By Dr. Murray J. Vimy DMD
Clinical Associate Professor
Faculty of Medicine,
University of Calgary.

Are mercury-based fillings slowly poisoning their owners? Evidence suggests that, far from being the best material to use in the mouth, these fillings should be banned.

The issue of mercury exposure from dental "silver" fillings has gained considerable notoriety in the general media during the last decade. Specific attention has focused on the potential for human health consequences and the general well-being of the global environment. The modern silver amalgam (amalgam meaning mixed with mercury), traditionally known as a "silver" filling, has been employed as the principal tooth restorative material for over 180 years and presently accounts for 75-80% of all tooth restorations.1 These "silver" fillings contain approximately 50% mercury by weight, 35% silver, 13% tin, 2% copper and a trace of zinc.2 Each tooth restoration has a mercury mass of about 750-1000 mg and should more properly be called a mercury filling. They have a functional life of approximately 7-9 years, after which they are usually replaced with another mercury filling.3,4 Hundreds of metric tonnes of mercury are placed into teeth world wide each year and some of this material, as particulate waste from the dental office, finds its way into the sewerage and refuse systems.

Within the dental profession, the issue of mercury filling safety has cyclically recurred. After the introduction of the modern dental amalgam in 1812 by a British chemist, a "silver paste", which was a combination of silver filings from coins and mercury, became fashionable for tooth restoration. Since the coins were not pure, expansion of the material often resulted in tooth fracture and/or a "high bite". In America during the 1800s, concern regarding the possibility for mercury toxicity caused the American Society of Dental Surgeons to make mercury usage an issue of malpractice, mandating that its members sign an oath not to use mercury-containing materials. However, mercury fillings usage increased because it afforded an economic advantage to those dentists employing it; it is user friendly; and because of its durability in the mouth. By 1856, the American Society of Dental Surgeons was forced to disband due to dwindling membership over the mercury filling issue. In its place arose the American Dental Association, founded by those who advocated silver amalgam - mercury use in dentistry.5-7 Again in the 1920s, a controversy erupted after the publication of articles and letters by a German chemistry professor, who attacked mercury filling usage for possible toxic effects.8-13 That debate abated and the dental profession's opinion still remains unchanged.

Today, 182 years later, the American Dental Association has amended its Code of Ethics to make the removal of serviceable mercury fillings an issue of unethical conduct, if the reason for removal is to eliminate a toxic material from the human body and if this recommendation is made solely by the dentist.14 In the American Dental Association's view, a dentist is "ethical" to place the mercury material and recommend its safety. But, if the dentist suggests that the mercury fillings are potentially harmful or that exposure to unnecessary mercury can result, then the dentist is acting "unethically". Clinically serviceable mercury fillings can be "ethically" removed if: done for aesthetic reasons; at the request of a physician; or at the patient's request (without prompting). *** Release of mercury from dental fillings. Mercury vaporizes continuously from dental fillings, being intensified by chewing,15,16 tooth brushing17 and hot liquids.18 After mastication or tooth brushing ceases, it takes almost 90 minutes for the rate of vaporization to decline to the lower prechewing level (Fig. 1).16 Also, the greater the number of fillings and the larger the chewing surface area, the larger the mercury exposure.15,16 Thus, the average individual is on a roller coaster of mercury vapor exposure during the day. Breakfast will cause the release rate to increase and just as the rate is slowing again it is time for the midmorning coffee break. Lunch, mid-afternoon coffee or tea, the evening meal, and a snack before bedtime all contribute to the daily exposure to mercury from dental fillings.

It is estimated that the average individual, with eight biting-surface mercury fillings, is exposed to a daily dose uptake of approximately 10 micrograms mercury per day from dental fillings.19 Select individuals may have daily doses 10 times higher (100 micrograms per day) because of factors which exacerbate the mercury vaporization. Some of these factors are: frequency of eating, chronic gum chewing, chronic tooth grinding behavior (usually during sleep), the chewing pattern of the individual, consumption of hot foods and drinks, mouth and food acidity.16 Corroborating human autopsy evidence20-22 showed that brain and kidney tissues contained significantly higher mercury in individuals who had mercury fillings. Furthermore, the concentration of brain mercury in the subjects with mercury fillings correlated with the number of these fillings present.

