Mercury Exposure Levels from Amalgam Dental Fillings

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Introduction

Toxic metals such as mercury, lead, cadmium, etc. have been documented to be neurotoxic, immunotoxic, as well as reproductive/developmental toxins that, according to U.S. governmental agencies, cause adverse health effects and learning disabilities in the U.S. each year. Exposure of humans and animals to toxic metals, such as mercury, cadmium, lead, copper, aluminum, arsenic, chromium, manganese, etc., is widespread and is, in many areas, increasing. A 2009 study found that inorganic mercury levels in people have been increasing rapidly in recent years. The study used data from the U.S. Centers for Disease Control and Prevention’s National Health Nutrition Examination Survey (NHANES), finding that while inorganic mercury was detected in the blood of 2% of women aged 18 to 49 in the 1999-2000 NHANES survey, the level rose to 30% of women by 2005-2006. Surveys that used hair tests in all states have found dangerous levels of mercury in an average of 22% of the population, with over 30% in some states including Florida and New York.

The U.S. Center for Disease Control ranks toxic metals as the number one environmental health threat to children. According to an EPA/ATSDR assessment, the toxic metals mercury, lead, arsenic, and cadmium are all ranked in the top seven toxins that have the most adverse health effects on the public (based on toxicity and current exposure levels in the U.S.), with nickel and chromium also highly listed. The U.S. EPA indicates that approximately 25% of U.S. infants are exposed to dangerous levels of mercury. A National Academy of Sciences report in July 2000 and other studies found that even small levels of mercury in fish or levels of mercury in the blood of women below 10 micrograms per liter (ug/l) appear to result in developmental effects and represent unacceptable risks of birth defects and developmental effects in infants. The National Academy of Sciences safety limit is 5 micrograms per liter. However, blood level is also documented to not be a reliable indicator of mercury toxicity since mercury vapor passes out of the blood in a very short time. In addition, mercury amalgam dental fillings have been found to be the largest source of both inorganic and methylmercury in those who have several amalgam fillings.

The main factors determining whether chronic conditions are induced by metals appear to be exposure and genetic susceptibility, which determines individuals’ immune sensitivity and ability to detoxify metals. Very low levels of exposure have been found to seriously affect relatively large groups of individuals who are immune sensitive to toxic metals or have an inability to detoxify metals due to such as deficient sulfoxidation or metallothionein function or other inhibited enzymatic processes related to detoxification or excretion of metals. For those with chronic conditions, fatigue regardless of the underlying disease is primarily associated with hypersensitivity to inorganic and organic mercury, nickel, and gold.

While there have been large increases of most neurological and immune conditions among adults over the last two decades, the incidence of neurotoxic or immune reactive conditions in infants such as autism, schizophrenia, ADD, dyslexia, learning disabilities, etc. have been increasing especially rapidly in recent years. A recent report by the National Research Council found that 50% of all pregnancies in the U.S. now result in prenatal or postnatal mortality, significant birth defects, developmental neurological or immune conditions, or otherwise chronically unhealthy babies. Exposure to toxic chemicals or environmental factors appears to be a factor in as much as 28% of the four million children born each year, with one in six having one of the neurological conditions previously listed. EPA estimates that over three million of these are related to lead or mercury toxicity, with approximately 25% of U.S. infants receiving dangerous levels of mercury exposure. A recent study found that prenatal Hg exposure is correlated with lower scores in neurodevelopmental screening, although more so in the linguistic pathway. A study at the U.S. CDC found “statistically significant associations” between certain neurologic developmental disorders such as attention deficit disorder (ADD) and autism with exposure to mercury from thimerosal-containing vaccines before the age of six months. A follow-up study using federal vaccine data bases confirmed that autism, speaking disorders, and heart arrest have increased exponentially with increasing exposures to mercury thimerosal-containing vaccines. Thimerosal has also been found to cause hormonal effects. Prenatal exposure to mercury has also been found to predispose animals and infants to seizures and epilepsy.

The health effects of toxic metals are synergistic with other toxic exposures, such as pesticides, endocrine-disrupting substances like organochlorine compounds, PCBs, etc. There are also synergistic effects with the various types of parasites, bacteria, and viruses to which people have common exposures. While there is considerable commonality to the health effects caused by these toxic metals and effects are cumulative and synergistic in many cases, this paper will concentrate on the health effects of elemental mercury from amalgam fillings. Studies have found considerable genetic variability in susceptibility to toxic metals as well. The public appears to be generally unaware that considerable scientific evidence supports that mercury is the metal causing the most widespread adverse health effects to the public, and amalgam fillings have been well documented to be the number one source of exposure of mercury to most people, with exposure levels often exceeding government health guidelines and levels documented to cause adverse health effects.

Toxicity and Health Effects of Mercury

Dental amalgam contains about 50% mercury, as well as other toxic metals such as tin, copper, nickel, palladium, etc. The average filling has one gram of mercury and leaks mercury vapor continuously due to mercury’s high volatility along with loss due to galvanic action of mercury with dissimilar metals in the mouth, resulting in significant exposure for most with amalgam fillings. Mercury vapor is transmitted rapidly throughout the body, easily crosses cell membranes, and like organic methylmercury has significant toxic effects at much lower levels of exposure than other inorganic mercury forms. The OSHA level for mercury vapor in air is 50% lower than for organic mercury in air. According to the U.S. EPA and ATSDR, mercury is among the top three toxic substances adversely affecting large numbers of people, and amalgam is the number one source of exposure for most people.

A large U.S. Centers for Disease Control epidemiological study, NHANES III, found that those with more amalgam fillings (meaning more mercury exposure) have significantly higher levels of chronic health conditions. The conditions where the dental amalgam surfaces are most highly correlated with disease incidence are MS, epilepsy, migraines, mental disorders, nervous system conditions, disorders of the thyroid gland, cancer, and infectious diseases. Other conditions where incidence was significantly correlated with having more than the average number of amalgam surfaces are: diseases of the male and female genital tracts, disorders of the peripheral nervous system, diseases of the respiratory system, and diseases of the genitourinary system. MS clusters in areas with high metals emissions.

As far back as 1996, it was shown that the lesions produced in the myelin sheath of axons in cases of MS were related to excitatory receptors on the primary cells involved called oligodendroglia. The loss of myelin sheath on the nerve fibers characteristic of these diseases is due to the death of oligodendroglial cells at the site of the lesions (called plaques). Further, these studies have shown that the death of these important cells is a result of excessive exposure to excitotoxins at the site of the lesions. Most of these excitotoxins are secreted from microglial immune cells in the central nervous system. This not only destroys these myelin-producing cells, but it also breaks down the blood-brain barrier (BBB), allowing excitotoxins in the blood stream to enter the site of damage. Some common exposures that cause proliferation of excitotoxins are mercury and aspartame, with additional effects from MSG and methanol. Mercury and other toxic metals inhibit astrocyte function in the brain and CNS, causing increased glutamate and calcium-related neurotoxicity, which are factors in neural degeneration in MS and ALS. There is evidence that astrocyte damage/malfunction is a major factor in MS. Mercury and increased glutamate activate free radical forming processes, like xanthine oxidase which produces oxygen radicals and causes oxidative neurological damage. Nitric oxide-related toxicity caused by peroxynitrite formed by the reaction of NO with superoxide anions, which results in nitration of tyrosine residues in neurofilaments and manganese Superoxide Dismutase (SOD), has been found to cause inhibition of the mitochondrial respiratory chain, inhibition of the glutamate transporter, and glutamate-induced neurotoxicity involved in ALS.

