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Mercury free dentists

Index of articles on Dental Amalgams:

ANILINE-INDUCED TOXICITIES FROM LOCAL ANESTHETICS - Technical, but informative.

MERCURY EXPOSURE FROM "SILVER" TOOTH FILLINGS: EMERGING EVIDENCE QUESTIONS A TRADITIONAL DENTAL PARADIGM
I recommend everyone to understand the issue before their next visit to the dentist.

DENTAL "SILVER" TOOTH FILLINGS: A SOURCE OF MERCURY EXPOSURE REVEALED BY WHOLE-BODY IMAGE SCAN AND TISSUE ANALYSIS

DENTAL "SILVER" TOOTH FILLINGS: A SOURCE OF MERCURY EXPOSURE REVEALED BY WHOLE-BODY IMAGE SCAN AND TISSUE ANALYSIS

THE DENTAL AMALGAM ISSUE

Dental amalgam--a mixture of elemental mercury and a silver-dominated metal alloy--has been the most widely used dental filling material for well over a century. Alternative materials exist but are not well suited for some important applications, and all are more expensive than amalgam. The toxic effects of occupational mercury exposure have long been known, but it was not until about 1980 that serious consideration was given to the possibility that mercury vapor escaping from amalgam fillings might be affecting health, specifically producing subtle effects on the central nervous system. Such effects have been reported among dentists and other dental personnel, whose exposures are well below industrial levels but above those from fillings alone.

No large studies have been completed that examine the effects of mercury exposure from dental amalgam fillings. In the face of inadequate evidence on the possible risks of dental amalgam, countries have reacted desperately. Sweden is phasing out amalgam entirely. Germany has produced guidelines for limiting its use, other countries have signaled their intention to reduce it, and others--the United States and Canada--have studied the matter but taken no action. Policy differences within Europe have made dental amalgam a test case for the European Community's new medical device regulations. Relatively little epidemiologic research has been initiated to try to answer the question of dental amalgam's possible health effects. An international effort to define and carry out a research agenda to guide public policy is called for.

The science & politics of dental amalgam. Gelband H. Int J Technol Assess Health Care 1998;14(1):123-134

MERCURY EXPOSURE FROM "SILVER" TOOTH FILLINGS: EMERGING EVIDENCE QUESTIONS A TRADITIONAL DENTAL PARADIGM

For more than 160 years dentistry has used silver amalgam, which contains approximately 50% Hg metal, as the preferred tooth filling material. During the past decade medical research has demonstrated that this Hg is continuously released as vapor into mouth air; then it is inhaled, absorbed into body tissues, oxidized to ionic Hg, and finally covalently bound to cell proteins. Animal and human experiments demonstrate that the uptake, tissue distribution, and excretion of amalgam Hg is significant, and that dental amalgam is the major contributing source to Hg body burden in humans. Current research on the pathophysiological effects of amalgam Hg has focused upon the immune system, renal system, oral and intestinal bacteria, reproductive system, and the central nervous system. Research evidence does not support the notion of amalgam safety.

Lorscheider FL, Vimy MJ, Summers AO. FASEB J 1995 Apr9(7):504-508

DOES AMALGAM AFFECT THE IMMUNE SYSTEM?

Although in use for more than 150 years, dental amalgam has been questioned more or less vigorously as a dental restoration material due to its alleged health hazard. Humans are exposed to mercury and the other main dental amalgam metals (Ag, Sn, Cu, Zn) via vapour, corrosion products in swallowed saliva, and direct absorption into the blood from the oral cavity. Dental amalgam fillings are the most important source of mercury exposure in the general population. Local, and in some instances, systemic hypersensitivity reactions to dental amalgam metals, especially mercury, occur at a low frequency among amalgam bearers. Experimental and clinical data strongly indicate that these and other subclinical systemic adverse immunological reactions to dental amalgam metals in humans will be linked to certain MHC genotypes, and affect only a small number of the exposed individuals. These individuals will be very difficult to detect in a mixed population of susceptible and resistant individuals, including persons with alleged symptoms due to dental amalgam fillings, where many of the individuals are likely to suffer from conditions with no proven immunological background such as multiple chemical sensitivity syndrome. Intensified studies should be performed to identify such susceptible MHC genotypes, taking advantage of the reported cases of more heavily metal-exposed humans with systemic autoimmune reactions.

