This paper was originally published in the Autumn 1986 edition of the peer reviewed journal

Download 99.36 Kb.
Date conversion23.11.2016
Size99.36 Kb.
(This paper was originally published in the Autumn 1986 edition of the peer reviewed journal Research Forum by Palmer College of Chiropractic)

A chiropractic perspective on the dental amalgam controversy

Kristopher Keller


Dental amalgams, commonly known as silver fill­ings, account for 75 percent of all single tooth restorations. Amalgams are composed of several metals, most notably mercury, which comprises about 50 percent of the typical filling by weight. Several recent studies have revealed that mercury vapor is released from these fillings under the con­ditions normally present in the oral environment.

The concentration of mercury in the oral air of some subjects exceeded government established standards for occupational exposure to mercury vapor. Other studies indicate that psychological and behavioral changes can occur in humans at exposure levels below these government standards. Genetic, dietary and other factors make individual sensitivity to mer­cury unpredictable. Though no major study has ever attempted to find a link between amalgams and any specific pathology resulting from mercury toxicity, the available evidence raises concerns about its safety.
Key Words: Chiropractic, dental amalgam, dental materials, intra-oral galvanism, mercury, mercury poisoning, selenium.

Amalgam is defined as an alloy of two or more metals, one of which is mercury (Hg). Dental amalgams, commonly known as "silver fillings," contain mercury, silver, tin and sometimes copper and zinc. (II First introduced in North America in 1833, dental amalgam is now estimated to represent 75 percent of all single tooth restorations (fillings)y.J) There are several manufacturers of amalgam, each with a slightly different formula.(4)
Below are the approximate percentages of the com­ponent elements:

Mercury (Hg) 50%

Silver (Ag) 35 %

Tin (Sn) 13%

Copper (Cu) 0-3 %

Zinc (Zn) 0-1%

Liquid elemental mercury (Hg) is added in equal parts by weight to the other ingredients to produce a mass that is pliable enough to be forced into the prepared cavity. Excess Hg is squeezed out of the amalgam usually by manual pressure. The filling then cures; ideally it hardens in about a day. The final mass contains about 45-50% Hg by weighus.6)
Recent research shows that amalgam is not en­tirely chemically stable after curing. In contrast to earlier studies, recent evidence suggests that amalgam in the oral environment constantly releases small quantities of cytotoxic corrosion products and Hg vapor. (4,7,8,9,10) The Hg vapor levels are greatly in­creased by mildly abrasive action such as chewing gum and brushing. Ingestion of hot beverages also increases the vapor release. The elevated vapor release continues after the removal of the stimula­tion, gradually tapering off over the next few hours. The current point of controversy is whether or not the levels released are great enough to be hazardous to the health of the patient. The American Dental Association and associated organizations have released statements to the effect that except in rare cases of allergic hypersensitivity, the levels of release are too low for concern. Recent studies revealing psychological and teratogenic effects at levels of Hg exposure considered safe by current standards have caused some professionals to question the validity of those standards.

Biological Indicators of Hg Intoxication
A major problem in verifying or refuting the danger of amalgam is the lack of reliable biological indicators of Hg intoxication and variations in in­dividual sensitivity to Hg exposure. (2,13,22,24). There has been little success in finding correlations between blood and urine Hg levels with clinical signs or symptoms. There is also disagreement about whether urine and blood levels reflect current exposure or are a delayed expression of exposure over the period of a year. It is generally agreed that urine and blood levels of Hg are very poor predictors of intoxica­tion. Individual sensitivity and selective tissue accumulation may cause an unpredictable response in a patient, while renal damage from Hg exposure will affect the urine and blood levels. (13,23,24,25) In popula­tions with similar exposure, however, careful studies have shown some dose/response relationship within narrow ranges of urine and blood Hg. (18,25,26,27)
Because of its strong affinity for sulfur contain­ing proteins, Hg concentration in the hair is a fairly good indicator of chronic exposure but is subject to error from environmental contaminants and some shampoos and hair treatments.(13,28) Hair analysis seems to be the preferred method of evaluating body burden of Hg, as long as care is taken in collecting and testing. Hair gives a profile of exposure over several months; this is a sufficient time to gauge most body tissues' burden because the average half-life of Hg in the body is usually quoted at 58 days. (13,22) Some tissues, most notably the CNS, have much longer half-life for Hg and therefore care must be taken in evaluation of CNS related disorders by hair sampling.
With amalgams the level of exposure can be tested directly by analysis of Hg concentration of air in the mouth. Several machines developed primarily for industry are available to do this; the best for this purpose is known as the Jerome Mercury Vapor Analyzer. (13) Some question exists as to the significance of oral vapor levels if the subject nor­mally breathes through the nose.
At present the diagnosis of Hg poisoning must be made primarily on the basis of physical examina­tion and history of exposure with secondary em­phasis on laboratory tests. (24)

