough it off. Thismercury may also contribute to the formation of free radicals which also leads to ageing anddementia.
Mercury’s well known and scientifically documented affinity for thiols is particularly significantin light of the above studies as they provide a pathway for the widespread distribution of mercurythroughout the body. Thiols are any organic compound containing a univalent radical called asulhydryl and identified by the symbol -SH. They are ubiquitous throughout the body and areinvolved in all of the following pathways... amino acids, tissue cell receptor sites, hormones andenzymes, erythrocytes, glutathione and glutathione peroxidase, coenzyme ‘a’ and succinylcoenzyme ‘a’, myosin, heart muscle, factor xiii and thioredoxin. Mercury competes for the -SHsites in all of the pathways listed.
The continuing and chronic release of mercury from dental amalgams ensures that the mercurylevels build up in tissues throughout the body over many years, interfering with a variety of bodyfunctions. It is this chronic longterm heavy metal poisoning which is the problem, not the one-offbrief and acute exposure.
Professor Moore does not address the point that ASOMAT is making, presumably accepting it tobe accurate, which is that mercury from dental amalgams is transported throughout the body andthat it accumulates in the tissues. This has been irrefutably confirmed by animal and humanautopsy studies (57,87,88).
Professor Moore’s comments do not refute ASOMAT’s statement.ASOMAT SUBMISSION 10: Human autopsy studies have shown that the concentration of
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mercury in the brain is directly related to the number, size and age of amalgam fillings in themouth.
Professor Moore: Unsurprising, but the form of the Hg deposits and their amountswould be insignificant in relation to possible health effects.
ASOMAT RESPONSE: Prof. Moore’s statement is totally speculative and without any validscientific basis. He has presented no scientific evidence to support his assertion. References havealready been cited by ASOMAT earlier which demonstrate the exact opposite.
Professor Moore’s comments do not refute ASOMAT’s statement.
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ASOMAT SUBMISSION 11: Mercury has been shown to interfere with tubulin synthesisresulting in "neurofibril tangles" in the brain. Mercury, specifically from dental amalgam, placedin rats' teeth, has been shown to affect tubulin synthesis.
Professor Moore: Hg in any form is well known to inhibit protein synthesis inneurones and this would include tubulin. I don't see how this is related to theformation of the neurofibrillary tangles of dementia.
ASOMAT RESPONSE: The relationship of mercury in this matter is still not fully determined.There is however, a body of evidence which is strongly suggestive of a connection. InAlzheimer's diseased brain the tubulin is present in normal levels, so synthesis is not theproblem. However, tubulin in Alzheimer's diseased brain is inactive and unable to bind itsnatural substrate, GTP, and this can be mimicked by addition of mercury (as the cation orvapour) to get Hg into the brain tissue. Also, tubulin in Alzheimer's disease is not in the correctplace (the cytosol, where it is found in normal brain). Instead it is found in the particulatefraction where the neurofibrillary tangles are found. Adding Hg to normal brain tissues causes2+
tubulin to not bind GTP, and to partition into the particulate fraction as is observed inAlzheimer's disease brain (274).
ASOMAT does NOT assert that mercury causes Alzheimer’s. ASOMAT does believe however,in the light of recent research (10,90,100,101,102,103), that it is quite possible that low levels ofmercury present in the brain could cause normal cell death, and that in susceptible people thiscould lead to dementia which would be similar to Alzheimer's disease. This would be entirelyconsistent with what is known in the literature about mercury’s neurotoxicity.
Professor Moore’s comments do not refute ASOMAT’s statement.
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ASOMAT SUBMISSION 12: Mercury from dental amalgams has been shown to be related toantibiotic resistance in the gut and oral cavity.
Professor Moore: Mercuric chloride was often used to sterilise infected apparatusin the past and as a cytotoxic agent. Mercury in the oral cavity might be expectedto support antibiotic action rather than promote antibiotic resistance inorganisms.
ASOMAT RESPONSE: The point of Prof. Moore’s comment is a little obscure. Prof. Moorehas not addressed the statement but has, yet again, made an assertion with no support from thescientific literature. What evidence does Prof. Moore have to justify what he has said? Is hereally asserting that amalgams are having an antibiotic effect in the oral cavity? Is he assertingthat this is in some way beneficial? Prof. Moore is obviously unfamiliar with the relevantresearch. Penicillin is an antibiotic and continued use of penicillin has led to penicillin resistance,one of modern medicine’s greatest problems. Published research (104,105,106,107) nowdemonstrates that mercury from dental amalgam may be a significant factor in antibioticresistance. The experiments also demonstrated that when the amalgam fillings were removedthere was a rapid return of non-antibiotic resistant organisms in the gut and the mouth. This issueis not yet resolved beyond dispute, but the published literature on the subject deserves a moreconsidered and thoughtful approach from Prof. Moore than he has so far demonstrated.
Professor Moore’s comments do not refute ASOMAT’s statement.
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ASOMAT SUBMISSION 13: Both Health Canada (1996a) and the World Health Organization(1991) consider dental amalgam to be the single largest source of mercury exposure for thegeneral public, with amalgam potentially contributing up to 84% (WHO, 1991) of total dailyintake of all forms of mercury from all sources. Therefore, the level of exposure resulting fromamalgam is not an issue of contention. The WHO also noted that for mercury vapour "a specificno-observed-effects level (NOEL) cannot be established, ie. NO level of Mercury Vapour hasbeen found that can be considered harmless.
Professor Moore: Of course Hg from amalgam is the most common source of Hgexposure in people - who could deny it - but the degree of exposure whileproportional to the amount of fillings is still small. It would be better to usedental materials other than amalgam. The dental profession has a vast researchbase addressing this.
ASOMAT RESPONSE: Interestingly enough and despite the available evidence, it is the dentalassociations, including the Australian Dental Association, who deny the above. Clearly Prof.Moore has not been reading the publications of the Australian Dental Association, even thoughhe has publicly supported their position on amalgams. ASOMAT applauds Prof. Moore’sagreement with the ASOMAT statement, and his acknowledgment that dental amalgam is thegreatest source of mercury to the non-occupationally exposed person. We also applaud ProfessorMoore's statement that it would be better to use non amalgam filling materials. We also agreethat the amount of exposure is small. We point out however, that in toxicological terms, ‘small’needs to be relative to the threshold for effects. Where no threshold has been defined (as with Hgvapour) it must be compared to a regulatory reference dose. The total dose may be small butwhere the reference dose is smaller, then the exposure can still be detrimental. Current research,using solid biochemical data, shows that ‘small’ as it is, it is still enough to compromise bodyhealth.
Professor Moore’s comments do not refute ASOMAT’s statement..
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ASOMAT SUBMISSION 14: Amalgam fillings have been associated, in the scientificliterature, with a variety of problems such as periodontal problems (pyorrhea), allergic reactions,oral lichen planus, interference with the immune system, as measured by the T-lymphocytecount, multiple sclerosis, fatigue, cardiovascular problems, skin rashes, endocrine disorders, eyeproblems. Blood mercury levels, significantly higher in amalgam patients than in non-amalgampatients, correlate with number and size of the fillings but return to normal when the fillings arereplaced.
Professor Moore: Bad dentistry causes periodontal disease rather than the use ofamalgam fillings - properly inserted. Anyone can become sensitised to Hg and ifthis is identified, the use of amalgam for dental reconstruction should be avoided -and replacement of amalgam filling with other materials justified. Mercury levelsin blood are normally extremely low. In a study in the 1970's we analysed 100random samples of blood bank blood and on all samples Hg concentration was below the then level of detection with the AAS. In those days most of these bloodsamples would have come from donors carrying amalgam fillings. It would seemthat people are not being unduly exposed - even those prone to eating fish. Catssampled at the same time had measurable blood levels of Hg but none showed anysigns of Hg intoxication.
ASOMAT RESPONSE: Periodontal disease begins as gingivitis, a symptom put forward byProf. Moore himself (statement #4) as one of the effects of mercury exposure. It seemsinconsistent to then deny, or at least ignore the possibility of a connection between periodontaldisease and mercury exposure from amalgams.
Professor Moore’s comments are not illuminating. He makes no mention of any attempt tocorrelate symptoms with mercury exposure or tissue mercury levels, only of measuring bloodlevels. Even then there is no information on the number of amalgam fillings, only thepresumption that the ‘blood samples would have come from donors carrying amalgam fillings’. It is not clear how the above study contributes to our understanding of this issue, nor is it clearhow it relates to the statement made at the beginning of this section. Blood mercury levels,significantly higher in amalgam patients than in non-amalgam patients, correlate with the numberand size of the fillings but return to normal when the fillings are replaced (200,201,202). In onestudy (203) , the daily intake of mercury from amalgams in the subjects was estimated to be at least1.5ug. Scientific research has clearly established that mercury vapour passes very rapidly fromblood to tissue and that levels of mercury in blood or urine are not reflective of the mercury inthe body (204,205,206).
While bad dentistry can be ONE reason for periodontal problems, it is by no means the onlycause. Amalgam, as reported in peer reviewed literature, is also a cause.
(See appendix 7 for further discussion on amalgams and periodontal disease )
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ASOMAT SUBMISSION 14 continued:
Professor Moore's response has ignored the ASOMAT observation of other effects of mercury,specifically in the areas of allergic reactions, (109,110,111,112,113,114,115,116,117, 118,119,121,122 ). Orallichen planus, and interference with the immune system as measured by the T-lymphocyte count(123,124,125,126,127,128,129,130,131,132,133), multiple sclerosis (134,135,136,137, 138,139), fatigue(142,143,144,145,146,147,148,149,150,151), cardiovascular problems (142,152,153,154,155, 156,157,158,
Professor Moore’s comments do not refute ASOMAT’s statement.
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ASOMAT SUBMISSION 15: Claims by the Australian and American Dental Associations thatthe incidence of mercury allergy is less than 1% have never cited any references. Such claims aretotally refuted by the scientific literature. Published peer reviewed studies show allergic reactionsrange from 5%-8% (Nth Am Derm Gp) up to 39% (Miller et al).
Professor Moore: Hg related allergy is irrelevant to the problem of chronic Hgtoxicity - especially as it affects the CNS.
ASOMAT RESPONSE: Peer reviewed published research has reported allergy levels of 5%-8%(Rudner) 27% (Djerrasi & Berova), 2%-10.8 % (White & Brandt), 31%, 27%, 32%, 39% (Miller et al),11.3% (Brun), 9.6 % (Nebenfuher et al), 13% (Sato et al) (119, 275,276, 278,279,280). Despite thisresearch, the dental associations, including the Australian Dental Association, have, withoutoffering any supporting evidence, falsely stated, and continued to maintain, that the true incidenceof mercury allergy is much less than 1% (Dr. Sheldon Newman “Amalgam best material, Expert Reports”
AmDA News September1,1986). They continue to publicly claim that amalgam is only dangerous tothose 'rare individuals' who are allergic to amalgam. Such comments are blatantly false andmisleading. (Even Caulk Co., the manufacturers of the Dispersalloy brand of amalgam warn:"Allergic reactions that may occur in previously exposed persons include dermatitis,encephalitis, and death”).
As cited above, the research shows allergy levels of up to 39%. Prof. Moore asserts that Hgrelated allergy is irrelevant to the problem of chronic Hg toxicity. Hg allergy is, however, VERYrelevant in the context of health effects and mercury exposure. It is relevant because mercuryallergies are caused by mercury binding to a host protein, forming a P-S-Hg-X complex that thebody’s immune system recognizes as a foreign protein and which it attacks. Low level chronicexposure would sensitize the immune system of anyone with the genetic make-up predisposingthem to having this problem. It is similar to the penicillin sensitivity that many individuals have. The sensitivity is not to penicillin but to host proteins that are covalently modified by penicillinand appear as foreign proteins to the immune system. Assuming half of the Australian populationhave amalgam fillings and 13% (119) of them showed symptoms caused by true allergy tomercury, this would mean that over 1,700,000 people have had their immune systemcompromised to some extent, either minor or significant, by a toxic substance, the most commonsource of which, as Prof. Moore has unequivocally acknowledged (statement 13), is dentalamalgams!
(See Appendix 8 for further discussion on allergy and amalgams including discussion of OralLichenoid reactions)
Professor Moore’s comments do not refute ASOMAT’s statement.
ASOMAT SUBMISSION 16: The earliest symptoms of long term, low level mercury poisoning
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are sub-clinical and neurological. Consequently, due to their subtlety, these symptoms are easilymisdiagnosed.