Further studies will also be needed to ascertain whether the combined exposure to the metals in dental amalgam may lower the threshold for adverse immunological reactions, since recent studies have shown that the metals in alloy, especially silver, may induce autoimmunity in genetically susceptible mice.

Enestrom S, Hultman P. Int Arch Allergy Immunol 1995 Mar;106(3):180-203

DENTAL "SILVER" TOOTH FILLINGS: A SOURCE OF MERCURY EXPOSURE REVEALED BY WHOLE-BODY IMAGE SCAN AND TISSUE ANALYSIS

Mercury (Hg) vapor is released from dental "silver" tooth fillings into human mouth air after chewing, but its possible uptake routes and distribution among body tissues are unknown. This investigation demonstrates that when radioactive 203Hg is mixed with dental Hg/silver fillings (amalgam) and placed in teeth of adult sheep, the isotope will appear in various organs and tissues within 29 days. Evidence of Hg uptake, as determined by whole-body scanning and measurement of isotope in specific tissues, revealed three uptake sites: lung, gastrointestinal, and jaw tissue absorption. Once absorbed, high concentrations of dental amalgam Hg rapidly localize in kidneys and liver.

Hahn LJ, Kloiber R, Vimy MJ, Takahashi Y, Lorscheider FL. FASEB J 1989 Dec;3(14):2641-2646

MERCURY FROM MATERNAL "SILVER" TOOTH FILLINGS IN SHEEP AND HUMAN BREAST MILK. A SOURCE OF NEONATAL EXPOSURE

Neonatal uptake of mercury (Hg) from milk was examined in a pregnant sheep model, where radioactive mercury (Hg203)/silver tooth fillings (amalgam) were newly placed. A crossover experimental design was used in which lactating ewes nursed foster lambs.

In a parallel study, the relationship between dental history and breast milk concentration of Hg was also examined in 33 lactating women. Results from the animal studies showed that, during pregnancy, a primary fetal site of amalgam Hg concentration is the liver, and, after delivery, the neonatal lamb kidney receives additional amalgam Hg from mother's milk.

In lactating women with aged amalgam fillings, increased Hg excretion in breast milk and urine correlated with the number of fillings or Hg vapor concentration levels in mouth air. It was concluded that Hg originating from maternal amalgam tooth fillings transfers across the placenta to the fetus, across the mammary gland into milk ingested by the newborn, and ultimately into neonatal body tissues. Comparisons are made to the U. S. minimal risk level recently established for adult Hg exposure. These findings suggest that placement and removal of "silver" tooth fillings in pregnant and lactating humans will subject the fetus and neonate to unnecessary risk of Hg exposure.

Vimy MJ, Hooper DE, King WW, Lorscheider FL. Biol Trace Elem Res 1997 Feb;56(2):143-152

ANILINE-INDUCED TOXICITIES FROM LOCAL ANESTHETICS

Aniline compounds are well-documented human poisons 5: classic human carcinogens 21,31 and neurotoxins. The most effective route of delivery is injection into the human blood stream 6. Symptoms of anilism poisoning develop at ingestion levels greater than I gram, manifesting as methemoglobanemia, headache, paresthesia, hyperalgesia, polyneuritis, cardiac arrhythmias, dizziness, hypotension, convulsion, muscle weakness, and/or digestive derangement. German literature32 states that the hydroxyaniline form induces allergies in humans in addition to other known neurotoxicities.

Experimental neurotoxicity of these nitrobenzene compounds (C6H5NO2) includes animal evaluation of nystagmus, opisthotonus, loss of righting reflex, tremors, paralysis, and coma. Cerebellar Purkinje cell degeneration in animals is observed in addition to focal malacia with reactive gliosis or vacuolization in cerebellar peduncles and medulla oblongata. Of serious concern in its implications for human beings is the ability of the aniline derivative of lidocaine, 2,6-dimethylaniline, to easily cross over to brain tissue and alter gross neurocellular structures in animals33.