Factors of Exposure
The major route of entry for Hg vapor is through the lungs. Seventy to 100 percent of the Hg vapor that is inhaled is retained in the lungs. (11,22) The Hg then diffuses into the capillaries, 50 percent binding to the plasma proteins and 50 percent to the hemoglobin in the RBC's. The Hg is then quickly carried to the CNS and other tissues of the body via the blood circulation. (17)
Elemental Hg is much less toxic when swallowed than inhaled because very little absorption of elemental Hg takes place in the GI tract. For this reason, Hg that is swallowed during placement and removal of amalgam is not considered a hazard. (22) The elevated vapor levels present during these pro­cedures is potentially a risk to both doctor and patient. (37)
Although the primary route of entry is most likely the lungs, several other routes of entry for amalgam generated Hg have been proposed. The direct ab­sorption into oral mucosa does occur but seems to remain fairly localized. (20) Hg is known to penetrate into the dental pulp one to seven days after place­ment of the amalgam. (11) Ingalls has suggested Hg may enter the nerves in the tooth and be transported via axoplasmic flow directly to the brain. (30) Similarly, Nylander has proposed that Hg vapor may be absorbed into the olfactory nerves and then transported by axoplasmic flow to the brain. (31) Autopsy studies by Nilner, et al, however, found no consistent correlation between Hg concen­trations in alveolar nerve tissue and the presence of amalgam fillings. (47)
Symptoms displayed seem to be dependent at least in part on two factors: 1) The ability of the kidneys to eliminate Hg from the body and 2) The rate of retention and elimination of various organs. At low levels of exposure the kidneys seem able to eliminate Hg readily with little sign of renal damage. (12) At these low levels, however, certain systems are known to retain Hg and build up considerable concentra­tions. The blood brain barrier and placenta are permeable to Hg. Once inside the CNS and fetus, Hg is rapidly oxidized to a less permeating form. Hg is thereby trapped in these tissues and builds up to levels far above that indicated by the blood levels. (17,22) This would be consistent with the findings of CNS and em­bryological disorders found at low exposure levels. (8,25,26,28)
At higher levels of acute exposure or chronic ex­posure to lower levels, the kidneys begin to lose the ability to excrete Hg. The exact mechanism is not understood. It may have some relationship to find­ings that Hg accumulates in the distal and convoluted tubules. (17) Therefore, while blood and tissue levels increase, urine samples actually show a lower Hg

concentration. Patients exhibiting signs of Hg poisoning may actually have little or no Hg in the urine.(13,23,24) Psychomotor changes are common; other systemic manifestations may be present as well, such as anorexia, chest pains, insomnia and bleeding gums. (22)

Heavy exposure most likely will manifest first in bronchial damage and pneumonitis.(22,23) Severe renal damage with nephrotic syndrome is likely, with the pattern of urinary Hg reversing again and ex­tremely high levels of Hg being excreted. Even at these high levels there is very little correlation be­tween signs and symptoms of intoxication and urine Hg concentration. (27) Severe CNS damage with serious psychomotor and psychological dysfunction­ing will occur. The prognosis at this stage is poor with death possible.
Individual response and individual organ or system dysfunction may vary greatly from the norm for a variety of known and unknown reasons.