Professor Moore: How is sub-clinical neurological damage - (if it is due to Hgexposure) recognized. By definition this would be pre-symptomatic
ASOMAT RESPONSE: This is a challenge to our approach to health care and requires adifferent awareness of prevention. If all symptoms were totally reversible, with no enduringdamage to the patient, then the problem would be relatively straightforward. Unfortunately, bythe time chronic mercury toxicity is accurately recognised, the damage is done and often NOTtotally reversible, even though significant improvements can be achieved with appropriatetreatment. A contemporary example of this is Pink’s disease where those patients affected byexposure to mercury as children are still being affected, even though the original source ofexposure is now absent.
The fact that such potential irreversibility exists is the reason that prevention and caution must bethe dominant sentiments in national health policy, and why the onus of proof of safe levelsMUST be on those who advocate the use of this material and not on those in whose mouths it isplaced. The consequences of getting it wrong (most recently demonstrated by the Faroe Islandsstudy, cited in Appendix 3, in which neurological damage by methyl mercury was shown at levelspreviously considered safe) are too debilitating and too long lasting. We must begin to think interms of potential and pre-symptomatic effects. In studies in which rats were exposed to mercuryvapour, it was found that they showed few clinical symptoms, even though 41% to 75% of theirbrain tubulin was dysfunctional. In amyotrophic lateral sclerosis (ALS), over one half of theneurons were destroyed before the patients showed signs of clinical distress.
What constitutes clinical versus sub-clinical health impairment? In the case of lead exposure inchildren for example, no clinical measurement or test can be applied to the individual children tomeasure impairment of IQ due to lead exposure. However, groups of children exposed to leadhave a slightly lower average IQ than do children with no lead exposure. Is the effect clinical orsub-clinical? Does this make low level lead exposure less biologically (or societally) significant? The answer must surely be NO. Similar results have already been reported with low levels ofmercury exposure (Faroe Islands Study (50), Marlowe et al. (52) in Appendix 3).
There is obviously a lot of neural redundancy in the body but is it really Prof. Moore’s contentionthat we should casually, and with a cavalier attitude, take known and universally acknowledged toxins into our body just because we can withstand a certain amount before obvious, but oftenirreversible, symptoms become apparent? Is such a position morally and ethically justified whensafer alternatives have been available for many years? It is widely acknowledged within the dentalprofession that the main obstacle to universal use of the alternatives in Australia is the inadequateskill levels of the majority of practising dentists. The response must be more concentrated trainingof the dental profession, not a resigned acceptance that toxic contamination of the population isan acceptable trade-off for more ‘easy to use’ materials.
Professor Moore’s comments do not refute ASOMAT’s statement.
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ASOMAT SUBMISSION 17: Some recent studies show that at least 50% of dentists withelevated mercury levels had peripheral nervous disorders and that dentists have twice the rate ofGlioblastomas than non-dentists.
Professor Moore: Peripheral nervous disorders in dentists have to be properlyevaluated as to aetiology and not necessarily land at the door of Hg exposure. Renal damage would become evident before any sign of a peripheral neurologicaldisorder due to mercuric ion.
ASOMAT RESPONSE: The studies referred to, Ahlbom, (281) and Shapiro (222), WERE properlyevaluated and DID show what is stated above. Ahlbom made no observations about the cause ofthe tumours other than saying that there must be some factor in the practice of dentistry whichwas responsible. A possible clue that mercury is responsible comes from research by Arrhenius1971 (282), who hypothesised that methyl mercury might enhance the tumour inducing effect ofcertain amines, in vivo, by inhibition of enzymes involved in detoxification, thereby leading to anaccumulation of carcinogenic intermediates. Neither the tissue mercury levels, nor the dental stateof the subjects are known. Only conjecture is possible, but if their own mouths were filled withamalgams then their exposure to mercury could have been significant, with all the attendantbiochemical disruption. Nevertheless, while the Ahlbom report is clearly not an unequivocalexample of mercury induced problems, it clearly disproves the assertion that dental personnel areas healthy, if not healthier, than the general population, which was the main reason it was cited.On the other hand, Shapiro’s report is more definite. He wrote, "298 dentists, 30% of the highmercury dentists had polyneuropathies. No polyneuropathies were detected in the control group.The high mercury group had mild visuographic dysfunction; they also had moresymptom-distress than did the control group. These findings suggest that the use of mercury as arestorative material is a health risk for dentists."
The symptoms reported above are consistent with what is known about the neurotoxic effects ofmercury. Given this, and the fact that the source of mercury was mercury vapour and not mercurycation, the proposition that mercury is responsible, in the absence of a reasonable alternativeexplanation from Prof. Moore, is a sound and reasonable one.
See Appendix 9 for further discussion on dentist’s health
Professor Moore’s comments do not refute ASOMAT’s statement.
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ASOMAT SUBMISSION 18: Research shows female dental personnel have twice the rate ofinfertility, miscarriage and spontaneous abortion than the rest of the population.
Professor Moore: Again, fertility problems in women have to be properly evaluated in relation toaetiology and not automatically charged to mercury exposure.
ASOMAT RESPONSE: We agree with Prof. Moore’s comment. The point was made todemonstrate the inaccuracy of constant assertions that the health of dentists and dental personnelwas as good as, if not better, than the general population. The studies referred to (283, 284, 285, 286)
in the above point clearly show that such assertions are not factually based.
Professor Moore’s comments do not refute ASOMAT’s statement.
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ASOMAT SUBMISSION 19: Mercury from dental amalgams crosses the placenta,accumulating in the foetus, and is also transferred through the breast milk to neonates.
Professor Moore: Of course Hg in tiny amounts can get into any tissues includingthe foetus but would in these amounts be rendered harmless and has never beenshown to cause disease.
ASOMAT RESPONSE: Professor Moore's comments are that Hg would be rendered harmlessif it got into any tissue in the foetus. Major scientific bodies and institutions throughout the worldhave long ago agreed that there is no known safe level of mercury in the body. Where is Prof.Moore’s evidence to the contrary? Where is his evidence that mercury in neonates is renderedharmless? Prof. Moore’s comments are not scientific fact. They are personal speculation andopinion, unsupported by any of the scientific literature.
The facts are that disease has never been shown because it has never been fully investigated.Animal studies demonstrate potential neurobehavioural deficits in offspring due to exposure ofpregnant animals to mercury vapour. This was one of the major concerns of Professor Mats Berlinin his recent review of the literature for the Swedish Government’s Council for Planning andCoordinating Research. In the absence of proper investigation, absence of proof cannot be seenas proof of absence. Mercury is known to cause genetic damage in animals. How can we assumethat similar results will NOT occur in humans, particularly when there is already some evidence(referred to in statement #4 and Appendix 3) that similar effects are present in humans. What level ofirreversible damage does Prof. Moore feel is acceptable as a trade-off for easier-to-use dentalmaterials?
As far back as 1984 the USEPA stated that “Women chronically exposed to mercury vapourexperienced increased frequencies of menstrual disturbances and spontaneous abortions”, and ...“A high mortality rate was observed among infants born to women who displayed symptoms ofmercury poisoning” (240). Many other studies also support these findings (151,241,242,243,244).
Professor Moore’s comments do not refute ASOMAT’s statement.
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ASOMAT SUBMISSION 20: Wolf et al in 1983 in the journal 'Neurotoxicology' stated, “It isgenerally agreed that if amalgam was introduced today as a restorative material, it would neverpass FDA approval".
Professor Moore: Agreed - given the ridiculous official and public perceptions,and of over reaction to toxicity at present.
ASOMAT RESPONSE: The reason that amalgam would not pass FDA approval is due to itshighly toxic nature. It has nothing to do with perceptions. Prof. Moore’s assessment ofperceptions being ‘ridiculous’ is a personal view and does not constitute scientific evaluation ofthis issue. Prof. Moore might like to read Science V279, 20 March 1998, page 1850, where proofof a mercury-malarial link was uncovered in Brazil among natives living near gold mines. Perhaps Prof. Moore is under reacting.
Professor Moore’s comments do not refute ASOMAT’s statement.
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ASOMAT SUBMISSION 21: The German and Norwegian Health Departments have directedtheir dental professions to NOT use amalgams in pregnant women, and the German HealthDepartment has also directed that children not receive dental amalgams.
Professor Moore: The Germans and Norwegians are prone to over reactionespecially where the environment is concerned. Their views should be taken withconsiderable reservation.
ASOMAT RESPONSE: Professor Moore’s comment is irrelevant, unsubstantiated andinappropriate.
Professor Moore’s comments do not refute ASOMAT’s statement.
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ASOMAT SUBMISSION 22: Canada Health, in the wake of the Richardson report, has statedsimilar views and has also added that people with kidney problems should not have amalgamfillings placed.
Professor Moore: Canada Health is more reliable and their reasoning inrelationship to renal disease is more reasonable.
ASOMAT RESPONSE: Given that Prof. Moore feels the Canadian position on renal disease ismore reasonable, can we assume that he also endorses Canada Health’s recommendations aboutthe use of amalgams in young children and pregnant women? Does he then endorse the amalgammanufacturer’s warnings, which include kidney disease as a contraindication to the use of dentalamalgams? Is Prof. Moore willing to advise the Australian Dental Association to that effect?Curiously, Prof. Moore rejects the position of the German and Norwegian governments, eventhough their recommendations are almost the same as those of Canada Health. Why?
Professor Moore’s comments do not refute ASOMAT’s statement.
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Appendices
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Appendix 1: THE SYNERGISM OF MERCURY and VARIOUS OTHER SUBSTANCES.
In a study (24) which looked at a common amalgam (Dispersalloy), the researchers reported....“Dispersalloy was severely cytotoxic initially when Zn release was greatest, but was less toxicbetween 48 and 72 hours as Zn release decreased.” Zn, at the amount released from an amalgam,should not reach cytotoxic levels. It does however, potentiate the toxicity of the mercury releasedby tying up protective mercury chelators due to the fact that Zn and Hg both have a high affinityfor sulfhydryls. In experiments investigating this effect, it was found that addition of non-toxicamounts of Zn2+ (5-10 micromolar) enhanced the toxicity of mercury about 5-fold. (Personal
communication: Prof. Boyd Haley. Prof. and Chair, Dept of Chemistry, Univ of Kentucky)
The effects of mercury and lead combined have also been reported. One study showed that whena lethal dose (LD1) of mercury was combined with 1/20 LD1 of lead, the combination of the tworesulted in a LD100 in the test animals(44). This has not been investigated in human subjects butit is clearly reasonable to assume the possibility of similar effects in amalgam-bearing humans.
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Appendix 2: ATSDR
The Agency for Toxic Substances and Disease Registry (ATSDR) is an agency mandated by theUnited States Government to develop, jointly with the US EPA, a list of hazardous substances,and to rank them in order of priority. In response to this mandate the ATSDR developed ‘MinimalRisk Levels’ (MRL’s). MRL’s are an estimate of the daily human exposure to a hazardoussubstance that is likely to be without appreciable risk of adverse non-cancer health effects over aspecified duration of exposure.
The toxicological profiles include an examination, summary and interpretation of toxicologicalinformation and epidemiological evaluations of a hazardous substance. During the developmentof toxicological profiles, MRL’s are derived when ATSDR determines that reliable and sufficientdata exists to identify the target organ(s) which are affected, as well as the most sensitive healtheffects for a specific duration for a given route of exposure to the substance.
Proposed MRL’s undergo a rigorous review process. They are reviewed by the Health Effects MRL Workgroup within the division of Toxicology, an expert panel of external peer reviewers,the agency wide MRL workgroup, and with participation from other federal agencies, includingthe EPA, and are submitted for public comment through the toxicological profile publiccomment period.
The ATSDR list mercury as one of the twenty most hazardous substances known to man. TheATSDR has established "Minimal Risk Levels" (MRL's) for the various forms of mercury relatedto their route of exposure. The current (1994) MRL for acute inhalation exposure to metallicmercury vapour is 0.02 mcg Hg/m3 and for chronic inhalation exposure it is 0.014 mcg Hg/m3.These levels should be kept in mind when noting published levels in some studies (40,42,47,48,49,51),
of mercury vapour of 87mcg/m3, where some individuals measured as high as 100mcg/m3 (37).
SYMPTOMS of Hg EXPOSURE and REVERSIBILITY.