It is now known that the cause of the destruction of the myelin in the lesions is over-activation of the microglia in the region of the myelin. An enzyme that converts glutamine to glutamate called glutaminase increases tremendously, thereby greatly increasing excitotoxicity. Any dietary excitotoxin can activate the microglia, thereby greatly aggravating the injury. This includes the aspartate in aspartame and MSG, which is in many processed foods. The methanol in diet drinks adds to this toxicity as well. Now, the secret to treatment appears to be reducing microglia inflammation.

Mercury and cadmium inhibits magnesium and zinc levels as well as inhibits glucose transfer. These are other mechanisms by which mercury and toxic metals are factors in metabolic syndrome and insulin resistance/diabetes. Reduced levels of magnesium and zinc are related to metabolic syndrome, insulin resistance, and brain inflammation.

According to neurologist Dr. RL Blaylock, the good news is that there are supplements and nutrients that calm the microglia. The most potent are: silymarin, curcumin and ibuprophen. Phosphatidylcholine helps re-myelinate the nerve sheaths that are damaged, as does B12, B6, B1, vitamin D, folate, vitamin C, natural vitamin E (mixed tocopherols) and L-carnitine. DHA plays a major role in repairing the myelin sheath. Vitamin D may even prevent MS, but it acts as an immune modulator, preventing further damage—the dose is 2000 IU a day. Magnesium, as magnesium malate, is needed in a dose of 500 mg two times a day. Patients must avoid all excitotoxins, even natural ones in foods, such as soy, red meats, nuts, mushrooms, and tomatoes. Avoid all fluoride and especially all vaccinations since these either inhibit antioxidant enzymes or trigger harmful immune reactions.

Mercury is the most toxic of the toxic metals. Mercury (vapor) is carried by the blood to cells in all organs of the body where it:

  1. is cytotoxic (kills cells).
  2. penetrates and damages the blood brain barrier, resulting in accumulation of mercury and other substances in the brain.
  3. accumulates in the motor function areas of the brain and CNS.
  4. is neurotoxic (kills brain and nerve cells): damages brain cells and nerve cells; generates high levels of reactive oxygen species (ROS) and oxidative stress, depletes glutathione and thiols causing increased neurotoxicity from interactions of ROS, glutamate, and dopamine; kills or inhibits production of brain tubulin cells inhibits production of neurotransmitters by inhibiting: calcium-dependent neurotransmitter release, dihydroteridine reductase, nitric oxide synthase, blocking neurotransmitter amino acids, and effecting phenylalanine, serotonin, tyrosine and tryptophan transport to neurons.
  5. is immunotoxic(damages and inhibits immune T-cells, B-cells, neutrophil function, etc.) and induces ANA antibodies and autoimmune disease.
  6. is nepthrotoxic (toxic to kidneys).
  7. is endocrine system-disrupting chemical(accumulates in pituitary gland and damages or inhibits pituitary glands hormonal functions at very low levels, adrenal gland function, thyroid gland function, thymus gland function, and disrupts enzyme production processes at very low levels of exposure.
  8. causes rapid transmittal through the placenta to the fetus and significant developmental effects—much more damage to the fetus than for maternal exposure to inorganic mercury and at lower exposure levels than for organic mercury.
  9. is a reproductive and developmental toxin; damages DNA and inhibits DNA; RNA synthesis; damages sperm, lowers sperm counts and reduces motility; causes menstrual disturbances; reduces bloods ability to transport oxygen to fetus and transport of essential nutrients including amino acids, glucose, magnesium, zinc and Vit B12; depresses enzyme isocitric dehydrogenase (ICD) in fetus, causes reduced iodine uptake; hypothyroidism; causes learning disabilities and impairment, and reduction in IQ, causes infertility, causes birth defects.
  10. prenatal/early postnatal exposure affects level of nerve growth factor in the brain, impairs astrocyte function, and causes imbalances in development of brain causes cardiovascular damage and disease: including damage to vascular endothelial cells, damage to sarcoplasmic reticula, sarcolemma, and contractile proteins, increased white cell count, decreased oxyhemoglobin level, high blood pressure, tachycardia, inhibits cytochrome P450/heme synthesis, and increased risk of acute myocardial infarction.
  11. causes immune system damage resulting in allergies, asthma,lupus, schleraderma, chronic fatigue syndrome (CFS), and multiple sensitivities (MCS) and neutrophil functional impairment.
  12. causes interruption of the cytochrome C oxidase system/ATP energy function and blocks enzymes needed to convert porphyrins to adenosine tri phosphate (ATP) causing progressive porphyrinuria, resulting in low energy, digestive problems, and porphyrins in urine. m. inhibition of immune system facilitates increased damage by bacterial, viral, and fungal infections, and increased antibiotic resistance.
  13. mercury causes significant destruction of stomach and intestine epithelial cells, resulting in damage to stomach lining which along with mercury’s ability to bind to SH hydroxyl radical in cell membranes alters permeability and adversely alters bacterial populations in the intestines causing leaky gut syndrome with toxic, incompletely digested complexes in the blood and accumulation of heliobacter pylori, a suspected major factor in stomach ulcers and stomach cancer and candida albicans, as well as poor nutrient absorption.
  14. forming strong bonds with and modification of the-SH groups of proteins causes mitochondrial release of calcium, as well as altering molecular function of amino acids and damaging enzymatic process resulting in improper cysteine regulation(194), inhibited glucose transfer and uptake, damaged sulfur oxidation processes, and reduced glutathione availability (necessary for detoxification).
  15. HgCl2 inhibits aquaporin-mediated water transport in red blood cells.

Mercury has been well documented to be an endocrine system-disrupting chemical in animals and people, disrupting function of the pituitary gland, thyroid gland, reproduction processes, and many hormonal functions at very low levels of exposure. Mercury (especially mercury vapor) rapidly crosses the blood brain barrier and is stored preferentially in the pituitary gland, thyroid gland, hypothalamus, and occipital cortex in direct proportion to the number and extent of dental amalgam surfaces. Thus mercury has a greater effect on the functions of these areas. Studies have documented that mercury causes hypothyroidism, damage of thyroid RNA, autoimmune thyroiditis, and impairment of conversion of thyroid T4 hormone to the active T3 form.

An overactive thyroid gland, or hyperthyroidism, can trigger restlessness, hyperactivity, insomnia and irritability—symptoms that could be mistaken for mania. On the other hand, a thyroid gland that responds sluggishly in a hypothyroid state may result in feelings of coldness, depression, pain, and low energy. Overt autoimmune thyroiditis is preceded by a rise in levels of thyroid peroxidase antibodies. Without treatment, many of the women with thyroiditis go on to develop overt clinical hypothyroidism as they age and, eventually, associated complications such as cardiovascular disease. About 5% of pregnant women develop thyroiditis after birth.