Factors of Individual Sensitivity
The body has several methods of dealing with tox­ic substances. It may try to change them chemical­ly or it may attempt to eliminate them by some ex­cretory process. It may attempt to isolate the toxin and store it. Most likely a combination of the above will be employed. Occasionally the methods will backfire and a more toxic substance will be produced or the stored chemical will be of such a quantity that it will re-enter the system or damage the tissue.
Hg is excreted in other ways besides the urine. It is excreted in the bile, feces, sweat, saliva, hair and nails, and vapor in the breath. (11,24) Urine is by far the most important route of excretion for elemen­tal or inorganic forms of Hg.
It is possible that some of the elemental Hg is con­verted to the more toxic methyl or organic form in the body. Bacteria native to the human oral environ­ment are known to be able to methylate Hg, or methylation may take place within the body itself. (12,23) But, based on the relative amounts of methylated Hg found in exposed individuals, it seems that inorganic HG is either methylated in small quan­tities or it is eliminated rapidly from the body.(9) Autopsies on retired workers from an Hg mine were found to have enormous quantities of inorganic Hg in thyroid, pituitary, kidney, brain and lung tissue, but levels of methyl Hg were just slightly above con­trol subjects. (34)
The same study of miners revealed what is thought to be a major detoxification tool for Hg. A near equimolar concentration of Selenuim (Se) to that of Hg was found in the tissues tested. (34) This same ratio has been discovered for ocean fish such as tuna.
Fresh and saltwater fish taken from Hg polluted waters do not seem to be able to maintain this balance and exhibit elevated Hg/Se ratios.(35) Dietary Se has been found to protect laboratory: animals from high levels of Hg exposure. Se does not reduce the quantity of Hg retained in the body, in fact Se may actually cause increased retention in the brain and kidneys while reducing the toxicity. Se itself is a very toxic mineral and its toxicity is reduced by the presence of Hg. The Se-Hg connec­tion may explain why people who consume large amounts of seafood have been found to have high concentrations of Hg in their blood with apparent­ly no ill effects. It has been found that some species of fish have high enough amounts of Se to act as protection against Hg from other sources. (36)
Se poisoning was once thought to be a major health hazard, but more recent studies have shown that Se deficiency in the diet may be a more com­mon occurrence. (36) Many agricultural soils are defi­cient in Se and a diet dependent on those foods could conceivably lead to greater sensitivity to Hg poisoning. (44)
Vitamin E plays a major role in detoxifying Hg in the body. It is thought to act as an anti-oxidant or radical scavenger and in some way assists Se.(35,36) Other dietary factors may also have an im­pact on Hg toxicity. There is some evidence that sulfur containing amino acids may have an effect on reducing toxicity. (35) Vitamin C is sometimes recommended as reducing. the effects of Hg hypersensitivity. (5)
Conversely, lead (Pb) is known to increase the tox­ic effects of Hg and vice versa. Therefore, sub-acute doses of both of these minerals could result in acute reactions. (28)
Hypersensitivity Versus Toxicity
Hypersensitivity to Hg from dental amalgam ex­posure is well documented. (11,12) The most common form of reaction is contact dermatitis. Hg is thought to act as a hapten, combining with oral mucosa pro­teins to produce an antigen to which the body responds in a cell mediated antibody reaction. (13) Mobacken et al found a high correlation between the presence of oral lichen planus lesions and amalgam restorations. In 64 of the 67 cases studied, the lesion was in direct contact with an amalgam filling. (14) The documented cases of hypersensitivity to amalgam almost always follows a previous ex­posure to Hg. Most of these reactions are self limiting and usually require only palatal care. But, some cases are cleared up only with the removal of the amalgam. (11)
Systemic hypersensitivity to amalgam is also well documented. (15) This most often takes the form of diffuse erythema or dermatitis. Other signs and symptoms of hypersensitivity to amalgam that are reported are given in Table 1. The use of skin patch tests for determination of potential allergic reaction has been discouraged because of poor accuracy and the possibility of the test itself sensitizing the patient to further Hg exposure. (13,16)
Actual toxicity from Hg is often difficult to diagnose even at relatively high levels of exposure because of individual variability in sensitivity and the non-specific clinical picture, as listed in Table 2. The toxicity of Hg is in its ability to bind to en­zymes, especially those with -SH groups at the ac­tive site, thereby altering or blocking their actions. Hgis known to stimulate and then completely block acetycholine release from neurons, (17,18) block pro­gesterone binding sites, (19) reduce synthesis of col­lagen by fibroblasts and epithelial cells, (11,20) and reduce RNA concentrations in the hypothala­mus. (21) Hg also binds to hemoglobin and plasma proteins very rapidly. (11)
Study of the Hg toxicity syndrome known as acrodynia (Table 5) shows that a mechanism of hypersensitivity exists which can exhibit the signs and symptoms of acute Hg poisoning at very low exposure levels. (24,32,33) This is in contrast to the dermatological presentation of antigen-antibody hypersensitivity. One mechanism for variations in individual sensitivity is suggested by the Se/Hg detoxification interaction. The actual biochemical relationship is poorly understood, but the ability to use the mechanism has been shown in rats to be a sex linked characteristic. (36) This indicates the possibility of genetic variations in Hg sensitivity. As stated earlier, dietary variations in Se consumption can affect Hg sensitivity. This is an area that has received considerable attention in animal research, but little in the way of human studies. (35,36)
There are examples in the literature of case studies that seem to be non-allergic hypersensitivity reac­tions to amalgam derived Hg. (5)