Regarding the clinical signs of mercury vapour exposure, it is important to distinguish betweenlarge acute exposures and those of long-term, low-level chronic exposure, known asmicro-mercurialism. For acute exposure, Prof. Moore's assertions may be valid, but theassumption that the symptoms are reversible by removing the person from the source of themercury, is limited and not necessarily the case. Intention tremor must be regarded as indicativeof serious neurological damage and is not always reversible. Micromercurialism is characterisedby many symptoms, the earliest of which are subclinical and neurological (43). Mercury vaporizescontinuously from dental fillings, and this is intensified by chewing, tooth brushing and hotliquids (45, 48). After mastication or tooth brushing ceases it takes almost 90 minutes for the rateof vaporisation to decline to the lower pre-chewing level. Also, the greater the number of fillingsand the larger the chewing surface area, the larger the mercury exposure (48). Thus, the averageindividual is on a roller coaster of mercury vapour exposure during the day. Breakfast will causethe release rate to increase and just as the rate is slowing again, it is time for the mid-morningcoffee break. Lunch, the evening meal and bedtime snacks all contribute to the daily exposure tomercury from dental fillings. Even the manufacturer, Caulk Company, has listed on their MaterialSafety Data Sheet, many of the symptoms of
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Appendix 2 continued:
micromercurialism: "Section VIII - Control Measures, Inhalation, Chronic: Inhalation of mercuryvapour over a long period may cause mercurialism, which is characterized by fine tremors anderethism. Tremors may affect the hands first, but may also become evident in the face, arms, andlegs. Erethism may be manifested by abnormal shyness, blushing, self consciousness, depressionor despondency, resentment of criticism, irritability or excitability, headache, fatigue, andinsomnia. In severe cases, hallucinations, loss of memory, and mental deterioration may occur.Concentrations as low as 0.03 mg/m3 have induced psychiatric symptoms in humans. Renalinvolvement may be indicated by proteinuria, albuminuria, enzymuria, and anuria. Other effectsmay include salivation, gingivitis, stomatitis, loosening of the teeth, blue lines on the gums,diarrhoea, chronic pneumonitis and mild anaemia. Repeated exposure to mercury and itscompounds may result in sensitisation. Intrauterine exposure may result in tremors andinvoluntary movements in the infants. Mercury is excreted in breast milk. Paternal reproductiveeffects, and effects on fertility, have been reported in male rats following repeated inhalationexposures. "The Caulk Co. also warns that mercury may be a skin sensitizer, pulmonarysensitizer, nephrotoxin and neurotoxin, and further cautions that the number of amalgamrestorations for one patient should be kept to a minimum.The above symptoms are not new. Even the dental industry has given warnings to the dentalprofession regarding the dangers of inhaling low levels of mercury vapour over a long period.“Mercury Contamination in the Dental Office. A Review” (The NYS Dental Journal, November1979, pp 457-458), stated...“The symptoms of mercury poisoning from chronic inhalationdevelop gradually and thus, may be difficult to notice. With the exception of tremor, thesymptoms may be ignored by the victim or attributed to other causes. This lack of awareness isparticularly likely in the case of erethism, a condition characterized by irritability, outbursts oftemper, excitability, shyness, resentment of criticism, headache, fatigue and indecision.
Erethism is the most difficult manifestation of mercury poisoning to evaluate, especially iftremors are absent, and its symptoms may be attributed to anxiety or neuroasthenia. Other generalsymptoms associated with mercury poisoning include weakness, unusual fatigue, loss of weight,loss of appetite, insomnia and gastrointestinal disturbances.
A condition known as micromercurialism, is said to account for psychological changes observedin persons frequently exposed to low concentrations of mercury in the air, concentrations found inthe majority of dental offices surveyed. The syndrome is characterized by: decreasedproductivity, loss of memory, loss of self confidence, depression, fatigue and irritability.
In a study (46) which exposed rats to 0.3mg/m Hg for 4 hours a day for two weeks it was foundthat viable brain tubulin decreased between 41% to 75%. How would this compare to a lifetimeof chronic exposure? What are the implications for those individuals that are near that "thin redline" going over to Alzheimer-like dementia, whose brain tubulin is already compromised. Doesthe dental association only consider mercury toxicity effects on the totally healthy, or should weconsider the cumulative effects in the medically compromised of what is universallyacknowledged to be a potent neurotoxin?
Appendix 3: FAROE ISLANDS STUDY
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This study is included as an example where effects were measured at levels previously thought tobe safe, so we cannot assume that levels of exposure to mercury from amalgam are ‘safe’particularly since it is acknowledged that studies have not been performed for the appropriate endpoints (neurotox) on the appropriate at-risk population (people with amalgam). Secondly, becausethe mechanism of absorption into the brain is the same for methyl and elemental (vapour)mercury, it is likely that mercury vapour will accumulate as easily in the brain.
The publication of this widely discussed Faroe Islands study should have a dramatic impact onevaluation of mercury exposure to unborn babies. Obviously, the adverse effect is not detectableat birth, and shows a dramatic impact on quality of life for the affected individuals. Thesignificance to dentistry of this study is that methyl mercury and mercury vapour are the twoforms of mercury that readily penetrate cell membranes and accumulate in tissues of unbornbabies. Methyl mercury is derived primarily from consumption of fish and seafood, whereas theprimary contributor of mercury vapour to human body burdens comes from dental fillings.
This research, (50) also reported on in the Lancet, adds to the concern about effects of low levelsof mercury on children's development raised some time ago by Marlowe et al.(52) Their researchfound that low mercury levels correlated significantly and negatively with full scale, verbal, andperformance IQ and six subset scores of the intelligence test. They concluded that a continuing re-examination of mercury exposure was needed because mercury levels previously thoughtharmless and routinely encountered in the environment may be associated wth intellectualdecrements. Their concern about the adverse effects of low levels of mercury on the developmentprocess was influenced by several points. Firstly, the effects could signal the early stages of anongoing toxic process that becomes more disabling with age. Animal studies have shown thatanimals exposed at an early age showed only slight retardation but by adulthood overtneurological impairment, measured by co-ordination problems became evident. As the animalsapproached middle age, central nervous system involvement became obvious and behaviouraltests were no longer needed to identify exposed animals. When one appreciates the fact thatmercury amalgam fillings release mercury vapour over the entire life of the filling, theimplications of this research become even more significant. The second reason was that there isconsiderable individual variation to mercury, a variation that applies to most metal pollutants. Apollutant that produces subtle behavioural alterations in many children may produce a severelearning disorder in those who are especially susceptible because of genetic or other factors. Thethird reason was that behavioural effects of children affected by mercury could make the childdifficult to parent or instruct leading to tension that became aggravated over time. The difficultyin instructing would also presumably add to the problems caused by the neurological impairmentalready present. The implications of this study and the Faroe Islands study need to be consideredin conjunction with Drasch's recent studies (57, 86)
Prof. Drasch’s research has demonstrated that mercury from amalgam will be similarlytransported. Professor Drasch in 1994 demonstrated that the level of mercury in the foetus, new-born and young child is directly proportional to the number of amalgams in the mother’s mouth. It therefore does not matter if the woman falls pregnant 10 years after having her amalgamsplaced, the foetus is still exposed to both mercury and methyl mercury.
Appendix 3 continued:
Prof. Drasch stated "Future discussion on the pros and cons of dental amalgam should not be
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limited to adults or children with their own amalgam fillings, but also include foetal exposure.The unrestricted application of amalgam for dental restorations in women before and during thechild-bearing age should be reconsidered." In another paper he also concluded: "These resultsshow that amalgam fillings release silver as well.........Silver is a reliable marker for the fact thatthe elevated concentrations of inorganic mercury found in tissues of people with amalgam filings, derive mainly from these fillings and not from other theoretically possible sources."
Clearly, there is no place for mercury amalgams in the mouths of children, young and old,pregnant or fertile women or nursing mothers.
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Appendix 4: ACCUMULATION OF AMALGAM DERIVED MERCURY IN THE CNS
Uncharged mercury ions will be oxidised in the blood and, although this process is rapid, it is notimmediate. This is ample time for circulation and transport across the blood brain barrier. Onceinside the CNS it will be oxidised to Hg and in this form cannot escape back across the blood2+
brain barrier. This is one of the mechanisms by which mercury is locked into the CNS. Tosuggest that mercury vapour does not readily pass into the CNS is incorrect. It is well documentedthat CNS is one of the main target organs for both mercury vapour and inorganic mercury.
Three mechanisms are known by which mercury is transported into the CNS:
a) Inhaled mercury is absorbed from the lungs and into the blood, by which route it is transportedthroughout the body and across the blood brain barrier. (53,54,55,56) .b) Stortebecker and others (43) have demonstrated that mercury vapour in the oral cavity willadhere to the oro-nasal mucosa and pass directly through the bone at the base of the skull to enterthe brain.c) Some mercury from amalgams will be transported through the tooth and also from the oralmucosa, and undergo retrograde axonal transport back to the brain. Transport along nerve fibreshas been shown to be at a rate of approximately 10mm per day (58,59,60) .
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Appendix 5: MERCURY AND BREAST MILK
The ability of metal ions to concentrate in mothers' milk has been scientifically established foryears, as has the ability for methyl mercury to transfer to breast milk and cause neurologicdamage to infants (69) .The investigation of the possible transfer of mercury specifically fromamalgam dental fillings to mothers' milk, began in 1990. A study by Vimy et al (236) implantedamalgam fillings, seeded with radioactively labelled mercury, into pregnant ewes. Sinceradioactively labelled mercury does not occur naturally, it was possible to detect mercury intissues that were specifically derived from the amalgam dental fillings. The amalgam mercurywas found to quickly accumulate in tissues of mothers and foetuses, appearing in foetal tissuewithin two days of the amalgams being placed in the mother's teeth. In the lactating ewes, thelevels of labelled mercury in milk were as much as six times higher than the levels of labelledmercury in their blood. Another recent study by Vimy, MJ; et al, (237) evaluated mercury related to amalgam dentalfillings transferring to breast milk in both animals and humans. In the animal study, lactatingewes with amalgam fillings nursed foster lambs from ewes without amalgam fillings. Theamalgam fillings contained a portion of radioactively labelled mercury, which was found in thetissues of the foster lambs. This confirmed the transfer of mercury from the amalgam fillings ofthe mothers, into the breast milk, then into the tissues of the foster lambs. The human studyexamined mercury levels in breast milk of 33 lactating women. The mercury levels correlatedwith the number of amalgam fillings or mercury vapour concentration levels in mouth air. Theinfant exposure levels were compared to the United States Public Health Service Minimal RiskLevel (MRL) standard for adults, and caution was urged. The combination of prenatal mercuryexposure and lactating exposure to maternal amalgam mercury was addressed. Other importantfactors addressed were mercury exposures related to the differences in body mass between infantsand adults and the particular sensitivity of infants to heavy metal toxic effects. The findingssuggested that placement and removal of "silver" tooth fillings in pregnant and lactating humanswill subject the foetus and neonate to unnecessary risk of Hg exposure.
Schumann 1990, Yoshida, M. et al 1994, Oskarsson, A. et al 1995, 1996, (235,245,221) found thatany form of mercury can transfer to breast milk and, from there, into the tissues of infants,although the fat soluble forms of mercury (methyl mercury and mercury vapour) will concentratemore in brain tissue of infants. The Schumann study pointed out that milk increases thebioavailability of Hg , as the ionic mercury is bound to a greater extent in the red blood cells of2+
the suckling infants. In an evaluation of lactating human females, the study by Oskarsson andAssociates found that dental amalgam mercury transferred to mothers' milk, but that methylmercury from consumption of fish correlated to mercury levels in blood but not to levels in milk.In the portion of the study on rats and mice, the mercury was found to cause pathologic effects inthe offspring, including alteration of the thymocytes, increased lymphocyte activities, and effectson noradrenaline and nerve growth factor in the developing brains. These effects occurred in theanimals exposed to methyl mercury.
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Appendix 5 continued:
It has been well established scientifically that mercury vapour, being lipid soluble, functions verysimilar to methyl mercury pathologically. There have been other studies confirming the harmfuleffects of mercury vapour on unborn babies and developing infants (214,220,238) It should beemphasised that the studies cited herein clearly show that mercury damage to unborn babies andinfants is not readily observable early on. The neurological damage is develop- mental in nature,primarily affecting learning, behavior and neurological function. These effects can dramaticallyalter the functioning of the individual throughout life. Schumann (235) found
that early exposure to inorganic or organic mercury can even result in mental retardation. In asubsequent study, Oskarsson et al (68) confirmed the accumulation of dental amalgam mercury inmothers' milk. This study found that amalgam mercury dental fillings were the main source ofmercury in the milk of lactating humans, related the exposure to the World Health Organizationstandard for daily intake for adults, and concluded it to be significant enough to be a risk toinfants.