According to survey tests, 8 to 10% of untreated women were found to have thyroid imbalances so the actual level of hypothyroidism is higher commonly recognized. Even larger percentages of women had elevated levels of antithyroglobulin (anti-TG) or antithyroid peroxidase antibody (anti-TP). Studies indicate that slight imbalances of thyroid hormones in expectant mothers can cause permanent neuropsychiatric damage in the developing fetus. Low first trimester levels of free T4 and positive levels of anti-TP antibodies in the mother during pregnancy have been found to result significantly reduces IQs. Hypothyroidism is a well-documented cause of mental retardation. Women with the highest levels of thyroid-stimulating-hormone (TSH) and lowest free levels of thyroxine seventeen weeks into their pregnancies were significantly more likely to have children who tested at least one standard deviation below normal on an IQ test taken at age eight.

Based on study findings, maternal hypothyroidism appears to play a role in at least 15% of children whose IQs are more than one standard deviation below the mean. Studies have also established a “clear association” between the presence of thyroid antibodies and spontaneous abortions, as well as a connection between maternal thyroid disease and babies born with heart, brain, and kidney defects. Levels of recurrent abortions in a population with positive levels of thyroid antibodies in one study were 40%, five times the normal rate. Hypothyroidism is a documented risk factor in spontaneous abortions and infertility. Another study of pregnant women who suffer from hypothyroidism (underactive thyroid) found a greater risk for miscarriage during the second trimester than those who do not, and women with untreated thyroid deficiency were more likely to have a child with developmental disabilities and lower I.Q. The American Association of Clinical Endocrinologists advises that all women considering becoming pregnant should get a serum thyrotropin test so that hypothyroidism can be diagnosed and treated early.

Mercury blocks thyroid hormone production by occupying iodine binding sites and inhibiting hormone action even when the measured thyroid level appears to be in proper range. The thyroid and hypothalamus regulate body temperature and many metabolic processes including enzymatic processes that when inhibited result in higher dental decay. Mercury damage thus commonly results in poor bodily temperature control, in addition to many problems caused by hormonal imbalances such as depression. Such hormonal secretions are affected at levels of mercury exposure much lower than the acute toxicity effects normally tested, as previously confirmed by hormonal/reproductive problems in animal populations. Mercury also damages the blood brain barrier and facilitates penetration of the brain by other toxic metals and substances. Thyroid imbalances, which are documented to be commonly caused by mercury, have been found to play a major role in chronic heart conditions, such as clogged arteries, mycardial infarction, and chronic heart failure.

Mercury can have significant effects on thyroid function even though the main hormone levels remain in the normal range, so the usual thyroid tests are not adequate in such cases. Prenatal methylmercury exposure severely affects the activity of selenoenzymes, including glutathione peroxidase (GPx) and 5-iodothyronine deiodinases (5-Di and 5′-DI) in the fetal brain, even though thyroxine (T4) levels are normal. Gpx activity is severely inhibited, while 5-DI levels are decreased and 5′-DI increased in the fetal brain, similar to hypothyroidism. Thus normal thyroid tests will not pick up this condition.

The pituitary gland controls many of the body’s endocrine system functions and secretes hormones that control most bodily processes, including the immune system and reproductive systems. One study found mercury levels in the pituitary gland ranged from 6.3 to 77 ppb, while another found the mean level to be 30 ppb—levels found to be neurotoxic and cytotoxic in animal studies. Some of the effect on depression is related to mercury’s effect of reducing the level of posterior pituitary hormone (oxytocin). Low levels of pituitary function are associated with depression and suicidal thoughts and appear to be a major factor in suicide of teenagers and other vulnerable groups. A study by a neuroscience researcher found a connection between the levels of pituitary hormone lutropin and chronic mercury exposure. The authors indicated that inorganic mercury binding to luteinizing hormone can impair gonadotrophin regulation affecting fertility and reproductive function, as well as immune function and has been found to accumulate in the brain and stay there for years, which may help explain mercury’s link to neurodegenerative disease.

The pituitary glands of a group of dentists had 800 times more mercury than controls. This may explain why dentists have much higher levels of emotional problems, depression, suicide, etc.
Amalgam fillings as well as nickel and gold crowns are major factors in reducing pituitary function. Supplementary oxytocin extract has been found to alleviate many of these mood problems, along with replacement of metals in the mouth. The normalization of pituitary function often normalizes menstrual cycle problems, endometriosis, and increases fertility.

The thymus gland plays a significant part in the establishment of the immune system and lymphatic system from the 12th week of gestation until puberty. Inhibition of thymus function can thus affect proper development of the immune and lymphatic systems. Lymphocyte differentiation, maturation, and peripheral functions are affected by the thymic protein hormone thymulin. Mercury at very low concentrations has been seen to impair some lymphocytic functions, causing subclinical manifestations in exposed workers. Animal studies have shown mercury significantly inhibits thymulin production at very low micromolar levels of exposure.
The metal allergens mercuric chloride and nickel sulfate were found to stimulate DNA synthesis of both immature and mature thymocytes at low levels of exposure, so chronic exposure can have long term effects. Also, micromolar levels of mercuric ions specifically blocked synthesis of ribosomal RNA, causing fibrillarin relocation from the nucleolus to the nucleoplasm in epithelial cells as a consequence of the blockade of ribosomal RNA synthesis. This appears to be a factor in deregulation of basic cellular events and in autoimmunity caused by mercury. There were specific immunotoxic and biochemical alterations in lymphoid organs of mice treated at the lower doses of mercury. The immunological defects were consistent with altered T-cell function as evidenced by decreases in both T-cell mitogen and mixed leukocyte responses. There was a particular association between the T-cell defects and inhibition of thymic pyruvate kinase, the rate-limiting enzyme for glycolysis. Pyruvate and glycolysis problems are often seen in mercury toxic children being treated for autism. L-arginine restored thymulin activity, TEC proliferation, NKT cytotoxicity, cytokine profiles and nitrite and nitrate plasma levels both in vivo and in vitro.

Mercury’s biochemical damage at the cellular level include DNA damage; inhibition of DNA and RNA synthesis; alteration of protein structure; alteration of the transport of calcium; inhibition of glucose transport, enzyme function, and other essential nutrient transport; induction of free radical formation; depletion of cellular glutathione (necessary for detoxification processes); inhibition of glutathione peroxidase enzyme; endothelial cell damage; abnormal migration of neurons in the cerebral cortex; and immune system damage. Part of the toxic effects of mercury, cadmium, lead, etc. is through their replacement of essential minerals such as zinc at their sites in enzymes, disabling the necessary enzymatic processes.

There has been a huge increase in the incidence of degenerative neurological conditions in virtually all Western countries over the last two decades. The increase in Alzheimer’s has been over 300% while the increase in Parkinson’s and other motor neuron disease has been over 50%. The primary cause appears to be increased exposures to toxic pollutants.