The historically espoused opinion of dentistry insists that, once mixed, the mercury is locked into the fillings.23 The aforementioned body of experimental evidence suggests that their opinion is totally without merit. Despite these replicated research findings, many national dental trade associations still claim that mercury fillings are safe.24 They base their conviction on the anecdotal facts that mercury fillings have been used for over 150 years, billions of fillings have been placed, and they do not see sickness or death from the mercury exposure.25 But, the diagnosis of mercury toxicity lies outside the purview of dentistry, falling more appropriately within the jurisdiction of medicine. Dental institutions do not have the scientific expertise or the resources to undertake the necessary studies to scientifically resolve this issue. Thus, the issue of mercury filling safety has not been suitably addressed until recently, when academic medicine became aware of this insidious exposure to mercury. From the medical perspective, dental amalgam fillings are a significant mercury source, having potential medical consequences.

Tissue uptake of mercury from dental fillings. Recent investigations in sheep and monkey animal models demonstrate that dental mercury accumulates in all tissues of the adult, being highest in the kidney and liver. This accumulation is so extensive that it can be visualized on a whole-body image scan (Fig. 2).26,27 Research also shows that a high level of dental amalgam mercury in monkey kidney is still present at one year after mercury filling placement.28 Also, mercury from dental amalgam will cross the placenta and begin accumulating in the developing fetus within two days after the filling placement in pregnant sheep and is highest in the fetal liver then the kidney. The mother's milk also showed evidence of mercury, suggesting that the newborn would have an additional exposure to mercury.29 Recent human chelation studies show a association between urinary mercury excretion and the presence of mercury fillings.30-33 For example, one study showed that, after a chelation challenge with DMPS, urinary mercury excretion is significantly higher from subjects with mercury fillings than from those with no such fillings. It was concluded that at least two-thirds of the excreted mercury originates from the dental restorations.30

On the basis of the research cited here, there is now international scientific consensus that the mercury from dental tooth restorations constitutes the largest non-occupational source of mercury in the general population, being greater than all other environmental sources combined!34-36 Yet, the dental profession still insists, without evidence, that the exposure is insignificant and has no potential to produce harm.

Pathophysiological consequences of mercury from dental fillings. During the last several years, medical research has demonstrated a relationship between mercury exposure and pathophysiology in various animal models.

In sheep exposed to mercury from in situ tooth fillings, kidney function has been shown to be impaired. After 30 days of chewing the sheep lost 50% of their kidney filtration ability; they began to have difficulty regulating sodium and they demonstrated a reduced albumin excretion. Control sheep treated with non-mercury dental fillings did not show such effects.37 In a study of 10 humans with mercury fillings, it was demonstrated that the plasma mercury level dropped by 50% and the urinary mercury level declined by 25% over a twelve month interval after filling removal compared to the pre-removal level. Most notable was the finding that 12 months after filling removal, the urinary albumin level was significantly higher than the level 4 months prior to removal.38 In the sheep, the placement of mercury fillings caused a fall in the urinary albumin, signifying renal pathophysiology. In humans, the removal of mercury fillings results in an elevation in urinary albumin, indicating a renal homeostatic readjustment. The agreement between this sheep and human data is remarkable.

In a recent collaborative paper between three North American universities, it was demonstrated in a primate model that oral and intestinal bacteria (eg. streptococci, enterococci, enterobacteriaceae) exhibit a significant increase in mercury and antibiotic resistance within two weeks following mercury filling placement.39 The mercury resistant bacterial species exhibited resistance to various antibiotics such as, ampicillin, tetracyclines, streptomycin, kanamycin, erythromycin, and chloramphenicol, which they had not demonstrated prior to placement.. This is the first direct experimental confirmation of a non-antibiotic factor, mercury, producing antibiotic resistance. This occurs because in some bacteria mercury-resistance and antibiotic-resistance are encoded on adjacent small genetic sites within plasmids.40 When exposed to environmental mercury, this genetic material is activated to protect the bacteria from the lethal mercury. The plasmid is also replicated and passed on to other bacteria, insuring species survival. In so doing, the antibiotic resistance also spreads to the other bacteria. Antibiotic resistance is a important issue in medicine today.41 It has been estimated that 80% of mercury-resistant bacterial strains also show an increased resistance to one or more conventional antibiotics. Thirty percent of all hospitalized patients in North America receive antibiotic therapy42 and antibiotics compromise 10% of the total $5.1 billion drug sales in Canada during 1992.43 Moreover, ten of the top 20 generic drugs prescribed during 1990 in the U.S.A. were antibiotics.44 Yet, antibiotics appear to be losing their clinical potency and stronger antibiotic medications at increasing dosages are necessary to combat many common infections.41