Table 1

Symptoms of Allergic Hypersensitivity to Amalgam Fillings


Absence of lingual papillae

Dermatitis of extremities,

eyes, lips and gingiva
Dry mouth






Loss of taste




Swelling of lips,

tongue and oral mucosa

Table 2

Signs and Symptoms of Mercurial Poisoning





Decreased mental ability


Easy embarrassment



Lack of concentration

Loss of memory Loss of sex drive



Personality changes

Psychic disturbances

Other PNS and CNS Related Dysfunctions

ALS type syndrome


Anorexia Paresthesia


Ataxia Polyneuropathy

Cardiac arrythmia

Excessive salivation



Increased deep tendon


Muscular weakness

Peripheral neuritis

Profuse sweating

Tremors of hands, lips,tongue and feet

Kidney Related Disorders




Nephrotic syndrome

Oliguria Proteinuria

Renal damage

Thirst - Excessive

GI Tract and Other Signs and Symptoms

Abdominal Cramps


Blue line on gums around tooth


Dermatltus Rhinitis

Diarrhea Sialorrhea

Erythema Stomatitis


Mercurilentis (Hg deposits on lens of eyes)

Metallic taste

Mucocutaneous lymph node syndrome (Kawasaki's Disease)

Weight loss

Heavy Exposure to Hg Vapor


Chest Pain







Interstitial pneumonitis




Table 3

Signs and symptoms of Mercurial Toxicity Reported From Occupational Exposure In Dentists and Dental Assistants



Burning tongue


Decreased reflexes Depression


Digestive disturbances Emotional instability Erethism

EX<4essive salivation Fatigue


Fine motor control loss Gingivitis


Hopeless feeling




Memory loss

Metallic taste


Nasal secretion Increase


Nephrotic syndrome

Red palms


Sore mouth



Visual disturbances

Including focusing Weakness

Table 4

Signs Associated With Acrodynia



Digestive disturbances

Erythema of cheeks and nose Irritability

Lesions of skin on hands and feet

Muscle weakness




Profuse salivation

Swelling of extremities


Table 5

Signs and Symptoms Ascribed In Anecdotal Reports to Hg Poisoning in Patients with Amalgams



Depressed WBC count

Difficulty breathing

Elevated WBC count

Emotional instability


Excessive shyness

Gall bladder dysfunction


Lack of energy

Uver dysfunction

Painful menstruation

Severe chest pains

Subnormal body temperature


Thyroid dysfunction

Weight loss

Toxicity From Amalgam and Equivalent Ex­posure levels
Dentists and dental assistants are known to be at risk of Hg poisoning. (Table 3) Ten to twenty-five percent of dental offices have been found to exceed acceptable levels of Hg vapor in the air. (20) Cases of Hg poisoning of dentists and assistants are well documented. (2,12) Periodic studies of urine Hg levels in dentists in the U.S. show that approximately 1.3% have levels in excess of those known to cause physiological changes. Dental students are found to have significant increases in allergic sensitivity to Hg as they progress through school. (37,44)


Nylander found increased levels of Hg in the pituitary glands of cadavers of dentists compared to controls with no known Hg exposure. (31) ln one case the amount of Hg in the pituitary gland of a dentist was 60 times that of a control with no known exposure. A study in Sweden found that the rate of glioblastomas for dentists and assistants was about twice that of the general population. The study did not prove a relationship specifically with Hg, but only with some factor associated with the dental pro­fession, such as amalgam, chloroform, or radiography. (38)