Oxidative stress and reactive oxygen species (ROS) have been implicated as major factors in neurological disorders, including stroke, PD, MS, Alzheimer’s, ALS, MND, FM, CFS, etc. Mercury-induced lipid peroxidation has been found to be a major factor in mercury’s neurotoxicity, along with decreased levels of glutathione peroxidation and superoxide dismutase (SOD). Metalloprotein (MT) is involved in metals transport and detoxification. Mercury inhibits sulfur ligands in MT and in the case of intestinal cell membranes inactivates MT that normally binds cuprous ions, thus allowing buildup of copper to toxic levels in many and malfunction of the Zn/Cu SOD function. Exposure to mercury results in changes in metalloprotein compounds that have genetic effects, having both structural and catalytic effects on gene expression. Some of the processes affected by such MT control of genes include cellular respiration, metabolism, enzymatic processes, metal-specific homeostasis, and adrenal stress response systems. Significant physiological changes occur when metal ion concentrations exceed threshold levels. Such MT formation also appears to have a relation to autoimmune reactions in significant numbers of people. In a population of over 3,000 tested by the immune lymphocyte reactivity test, 22% tested positive for inorganic mercury and 8% for methylmercury.

Programmed cell death (apoptosis) is documented to a major factor in degenerative neurological conditions like ALS, Alzheimer’s, MS, Parkinson’s, etc. Some of the factors documented to be involved in apoptosis of neurons and immune cells include inducement of the inflammatory cytokine Tumor Necrosis Factor-alpha (TNFa), reactive oxygen species and oxidative stress, reduced glutathione levels, inhibition of protein kinase C, nitric oxide and peroxynitrite toxicity, excitotoxicity and idation, excess free cysteine levels, excess glutamate toxicity, excess dopamine toxicity, beta-amyloid generation, increased calcium influx toxicity, DNA fragmentation, and mitochondrial membrane dysfunction.

TNFa is a cytokine that controls a wide range of immune cell response in mammals, including apoptosis. This process is involved in inflammatory and degenerative neurological conditions like ALS, MS, Parkinson’s, rheumatoid arthritis, etc. Cell signaling mechanisms like sphingolipids are part of the control mechanism for the TNFa apoptosis mechanism. Gluthathione is an amino acid that is a normal cellular mechanism for controlling apoptosis. When glutathione is depleted in the brain, reactive oxidative species increased, and CNS and cell signaling mechanisms are disrupted by toxic exposures such as mercury, neuronal cell apoptosis results, and neurological damage. Mercury has been shown to induce TNFa and deplete glutathione, causing inflammatory effects and cellular apoptosis in neuronal and immune cells.

Another neurological effect of mercury that occurs at very low levels is inhibition of nerve growth factors, for which deficiencies result in nerve degeneration. Mercury vapor is lipid soluble and has an affinity for red blood cells and CNS cells. Only a few micrograms of mercury severely disturb cellular function and inhibit nerve growth. Prenatal or neonatal exposures have been found to have life-long effects on nerve function and susceptibility to toxic effects. Prenatal mercury vapor exposure (levels of only four parts per billion in newborn rat brains) was found to cause decreases in nerve growth factor and other effects. This is a level that is common in the population with several amalgam fillings or other exposures. Insulin-like-growth factor I (IGF-I) are positively correlated with growth hormone levels and have been found to be the best easily measured marker for levels of growth hormone, but males have been found more responsive to this factor than women. IGF-I controls the survival of spinal motor neurons affected in ALS during development as well as later in life. IGF-I and insulin levels have been found to be reduced in ALS patients with evidence this is a factor in ALS. Several clinical trials have found IGF-I treatment is effective at reducing the damage and slowing the progression of ALS and Alzheimer’s with no medically important adverse effects. It has also been found that in chronically ill patients the levels of pituitary and thyroid hormones that control many bodily processes are low, and supplementing both a thyrotropin-releasing hormone and a growth control hormone is more effective at increasing all of these hormone levels in the patient.

A direct mechanism involving mercury’s inhibition of cellular enzymatic processes by binding with the hydroxyl radical (SH) in amino acids appears to be a major part of the connection to allergic/immune reactive conditions, such as autism, schizophrenia, lupus, scleroderma, eczema and psoriasis, and allergies. For example, mercury has been found to strongly inhibit the activity of dipeptyl peptidase (DPP IV) which is required in the digestion of the milk protein casein as well as of xanthine oxidase. Studies involving a large sample of autistic and schizophrenic patients found that over 90% of those tested had high levels of the milk protein beta-casomorphin-7 in their blood and urine and defective enzymatic processes for digesting milk protein. Elimination of milk products from the diet has been found to improve the condition. Such populations have also been found to have high levels of mercury and to recover after mercury detox. As mercury levels are reduced, the protein binding is reduced and improvement in the enzymatic process occurs. Additional cellular level enzymatic effects of mercury’s binding with proteins include blockage of sulfur oxidation processes, enzymatic processes involving vitamins B6 and B12, effects on the cytochrome-C energy processes, along with mercury’s adverse effects on cellular mineral levels of calcium, magnesium, zinc, and lithium. Along with these blockages of cellular enzymatic processes, mercury has been found to cause additional neurological and immune system effects in many through immune/autoimmune reactions. Most doctors treating such conditions also usually recommend supplementing the deficient essential minerals previously noted that mercury affects.

However, the effect on the immune system of exposure to various toxic substances such as toxic metals and environmental pollutants has also been found to have additive or synergistic effects and to be a factor in increasing eczema, allergies, asthma, and sensitivity to other lesser allergens. Most of the children tested for toxic exposures have found high or reactive levels of other toxic metals, and organochlorine compounds. Much mercury in saliva and the brain is also organic since mouth bacteria and other organisms in the body methylate inorganic mercury to organic mercury.

Studies and clinical tests have found amalgam to be the largest source of methylmercury in most people. Bacteria also oxidize mercury vapor to the water soluble, ionic form Hg (II). A clinical study found that methylmercury in saliva is significantly higher in those with amalgam fillings than those without. The average level of methylmercury in the blood of a group with amalgam was more than four times that of groups without amalgam or that had amalgam replaced. Total mercury in those with amalgams was over ten times that of those without amalgam. Other studies have found similar results.

Because of the extreme toxicity of mercury, only ½ gram is required to contaminate a ten acre lake to the extent that a health warning would be issued by the government to not eat the fish. Over half the rivers and lakes in Florida have such health warnings banning or limiting eating of fish, and most other states and four Canadian provinces have similar health warnings. Wisconsin has fish consumption warnings for over 250 lakes and rivers and Minnesota even more, as part of the total of over 50,000 such lakes with warnings.