Recently, investigations have suggested that mercury may be involved in common brain pathologies and that the source of the mercury is likely the dental fillings45-47 In a human autopsy study, brain tissue from persons having Alzheimer's Disease at death were compared to an age-matched group of control brains from subjects without Alzheimer's Disease. The only significant difference in metal content between the two groups was mercury, being considerably higher in the Alzheimer group. The mercury concentration was prominent in the hippocampus, the amygdala and particularly in the nucleus basalis, all brain structures involved in memory function. Other metals examined were not significantly different in the two groups of subjects. The effect of mercury on central nervous system neuron membrane integrity has been examined and shown that mercury specifically affects tubulin, a brain neuronal dimer protein responsible for proper microtubule formation of brain neurons.48 Both in vivo and in vitro experiments demonstrated that mercury chelated to amino acids maintains an abnormal polymerization state of tubulin. This effect may produce neurofibrillar tangles. Such tangles are a recognized lesion of Alzheimer's Disease. Inorganic mercury affects ADP-ribosylation of the rat brain neuronal proteins tubulin, actin and B-50, in both in vivo and in vitro experiments.49 ADP-ribosylation is the rate limiting process involved in polymerization of tubulin and actin monomers into the structure of the neuron membrane. Most recently, our laboratory has demonstrated that ionic mercury and elemental mercury vapour markedly diminishes the binding of tubulin to GTP and thus inhibits the polymerization of tubulin which is essential for the formation of microtubule in the central nervous system50 These studies are direct quantitative evidence for a connection between mercury exposure and neurodegeneration.

Other investigations have examined the mercury hypersensitivity from dental amalgam in patients with and without oral lichen planus lesions.51-53 These studies showed that patient groups having oral lichen planus had a much higher incidence of mercury patch-test reactivity (16-62%) than did control groups (3-8%). Removal of the mercury fillings resulted in amelioration of the oral symptoms.

Governmental regulatory action concerning mercury fillings. In 1987, the government of Sweden commissioned an "expert panel" to evaluate the available evidence regarding mercury filling safety. The panel concluded that mercury fillings were "unsuitable from a toxicological point of view". Based on this panels advice, the Swedish Socialstyrelsen announced that steps would be taken to eliminate dental amalgam usage and recommended that comprehensive mercury filling treatment on pregnant women should be stopped to prevent mercury damage to the fetus.54 Shortly thereafter, the German Ministry of Health (Bundesgesundheitsamt, BDA) issued an similar advisory.55 In October of 1989, the Swedish Director of Chemical Inspection (KEMI), responsible for environmental protection, declared that amalgam would be banned.56 In January of 1992, the German Ministry of Health (BDA) informed manufacturers of its intention to ban the production of amalgam.57 The BDA removed low copper non-gamma-2-amalgam from the market and published a pamphlet recommending avoiding mercury filling use in individuals with kidney disease, children to age 6, and pregnant women.58 In August of 1992, the Swedish government suggested a timetable to phase out mercury fillings. Environmental concerns were used as the official reason for amalgam discontinuation, but the government did acknowledge the toxicological risk to patients and stated that mercury fillings should no longer be used in children by July 1993, in adolescent to age 19 by July 1995, and in all Swedish citizens by 1997.59 The Austrian Minister of Health announced that the use of mercury fillings in children would be banned in 1996 and discontinued in all Austrians by the year 2000.60 In 1994, the Swedish Dental Association acknowledged that its leadership had previously been incorrect in their position regarding mercury filling safety. They now support a discontinuation of mercury use in dentistry.61 Other industrialized countries, for what ever reason, appear to be side stepping the issue.

Conclusions. As one might expect, the dental profession has not responded well to these data. Some national dental associations have attempted to influence public and governmental opinion by endorsing quasi academic symposia pervaded with amalgam advocates. These gatherings are non-consensus meetings often under government auspices, where the moderators responsible for drawing the conclusions are typically inclined toward the prevailing dental orthodoxy and the conclusions reached often blatantly disregard the experimental data presented.62 Most damning to the dental profession is that they have not advanced any reputable experimental evidence of their own to support their belief in mercury filling safety.

The medical research evidence has been clear for some time. Dental amalgam - mercury fillings - constitute a significant source of chronic exposure to mercury in the general population. This exposure is unnecessary and can not be justified by risk/benefit analysis. While incriminating medical research continues to be published, the dental profession persists in placing itself in the untenable predicament of advocating an anecdotal position of mercury filling safety. The mercury filling advocates can be criticized for their shortage of supporting research evidence; however, so can many mercury filling opponents, who irresponsibly go far beyond the limits of the experimental data, by suggesting that miraculous cures will occur after removal of the fillings. Still, the mercury exposure from dental silver amalgam is toxicologically significant and research into its possible effects is at an early stage. Perhaps a 1000 years from now, historians will look back and draw comparisons between the chronic lead poisoning of the Roman Empire and the insidious mercury poisoning from our toxic teeth.