Research on Hg toxicity from amalgams in dental patients is in its infancy. Direct relationship between amalgam and pathologies has not been proven, but available evidence shows that subjects with amalgams have associated increases in Hg in body tissues. Nylander found that cadavers of pa­tients with amalgam fillings had concentrations of Hg in their pituitary glands as high as 19 times that found in non Hg exposed controls. (31) Friberg, et al, indicated that cadavers with an average number of amalgams had about three times as much Hg in their brains as did those tested without amalgams.(9)
Because there have been no studies done to deter­mine if there is a significant increase in pathologies in subjects with amalgams, we must look at the possibilities suggested by exposure levels in the same range as those produced by amalgams. Recommend­ed maximum exposure levels for occupational ex­posure, eight hours/day and five days/week, have been established by the National Institute for Oc­cupational Safety and Health (NIOSJ-i) and the World Health Organization (WHO). (10,48) The NIOSH level is set at 50 Ng Hg/L air, the WHO level is set at 25 Ng Hg/L air. The WHO standard, when adjusted for 24 hours/day, seven days/week ex­posure, is equal to 7.7 Ng Hg/L air.
Several studies have shown Hg vapor levels in excess of these limits in the oral air of people with amalgam fillings. Mechanical stimulation significantly increases the levels of Hg vapor produced so most studies are run before and after some. mechanical stimulation such as brushing teeth or chewing gum for 10 minutes. Ou, et al, found levels as high as 12.7 Ng/L before brushing and 62.0 after brushing.nol Svare, et al, found levels as high as 85.5 Ng/L after chewing gum for 10 minutes.(10) Higher concentration levels are present during in­stallation and removal of amalgams. In some cases removal of amalgams can produce levels in excess of those established as maximum permissible for any exposure period. (37)
Research on workers exposed to Hg vapor found a correlation between changes in short term memory and urine Hg concentration at very low levels of urine Hg. (25) The average levels tested were above those associated with amalgam exposure, but some subjects in the test had urine Hg in the same range as found in amalgam studies. Two interesting side notes from this study are: 1) Workers with the longest exposure (i.e. the oldest workers) were among those with the lowest urine Hg levels and were eliminated from the test group; 2) One method of evaluating memory deficiency that is commonly

used in this type of testing was found to be too in­accurate to reveal a significant correlation. (25)

Several specific maladies have been noted to oc­cur in association with extremely low levels of Hg exposure. A significant correlation was found be­tween increased stillbirths and malformed infants and prenatal blood concentrations of Hg similar to those found in relation to amalgams. (8) Similarly, a Danish study found that women exposed to Hg

in the workplace had a higher incidence of infertility.(26)

A study of school children in Wyoming found a significant correlation between emotional distur­bance and increased Hg exposure as indicated by hair analysis. The levels of Hg in the hair of both con­trol and disturbed children were far below the level considered toxic and well within normal limits stated in the literature.(13,24,28) No source of Hg exposure was postulated.
Studies in the Russian literature report that rats and rabbits exposed for several months to Hg vapor levels equivalent to those produced by amalgams showed pathological changes in the CNS, the thyroid and adrenal glands, the heart, and the liver.(22) How the sensitivity of these laboratory animals com­pares to that of humans is not clear.

Amalgam and other metallic dental materials are known to produce small amounts of electric current. Metals in contact with saliva make up an elec­trochemical cell.(40) The chemical reactions that have been suggested to produce the current include some in which salts and ions of the metals involved are released into the oral environment. Studies that have tried to correlate the amount of galvanic ac­tion with saliva Hg concentrations have found very little relationship. Saliva Hg concentrations are found to be more closely related to blood Hg con­centrations. The relationship between galvanism and ­oral Hg vapor levels has not been studied. (41)