Over 30% of all U.S. lakes have mercury health warnings and 15% of all U.S. rivers. All Great Lakes as well as many coastal bays and estuaries and large numbers of salt water fish carry similar health warnings. Some wading birds and Florida panthers that eat birds and animals that eat fish containing very low levels of mercury (about one part per million) have died from chronic mercury poisoning. Since mercury is an estrogenic chemical and reproductive toxin, the majority of the rest cannot reproduce. The average male Florida panther has higher estrogen levels than females, due to the estrogenic properties of mercury. Similar is true of some other animals at the top of the food chain like alligators, polar bears, minks, seals, and beluga and orca whales, which are affected by mercury and other hormone disrupting chemicals.

Mercury accumulates in the pituitary glands, ovaries, testes, and prostate gland. In addition to having estrogenic effects, mercury has other documented hormonal effects including effects on the reproductive system resulting in lowered sperm counts, defective sperm cells, damaged DNA, aberrant chromosome numbers rather than the normal 46, chromosome breaks, and lowered testosterone levels in males and menstrual disturbances and infertility in women. Another result is increased neurological problems related to lowered levels of neurotransmitters dopamine, serotonin, noreprenephrine, and acetylcholinesterase. The reduced neurotransmitter levels in those with amalgam appear to be a factor encouraging smoking since nicotine increases these neurotransmitter levels and a much higher percentage of those with amalgam smoke than in those without amalgam.

An average amalgam filling contains over ½ gram of mercury, and the average adult had at least five grams of mercury in fillings (unless most has vaporized). Mercury in solid form is not stable, having low pressure and being subject to galvanic action with other metals in an oral environment, so that within ten years up to half has been found to have been transferred to the body of the host. In patients with galvanic cell in their oral cavity, researchers found decreased levels of anti-inflammatory markers, such as secretory IgA, IgA 1, IgA 2, and lysozyme, and increased levels of the pro-inflammatory marker albumin. The amount of mercury released by a gold alloy bridge over amalgam over a ten year period was measured to be approximately 101 milligrams (mg) (60% of total) or 30 micrograms(ug) per day.

Elemental mercury vapor is more rapidly transmitted throughout the body than most other forms of mercury and has more much toxic effects on the CNS and other parts of the body than inorganic mercury due to its much greater capacity to cross cell membranes, according to the World Health Organization and other studies. Mercury vapor rapidly crosses the blood-brain barrier and placenta of pregnant women. Developmental, learning, and behavioral effects have been found from mercury vapor at much lower levels than for exposure to methyl mercury.

Running shoes with ½ gram of mercury in the heels were banned by several states because the amount of mercury was considered dangerous to public health and created a serious disposal problem. Mercury from dental offices and human waste from people with amalgam fillings has much higher levels and is a major source of mercury in Florida and U.S. waters. Nationwide, the dental industry is the third largest user of mercury, using over 45 tons of mercury per year, and most of this mercury eventually ends up in the environment. Amalgam from dental offices is by far the largest contributor of mercury into sewers and sewer plants, with mercury from replaced amalgam fillings and crown bases the largest source. One study found dental offices discharge into waste water between 65 and 842 milligrams per dentist per day, amounting to several hundred grams per year per office. This is in addition to air emissions. In Canada, the annual amount discharged is about two tons per year, with portions ending up in water, some in landfills and cropland, and some in air emissions. When amalgam fillings are removed by standard practice methods using primary and secondary solids collectors, approximately 60% of the amalgam metals by weight end up in sewer effluent. As much as 10% of prepared new amalgam becomes waste. This mercury also accumulates in building sewer pipes and septic tanks or drain fields where used, creating toxic liabilities. The recently enacted regulations on dental office waste in Canada are expected to reduce emissions by at least 63% by 2005, compared to 2000.

Mercury excreted into sewers by those with amalgam fillings was found by government agencies to be the second largest source of mercury in sewers. In a Finnish study, over 20% of those with amalgam excrete so much to home sewers that the EEU standard for mercury in sewers (50 ug/L) is exceeded. The percentage exceeding the standard doubled for each additional ten amalgam surfaces.

Additionally cremation of those with amalgam fillings adds to air emissions and deposition onto land and lakes. A study in Switzerland found that in Switzerland, cremation released over 65 kilograms of mercury per year as emissions, often exceeding site air mercury standards, while another Swiss study found mercury levels during cremation of a person with amalgam fillings as high as 200 micrograms per cubic meter (considerably higher than U.S. mercury standards).

The amount of mercury in the mouth of a person with fillings was on average 2.5 grams, enough to contaminate five ten-acre lakes to the extent there would be dangerous levels in fish. A Japanese study estimated mercury emissions from a small crematorium as 26 grams per day. A study in Sweden found significant occupational and environmental exposures at crematoria, and since the requirement to install selenium filters, mercury emission levels in crematoria have been reduced 85%.

Studies have found that levels of exposure to the toxic metals mercury, cadmium, and lead have major effects on classroom behavior, learning ability, and also in mental patients and criminals behavior. Studies have found that both genetic susceptibility and environmental exposures are a factor in xenobiotic related effects and disease propagation. Large numbers of animal studies have documented that genetically susceptible strains are more affected by xenobiotic exposures than less susceptible strains. Some genetic types are susceptible to mercury-induced autoimmunity, and some are resistant and thus much less affected. Studies found that mercury causes or accelerates various systemic conditions in a strain dependent manner, and that lower levels of exposure adversely affect some strains but not others, including inducing autoimmunity. When a condition has been initiated and exposure levels decline, autoimmune antibodies also decline in animals or humans. One genetic factor in Hg induced autoimmunity is major histocompatibility complex (MHC) linked. Both immune cell type Th1 and Th2 cytokine responses are involved in autoimmunity. Mercury has been found to affect both Th1 and Th2 cytokines causing an increase in inflammatory Th2 cytokines. In the pancreas, the cells responsible for insulin production can be damaged or destroyed by the chronic high levels of cytokines, with the potential of inducing type II diabetes—even in otherwise healthy individuals with no other risk factors for diabetes. Mercury inhibits production of insulin and is a factor in diabetes and hypoglycemia, with significant reductions in insulin need after replacement of amalgam fillings and normalizing of blood sugar.

Diabetes incidence is increasing drastically. For individuals born in 2000, the lifetime risk of diabetes in the U.S. is 33% and over 16 million currently have diabetes. Several studies have documented that lipoic acid (an antioxidant and chelator) resulted in improvement in the majority of diabetes cases it was used for, by improving glucose metabolism, increasing insulin sensitivity, and reducing nerve damage (including in diabetic neuropathy).

Another genetic difference found in animals and humans is cellular retention differences for metals related to the ability to excrete mercury. For example, it has been found that individuals with genetic blood factor type APOE-4 do not excrete mercury readily and bio-accumulate mercury, resulting in susceptibility to chronic autoimmune conditions such as Alzheimer’s, Parkinson’s, etc. as early as age forty, whereas those with type APOE-2, which contains two cysteine molecules, readily excrete mercury and are less susceptible. Those with type APOE-3 are intermediate to the other two types. The incidence of autoimmune conditions has increased to the extent this is now one of the leading causes of death among women.

Long-term occupational exposure to low levels of mercury can induce slight cognitive deficits, fatigue, decreased stress tolerance, etc. Higher levels have been found to cause more serious neurological problems. Occupational exposure studies have found mercury impairs the body’s ability to kill Candida albicans by impairment of the lytic activity of neutrophils and myeloperoxidase in workers whose mercury excretion levels are within current safety limits.