A Brief History of Aniline Homolog Cancer Induction

The study of chemical carcinogenesis begins in 1775 when Dr. Percivall Pott, a surgeon at St. Bartholomew's Hospital in England, ascribed cancer scroti to contamination of the skin by chimney soot. One hundred years later in 1875, Von Volkmann observed occupational skin tumors among workers in the tar and paraffin industry at Halle. In 1876 Joseph Bell of Edinburgh described the "paraffin cancer" of Scotland. The coal tar dye industry founded by William Henry Perkins in 1856 was quickly controlled by the Germans who owned 80% of the market up to World War I. Bladder cancer among aniline dye workers was first described by Dr. Ludwig Rehen of Germany in 1895.

In 1915 Yamagiwa and Ichikawa deliberately produced malignant epithelial tumors by application of coal tar to the ears of rabbits. In 1922 Passey produced malignant growths by painting the skins of mice with coal tar ethereal extracts. In 1938, Hueper, Wiley, and Wolfe first reported successful induction of bladder cancer in dogs by repeated injections of 2-napthylamine. Smaller doses and relatively short exposures to 2-napthylamine are very hazardous in man 5,7. Tumors induced by coal tar dyes develop from 3 to 36 years after exposure 5,6. It is worthy of note that it was in 1905, that Einhorn developed the local anesthetic, novacaine, from the aniline homolog, hydroxyaniline.

Biochemistry of Local Anesthetics

The receptor site of action for aniline based injectable local anesthetics, both esters and amides, is the membrane ion channel of a neuron. Ion channels are complex helical transmembrane "pores" capable of a "gating" action to admit or prohibit the passage of ions which creates the nerve impulse. This gating action is dependent on thermally induced coiling and uncoiling of the alpha helical proteins which make up the channel. The thermal requirements for this process are provided by known intracellular energy transport biochemical mechanisms 8,9,10. Neurotransmiter action in the ion channel is terminated by the action of two acetylcholine intrachannel enzyme esterase sites 11. The presence of a local anesthetic in the ion channel has been found in bovine molecular models to produce anesthesia by preventing the uncoiling of the alpha helical proteins which allows the gating mechanism to "open".

Anesthesia action is reversed by enzymatic hydrolysis of the local anesthetic within the pore structure. Modeling of this metabolic activity can be observed in the bovine where the metabolic conversion of local anesthetics to aniline derivatives is rate dependent on a thermally induced response of membrane sodium ion channel proteins. Increased environmental temperatures, then, may change rates of aniline production and increase toxicity 8. At the point that the local anesthetic molecule is hydrolyzed, biologically active metabolic products are produced in the membrane pore and may migrate extra- or intracellularly. In the latter case anilines are given access to the cellular genetic apparatus, explaining genotoxic long-term cellular damage associated with anilines.

In the case of existing clinical anesthetics, their hydrolysis within the pore structure will result in alcohol and aniline derivatives, e.g. 2,6-dimethylaniline, ortho-toluidine, or hydroxyaniline. Intracellular genetic damage to both sensory and parasympathetic neurons can be expected to result. Cancer is one expression of this genetic damage 8,12. Both ortho-toluidine and 2,6-dimethylaniline (the anilines on which prilocaine and lidocaine are based) give positive results in Ames tests under conditions of metabolic activation. (The Ames test evaluates the mutagenic potential of a material by measuring the ability to induce reverse mutations at selected loci of several strains of 'Salmonella tymphimurium 20. Extracellular metabolism of local anesthetics includes liver and serum mediated esterase conversion to aniline derivatives. Human hemaglobin adducts for lidocaine do show high circulating levels of 2,6-dimethylaniline after lidocaine injection 16. Human liver membrane systems have clearly demonstrated their ability to convert a parent anesthetic molecule to 2,6-dimethylaniline 13, and human liver-mediated detoxification of 2,6-dimethylaniline by demethylation to 2-methylaniline (ortho-toluidine) and finally to hydroxyaniline would expose the individual to all these anilines and to the ailments in which they have been implicated. For example, laboratory animal studies for ortho-toluidine demonstrating increased mammary gland adenocarcinoma (P less than 0.001) 14,15 are applicable to any compound having 2,6-dimethylaniline as its parent molecular predecessor. Data on aniline derivative metabolite excretion is deficit, but at human in vivo temperature these aniline compounds can be expected to, for the most part, follow a volatile pathway of excretion (e.g. lung rather than kidney).