The greatest flow of current will be between fill­ings with large differences in electrical potentials. This current flow is known to be responsible for in­creased rate of corrosion in amalgams, but con­troversy exists as to whether these currents are responsible for certain types of oral lesions.(29,42,44) Amalgams are found to have potentials in the range of +50mv to -500mv. Gold fillings and others are found to have potentials from + 100mv to -200mv.(39) Contact between amalgam and any other type of material increases the likelihood of cur­rent flow because of the different potential ranges. Other factors affect the rate of current such as con­tact surface area and internal resistance of the amalgam.(29) Currents between amalgams have been measured as high as 100 ua.(42,45)

The NIOSH and WHO recommended maximum exposure levels are based, for the most part, on studies of physiological changes in workers expos­ed to Hg vapor in an industrial setting. The popula­tions used to determine safe levels of exposure have been those populations who have had heavy ex­posure in industry for years and were still capable of performing their jobs. (22) The question comes to mind of how many others were forced to leave these jobs because of Hg related health problems and thus were left out of the studies. It is possible that the levels being accepted as safe are skewed toward the higher end of the scale by a hypertolerant test population. Additionally, are we to accept physiological effects as the criterion of intoxication? Psychological and embryological changes are known to occur at very low exposure levels. These should also be considered when establishing permissible ex­posure levels.
Several aspects of Hg poisoning could be con­sidered to be chiropractic related. The CNS effects of Hg poisoning are obviously of interest. (17,18) Degenerative joint disease and skeletal disorders may also have Hg connection. Hg is known to block collagen synthesis by fibroblasts and epithelial cells. (11,22) One aspect of acrondynia is polyarthritis and muscle weakness. The effects of galvanism may also have significance chiropractically. What effect might electrical potentials of 400mv or more have on the nerves in the tooth pulp that are in contact with the amalgam? What effect on reflex mechanisms would stimulation of these nerves have? A dramatic demonstration of galvanic action can be performed by biting down on a piece of aluminum foil between two amalgams. The same neuronal pathways are be­ing stimulated or at least potentiated every time those same teeth are in close proximity. Is there a possibility of reflex muscle contraction in the head and neck in response to this micro-stimulation? Could this lead to excessive fixation and reduced function in the cervical region?
Several epidemiological studies in the U. S. have found statistical and geographical correlations be­tween amalgam fillings and the incidence of multi­ple sclerosis (MS). (30) These relationships do not prove a cause and effect, of course. The ability of Hg from amalgam to accumulate in the CNS and its ability to cause antigen-antibody reactions do lend some credibility to the theory. Additionally, the resemblance between chronic Hg poisoning and amyotrophic lateral sclerosis (ALS), a syndrome similar to MS, is often mentioned in the literature.(24)
The question for chiropractic seems to be how this fits into our scope of practice. Some dentists have been accused of practicing medicine for suggesting that patients with suspected Hg toxicity have their amalgams replaced. Would it be practicing medicine for a chiropractor to refer a patient with suspected Hg poisoning to a dentist for evaluation? The duty

of a primary health care provider is to do what is in the best interest of the patient. The evidence in no way suggests that everyone with amalgam fill­ings should have them replaced, yet there is enough evidence to make one suspect that it could help some people. Certainly the evidence is strong enough to make one very cautious about the installation of new amalgam especially in children who would then face a life-long exposure to a known toxin.

Until recently there were no acceptable substitutes for amalgam other than expensive gold fillings. In the last year, several new posterior composites have been at least provisionally approved. Composites have been in use for about 20 years as cosmetically acceptable materials for front, low-load bearing teeth. The composites, a combination of synthetic resin and powdered silica or quartz, closely match the appearance of natural teeth and improvements in the technology have made them nearly as durable as amalgam. Though they are more difficult to in­stall the overall cost of restoration with composites is not much different than with amalgam.
Aside from the hypersensitive patient there is no conclusive proof yet that amalgam is hazardous when used judiciously. But does it make sense to knowingly add to the body's burden of a toxic chemical? For this reason it is questioned in the­literature whether amalgam would ever pass FDA approval if introduced as a new material today. (6) It is the author's desire that increased public and pro­fessional awareness of the questions surrounding the use of amalgam will stimulate further research into their possible toxic effects especially in the areas of emotional and behavioral disorders and infertility.