At this point, the scientific evidence clearly establishes that mercury transfers from amalgamdental fillings to the tissues of unborn babies and to mothers' milk; from the milk to body tissuesof infants, and, according to existing standards, presents a health risk to the infants. Thecombination of prenatal exposure and neonatal exposure from nursing presents an undeniableconcern. Oskarsson et al (68) stated: "We concluded that efforts should be made to decreasemercury burden in fertile women."
It is also now documented (50) that mercury in the developing infant and foetus can lead topermanent and irreversible brain damage and is discussed in Appendix 3
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Appendix 6: TOXICITY OF MERCURY
Chronic exposure to mercury vapour produces neurological effects which include excitation,tremors, insomnia, vasomotor disturbances, gingivitis and kidney dysfunction. Toxicity ofinorganic mercury includes inflammation of mucosal surface of the mouth, gingivitis withswelling, and kidney dysfunction (nephrotic syndrome) (71,72,73,74,75,76).
Neurological damage is sustained by chronic exposure to mercury vapour. This is relevant notonly for the patients receiving amalgam fillings but also for the future children of women withamalgam fillings. It is also relevant to dentists who place it. Many studies have demonstratedneurological damage to dental personnel (12,77,78,79,80,81,82,83,84,85)
In another recent study (5), the authors included a significant comment:
"We once stated that our experimental results can not be used to support either side of thecontroversy dealing with whether mercury vapour liberated from dental amalgam is harmful orinvolved in the etiology of disease(s). In the present study, however, in which dental technicianswere exposed to mercury vapour as a result of their working with amalgams, the mean urinarymercury level after the DMPS challenge was adversely and statistically associated with functionsrelated to complex attention, a psychomotor task, mood and symptoms in a linear dose-effectmanner. Of singular importance, this investigation establishes a firm protocol for the evaluationof dental personnel regarding potential adverse neurological effects from occupational exposureto amalgam mercury"
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Appendix 7: AMALGAM FILLINGS AND PERIODONTAL PROBLEMS
Periodontal disease produces hydrogen sulfide and methylthiol compounds as evidenced bynumerous publications (and breath odor). Hydrogen sulfide (H2S) reacts with mercury vapour toproduce mercury sulfide (HgS) which produces the "amalgam tattoo" often seen around infectedteeth in the mouths of individuals with amalgams (note HgS is the mineral cinnabar from whichHg is mined, HgS is classified as extremely toxic). More importantly, methylthiol reacts with Hgto form methylthiol-mercury which is extremely cytotoxic, like methyl-mercury and dimethylmercury. These mercury methylthiol compounds are more lethal than Hg . 2+
(from Prof Boyd Haley report. See Appendix 12 for more detailed discussion)
There are several published studies linking the presence of amalgam fillings and periodontalproblems. Catsakis and Sulica,(108) from the Georgetown University School of Dentistry inWashington D.C. reported a case of persistent periodontitis which did not clear up, despiteconstant periodontal therapy up to and including periodontal surgery, until all the amalgams wereremoved. The periodontal problem had persisted for seven years but after the amalgams wereremoved, the periodontal condition healed quickly and the tissues remained healthy for a periodof more than two years up to the time of publication of that report.
Fisher et al. (247) reported a study where 54 amalgams were placed in 43 patients and followed up,for up to four years. Yearly measurements were made between the alveolar crest and the apicalmargin of the fillings in the experimental group and the cementoenamel junction and the alveolarcrest in the control group. They found that in the experimental group the level of alveolar crestresorption was almost twice that of the control group, i.e. 0.8 mm vs 0.45 mm. This study needsto be considered in the light of the work of Freden in 1974.(248) He measured the amount ofmercury in tissues in contact with amalgams and found average levels 49 times higher thancontrol tissues from the same mouth. Is it reasonable to postulate, in light of our knowledge of theextreme toxicity of mercury, that some deleterious effect could be expected in tissues that have 49times more mercury compared with tissues which have no mercury? Is it even more reasonablewhen one considers research has shown that mercury in a concentration as low as 20 parts perbillion (ppb) was sufficient to stop osteoblastic activity. (Personal communication in Oct 1985regarding preliminary studies at the Department of Biology, University of Colorado, ColoradoSprings). Ellender et al (246) reported that nickel needed a concentration of 200 ppb to achieve thesame result. Finally, consider the findings of Koivumma & Makila (249) who reported that, of avariety of materials, amalgam, in a human mouth, attracted more plaque than any other material.
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Appendix 8: AMALGAMS, ALLERGIC REACTIONS and ORAL LICHENOID REACTIONS.
True allergy is only one of the possible immune reactions to mercury. General sensitivity to themetals in amalgams also exist. Mercury from amalgams has been implicated in immune disease.Lindquist &Mornstad (250) concluded that "It thus seems that mercury released from amalgamfillings may inititate or support an ongoing immune disease" and called for further research.
In 13 studies (251,252,253,254,255,256,257,258,259,260,261,262,263) 65%-100% of patients suffering fromOral lichenoid reactions experienced an improvement or total remission of their symptoms aftertheir amalgams were removed. In 9 of those studies they tested for allergic reactions to mercury.In 3 of them the reseachers reported 100% of the participants as testing allergic to mercury andthe others reported 19%-62% of the subjects showing allergic responses.
In the absence of any large studies to look at this problem one can only speculate on the financialcost to the community and the health care system of such a widespread effect on people’simmune systems. Few medical practitioners, and virtually no dentists, have the training todiagnose such an allergy. It would be unfortunate if the influence of dismissive opinions such asthose expressed by Professor Moore prevailed as a substitute for a serious attempt to study thisissue.
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Appendix 9: HEALTH OF DENTISTS
Many other studies also show health effects on dental personnel as a result of exposure tomercury vapour and the mercury derived from their own fillings (12,80,81,82,84,85,151,178,209,210, 211,
The higher suicide rates of the dental profession are also well known and have been commentedon many times (219,228,233,264,265,266,267). It is not known why this is so but it is foolish to ignorewhat IS known about the neurological, psychological and emotional effects of mercury vapourexposure. It is recognised and accepted that such effects include depression and suicidaltendencies. It is noteworthy that Simpson et al (1983) pointed out the probability that, for avariety of methodological and cultural reasons, the real incidence of suicide has been significantlyunder reported, perhaps by as much as 35%.
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Appendix 10: Text of letter from Dr. MARK RICHARDSONresponding to Eley’s criticism cited by Prof. Moore
Dear Dr. Lohyn:
Re: Criticism of my risk assessment of dental amalgam by Dr. B.M. Eley
At your request, I have reviewed a series of papers authored by Dr. B. M. Eley in the BritishDental Journal. These articles are entitled: “The future of dental amalgam: a review of theliterature, Part 1 through Part 7". I will restrict my comments to parts 4 and 5 in which Dr. Eley comments on and criticizes my risk assessment for Health Canada. As you know, my riskassessment is a Health Canada document, distributed by the department, as well as beingpublished in a peer-reviewed scientific journal.
Interestingly, unbeknownst to me at the time, two Swedish researchers also conducted andpublished an assessment of mercury exposure from dental amalgam (Weiner and Nylander,1995). Independently from me, they employed the same methodology as I did in estimatingexposure from urinary mercury levels. The publication of their assessment in a peer-reviewedSwedish journal adds further validity to the methods I employed in my risk assessment. Dr. Eley’s criticisms are primarily those developed by the Canadian Dental Association (CDA)and their “International Panel”. Dr. Eley was a member of that panel. The CDA panel reportwas submitted to Health Canada in response to my study. When their report was submitted, theCDA requested that it be appended to my risk assessment or be distributed by Health Canada. Health Canada refused both requests. I would speculate that the criticisms were not ofsufficient quality or validity to warrant departmental support or acceptance. I find it somewhat difficult to take Dr. Eley’s criticisms too seriously. Firstly, my riskassessment has undergone the most rigorous peer review possible, including 16 national andinternational scientists, regulators and risk assessment specialists, as well as three additionalanonymous peer reviewers prior to its acceptance and publication in the journal Human and Ecological Risk Assessment. Secondly, Dr. Eley’s papers are fraught with factual errors and contradictions. Of greatest note,he claims my study results to be invalid and then in Table IX of part 4 he presents what hepurports to be the more accurate estimates of exposure. Note that Table IX does not containdata from Mackert, as the Table legend suggests, but rather presents the results of my ownexposure calculations from my report for Health Canada. The data that he presents in TableVIII, which he attributes to me, is fictitious. I have no idea where the data in Table VIII comesfrom but it most certainly is not from my published study. Dr. Eley obviously believes that thedata in Table IX are correct. Therefore, he supports the results of my study. What more needsto be said.
The other major contradiction that I repeatedly encountered is Dr. Eley’s criticism of smallsample sizes in certain studies I have employed, and then he sites other ‘preferred’ studieswhich, upon examination, have similarly small, or smaller, sample sizes than the studies Iemployed.
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Richardson letter page 1 of 3
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Dr. Eley makes numerous criticisms of the assumptions I employed to estimate exposure tomercury from amalgam, and he (as well as others) contend that these criticisms somehowinvalidate the exposure estimates. However, Dr. Eley lauds the work of the U.S. Public HealthService in their review conducted in 1993 (CCEHRP, 1993). If you examine my estimates of exposure and those of the U.S. Public Health Service (CCEHRP, 1993), we are in virtually totalagreement as to the range of exposures which result from dental amalgam. Dr. Eley incorrectlyreports that the U.S.PHS estimated exposure to be 1 to 2 ug/day. In fact, they state thatexposure is from 1 to 5 ug/day for persons with 7 to 10 amalgam fillings. The reported maximum number of fillings being 25, at least in Canada, then this would suggest a range of 1to 12.5 ug/day for up to 25 amalgam fillings. My estimates for adult exposure from amalgamrange from 0.2 to 11.6 ug/day, virtually the same as U.S.PHS estimates for up to 25 fillings. Based on the comparability of exposure estimates, I find Dr. Eley’s contention that my resultsare somehow invalid quite confusing. Dr. Eley states that “the recent consensus view is that mercury vapour from dental amalgamrestorations results in the absorption of approximately 1 ug/day”. What consensus is hespeaking of? His own review examines numerous articles that assess exposure and there isanything but consensus. Estimates in the various papers range from 1 ug/day to about 30 ug/day. If any consensus has emerged, it is that exposure ranges from something slightly more than 0ug/day (for 1 filling) up to about 12 to 17 ug/day (for a high number of fillings, perhaps 25). This general range is supported by the work of the U.S.PHS (CCEHRP, 1993), the WHO(1991) and my own risk assessment (Richardson and Allan, 1996). Dr. Eley lauds the U.S.PHS study indicating its exposure assessment reviewed over 500articles. However, this is not correct. For their exposure assessment, Appendix III of theU.S.PHS report, the references are consecutively numbered and total 119. My own report toHealth Canada included 210 references. Dr. Eley relies extensively on comments provided by Dr. R. Mackert Jr. on my risk assessment. Dr. Mackert provided some valuable, substantive advice regarding my exposure models andmany of his comments were incorporated. However, not all of Dr. Mackert’s comments werefollowed. You must keep in mind, though, that his interest and involvement in this issue wasnot unbiased. Dr. Mackert was hired by Sybron Inc., one of North America’s largestmanufacturers of amalgam, to review and criticize my study. In fact, Sybron Inc. flew Dr.Mackert to Ottawa in their corporate jet on two separate occasions to meet with me and to tryand convince me of alternate assumptions which were all at the extreme low end of thespectrum of published values for the various assumptions required for my exposure models. Therefore, it should not be surprising that not all of Dr. Mackert’s comments were accepted asvalid, nor is it surprising that Dr. Mackert would find my analysis wanting because of it.
Table II in part 4 purports to list all the variables included in the Olsson and Bergman model(Olsson and Bergman, 1992). In fact, this is incorrect. The variables listed in Table II are thoserequired by myself and my co-investigator, Margaret Allan, for our ‘modified’ Olsson and Bergman model as developed in our risk assessment (Richardson and Allan, 1996). I can onlywonder if Dr. Eley actually read the paper by Olsson and Bergman.