Metabolic Conversion of Local Anesthetics (preliminary data and background)

In writing a review of the history of chemical carcinogenesis, Dr. M.B. Shimkin recognized in 1967 that if metabolic conversion of aniline derivative pharmaceuticals to their aniline homologs was demonstrated, these compounds could no longer be considered safe. Once incorporated into their local anesthetic forms, however, anilines were believed to have been rendered harmless, transformed into benign, utilitarian pain relievers with few and minor side effects and now used liberally in medicine and dentistry throughout much of the world. Sales of local anesthetics total $500,000,000 each year in the United States alone.

But the theory that the local anesthetic molecule is always excreted from the body intact is unsupported in the scientific literature. It is apparently based on the assurances of pharmaceutical companies, usually foreign, that manufacture local anesthetics and a study which found that 10% of injected local anesthetic was recoverable from the urine; the fate of 90% of the injected local anesthetic was not determined 17. In 1972, Keenaghan and Boyes identified 2,6dimethylaniline as a metabolite in the urine of rats, guinea pigs, dogs, and humans administered lidocaine orally, evidence of the metabolic conversion of lidocaine to its aniline derivative on excretion 18.

The implications of this study are still widely ignored by the medical and dental communities. Although in retrospect Dr. Nickel observed metabolic conversion of lidocaine and prilocaine in a bovine molecular model system studied in 1971, the focus of this research was the functional mechanism of the sodium ion channel alpha helical proteins that are the target of action of local anesthetics, and the significance of the metabolic conversion was only realized some 20 years later. (It is now published as a patent pending: PCT US93 05792.) A case-control study by Dr. Nickel of 4987 oral surgery patients (3071 third molar extraction patients) demonstrated that paresthesia, a complication of oral surgery in from 1% to 5% of cases, is actually a toxic effect of the local anesthetic used, probably induced by the alcohol and/or aniline derivative released in hydrolytic metabolism of the local anesthetic molecule 19. This study, published in 1990, is the first evidence of the existence of local anesthetic metabolic conversion to toxic metabolites in human tissues preceding the organs of metabolic excretion. It confirms the fears that Dr. Shimkin expressed back in 1967. In 1994, direct evidence of local anesthetic metabolic conversion was presented to the Anesthetic and Life Support Drugs Advisory Committee for the Food and Drug Administration.

When lidocaine was incubated with fresh human liver slices for four hours, 67% of the lidocaine was converted to its aniline homolog, 2,6-dimethylaniline, an established animal and probable human carcinogen 12,13. A second study published that same year demonstrated significantly elevated human hemoglobin adduct levels of 2,6-dimethylaniline in patients who had received lidocaine in accepted clinical treatment for cardiac problems 16. The FDA ruled that the package insert for EMLA, a dermatologic cream containing lidocaine and prilocaine, would contain this warning: "Metabolites of both lidocaine and prilocaine have been shown to be carcinogenic in animals...The [ortho-toluidine induced] tumors included hepatocarcinomas/adenomas in female mice, multiple occurences of hemangiosarcomas/ hemangiomas in both sexes of mice, sarcomas of multiple organs, transitional cell carcinomas/papillomas of urinary bladder in both sexes of rats, subcutaneous fibromas/ fibrosarcomas and mesotheliomas in male rats, and mammary gland fibroadenomas/adenomas in female rats. The lowest dose tested (900 mg/m ; 60 times SDA) was carcinogenic in both species.

Thus the no effect dose must be less than 60 times SDA." 21. Both the International Agency for Research on Cancer (IARC) and OSHA recommend a maximum long-term daily occupational exposure of skin and lungs to aniline homologs in humans of 10 mg per cubic meter 22,23. Twenty mg per cubic meter for short term exposure is acceptable by some standards 34. In routine clinical use of local anesthetics, the maximum recommended, daily occupational exposure level for anilines is frequently exceeded.