1. Dorlands Illustrated Medical Dictionary. 26th

Ed. Philadelphia: W. B. Saunders Company,


2. Donovan TE, Handlers JP. A rational'policy on

the use of dental amalgam. CDA Journal 1984;


3. Department of Biomaterials. Consequences of mercury exposure in dentistry: A review of the Literature. Florida Dental Journal 1983, Winter; 54(4):17-21.

4. Milleding P, Wennberg A, Hasselgren G. Cytotoxicity of corroded and non-corroded dental silver amalgams. Scand J Dent Res 1985; 93:76-83.

5. Huggins HA, Mercury - A factor in mental disease? The Journal of Orthomolecular

Psychiatry 1982; 11(1). .

6. Wolff M, Osborne IW, Hanson AL. Mercury toxicity and dental amalgam. NeuroToxicology 1983; 4(3):201-204.

7. Ou KHR, Log F, Kroncke A. Zur Quecksilberb­nelastung durch Amalgamfullungen. Dtsch Zahnarztl Z 1984; 39:199-205.

8. Abraham JE, Svare CW, Frank CWo The effects of dental amalgam' restorations on blood mer­cury levels. J Dent Res 1984, January; 63(1):71-3.

9. Friberg L, Kullman L, Lind B. K vicksilver i cen­tral nervsystemet i relation till amalgamfylln­ingar. Lakartidningen 1986; 83(7):519-22.

10. Patterson JE, Weissberg BG, Dennison PI. Mer­cury in human breath from dental amalgams. Bull Environ Contam Toxico11985; 34:459-468.

11. Bauer JG, First HA. The toxicity of mercury in dental amalgam. CDA Journal 1982; Iune:47-60.

12. Bauer IG. Action of mercury in dental exposures to mercury. Operative Dentistry 1985; 10:104-13.

13. Cooley RL, Young JM. Detection and diagnosis of bioincompatibility of mercury. CDA Jour­na11984; October: 36-43.

14. Mobacken H, Hersle K, Sloberg K, Thilander H. Oral lichen planus: hypersensitivity to den­tal restoration material. Contact Dermatitis 1984; 10:11-5.

15. Nakayama H, Niki F, Shono M, Hada S. Mer­cury exanthem. Contact Dermatitis 1983; 9:411-7.

16. Mackert JR, Fisher AA. Hypersensitivity to mercury from dental amalgams. Journal of the American Academy of Dermatology 1985, May; 12(5):877-80.

17. Placidi GF, Dell'Osso L, Viola PL, Bertelli A. distribution of inhaled mercury (203 Hg) in various organs. Int J Tiss Reac 1983; V(2): 193-200.

18. Cooper GP, Manalis RS. Influence of heavy metals on synaptic transmission: A review. Neurotoxicology 1983; 4(4):69-84.

19. Greist RE, Coty WA. Binding of the chicken oviduct progesterone receptor to steroid affinity resins: resistance to elution with mercurial agents. J Steroid Biochem 1984; 21(1):29-34.

20. Payne RW, Bums RA, Davis WJ. The con­troversy of mercury in amalgam restorations: review of the literature. ODJ 1984; January:27-8.

21. Lach H, Srebro Z, Dziubek K, Krawczyk S, Szaroma W. The influence of mercury and lead compounds on the circadian rhythm of cytoplasmic RNA in hypothalamic neurons of mice. Folia Histochemica Et Cytochemica 1983; 21(3-4) :231-8.

22. World Health Organization. WHO study group on recommended health-based limits in occupa­tional exposure to heavy metals. World Health Organization, 1980; Geneva: WHO tecl)nical report series; No. 647.

23. Wyngaarden JB, Smith LH, eds. Cecil Textbook of Medicine. 17th edition. Philadelphia: W.B. Saunders, 1985:2309-10.

24. Arena JM. Poisoning: Toxicology, Symptoms, Treatments. 4th Edition, Springfield, IL: Thomas, cl979, pp. 144-9,272.

25. Smith PJ, Langolf GO, Goldberg J. Effects of occupational exposure to mercury on short term memory. British Journal of Industrial Medicine 1983, November; 40(4):413':9.

26. Rachootin P, Olsen J. The risk of infertility and delayed conception associated with exposure in the Danish workplace.

Journal of Occupational Medicine 1983, May; 25(5):394-402.