Richardson letter page 2 of 3
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With regard to the establishment of a tolerable daily intake (TDI) for mercury vapour, Dr. Eleycontends that my use of the study of Fawer et al. (1983) is “totally inappropriate”. The basis forthis is that the health effect measured was hand tremor. I am at a loss to understand how hand tremor is a totally inappropriate endpoint to consider. Putting my work aside, both the U.S.Environmental Protection Agency (U.S.EPA, 1997) and the U.S. Agency for Toxic Substancesand Disease Registry (ATSDR, 1994, 1997) consider this a valid endpoint, in fact the preferredendpoint, for derivation of regulatory reference exposure levels. However, Dr. Eley is not atoxicologist, risk assessor, nor a practising chemical evaluator for a regulatory agency. Therefore, I would not expect him to fully understand the methods and bases of TDIderivations. There is other evidence that Dr. Eley does not understand regulatory risk assessment nortoxicology. For example, Table VII of part 4 lists a variety of air concentrations which Dr. Eleypresents as LOAELs (lowest-observed-adverse-effect-level) or NOAELs (no-observed-adverse-effect-level). His understanding of toxicological terminology and thesubject matter in general are regrettably poor. First, he lists the ‘clinical mercurialism’threshold as a LOAEL. In fact, a threshold is defined as the theoretical upper NOAEL. If itwere a LOAEL, by definition having some measurable effect, then it could not possibly be aNOAEL. This same error in understanding is repeated with the ‘nephrotoxicity threshold’, italso being indicated as a LOAEL. In Table VII of part 4, Dr. Eley also presents air concentrations of mercury for the “generalpublic threshold” and the “children, pregnant, sick threshold”. These values have no regulatorystatus whatsoever in any jurisdiction that I am aware of. These values appear to be extractedfrom two 1977 reviews of mercury toxicity. This somewhat dumbfounds me because at onepoint Dr. Eley criticizes my use of the Fawer et al. (1983) study for it being ‘old’ when theliterature he is relying on is even older. Dr. Eley goes on to criticize my uncertainty factors as being ‘inappropriate’. His explanations,however, are unsupported. When employing a LOAEL to establish a reference exposure level,it is routine in Canada to apply an uncertainty factor of 10, since we don’t know what the threshold of effect is. Applying a further factor of 10 to account for sensitive members of thepopulation (or inter-individual variation in sensitivity) is also routine. Occupational studies arethe preferred basis for establishing reference exposure levels because they are studies of people,not of rats, mice, monkeys or other laboratory animals. However, occupational studies usuallyinclude only healthy adult males, which are not representative of the whole non-occupationalpopulation. In part 5 of his series of articles, Dr. Eley contends that an air concentration of 25 ug/m3 in airwill result in a urine concentration of 75 ug/l. In fact, Roels et al. (1987) has published thebenchmark paper on this issue and demonstrated by regression analysis that a workroom air concentration of 25 ug/m3 will result in a urine concentration of 25 ug/l, not 75 ug/l. Again, Dr.Eley is relying on older studies, in this case an article from 1970. Yours sincerely,
G. Mark Richardson Ph.D.
Richardson letter page 3 of 3
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Appendix 11: EXECUTIVE SUMMARY OF RICHARDSON REPORT
ASSESSMENT OF MERCURY EXPOSURE AND RISKS FROM DENTAL AMALGAM by G. Mark Richardson,PhD., Medical Devices Bureau, Environmental Health Directorate, Health Canada, August 18, 1995, Final Report(released November 27, 1995, in Toronto, at the stakeholders' meeting)
Executive Summary For Canadians with amalgam-filled teeth, it was estimated that total mercury (Hg) exposureaverages: 3.3 ug Hg/day in toddlers (aged 3 to 4 years); 5.6 ug Hg/day in children (aged 5 to 11 years); 6.7 ug Hg/day in teens (aged 12 to 19 years); 9.4 ug Hg/day adults (aged 20 to 59 years; and 6.8 ug Hg/day in seniors (aged 60+ years). Ofthis exposure, amalgam was estimated to contribute 50% to total Hg exposure in adults, and 32 to 42% for other agegroups. Estimates, based on two independent models, of exposure from amalgam alone were: 0.8 - 1.4 ug Hg/day intoddlers; 1.1 - 1.7 ug Hg/day in children; 1.9 -2.5 ug Hg/day in teens; 3.4- 3.7 ug Hg/day in adults and 2.1 - 2.8 ugHg/day in seniors.
There are insufficient published data on the potential health effects of dental amalgam specifically to support or refutethe diverse variety of health effects attributed to it. Numerous studies constantly report effects on the central nervoussystem (CNS) in persons occupationally exposed to Hg. Virtually all studies failed to detect a threshold for the effectsCNS measured. A tolerable daily intake (TDI) of 0.014 ug Hg/kg body weight/day was proposed for mercury vapour, theprincipal form of mercury to which bearers of amalgam fillings are exposed. This TDI was based on a published accountof sub-clinical (i.e. not resulting in overt symptoms or medical care) CNS effects in occupationally exposed men, expressed as a slight tremor of the forearm. An uncertainty factor of 100 was applied to these data, to derive a referencedose (TDI) which should, in all probability, prevent the occurrence of CNS effects in non-occupationally- exposedindividuals bearing amalgam fillings.
The number of amalgam-filled teeth, for each age group, estimated to cause exposure equivalent to the TDI
were: 1 filling in toddlers; 1 filling in children; 3 fillings in teens; and 4 fillings in adults and seniors. It was
recognized that filling size and location (occlusal versus lingual or buccal) may also contribute to exposure.
However, data suggest that no improvement in prediction of exposure is offered by any particular measure of
amalgam load. Therefore, the estimates of exposure derived from the number of filled teeth were considered as
reliable as those that might be based on size and position of amalgam fillings, were such data available for the
Canadian population.
Effects caused by allergic hypersensitivity to amalgam or mercury, including possible auto- immune reactions, can notbe adequately addressed by any proposed tolerable daily intake. Individuals suspecting possible allergic or auto-immunereactions should avoid the use of amalgam selecting suitable alternate materials in consultation with dental care (andpossibly health care) professionals.
Preface This report has been prepared in response to concerns that exposure to mercury from dental amalgam mayadversely impact on health. Recent reviews (USDHHS 1993, Swedish National Board of Health, 1994) have concludedthat there is no evidence to suggest that dental amalgam, specifically, is injurious to health. However, the data baserelating health impacts in humans or animals to amalgam specifically is small and weak. This suggests that indirectevidence relating mercury vapour exposure (the predominant form of mercury released by dental amalgam) to humanhealth effects (for which a large data base exists) is a necessary basis for an evaluation of the possible health risks ofdental amalgam. In the reports previously mentioned, exposure to mercury arising from amalgam was not adequatelyquantified, and a level of mercury vapour exposure which is, in all probability, tolerable to the vast majority of personsbearing amalgam fillings, was not defined. This report attempts to address these previous deficiencies.
This report is not exhaustive. Recent reviews on mercury (WHO 1990, 1991; IARC 1993; ATSDR 1994) adequatelyreview many aspects of mercury toxicity and exposure. Instead, this report focuses on studies which report on healtheffects in dental care practitioners and other occupational groups exposed to relatively low levels of mercury. This reportalso examines recent research which hypothesizes a link between mercury exposure, and thereby dental amalgam, andAlzheimers' Disease. This report concentrates on effects associated with long term mercury vapour exposure (viainhalation) in humans. Other reviews (WHO 1990, 1991; IARC 1993; ATSDR 1994) examined acute and sub-chronicexposure in animals, and all aspects of the toxicology of exposure to other forms of mercury via other routes of exposure(ingestion, dermal absorption), in extensive and adequate detail such that this is not repeated here.
Any medical or dental material, such as amalgam, will have associated with it some degree of health risk. The purposeof this report is to attempt some determination of what that risk is (i.e. what effect(s) it may cause), how significant it is(i.e. what level of exposure should be free from effect), and what proportion of the population might be at some degreeof risk (i.e. how many exceed the level considered to be free from effect).
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Appendix 12:
RESULTS FROM THE BOYD HALEY LABORATORY RELATING THE TOXICEFFECTS OF MERCURY TO EXACERABATION OF THE MEDICAL CONDITIONCLASSIFIED AS ALZHEIMER'S DISEASE
Professor Boyd Haley, Chairman and Professor, Dept of Chemistry with joint appointment inthe College of Pharmacy, University of Kentucky
Research regarding Alzheimer's disease (AD) in our laboratory has been directed towardsdetecting aberrancy in the nucleotide binding proteins of AD post-mortem brain versus agematched control brain samples. Basic to all of our findings is the following observation. Twovery important brain nucleotide binding proteins, tubulin and creatine kinase (CK), show greatlydiminished nucleotide binding ability and they are abnormally partitioned into the membranefraction of brain tissue (1,2). What tubulin and CK have in common is that both have a veryreactive sulfhydryl which, if modified, inhibits their biological activity. Mercury has a very highaffinity for sulfhydryls and has been proven to be a potent inhibitor of both of these proteinsbiological activity.
After our laboratory demonstrated that tubulin had diminished biological activity in AD brain,and only AD brain, we searched for possible toxicants that might mimic this biological problem. Our finding was simple and straight-forward. After testing numerous heavy metals we observedthat only mercury-II cation (Hg ) could mimic this effect in homogenates of normal brain at2+
concentrations that might be expected to be found under toxic conditions (3,4). The observationwas that Hg at 1-5 micromolar levels could selectively and totally abolish the binding activity2+
of tubulin without any noticeable effect on other proteins. This gave a nucleotide binding profilethat was identical to that observed in AD brain (4,5). Further, recent results in our laboratoryhave shown that the addition of Hg to control brain homogenates not only caused the decrease2+
in nucleotide interaction but also caused the abnormal partitioning of tubulin and CK into theparticulate fraction as observed in AD brain (7). This was especially effected in the presence ofother metals (see below).
The next set of experiments was to determine if mercury vapor, the form that escapes fromdental amalgams, could mimic the effect in rats exposed to such vapor for various periods oftime (5). Rats are different from humans in that their cells can synthesize vitamin C whereashumans have to ingest vitamin C. Vitamin C is thought to be somewhat protective against heavymetal toxicity and other oxidative stresses. However, we observed that the tubulin in the brainsof rats exposed to mercury vapor lost between 41 and 75 percent of their nucleotide bindingcapability demonstrating a Hg induced similarity to the aberrancy observed in AD brain (5). 2+
Consistent with this was a recent report by Dr. Michael Aschner of Wake Forrest University atthe 1998 Spring IAOMT meeting. He stated that Western blot analysis of brains of rats exposedto mercury vapor (as above) showed elevated levels of an enzyme called glutamine synthetase(GS) when compared to non-treated controls. This is consistent with a report published fromour laboratory in 1992 where we predicted that the elevation of GS in the cerebrospinal fluid ofAD patients had potential as a diagnostic marker for AD (12). We feel that, while this does not conclusively prove that mercury exposure causes AD, itdefinitely proves that such exposure would exacerbate the conditions of this disease.We were
Boyd Haley 1 of 4
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interested in the genetic research regarding AD and followed this work to see if it correlated toour results. That is, does susceptibility to heavy metal toxicity have any relationship to AD?
When we read the correlation of APO-E4 to age of onset of AD we were intrigued enough tolook at the primary structure of this protein and its alleles, APO-E2 and APO-E3. In general, thestory is this. Individual with APO-E2 or combinations of APO-E2 and E3 are much less likelyto get AD than are individuals who have inherited APO-E4 genes. Also, APO-E2 appears to bemore protective than APO-E3 against AD. What is the basic structural difference between thesethree alleles? Simply, the protective APO-E2 has two sulfhydryls (cysteines) which can bindmercury or other heavy metals. In APO-E3, one of these cysteines is replaced by an arginine andin APO-E4, both of the cysteines are replaced by arginine. Therefore, lack of protection againstAD follows loss of sulfhydryls from APO-E proteins (4). What does APO-E protein do. It isinvolved in cholesterol transport and all three forms work reasonably well at this. However,APO-E is classified as a "housekeeping protein". That is, in contrast to tubulin and CK whichare meant to stay inside of cells where they are synthesized, APO-E is meant to leave the cellcarrying out unwanted material for the body to dispose of. In the brain, APO-E protein leavesbrain cells and goes into the cerebrospinal fluid (CSF) and then crosses the blood brain barrierinto the blood plasma. It is cleared from the blood by processes that dispose of the unwantedmaterial that it is carrying. It is our hypothesis that while APO-E2 or E3 are leaving the braincells and traversing the CSF they likely bind any heavy metal or other sulfhydryl reactive toxinthat may have made it into the central nervous system (4). APO-E4 could not do this andtherefore loses the protective parameters that APO-E2 and E3 have. It is interesting to note thatthe second highest level of APO-E protein is in the CSF that bathes and protects the brain cells.