Such levels of mercury exposure were also found to inhibit cellular respiratory burst. A population of plant workers with average mercury excretion of 20 ug/ g creatinine was found to have long-lasting impairment of neutrophil function. Another study found such impairment of neutrophils decreases the body’s ability to combat viruses such as those that cause heart damage, resulting in more inflammatory damage. Another group of workers with average excretion rates of 24.7 ug/g creatinine had long lasting increases in humoral immunological stimulation of IgG, IgA, and IgM levels. Other studies found that workers exposed at high levels at least twenty years previous (urine peak levels above 600 ug/L) demonstrated significantly decreased strength, decreased coordination, increased tremor, paresthesia, decreased sensation, polyneuropathy, etc. Significant correlations between increasing urine mercury concentrations and prolonged motor and sensory distal latencies were established. Elemental mercury can affect both motor and sensory peripheral nerve conduction and the degree of involvement is related to time-integrated urine mercury concentrations. 30% of dentists with more than average exposure were found to have neuropathies and visual dysfunction compared to none in the control group. Other studies have also found a connection between mercury with peripheral neuropathy and paresthesia as well as with hearing loss. Mercury exposure has been found to commonly cause tremor, ataxia, and balance problems. Several doctors have found thiamin (B3), vitamin B6, inositol, and folic acid supplementation to alleviate peripheral neuropathies, pain, tinnitus, and other neurological conditions.

Another study found that many of the symptoms and signs of chronic candidiasis, MCS, and CFS are identical to those of chronic mercurialism and remit after removal of amalgam combined with appropriate supplementation and gave evidence to implicate amalgam as the only underlying etiologic factor that is common to all.

Other studies found that mercury at levels below the current occupational safety limit causes adverse effects on mood, personality, and memory, with effects on memory at very low exposure levels. More studies found that long-term exposure causes increased micro nuclei in lymphocytes and significantly increased IgE levels at exposures below current safety levels, as well as maternal exposure being linked to cognitive delays and birth defects.

Systemic Mercury Intake Level from Amalgam Fillings

The tolerable daily exposure level for mercury developed in a report for Health Canada is .014 micrograms/kilogram body weight (ug/kg) or approximately one ug/day for average adult. The U.S. EPA Health Standard for elemental mercury exposure (vapor) is 0.3 micrograms per cubic meter of air. The U.S. ATSDR health standard (MRL) for mercury vapor is 0.2 ug/M of air, and the MRL for methylmercury is 0.3 ug/kg body weight/day. For the average adult breathing 20 M of air per day, this amounts to an exposure of 4 or 6 ug/day for the two elemental mercury standards. The EPA health guideline for methylmercury is 0.1 ug/kg body weight per day or seven ug for the average adult or approximately 14 ug for the ATSDR acute oral toxicity standard. Since mercury is methylized in the body, some of both types are present in the body. The older World Health Organization mercury health guideline (PTWI) is 300 ug per week total exposure or approximately 42 ug/day. The EPA drinking water standard for mercury is two ppb. The upper level of mercury exposure recommended by the German Commission on Human Biomonitoring is one micrograms per liter in the blood, since adverse effects, such as increases in blood pressure and cognitive effects, have been documented as low as one ug/L cord blood, with impacts higher in low birth weight babies and commonly in adults with levels below 10 ug/l. The FDA limit for mercury in seafood is 1 ppm, with a warning at ½ ppm. The Japanese government’s limit for mercury contamination is 0.4 micrograms per gram, and studies have found adverse health effects eating fish at levels below 0.5 ppm. EPA and several medical labs suggest health safety guideline of 1 ppm. The EPA safety standard for mercury in blood is 5.8 ppb, and the EPA has found that since the fetus normally has mercury levels 70% above that of the mother’s blood, large numbers of infants are at risk of neurological damage.

Mercury in the presence of other metals in the oral environment undergoes galvanic action, causing movement out of amalgam and into the oral mucosa and saliva. Mercury in solid form is not stable due to high volatility and evaporates continuously from amalgam fillings in the mouth, being transferred over a period of time to the host. Mercury has a relatively high vapor pressure and vaporizes at room temperature. The rate of mercury volatilization is directly related to temperature so in the body it is even more volatile. The vapor saturation concentration in air of 20 milligrams of mercury per cubic meter of air is much higher than the safety limit. The ATSDR safety standard (MRL) for mercury is 0.2 micrograms of mercury per cubic meter of air. Thus mercury readily vaporizes to above the MRL level. The daily total exposure of mercury from fillings is from 3 to 1000 micrograms per day, with the average exposure being above 10 micrograms per day and the average uptake over 5 ug/day.

A large study was carried out at the University of Tubingen Health Clinic in which the level of mercury in saliva of 20,000 persons with amalgam fillings was measured. The level of mercury in unstimulated saliva was found to average 11.6 ug Hg/L, with the average after chewing being three times this level. Several were found to have mercury levels over 1100 ug/L, 1% had unstimulated levels over 200 ug/L, and 10 % had unstimulated mercury saliva levels of over 100 ug/L. The level of mercury in saliva has been found to be proportional to the number of amalgam fillings and generally was higher for those with more fillings, increasing by approximately 1.5 ug/L for each additional amalgam filling.

Saliva tests for mercury are commonly performed in Europe, and many other studies have been carried out with generally comparable results. Another large German study found significantly higher levels than the study summarized here, with some with exposure levels over 1000 ug/day.

These studies found that the amount of mercury in saliva increased about 1.5 to 2.5 micrograms for each additional amalgam filling. Some of the variability in these studies might be due to the fact that a more accurate measure of exposure such as amalgam surfaces augmented by also counting the number of metal crowns over amalgam. Metal crowns over amalgam have been found to produce as much exposure as an amalgam filling, due to galvanic currents in mixed metals. Three studies that looked at a population with more than twelve fillings found generally higher levels than this study, with average mercury level in unstimulated saliva of 29 ug/L, 32.7 ug/L, and 175 ug/day. The average for those with four or less fillings was eight ug/L. While it will be seen that there is a significant correlation between exposure levels and number of amalgam surfaces and exposure generally increases as number of fillings increases, there is considerable variability for a given number of fillings. Some of the factors that will be seen to influence this variability include composition of the amalgam, whether person chews gum or drinks hot liquids, bruxism, oral environmental factors such as acidity, type of toothpaste used, etc. Chewing gum or drinking hot liquids or use of bleaching products to whiten teeth can result in 10 to 100 times normal levels of mercury exposure from amalgams during that period.

The Tubingen study did not assess the significant exposure route of intraoral air and lungs. One study that looked at this estimated a daily average burden of 20 ug from ionized mercury from amalgam fillings absorbed through the lungs, while a Norwegian study found the average level in oral air to be 0.8 ug/M3. Another study at a Swedish University measured intraoral air mercury levels from fillings of from 20 to 125 ug per day, for persons with from 18 to 82 filling surfaces. Other studies found similar results, and some individuals have been found to have intraoral air mercury levels above 400 ug/M3. Most of those whose intraoral air mercury levels were measured exceeded U.S. government health guidelines for workplace exposure. The German workplace mercury limit is even lower than the U.S. guideline.