Extensive, repetitious dental or medical care may maintain large aniline doses for prolonged intervals. Moreover, local anesthetics are adminstered by injection, giving direct access to the blood stream and bypassing the barriers of gastrointestinal absorption and hepatic detoxification. Stoichiometrically, I cc of 2% lidocaine produces 10 mg of 2,6-dimethylaniline with maximal hydrolysis 24. Surgeons will administer as much as 50 cc of 2% lidocaine (500 mg 2,6dimethylaniline) for a routine orthopedic procedure or a vein stripping. A dentist can inject 14 cc 2% lidocaine (140 mg 2,6-dimethylaniline) for the extraction of 4 third molars and 5-8 cc 2% lidocaine per weekIy or biweekIy session for up to 6 months for a full mouth reconstruction case (50-80 mg 2,.6-dimethylanitine each session or 1.2 - 3.8 g over a 6 month period). Some aniline derivatives from local anesthetics are also in pesticides and tobacco. The amount of 2,6-dimethylaniline in a single unfiltered cigarette is 102 nanograms 25.

Thus it would be necessary to smoke a pack of unfiltered cigarettes a day for approximately 12.9 years to inhale an equivalent amount of 2,6-dimethylaniline to that injected in a single cc of 2% lidocaine. Weak Epidemiologic Associations with Breast Cancer (preliminary data) Many women undergo full mouth reconstruction in their forties after their children have become adults and the drain of third molar extractions and orthodontics on the family's dental budget has been reduced or has ceased. The effect on human breast cancer incidence of repetitious aniline exposure attendant to full mouth reconstruction has never been studied.

Although it is not possible to conclude from animal studies that anilines from local anesthetics will result in breast cancer in humans, the high animal breast cancer incidence rates seen in these studies coupled with the high rate of metabolic conversion of local anesthetics to these same animal carcinogens and the ubiquitous use of local anesthetics all would encourage a search for any possible link. The potential role of local anesthetic exposure in breast cancer induction has not been the subject of an epidemiologic investigation.

However, a preliminary survey of breast cancer incidence suggests that usage of local anesthetics might offer alternative explanations for observed data and identified risk factors:

1. Lidocaine came into widespread use in the U.K. in 1948-1949, ten years prior to its widespread use in the U.S. in 1958-1959 26. The mortality rate for breast cancer in each country peaked 22-25 years after adoption of lidocaine and reached a new steady-state level thereafter, the U.K. peak preceding the U.S. peak by, again, ten years. In both countries the graphed data demonstrate standard pharmaceutical toxicology curves 26.

2. Evaluation of data on breast cancer incidence from the Connecticut Tumor Registry (CTR) since 1940 reveals a straight line log plot that changes slope in 1982, reflecting an increased rate of incidence 27. Comparison of the published incidence rates of breast cancer in the U.S. leads to the observation that hydroxyaniline (from procaine) has a less virulent kinetic rate than its congener 2,6-di-methylaniline (from lidocaine). NIOSH found a similar differential rate of causation between hydroxyaniline and 2-methylaniline in animal studies 14,15.

3. Women of higher socioeconomic status are known to be at greater risk for breast cancer than women of low socioeconomic status 28. Greater economic status allows increased utilization of cosmetic dentistry and elective medical procedures as well as greater access to necessary dental and medical care which, in turn, may lead to greater exposure to the anilinebased local anesthetics which accompany this care.

4. Women who have never married also have an increased risk of developing breast cancer 29. Without dependents, they, too, may be able to dedicate a greater portion of their income to their medical and dental needs, again increasing exposure to local anesthetics. Hormonal factors may also be important here but these have been and are being studied, although they have not yet been shown to be rigorous risk factors.

5. The intriguing increasing incidence rates noted in developing countries 30 could also be related to improved access to modern, local anesthetic-mediated medical and dental care.

6. Our research team noted a curious and intriguing commonality among the 30 cancer patients evaluated at a recent meeting of the tumor board of one of the local hospitals. Each patient's dental history was visualized on the total body scans (crowns, fillings, etc. produce shadows on the film). The total body scans clearly demonstrated that each of the patients had undergone from 12 to 28 crown and bridge dental procedures, necessitating extensive exposure to local anesthetics. Could the dental exposure alone to aniline-based local anesthetics be enough to increase cancer incidence?

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Copyright 1996 by Alfred Nickel Aniline