Bibliography:
1. Baurer, J.G. and First, H.A., Calif. Dent. Assoc. J., 1982, 10, 47-61.
2. Skinner, E.W. and Phillips, R.W., The Science of Dental Materials, 6th ed., Philadelphia: W.B. Saunders Co., 1969., Chapt. 20, p. 303 and Chapt. 22, p. 332.
3. Paterson, N., Br. Dent. J. 157, 23-25.
4. Phillips, R.W., Hamilton, A.I. Jendresen, M.D. McHorris, W.H., and Schallhorn, R.G., J. Prosth. Dent., 1986, 55, 736-772.
5. American Academy of Dental Science, A history of dental and oral science in America. Philadelphia: Samuel White, publ., 1876
6. Bremmer, D.K., The story of dentistry, revised 3rd ed. Brooklyn: Dental Items of Interest Publishing Co Inc., 1954
7. Ring, M., Dentistry, an illustrated history. Harryu N. Abrams Inc., Publisher, New York, 1985.
8. Stock, A., Z Angew Chemie, 1926, 39, 984-989.
9. Stock, A., Z Angew Chemie, 1928, 41, 663-72.
10. Stock, A., Z Anorg Allgem Chemie, 1934, 217, 241-53.
11. Stock, A., Naturwissch, 1935, 28, 453-6.
12. Stock, A., Arch Gewerbepath Gewerbehygie, 1936, 7, 388-413.
13. Stock, A., Ber Dtsch Chem Ges, 1939, 72, 1844-57.
14. American Dental Association, Principle of ethics and code of professional conduct., section l-J; Representation of care and fees, 211 E. Chicago Avenue, Chicago IL U.S.A., 60611.
15. Vimy, M.J. and Lorscheider, F.L., J. Dent. Res., 1985, 64, 1069-71.
16. Vimy, M.J. and Lorscheider, F.L., J. Dent. Res., 1985, 64, 1072-5.
17. Patterson, J.E.; Weissberg, B.G.; and Dennison, P.J., Bull. Environ. Contam. Toxicol., 1985, 34. 459-68.
18. Fredin, B., Swed. Dent. J., 1988, 3, 8-15.
19. Vimy, M.J., and Lorscheider, F.L., J. Trace Elem. Exper. Med., 1990, 3, 111-123.
20. Schiele, R., Schellman, B., Schrodle, R. and Schaller, K.H., Amalgam aussagen von medizin und zahnmedizin; symposium, Koln, West Germany, March 1984, Abst. D29.
21. Nylander, M., Friberg, L., and Lind, B., Swed. Dent. J., 1987, 11, 179-187.
22. Eggelston, D.W. and Nylander, M., J. Prosth. Dent., 1987, 58, 704-707.
23. ADA News, Editorial and accompanying patient handout on the safety of dental amalgam., American Dental Association, Jan. 2, 1984.
24. Truono, E.J., Letter of Importance, J. Amer. Dent. Assoc., 1991, 122, 8-14.
25. American Dental Association News Release, 1990
26. Hahn, L.J., Kloiber, R., Vimy, M.J., Takahashi, Y., and Lorscheider, F.L., FASEB J., 1989, 3, 2641-2646.
27. Hahn, L.J., Kloiber, R., Leininger, R.W., Vimy, M.J., and Lorscheider, F.L., FASEB J, 1990, 4, 3256-3260.
28. Danscher, G. Horsted- Bindslev, P. and Rungby, J., Exp. Mol. Path., 1990, 52, 291-299.
29. Vimy, M.J., Takahashi, Y., and Lorscheider, F.L., Amer. J. Physiol., 1990, 258, R939-R945.
30. Aposhian, H.V., Bruce, D.C., Alter, W., Dart, R.C., Hurlbut, K.M. and Aposhian, M.M., FASEB J., 1992, 6, 2472-2476.
31. Gerhard, I., Waldbrenner, P. Thuro, H. and Runnebaum, B., Clin. Lab., 1992, 38, 404-411.
32. Zander, D., Ewers, U., Freier, I., and Brockhaus, A., Zbl. Hyg. Umwelt., 1992, 192, 447-54. 33. Zander, D., Ewers, U., Freier, I., and Brockhaus, A., Zbl. Hyg. Umwelt., 1992, 193, 318-328.