The studies also determined that the number of fillings is the most important factor related to mercury level, with age of filling being much less significant. Different filling composition and/or manufacturer can also make a difference in exposure levels. The authors of the Tubingen study calculated that, based on the test results with estimates of mercury from food and oral air included, over 40% of those tested in the study received daily mercury exposure higher than the WHO standard (PTWI). As can be seen, most people with several fillings have daily exposure exceeding the Health Canada TDE and the U.S. EPA and ATSDR health guideline for mercury, and many tested in past studies have exceeded the older and higher WHO guideline for mercury, without consideration of exposure from food, vaccinations, etc.

The main exposure paths for mercury from amalgam fillings are absorption by the lungs from intraoral air; vapor absorbed by saliva or swallowed; amalgam particles swallowed; and membrane, olfactory, sublingual venal, and neural path transfer of mercury absorbed by oral mucosa, gums, etc. The sublingual venal, olfactory, and neural pathways are direct pathways to the brain and CNS bypassing the liver’s detox system and appear to represent major pathways of exposure based on the high levels of mercury vapor and methylmercury found in saliva and oral cavity of those with amalgam. A study at Stockholm University made an effort to determine the respective parts in exposure made by these paths. It found that the majority of excretion is through feces, and that the majority of mercury exposure was from elemental vapor. Daily exposure from intraoral air ranged from 20 to 125 ug of mercury vapor, for subjects with number of filling surfaces ranging from 18 to 82. Other studies had similar findings. Most with several amalgams had daily fecal excretion levels over 50 ug/day. The reference average level of mercury in feces (dry weight) for those tested at Doctors Data Lab with amalgam fillings is .26 mg/kg, compared to the reference average level for those without amalgam fillings of .02 mg/kg.

The feces mercury was essentially all inorganic with particles making up at most 25%, and the majority being mercury sulfuhydryl compounds, likely originating as vapor. Their study and others reviewed found that at least 80% of mercury vapor reaching the lungs is absorbed and enters the blood from which it is taken to all other parts of the body. Elemental mercury swallowed in saliva can be absorbed in the digestive tract by the blood or bound in sulfhydryl compounds and excreted through the feces. A review determined that approximately 20% of swallowed mercury sulfhydryl compounds are absorbed in the digestive tract, but approximately 60% of swallowed mercury vapor is absorbed. At least 80% of particle mercury is excreted. Approximately 80% of swallowed methylmercury is absorbed, with most of the rest being converted to inorganic forms apparently. The primary detoxification/excretion pathway for mercury absorbed by the body is as mercury-glutathione compounds through the liver/bile loop to feces, but some mercury is also excreted though the kidneys in urine and in sweat. A high fiber diet has been shown to be helpful in mercury detoxification. The range of mercury excreted in urine per day by those with amalgams is usually less than 15 ug, but some patients are much higher. A large NIDH study of the U.S. military population with an average of 19.9 amalgam surfaces and range of 0 to 60 surfaces found the average urine level was 3.1 ug/L. The average in those with amalgam was four and a half times that of controls and more than the U.S. EPA maximum limit for mercury in drinking water. The average level of those with over 49 surfaces was over eight times that of controls. The same study found that the average blood level was 2.55 ug/L, with 79 % being organic mercury. The total mercury level had a significant correlation to the number of amalgam fillings, with fillings appearing to be responsible for over 75% of total mercury. From the study results, it was found that each ten amalgam surfaces increased urine mercury by approximately 1 ug/L. A study of mercury species found blood mercury was 89% organic and urine mercury was 87% inorganic, while another study found on average 77% of the mercury in the occipital cortex was inorganic. In a population of women tested in the Middle East, the number of fillings was highly correlated with the mercury level in urine, mean= 7 ug/L. Amalgam has also been found to be the largest source of organic mercury in most people. Nutrient transport and renal function were also found to be adversely affected by higher levels of mercury in the urine.

Mercury also bio-accumulates in the kidneys, liver, brain/CNS, heart, hormonal glands, and oral mucosa with the half-life in the brain being over twenty years. Studies have found dental amalgam, chewing on amalgam, and fish consumption were positively associated with urinary-HgC. In men, including workers occupationally exposed to mercury, U-HgC was positively associated with the kidney markers, especially with NAG, but to some extent also with A1M and albumin.

Elemental mercury vapor is transmitted throughout the body via the blood and readily enters cells and crosses the blood-brain barrier, and the placenta of pregnant women, at much higher levels than inorganic mercury and also higher levels than organic mercury. Significant levels are able to cross the blood brain barrier, placenta, and also cellular membranes into major organs such as the heart since the oxidation rate of Hg0, although relatively fast, is slower than the time required by pumped blood to reach these organs. Thus the level in the brain and heart is higher after exposure to Hg vapor than for other forms. While mercury vapor and methyl Hg readily cross cell membranes and the blood-brain barrier, once in cells they are rapidly oxidized to Hg+ inorganic mercury form that does not readily cross cell membranes or the blood brain barrier readily and is responsible for the majority of toxicity effects. Thus inorganic mercury in the brain has a very long half-life.

Thyroid imbalances, which are documented to be commonly caused by mercury, have been found to play a major role in chronic heart conditions such as clogged arteries, mycardial infarction, and chronic heart failure. In a recent study, published in the Annals of Internal Medicine, researchers reported that subclinical hypothyroidism is highly prevalent in elderly women and is strongly and independently associated with cardiac atherosclerosis and myocardial infarction. People who tested hypothyroid usually have significantly higher levels of homocysteine and cholesterol, which are documented factors in heart disease. 50% of those testing hypothyroid also had high levels of homocysteine (hyperhomocysteinenic), and 90% were either hyperhomocystemic or hypercholesterolemic. These are also known factors in developing arteriosclerotic vascular disease. Homocysteine levels are significantly increased in hypothtyroid patients and normalize with treatment.

The average amalgam filling has approximately 0.5 grams (500,000 ug) of mercury. As much as 50% of mercury in fillings has been found to have vaporized after five years and 80% by twenty years. Mercury vapor from amalgam is the single largest source of systemic mercury intake for persons with amalgam fillings, ranging from 50 to 90 % of total exposure, averaging about 80% of total systemic intake. After filling replacement levels of mercury in the blood, urine, and feces are increased typically temporarily for a few days, but levels usually decline in blood and urine within six months to from 60 to 85% of the original levels. Mercury levels in saliva and feces usually decline between 80 to 95%.