There was considerable debate concerning whether or not mercury reaches levels in the brainthat could be considered toxic. The determination of the levels of mercury toxicity that couldcause neurological disease has been done using animals, such as rats, under tightly controlledlaboratory conditions where the diet is carefully monitored to exclude other toxicants. However,humans do not live under such conditions and heavy metal imbalances in AD brains have beenreported (10,11). For example, lead (Pb) toxicity is not that uncommon in the inter-cityenvironment or for those exposed to leaded gasoline fumes for many years. The latest researchin our laboratory has shown that one can add various metals to human brain homogenates tolevels that do not affect nucleotide binding to tubulin. When we compare the toxicity of Hg in2+
brain homogenates as described above (refs. 3 & 4) the addition of low micromolar Zn2+ lowersby 2 to 5 fold the concentration of Hg that is required to totally abolish the nucleotide binding2+
to tubulin (7,13). In other words, mercury is much more toxic in the presence of other metals thatcompete with mercury for the binding sites on protective biomolecules (e.g., APO-E2 & E3,glutathione, metallo-thionine, ect.). This observation probably explains some observations onthe toxicity of solutions in which dental amalgams have been soaked. Wataha et al. (8) reportedthat extracts of the amalgam material (trade name, Dispersalloy) "was severely cytotoxic whenZn release was greatest, but less toxic between 48 and 72 hours as Zn release decreased". Zn isan essential metal needed for health and many times recommended by physicians to be taken insupplemental form. It is my opinion that the increased toxicity was not caused by direct Zntoxic effects. Rather, inhanced toxicity was due to the Zn potentiated toxicity of mercury causedby Zn2+ occupying biomolecule chelation sites resulting in a higher concentration of free Hg2+
capable of inhibiting the activity of critical nucleotide binding proteins such as tubulin and CK. This raises the question if mercury is released from amalgams under similar conditions. Chew etal. (9) tested the "long term dissolution of mercury from a non-mercury-releasing amlagam (tradename
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Boyd Haley 2 of 4
Composil)". Their results demonstrated "that the overall mean release of mercury was 43.5+/-3.2 micrograms/cm2/24hr, and the amount of mercury released remained fairly constantduring the duration of the experiment (2 years)". The bottom line is that mercury toxicity isenhanced by
the presence of other heavy metals and both are released from dental amalgams. Additionally,when one considers the toxicity of a certain body level of mercury it is somewhat meaninglessunless the body level of other heavy metals is also considered.
Many recent literature and popular press reports state that the presence of periodontal diseaseraises the risk factor or exacerbates the condition of several other seemingly unrelated diseasessuch as stroke, low birth weight babies, cardiovascular disease (See October 1996 issue ofPeriodontology). The anerobic bacteria of periodontal disease produce hydrogen sulfide (H2S)and methyl thiol (CH3SH) from cysteine and methionine, respectively. This accounts for the"bad breath" many individuals have. However, in a mouth that produces H2S, CH3SH and Hgo(from amalgam fillings) the very likely production of their reaction products, HgS (mercurysulfide), CH3S-Hg-Cl (methyl thiol mercury chloride) and CH3S-Hg-S-CH3 (Dimethylthiolmercury) has to occur. This is simple, un-refutable chemistry whose presence is supported byeasily observable amalgam tattoos. These tattoos are purple gum tissue surrounding certainteeth where the gum and tooth meet and caused by HgS as determined by mercury analysis ofsuch tissue. HgS is one of the most stable forms of mercury compounds and is the mineral formof mercury, called cinnabar, from which mercury is mined from the earth). All of thesecompounds are classified as extremely toxic and the latter compound, dimethylthiol mercury isvery hydrophobic and it solubility similar to dimethyl mercury. Dimethyl mercury was thecompound that was recently in the press where only a small amount spilled on the latex glovesof a Dartmouth University professor caused severe medical problems and finally death. Logicimplys that anyone with periodonatal disease, anaerobic bacterial infected teeth and mercurycontaining fillings would be exposed daily to these very toxic compounds. In our laboratory wesynthesized the two methylthiol-mercury compounds and tested them. They are extremelycytotoxic at 1 micromolar or less levels and are potent, irreversible inhibitors of a number ofimportant mamalian enzymes.
In summary, the data on the effects of mercury on the nucleotide binding properties and theabnormal partitioning of two very important brain nucleotide binding proteins suggests thatmercury must be considered as a contributor to the condition classified as AD. This is especiallytrue when mercury is present in combination with other heavy metals such as zinc (Zn) and lead(Pb). Bluntly, the determination of safe body levels of mercury by using animal data where theanimals have not been exposed to other heavy metals is no longer justifiable. Mercury is muchmore toxic to individuals with other heavy metal exposures. As I have been sent numerous labreports on levels of elements in the hair and other tissues of suspected mercury toxic patients Ihave noticed that many have exceedingly high Pb, Cu, Zn, etc. levels. It is my opinion that oneof the major questions left to be answered concerning the toxic effects of mercury is "does thecombination of mercury with different heavy metals lead to different clinical observations oftoxicity?" There can be little doubt that the elevated levels of other heavy metals increases thetoxicity of mercury. Further, the reaction of oral mercury from amalgams and the reaction ofthis mercury with toxic thiols produced by periodontal disease bacteria very likely enhances thetoxicity of the mercury being released. This makes any claim regarding the determination ofsafe levels of mercury as obtained under controlled conditions (e.g. in a system where otherheavy metals are excluded) very suspect when discussing toxic mercury effects in theuncontrolled environment that humans are exposed to.
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Bibliography attached to Boyd Haley report.
1. Khatoon, S., Campbell, S.R., Haley, B.E. and Slevin, J.T. Aberrant GTP ?-TubulinInteraction in Alzheimer's Disease. Annals of Neurology 26, 210-215 (1989).2. David, S., Shoemaker, M., and Haley, B. Abnormal Properties of Creatine kinase inAlzheimer's Disease Brain: Correlation of Reduced Enzyme Activity and Active SitePhotolabeling with Aberrant Cytosol-Membrane Partitioning. Molecular Brain Research accepted (1997).3. Duhr, E.F., Pendergrass, J. C., Slevin, J.T., and Haley, B. HgEDTA Complex Inhibits GTPInteractions With The E-Site of Brain ?-Tubulin Toxicology and Applied Pharmacology 122,273-288 (1993).4. Pendergrass, J.C. and Haley, B.E. Mercury-EDTA Complex Specifically Blocks Brain?-Tubulin-GTP Interactions: Similarity to Observations in Alzheimer"s Disease. pp98-105 inStatus Quo and Perspective of Amalgam and Other Dental Materials (International SymposiumProceedings ed. by L. T. Friberg and G. N. Schrauzer) Georg Thieme Verlag, Stuttgart-NewYork (1995).5. Pendergrass, J. C., Haley, B.E., Vimy, M. J., Winfield, S.A. and Lorscheider, F.L. MercuryVapor Inhalation Inhibits Binding of GTP to Tubulin in Rat Brain: Similarity to a MolecularLesion in Alzheimer's Disease Brain. Neurotoxicology 18(2), 315-324 (1997).6. Pendergrass, J. C., Haley, B.E., Vimy, M. J., Winfield, S.A. and Lorscheider, F.L. MercuryVapor Inhalation Inhibits Binding of GTP to Tubulin in Rat Brain: Similarity to a MolecularLesion in Alzheimer's Disease Brain. Neurotoxicology 18(2), 315-324 (1997).7. Pendergrass, J.C., David, S. and Haley, B. Aberrant GTP-Tubulin Interactions and Aberrant-Tubulin Partitioning in Alsheimer's Disease Brain are Induced In Vitro by Micromolar Mercury,Zinc and other Sulfhydryl Reactive Heavy Metals. (in preparation 1998).8. Wataha, J. C., Nakajima, H., Hanks, C. T., and Okabe, T. Correlation of Cytotoxicity withElement Release from Mercury and Gallium-based Dental Alloys in vitro. Dental Materials10(5) 298-303, Sept. (1994)9. Chew, C. L., Soh, G., Lee, A. S. and Yeoh, T. S. Long-term Dissolution of Mercury from aNon-Mercury-Releasing Amalgam. Clinical Preventive Dentistry 13(3): 5-7, May-June (1991).10. 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).11. Deibel, M. A., Ehmann, W.D., and Markesbery, W. R. Copper, Iron and Zinc Imbalancesin Severely Degenerated Brain Regions in Alzheimer's Disease: Possible Relation to OxidativeStress. J. Neurol. Sci. 143, 137-142 (1996).12. Gunnersen, D.J. and Haley, B. Detection of Glutamine Synthetase in the CerebrospinalFluid of Alzheimer's Diseased Patients: A Potential Diagnostic Biochemical Maker. Proc. Natl.Acad. Sci. USA, 88, 11949-11953 (1992).13. Pendergrass, J. C., Cornett, C.R., David, S. and Haley, B. Mercury and Zinc Levels inFrontal Pole and Hippocampus of Alzheimer's Disease Brain: Relationship to AbberantGTP-?-Tubulin Interactions. Submitted to Neurotoxicology (1998).
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Appendix 13:
Health Canada's Recommendations Concerning the Use of Dental Amalgam ( Health Canada, 1996a )
1. Non-mercury filling material should be considered for restoring the primaryteeth of children where the mechanical properties of the material are suitable.
2. Whenever possible, amalgam fillings should not be placed in or removed fromthe teeth of pregnant women.
3. Amalgam should not be placed in patients with impaired kidney function.
4. In placing and removing amalgam fillings, dentists should use techniques andequipment to minimize the exposure of the patient and the dentist to mercuryvapour, and to prevent amalgam waste from being flushed into municipal sewagesystems.
5. Dentists should advise individuals who may have allergic hypersensitivity tomercury to avoid the use of amalgam. In patients who have developedhypersensitivity to amalgam, existing amalgam restorations should be replacedwith another material where this is recommended by a physician.
6. New amalgam fillings should not be placed in contact with existing metaldevices in the mouth, such as braces.
7. Dentists should provide their patients with sufficient information to make aninformed choice regarding the material used to fill their teeth, includinginformation on the risks and benefits of the material and suitable alternatives.
8. Dentists should acknowledge the patient's right to decline treatment with anydental material.
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Appendix 14: Original Preliminary Submission by ASOMAT to NHAC (Sept 1997)
Some salient facts about mercury, dental amalgams and health effects.
Submitted by ASOMAT (Australasian Society of Oral Medicine and Toxicology)
For consideration by NHAC September 15 and September 16 , 1997th th
1. Dental amalgams are NOT a true alloy. They are made up of 50% mercury which is NOT locked into a set filling, but
escapes continuously during the entire life of the filling in the forms of vapour, ions and abraded particles. This release is
stimulated by chewing, brushing and hot fluids One study reported levels, of mercury vapour in the mouth, 54 times higher in
the mouth of a patient with amalgams, after chewing, than the levels in the mouth of a patient without amalgams after
chewing.
2. The absorption rate of inhaled mercury vapour is extremely high, approximately 80% of the inhaled dose, reaching the brain
tissue within one blood circulation cycle.
3. The extreme toxicity of mercury is well documented. Current research is clearly demonstrating that inorganic mercury is
just as toxic as organic mercury under various physiologic conditions.
4. The toxic threshold for mercury vapour has never been found. Even the US Environmental Protection Agency has so stated.
The existing occupational standards are all specifically declared to be estimates only on the appearance of CLINICALLY
OBSERVABLE SIGNS AND SYMPTOMS. Statements by the dental profession that the amount of mercury exposure
encountered by patients from dental amalgams is too small to be harmful are contradicted by the scientific literature and are
totally indefensible. Dentists receive no training at all which would enable them to even look for symptoms relating to
mercury toxicity.
5.Controlled, broad-scale scientific studies investigating the effects on the health of patients of mercury released from dental
amalgam fillings have NEVER been conducted. The true nature and full extent of effects are therefore unknown.
6. Mercury from amalgam fillings is stored principally in the kidneys, liver and central nervous system. This mercury has also
been shown to cross the placenta and collect in fetal tissue. Studies show the level of mercury in liver, kidney and brain tissue
of deceased Foetus, new-born and young children is proportional to the number of amalgam fillings in the mother’s mouth.