27. Roels H, Lauwerys R, Buchet JP, Bernard A, Barthels A, Oversteyns M, Gaussin J. Com­parison of renal function and psychomotor performance in workers exposed to elemental mer­cury. Int Arch Occup Environ Health 1982; 50:77-93.

28. Marlowe M, Errera J, Stellern L Beck D. Lead and mercury levels in emotionally disturbed children. Journal of Orthomolecular Psychiatry; Vol. 12, No.4, 1983.

29. Nilner K. Studies of electrochemical action in the oral cavity. Swedish Dental Journal Supple­ment 9, 1981.

30. Ingalls TH. Epidemiology, etiology, and preven­tion of multiple sclerosis. The American Jour­

nal of Forensic Medicine and Pathology 1983, . March; 4(1):55-61.

31. Nylander M. Mercury in pituitary glands of dentists. The Lancet, 1986, February; 22:442.

32. Thomas CL, ed. Tabers Cyclopedic MedicalDictionary. 12th edition Philadelphia; F .A.Davis Company 1977.

33. Arena JM. Poisoning: Toxicology, Symptoms,Treatments. 4th edition Springfield, IL. Thomascl979 p.608.

34. Kosta L, Byrne AR, Zalenko V. Correlation bet­ween selenium and mercury in man following exposure to inorganic

mercury. Nature 1975,March 20; 254:238.

35. Ganther HE. Interactions of vitamin E and selenium with mercury and silver. Annals New York Academy of Acience. 1980; Vol. 355.

36. Frost DV. Selenium and vitamin E as antidotes to mercury toxicity. International Conference on Mercury Hazards in Dental Practice; 1981.

37. Naleway, Sakaguchi, Mitchell, Muller, Ayer, Hefferren. Urinary mercury levels in U.S. den­tists, 1975-1983: Review of health assessment. JADA 1985, July; 111:37-42.

38. Ahlbom A, Norell S, Rodvall Y, Nylander M. Dentists, dental nurses, and brain tumors. British Medical Journal 1986, March 8; 292-662.

39. Bergman M, Ginstrup 0, Nillson B. Potentials of and currents between dental metallic restora­tions. Scand J Dent Res 1982; 90:404-8. '

40. Lundmark L, Johansson B, Stenman E, Bergman M. Convenient instrument for oral galvanism measurement. Scand J Dent Res 1982;


41. Nilner K, Glantz P. The prevalence of copper-,silver-, tin-, mercury- and zinc-ions in human saliva.

Swed Dent J 1982; 6:71-7.

42. Holland RI. Galvanic currents between gold and

amalgam. Scand J Dent Res 1980; 88:269-72.

43. Block JB. The signs and symptoms of chemical

exposure. Springfield, IL: Thomas, c1980.

44. Passwaer RA. Selenium as Food & Medicine.

Keats Publishing, c1980.

45. Ayres S. Amalgam and gold dental fillings:

Reaction from electrogalvanic current. Journal

of the American Academy of Dermatology

. (14(2) Part 1, Feb 1986.

46. Berkow R, ed. The Merck Manual. 14th edition.

Merck Sharp & Dome Research Laboratories


47. Nilner K, Akerman S, Klinge B. Effect of den­tal amalgam restorations on the mercury con­tent of nerve tissues. ACTA Odontol Scand 1985; 43:303-7.

48. Criteria for a recommended standard occupational exposure to inorganic mercury U.S. Department of Health, Education,

and Welfare Public Health Service. National Institute for Oc­cupational Safety and Health 1973.


My deepest gratitude to the many friends and associates who have supported and encouraged me in my labors. Unfortunately, there are too many to name individually; you know who you are.

Special thanks to the staffs of the Palmer Health Sciences Library and Palmer Research department for their expertise and professionalism.

Thanks to Susanne Olgaard and Dennis Miller for their translations. Thanks also to my advisors on this project, Dr. Saroja Reddy, Dr. Moin Ansari and Dr. Louis Freedman, for their patience and gentle criticism. Last but not least, thanks to Dr. Larry Sigulinsky for his artwork. .

(Kristopher Keller is a tenth quarter student at Palmer College of Chiropractic, 1000 Brady Street, Davenport, Iowa 52803. Correspondence or requests for reprints should be addressed to him at the college.)

The database is protected by copyright © 2016
send message

    Main page