34. Clarkson, T.W., Hursh, J.B., Sager, P.R., and Syversen, T.L.M., In: Biological Monitoring of Toxic Metals (Clarkson, T.W., Friberg, L., Nordberg, G.F., and Sager P.R., eds.), Plenum Press, New York., 1988, 199-246,
35. Vimy, M.J., and Lorscheider, F.L., J. Trace Elem. Exper. Med., 1990, 3, 111-123.
36. World Health Organization, Environmental Health Criteria 118, Inorganic Mercury., WHO, Geneva, 1991, 36.
37. Boyd, N.D., Benediktsson, H., Vimy, M.J., Hooper, D.E., and Lorscheider, F.L., Am. J. Physiol., 1991, 261, R1010-R1014.
38. Molin, M., Bergman, B., Marklund, S.L., Schutz, A. and Skerfving, S., Acta Odontol. Scand., 1990, 48, 189-202.
39. Summers, A.O., Wireman, J., Vimy, M.J., Lorscheider, F.L., Marshall, B., Levy, S.B., Bennett, S. and Billard, L., Antimicrob. Agents & Chemother., 1993, 37, 825-834.
40. Gilbert, M.P. and Summers, A.O., Plasmid, 1988, 20: 127-136.
41. Cohen, M.L., Science, 1992, 257, 1050-1055.
42. Gilman, H.G., Rall, T.W., Nies, A.S. and Taylor, P. Goodman and Gilman's: The Pharmacologic Basis of Therapeutics, 8th ed., Pergamon Press, Elmsford, New York, 1990, p. 1018.
43. Intercontinental Medical Statistics, IMS, Canada, 1992.
44. Pharmacy Times, April 1991, 58.
45. Khatoon, S., Campbell, S.R., Haley, B.E. and Slevin, J.T., Ann. Neurol., 1989, 26, 210-215.
46. Thompson, C.M., Markesbery, W.R., Ehmann, W.D., Mao, Y-X. and Vance D.E., Neurotoxicology, 1988, 9, 1-7.
47. Wenstrup, D., Ehmann, W.D. and Markesbery W.R., Brain Res., 1990, 533, 125-131.
48. Duhr, E., Pendergrass, C., Kasarskis, E., Slevin, J. and Haley, B., FASEB J., 1991, 5, A456.
49. Palkiewicz, P., Zwiers, H. and Lorscheider, F.L., J. Neurochem., 1994, 62, 2049-2052.
50. Lorscheider, F.L., Vimy., M.J., Pendergrass, J.C. and Haley, B.E., Abst. presented at the 12th International Neurotoxicology Conference, Univ. Arkansas Med. Center, Hot Spring, AR, Oct.30 - Nov.2, 1994.
51. Finne, K.; Goransson, K.; and Winckler, L., Int. J. Oral Surg., 1982, 11, 236-9.
52. Lundstrom, I.M.C., Int. J. Oral Surg., 1983, 12, 1-9.
53. Mobacken, H.; Hersle, K.; Sloberg, K.; and Thilander, H., Contact Dermatitis, 1984, 10, 11-5.
54. Socialstyrelsen (Sweden, Social Welfare and Health Administration). Redovisar; kvicksilver/amalgam halsorisker. Allanna Forlaget AB, Stockholm, 10 32-39, 1987.
55. Bundesgesundheitsamt (Germany, Ministry of Health), Machine Design, p. 274, August 25, 1988.
56. KEMI (Sweden, Chenical Inspection Agency), Amalgam will be banned. Dagens Nyheter, October 6, 1989.
57. Bundesgesundheitsamt (Germany, Ministry of Health), Letter to pharmacetical companies, January 29; Artezeitung (Physician's Daily), March 3, 1992
58. Bundesgesundheitsamt (Germany, Ministry of Health), Amalgame - nevbenwirkungen und bewertung der toxizitat, Zahnartzt Woche (DZW), 1992, 8, 1.
59. Socialstyrelsen (Sweden, Social Welfare and Health Administration), Press Release. August 28, 1992.
60. Austrian Minister of Health, Austria to be amalgam free by year 2000. FDI Dental World, March/April, 1993, p. 6.
61. Swedish Dental Association, Swedish News Bureau, TT, January 17, 1994. 62. Lorscheider, F.L. and Vimy, M.J., FASEB J., 1993, 7, 1432-1433.