One such study concludes that"the elevated concentrations of inorganic mercury found in tissues of people with amalgam
filings, derive mainly from these fillings and not from other theoretically possible sources
7. Mercury from dental amalgam will also be transported across the breast milk of lactating women. In fact it has been
demonstrated that breast milk increases the bio-availability of mercury to the newborn. Negative developmental effects have
been shown (in animal models) in relation to these sources and concentrations of mercury.
8.The halftime for the elimination of a single dose of mercury is extremely long, certainly at least 30 days for the whole body
and perhaps as long as 10,000 days for the brain. Multiple small doses will therefore result in body accumulation.
9. Sheep and monkey studies have confirmed that the mercury from dental amalgams enters and accumulates in the patient
throughout the body, including the brain.
10. Human autopsy studies have shown that the concentration of mercury in the brain is directly related to the number, size
and age of amalgam fillings in the mouth
11. Mercury has been shown to interfere with Tubulin synthesis resulting in “neurofibril tangles” in the brain.
Mercury specifically from dental amalgam, placed in rats’ teeth, has been shown to affect tubulin synthesis
12. Mercury from dental amalgams has been shown to be related to antibiotic resistance in the gut and oral cavity.
13.Both Health Canada (1996a) and the World Health Organization (1991) consider dental amalgam to be the single largest
source of mercury exposure for the general public, with amalgam potentially contributing up to 84% (WHO, 1991) of total
daily intake of all forms of mercury from all sources. Therefore, the level of exposure resulting from amalgam is not an issue
of contention.The WHO also noted that for mercury vapour "a specific no- observed-effects level (NOEL) cannot be
established ie. NO level of Mercury Vapour has been found, that can be considered harmless.
14. Amalgam fillings have been associated in the scientific literature with a variety of problems such as periodontal problems
(pyorrhea), allergic reactions, oral lichen planus, interference with the immune system as measured by the T-lymphocyte
levels, significantly higher in amalgam patients than in non-amalgam patients, correlate with number and size of the fillings
but return to normal when the fillings are replaced.
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15. Claims by the Australian and American Dental Associations that the incidence of mercury allergy is less than 1% have
never cited any references. Such claims are totally refuted by the scientific literature. Published peer reviewed studies show
allergic reactions range from 5%-8% (Nth Am Derm Gp) up to 39% (Miller et al)
16. The earliest symptoms of long term, low level mercury poisoning are sub clinical and neurologic. Consequently due to
their subtlety, these symptoms are easily misdiagnosed.
17. Some recent studies show that at least 50% of dentists with elevated mercury levels had peripheral nervous disorders and
that dentists have twice the rate of Glioblastoma than non-dentists.
18. Research shows female dental personnel have twice the rate of infertility, miscarriage and spontaneous abortion than the
rest of the population
19. Mercury from dental amalgams crosses the placenta, accumulating in the foetus, and is also transferred through the breast
milk to neonates.
20. Wolf et al in 1983 in the journal 'Neurotoxicology' stated.." It is generally agreed that if amalgam was introduced today as
a restorative material, it would never pass FDA approval "
21.The German and Norwegian Health Departments have directed their dental professions to NOT use amalgams in pregnant
women and the German Health Department has also directed that children not receive dental amalgams either.
22. Canada Health, in the wake of the Richardson report, has stated similar views and has also added that people with kidney
or neurological problems might consider alternative fillings as mercury is of particular concern in their cases.
23. A report, “Dental Amalgams and Human Health, current position” commissioned by the New Zealand Health Department
has just been submitted to the NZ Government. It concluded that in some circumstances some people could be adversely
affected by dental amalgam fillings.
Based on the peer-reviewed scientific literature we are currently able to state the following.
� Mercury from dental amalgams is released from the fillings continuously and almost totally absorbed
� Mercury from dental amalgams accumulates in the tissues throughout the body
� Mercury from dental amalgams is very toxic and interferes with a variety of physiologic systems
� Physiological effects and health changes can be demonstrated by the placement and removal of dental amalgams
� There is evidence of health problems, related to mercury exposure, in the dental profession
ASOMAT’s POSITION and CONCLUSION
It is ASOMAT’s position that dental amalgams do NOT cause any particular disease or illness. Rather it is our view that
dental amalgams promote heavy metal toxicity through a chronic and unrecognised accumulation of mercury in the body.
ASOMAT believes that this is a medical problem with a dental cause and that this needs to be managed by the medical
community. ASOMAT believes that recommendations which would stop or severely limit the use of dental amalgams in
pregnant and fertile women, children, and those patients with kidney or neurological problems would be an appropriate and
prudent preventive response based on the scientific literature of the moment. ASOMAT also believes that current alternative
materials negate the previous need for amalgams, allowing an immediate phase out of amalgams over a 2-3 year period which
would allow time for retraining of the dental profession and the teaching institutions. Training in the recognition of mercury
toxicity is also necessary.
It is appropriate to end this summary with a statement from the National Research Council of the United States of America,
which issued a report in 1978 entitled "An assessment of mercury in the Environment".
"Mercury compounds have no known normal metabolic function and their presence in the cells of living organisms, including
human beings, represents contamination from natural and anthropogenic sources. In view of the toxicity of mercury and the
inability of researchers to specify the threshold levels of toxic effects on the basis of present knowledge, all such
contamination must be regarded as undesirable and potentially hazardous."
No information has come to light since the publication of this statement in 1978 which alters this view
ASOMAT Contacts:
President Dr. Roman Lohyn B.D.S. 8/175 Collins Street, Melbourne ph: (03) 9650-1660 Fax: (03) 9650-8161
Secretary Dr. Robert Gammal B.D.Sc 102/222 Pitt Street, Sydney ph: (02) 9264-5195 Fax: (02) 9283-2230
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EXECUTIVE SUMMARY OF RICHARDSON REPORT
ASSESSMENT OF MERCURY EXPOSURE AND RISKS FROM DENTAL AMALGAM by G. Mark Richardson, PhD.,
Medical Devices Bureau, Environmental Health Directorate, Health Canada, August 18, 1995, Final Report (released
November 27, 1995, in Toronto, at the stakeholders' meeting)
Executive Summary For Canadians with amalgam-filled teeth, it was estimated that total mercury (Hg) exposure
averages: 3.3 ug Hg/day in toddlers (aged 3 to 4 years); 5.6 ug Hg/day in children (aged 5 to 11 years); 6.7 ug Hg/day in
teens (aged 12 to 19 years); 9.4 ug Hg/day adults (aged 20 to 59 years; and 6.8 ug Hg/day in seniors (aged 60+ years). Of
this exposure, amalgam was estimated to contribute 50% to total Hg exposure in adults, and 32 to 42% for other age
groups. Estimates, based on two independent models, of exposure from amalgam alone were: 0.8 - 1.4 ug Hg/day in
toddlers; 1.1 - 1.7 ug Hg/day in children; 1.9 -2.5 ug Hg/day in teens; 3.4- 3.7 ug Hg/day in adults and 2.1 - 2.8 ug Hg/day
in seniors.
There are insufficient published data on the potential health effects of dental amalgam specifically to support or refute
the diverse variety of health effects attributed to it. Numerous studies constantly report effects on the central nervous
system (CNS) in persons occupationally exposed to Hg. Virtually all studies failed to detect a threshold for the effects
CNS measured. A tolerable daily intake (TDI) of 0.014 ug Hg/kg body weight/day was proposed for mercury vapour, the
principal form of mercury to which bearers of amalgam fillings are exposed. This TDI was based on a published account
of sub-clinical (i.e. not resulting in overt symptoms or medical care) CNS effects in occupationally exposed men,
expressed as a slight tremor of the forearm. An uncertainty factor of 100 was applied to these data, to derive a reference
dose (TDI) which should, in all probability, prevent the occurrence of CNS effects in non-occupationally- exposed
individuals bearing amalgam fillings.
The number of amalgam-filled teeth, for each age group, estimated to cause exposure equivalent to the TDI were:
1 filling in toddlers; 1 filling in children; 3 fillings in teens; and 4 fillings in adults and seniors. It was recognized
that filling size and location (occlusal versus lingual or buccal) may also contribute to exposure. However, data
suggest that no improvement in prediction of exposure is offered by any particular measure of amalgam load.
Therefore, the estimates of exposure derived from the number of filled teeth were considered as reliable as those
that might be based on size and position of amalgam fillings, were such data available for the Canadian population.
Effects caused by allergic hypersensitivity to amalgam or mercury, including possible auto- immune reactions, can not be
adequately addressed by any proposed tolerable daily intake. Individuals suspecting possible allergic or auto-immune
reactions should avoid the use of amalgam selecting suitable alternate materials in consultation with dental care (and
possibly health care) professionals.
Preface This report has been prepared in response to concerns that exposure to mercury from dental amalgam may
adversely impact on health. Recent reviews (USDHHS 1993, Swedish National Board of Health, 1994) have concluded
that there is no evidence to suggest that dental amalgam, specifically, is injurious to health. However, the data base relating
health impacts in humans or animals to amalgam specifically is small and weak. This suggests that indirect evidence
relating mercury vapour exposure (the predominant form of mercury released by dental amalgam) to human health effects
(for which a large data base exists) is a necessary basis for an evaluation of the possible health risks of dental amalgam. In
the reports previously mentioned, exposure to mercury arising from amalgam was not adequately quantified, and a level of
mercury vapour exposure which is, in all probability, tolerable to the vast majority of persons bearing amalgam fillings,
was not defined. This report attempts to address these previous deficiencies.
This report is not exhaustive. Recent reviews on mercury (WHO 1990, 1991; IARC 1993; ATSDR 1994) adequately
review many aspects of mercury toxicity and exposure. Instead, this report focuses on studies which report on health
effects in dental care practitioners and other occupational groups exposed to relatively low levels of mercury. This report
also examines recent research which hypothesizes a link between mercury exposure, and thereby dental amalgam, and
Alzheimers' Disease. This report concentrates on effects associated with long term mercury vapour exposure (via
inhalation) in humans. Other reviews (WHO 1990, 1991; IARC 1993; ATSDR 1994) examined acute and sub-chronic
exposure in animals, and all aspects of the toxicology of exposure to other forms of mercury via other routes of exposure
(ingestion, dermal absorption), in extensive and adequate detail such that this is not repeated here.
Any medical or dental material, such as amalgam, will have associated with it some degree of health risk. The purpose of
this report is to attempt some determination of what that risk is (i.e. what effect(s) it may cause), how significant it is (i.e.
what level of exposure should be free from effect), and what proportion of the population might be at some degree of risk
(i.e. how many exceed the level considered to be free from effect).
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Health Canada's Recommendations Concerning the Use of Dental Amalgam ( Health Canada, 1996a )
1. Non-mercury filling material should be considered for restoring the primaryteeth of children where the mechanical properties of the material aresuitable.
2. Whenever possible, amalgam fillings should not be placed in or removed fromthe teeth of pregnant women.
3. Amalgam should not be placed in patients with impaired kidney function.
4. In placing and removing amalgam fillings, dentists should use techniques andequipment to minimize the exposure of the patient and the dentist tomercury vapour, and to prevent amalgam waste from being flushed intomunicipal sewage systems.
5. Dentists should advise individuals who may have allergic hypersensitivity tomercury to avoid the use of amalgam. In patients who have developedhypersensitivity to amalgam, existing amalgam restorations should bereplaced with another material where this is recommended by a physician.
6. New amalgam fillings should not be placed in contact with existing metaldevices in the mouth, such as braces.
7. Dentists should provide their patients with sufficient information to make aninformed choice regarding the material used to fill their teeth, includinginformation on the risks and benefits of the material and suitablealternatives.
8. Dentists should acknowledge the patient's right to decline treatment with any dental material.
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LIST OF RELEVANT REFERENCES
Richardson M. Assessment of mercury exposure and risks from dental amalgam. Final report Medical Devices Bureau, Environmental Health Directorate Health Canada
Hahn LJ, Kloiber R ,Leininger RW, Vimy MJ, Lorscheider FL: Dental Silver fillings: a source of mercury exposure revealed bywhole-body imagescan and tissue analysis FASEB J. 3: 2641-2646; 1989
JADA Workshop on biocompatibility of metals in dentistry July 1984Vimy.M.J., Lorscheider.F.L. Intraoral Air Mercury Released from Dental Amalgam J.Dent.Res. 64 pp 1069-1071 1985Svare. C.W, et al. The effect of dental amalgams on mercury levels in expired air. J.DentRes. 60: pp1668-1671 1981Svare.C.W, and Peterson.L.C. The effect of removing dental amalgams on mercury blood levels. IADR Abstracts no.896 1984Emler.M.C. An Assessment of Mercury in Mouth Air. J.Dent.Res. 64 Abstract # 652 pp 247 1985Gay.D.D, and Cox.R.D, Reinhardt.J.W. Letter, Chewing releases mercury from fillings. Lancet. 1: 8123: 985-986 1979Patterson.J.E., et al Mercury in human breath from Dental Amalgams. Bull. Envi. Contam. Toxicol 34 pp 459-468 1985 Moller.B. Reaction of the human dental pulp to silver amalgam restorations. Swedish Dent Jnl 2: 93-97 1978Freden.H, Hellden.L, Milleding.P. Mercury Content in gingival tissues adjacent to amalgam fillings. Odont. Rev. 25: 207-210 1974Till.T, and Maly.K. Zum Nachweis Der Lyse Von Hg Aus Silberamalgam Von ZahnfullungenSchiele et al. Studies on the mercury content in brain and kidney related to number and condition of amalgam fillings.Presented at a
symposium in Cologne in March 1984 and reported in Bio-Probe. 1:3 Dec 1984Hahn LJ, Kloiber R ,Leininger RW, Vimy MJ, Lorscheider FL: Dental Silver fillings: a source of mercury exposure revealed by
whole-body imagescan and tissue analysis FASEB J. 3: 2641-2646; 1989Hahn LJ, Kloiber R ,Leininger RW, Vimy MJ, Lorscheider FL: Whole body imaging of the distribution of mercury released from dental
fillings into monkey tissues FASEB J. 4: 3256- 3260; 1990Vimy MJ, Takahashi Y, Lorscheider FL ; Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings Am
J Physiol 1990 Apr 258 R939-R945Drasch et al; Mercury burdern of human fetal and infant tissues Eur J Pediatr (1994) 153:607-610Vimy MJ, Hooper DE, King WW, Lorscheider FL Mercury from Maternal “Silver” Tooth Fillings in Sheep and Human Breast Milk
Biological Trace Element Research 56: 143-152 1997 Rudner et al. Epidemiology of contact dermatitis in Nth. America Arch Derm 108 (4) 537-40 1973Djerrasi.E., Berova.N., The possibilities of allergic reactions from Silver Amalgam restorations Int Dent J 19:4 481-488 1969White.R., Brandt.R., Development of mercury hypersensitivity among dental students. JADA 92: 1204-1207 1976Miller.E., et al. Prevalence of mercury hypersensitivity in dental students J Dent Res 64:338 Special Abstracts #1472 1985Brun.R., Epidemiology of contact dermatitis in Geneva Contact Dermatitis 1:214-217 1975Nebenfuher.L., et al. Mercury Allergy in Budapest Contact Dermatitis 10(2) : 121-122 1983World Health Organization, Environmental Health studies. Criteria 118: Inorganic Mercury, Geneva, 1991.Abraham et al The effect of Dental Amalgam Restorations on blood mercury levels J.Dent Res 1984 63:1 71-73Magos L. Mercury-blood interaction and mercury uptake by the brain after vapor exposure. Environ Res. 1967: 1: 323-337Heintze.U, Edwardsson.S, Derand.R, and Birkhed.D. Methylation of mercury from dental amalgam and mercuric chloride by oral streptococci. Scand. J. Dent. Res. 91:2 pp 150-152 1983Cross.J.D, Dale.I.M, Goolvard.L, Lenihan.J.M.A, Smith.H. Letter, Lancet 2: 8084 pp 312-313 1978Racz.W.J, and Vanderwater.J.S. Perspectives on the central nervous system toxicity of methylmercury. Can.J.Physiol & Pharm. 60: pp 1037-1045 1982Siblerud R.L. “Relationship between mercury from dental amalgams and oral health”Ann Dent 1990; 49(2): 6-10Lindquist.B., Mornstad.H. Effects of removing amalgam fillings from patients with diseases affecting the immune system, Medical
Science Research 24: 1996Bratel J, Hakeberg M, Jontell Effect of replacement of dental amalgam on oral lichenoid reactions. J Dent 1996 Jan;24(1-2):41-45 Finne K, Goransson K, Winckler L Oral lichen planus and contact allergy to mercury. Int J Oral Surg 1982 Aug;11(4):236-239 Henriksson E, Mattsson U, Hakansson J Healing of lichenoid reactions following removal of amalgam. A clinical follow-up. J Clin Periodontol 1995 Apr;22(4):287-294 Ibbotson SH, Speight EL, Macleod RI, Smart ER, Lawrence CM The relevance and effect of amalgam replacement in subjects with
oral lichenoid reactions. Br J Dermatol 1996 Mar;134(3):420-423 James J, Ferguson MM, Forsyth A, Tulloch N, Lamey PJ Oral lichenoid reactions related to mercury sensitivity. Br J Oral Maxillofac Surg 1987 Dec;25(6):474-480Jameson MW, Kardos TB, Kirk EE, Ferguson MM Mucosal reactions to amalgam restorations. J Oral Rehabil 1990
Jul;17(4):293-301 Koch P, Bahmer FA Oral lichenoid lesions, Hg hypersensitivity and combined hypersensitivity to mercury and other metals: histologically-proven reproduction of the reaction by patch testing with metal salts. Contact Dermatitis 1995 Nov;33(5):323-328 Lind PO, Hurlen B, Stromme Koppang H Electrogalvanically-induced contact allergy of the oral mucosa. Report of a case Int J Oral Surg 1984 Aug;13(4):339-345 Lind PO, Hurlen B, Lyberg T, Aas E Amalgam-related oral lichenoid reaction. Scand J Dent Res 1986 Oct;94(5):448-451Pang BK, Freeman S Oral lichenoid lesions caused by allergy to mercury in amalgam fillings. Contact Dermatitis 1995
Dec;33(6):423-427Skoglund A, Egelrud T Hypersensitivity reactions to dental materials in patients with lichenoid oral mucosal lesions and in patients
with burning mouth syndrome. Scand J Dent Res 1991 Aug;99(4):320-328 Smart ER, Macleod RI, Lawrence CM Resolution of lichen planus following removal of amalgam restorations in patients with proven
allergy to mercury salts: a pilot study. Br Dent J 1995 Feb 11;178(3):108-112Stejskal VD, Forsbeck M, Cederbrant KE, Asteman O Mercury-specific lymphocytes: an indication of mercury allergy in man. J Clin Immunol 1996 Jan;16(1):31-40 Arvidson B, Arvidsson J, Johansson K Mercury deposits in neurons of the trigeminal ganglia after insertion of dental amalgam in rats
Biometals 1994 Jul 7(3): 261-263
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Langworth S. Stromberg R. A case of high mercury exposure from dental amalgams Eur J Oral Sci 1996: 104: 320-321Summers AO, et al. Mercury released from dental "silver" fillings provokes an increase in mercury and antibiotic-resistant bacteria in
oral and intestinal floras of primates. Antimicrob Agents Chemother 1993 Apr;37(4):825-834 Siblerud RL The relationship between mercury from dental amalgam and the cardiovascular system. Sci Total Environ 1990 Dec
1;99(1-2):23-35 Siblerud RL, Kienholz E Evidence that mercury from silver dental fillings may be an etiological factor in multiple sclerosis. Sci Total
Environ 1994 Mar 15;142(3):191-205 Siblerud RL The relationship between mercury from dental amalgam and mental health. Am J Psychother 1989 Oct;43(4):575-587 Siblerud RL, Kienholz E, Motl J Evidence that mercury from silver dental fillings may be an etiological factor in smoking. Toxicol
Lett 1993 Jun;68(3):307-310 Hultman P, Johansson U, Turley SJ, Lindh U, Enestrom S, Pollard KM Adverse immunological effects and autoimmunity induced by
dental amalgam and alloy in mice. FASEB J 1994 Nov;8(14):1183-1190 Boyd ND, Benediktsson H, Vimy MJ, Hooper DE, Lorscheider FL Mercury from dental "silver" tooth fillings impairs sheep kidney
function. Am J Physiol 1991 Oct;261(4 Pt 2):R1010-R1014 Lorscheider FL, Vimy MJ, Summers AO, Zwiers H The dental amalgam mercury controversy--inorganic mercury and the CNS;
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Contact Dermatitis. 10: pp 11-15 1984White.R, and Brandt.R.L. Development of mercury hypersensitivity among dental students. JADA 92: pp 1204-1207
1976Miller.E.G., Perry.W.L., Wagner.M.J. Prevalence of mercury hypersensitivity in dental students. J.Dent.Res 64:338 Special issue abstracts #1472, March 1985
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paper presented at the International Conference on Mercury Hazards in Dental Practice. Glasgow, Scotland. Sept. 1981Heintze.U, Edwardsson.S, Derand.R, and Birkhed.D. Methylation of mercury from dental amalgam and mercuric
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642-643 1983 Vimy.M.J., Lorscheider.F.L. Serial measurements of Intraoral Air Mercury: Estimation of daily dose from dental amalgams.
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Biochemical & Biophysical Research Communications 128 (3) pp 1145-1151 1985105.Varshaeve et al. Genetic damage induced by occupational low mercury exposure. Environ. Research 12 pp 306-316 1976 Wolff.M. et al. Mercury toxicity from dental amalgam. Neurotoxicology (4) pp 203 1983Ahlbom.A., Norell.S., Nylander.M., Rodvall.Y. Dentists, Nurses and Brain Tumours. 4th International Symposium Epidemiology
Occupational Health Como, Italy, 10-12 September 1985 (Abstracts)Symington.I.S., Cross.J.D., Dale.I.M., Lenihan.J.A. Mercury poisoning in Dentists. J. Soc. Occup. Med. 30 pp 37-39 1980Koos.B.J, and Longo.L.D. Mercury toxicity in the pregnant woman, fetus, and newborn infant Am.Jnl. of Obstet.Gynecol. 126:3
390-409 1976
ASOMAT Contacts:
President Dr. Roman Lohyn B.D.S. 8/175 Collins Street, Melbourne ph: (03) 9650-1660 Fax: (03) 9650-8161
Secretary Dr. Robert Gammal B.D.Sc 102/222 Pitt Street, Sydney ph: (02) 9264-5195 Fax: (02) 9283-2230
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Appendix 15: Copy of Professor Moore's review of ASOMAT submission
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to be inserted as soon as receive copy from NHMRC
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page 2
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Bibliography
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BIBLIOGRAPHY
1 Caulk state that dental amalgam should not be used:
* In proximal or occlusal contact to dissimilar metal restorations.
* In patients with severe renal deficiency.
* In patients with known allergies to amalgam.
* For retrograde or endodontic filling.
* As a filling material for cast crown.
* In children 6 and under.
* In expectant mothers.
2 Maiorino RM Gonzalez-Ramirez D Zuniga-Charles M Xu Z Hurlbut KM Aposhian MM Dart RC Woods
JS Ostrosky-Wegman P Gonsebatt ME Aposhian HV Sodium 2,3-dimercaptopropane-1-sulfonate challenge
test for mercury in humans. III. Urinary mercury after exposure to mercurous chloride. J Pharmacol Exp Ther
(1996 May) 277(2):938-44
3 Keith RL Setiarahardjo I Fernando Q Aposhian HV Gandolfi A Utilization of renal slices to evaluate the
efficacy of chelating agents for removing mercury from the kidney. Toxicology (1997 Jan 15) 116(1-3):67-75
4 Aposhian MM Maiorino RM Xu Z Aposhian HV Sodium 2,3-dimercapto-1-propanesulfonate (DMPS)
treatment does not redistribute lead or mercury to the brain of rat. Toxicology (1996 May 3) 109(1):49-55
5 Aposhian HV Bruce DC Alter W Dart RC Hurlbut KM Aposhian MM Urinary mercury after
administration of 2,3-dimercaptopropane-1- sulfonic acid: correlation with dental amalgam score. FASEB J
(1992 Apr) 6(7):2472-6
6 Aposhian HV Maiorino RM Rivera M Bruce DC Dart RC Hurlbut KM Levine DJ Zheng W Fernando Q
Carter D et al Human studies with the chelating agents, DMPS and DMSA. J Toxicol Clin Toxicol (1992)
30(4):505-28
7 Herrmann-M; Schweinsberg-F Biomonitoring for the evaluation of a mercury burden from amalgam fillings.
Mercury determination in urine before and after oral doses of 2,3-dimercapto-1-propanesulfonic acid (DMPS)
and in hair Abteilung Allgemeine Hygiene und Umwelthygiene, Universitat