Having dissimilar metals in the teeth (e.g., gold and mercury) causes galvanic action, electrical currents, and much higher mercury vapor levels and levels in tissues. Average mercury levels in gum tissue near amalgam fillings are about 200 ppm and are the result of flow of mercury into the mucous membrane because of galvanic currents with the mucous membrane serving as cathode and amalgam as cathode. Average mercury levels are often 1000 ppm near a gold cap on an amalgam filling due to higher currents when gold is in contact with amalgam. These levels are among the highest levels ever measured in tissues of living organisms, exceeding the highest levels found in chronically exposed chloralkali workers, those who died in Minamata, or animals that died from mercury poisoning. German oral surgeons have found levels in the jaw bone under large amalgam fillings or gold crowns over amalgam as high as 5760 ppm with an average of 800 ppm. These levels are much higher than the FDA/EPA action level for prohibiting use of food with over one ppm mercury. Likewise the level is tremendously over the U.S. Dept. Of Health/EPA drinking water limit for mercury, which is two parts per billion. Amalgam manufacturers, government health agencies such as Health Canada, dental school texts, and dental materials researchers advise against having amalgam in the mouth with other metals such as gold, but many dentists ignore the warnings.

Concentrations of mercury in oral mucosa for a population of patients with six or more amalgam fillings taken during oral surgery were twenty times the level of controls. Studies have shown mercury travels from amalgam into dentin, root tips, and the gums, with levels in root tips as high as 41 ppm. Studies have shown that mercury in the gums such as from root caps for root canaled teeth or amalgam tattoos result in chronic inflammation, in addition to migration to other parts of the body. Mercury and silver from fillings can be seen in the tissues as amalgam “tattoos,” which have been found to accumulate in the oral mucosa as granules along collagen bundles, blood vessels, nerve sheaths, elastic fibers, membranes, striated muscle fibers, and acini of minor salivary glands. Dark granules are also present intracellular-ly within macrophages, multinucleated giant cells, endothelial cells, and fibroblasts. There is in most cases chronic inflammatory response or macrophagic reaction to the metals, usually in the form of a foreign body granuloma with multinucleated giant cells of the foreign body and langhans types. Most dentists are not aware of the main source of amalgam tattoos, oral galvanism where electric currents caused by mixed metals in the mouth take the metals into the gums and oral mucosa, accumulating at the base of teeth with large fillings or metal crowns over amalgam base. Such metals are documented to cause local and systemic lesions and health effects, which usually recover after removal of the amalgam tattoo by surgery. The high levels of accumulated mercury also are dispersed to other parts of the body. It is well documented that amalgam fillings are a major factor in gingivitis, oral gum tissue inflammation, bleeding, and bone loss. Mercury also accumulates in the trigeminal ganglia and can cause trigeminal neuralgia from which patients recover after amalgam replacement. Cavitations from improperly healed tooth extractions also commonly cause trigeminal neuralgia and most such recover after cavitation surgery.

The periodontal ligament of extracted teeth is often not fully removed and results in incomplete jawbone regrowth, resulting in a pocket where mouth bacteria in anaerobic conditions along with similar conditions in the dead tooth produce extreme toxins similar to botulism which like mercury are extremely toxic and disruptive to necessary body enzymatic processes at the cellular level, comparable to the similar enzymatic disruptions caused by mercury and previously discussed. The component mix in amalgams has also been found to be an important factor in mercury vapor emissions. The level of mercury and copper released from high copper amalgam is as much as fifty times that of low copper amalgams. Studies have consistently found modern, high copper, non-gamma-two amalgams have a high negative current and much greater release of mercury vapor than conventional silver amalgams and are more cytotoxic. Clinics have found the increased toxicity and higher exposures to be factors in increased incidence of chronic degenerative diseases. While the non-gamma-two amalgams were developed to be less corrosive and less prone to marginal fractures than conventional silver amalgams, they have been found to be unstable in a different mechanism when subjected to wear/polishing/chewing/brushing. This has also been found to be a factor in the much higher release of mercury vapor by the modern non-gamma-two amalgams. Recent studies have concluded that, because the high mercury release levels of modern amalgams, mercury poisoning from amalgam fillings is widespread throughout the population. Numerous other studies also support this finding.

Amalgam also releases significant amounts of silver, tin, and copper which also have toxic effects, with organic tin compounds formed in the body being even more neurotoxic than mercury. Alloys containing tin such as amalgam were found to have the highest galvanic corrosion rates, while alloys containing copper or iron were very corrosive in acid environments. Metals tend to cause cellular acidic conditions which lead to disease and measuring urine acidity is useful in this regard. Normal acidity is PH of about 6.8.

The number of amalgam surfaces has a statistically significant correlation to

  • blood plasma mercury level (usually not as strong as other measures),
  • urine mercury level,
  • oral air,
  • saliva and oral mucosa,
  • feces mercury,
  • pituitary gland,
  • brain occipital cortex and frontal lobe,
  • renal (kidney) cortex,
  • liver,
  • motor function areas of the brain, and
  • fetal and infant liver/brain levels related to maternal fillings.

The blood and urine mercury load of a person with amalgam fillings is often five times that of a similar person without. The average blood level for one large population was five ug/l. Normal blood levels are less than 20 ppb, but health effects have been observed in patients in the upper part of this range. A Swedish study estimated the total amount mercury swallowed per day from intra-oral vapor was ten micrograms per day, and a large German study found median exposure through saliva alone for those with fillings to be about ten ug/day. Other studies have found similar amounts.

Teeth are living tissue and have massive communication with the rest of the body via blood, lymph, and nerves. Mercury vapor (and bacteria in teeth) has paths to the rest of the body. German studies of mercury loss from vapor in unstimulated saliva found the saliva of those with amalgams had at least five times as much mercury as the controls. Mercury (especially mercury vapor) rapidly crosses the blood brain barrier and is stored preferentially in the pituitary gland, hypothalamus, thyroid gland, adrenal gland, and occipital cortex in direct proportion to the number and extent of amalgam surfaces. Thus mercury has a greater effect on the functions of these areas. The range in one study was 2.4 to 28.7 ppb, and one study found on average that 77% of the mercury in the occipital cortex was inorganic. Autopsy studies have found higher levels of mercury in the brain of infants than of adults from the same population and much higher levels in adults who have amalgam fillings. Infants of mothers who had dental work involving amalgam during pregnancy had significantly higher levels of mercury in hair tests.
Some mercury entering nasal passages is absorbed directly into the olfactory lobe and brain without coming from blood. Mercury also is transported along the axons of nerve fibers. Mercury has a long half-life in the body and over 20 years in the brain.

Methylmercury is more toxic to some body processes than inorganic mercury. Mercury from amalgam is methylated by bacteria, galvanic electric currents, and candida albicans in the mouth and intestines. The level of organic mercury in saliva is significantly related to the number of amalgam fillings. Oral bacteria streptococommus mitior, S. mutans, and S. sanguis were all found to methylate mercury. High levels of vitamin B12 in the system also have been found to result in increased methylmercury concentrations in the liver and brain. Methylmercury is ten times more potent in causing genetic damage than any other known chemical and also crosses the blood-brain barrier readily. Once mercury vapor or methylmercury are converted to inorganic mercury in cells or the brain, the mercury does not readily cross cell membranes or the blood-brain barrier. Thus mercury has a very long half-life in the brain. N-acetylcysteine (NAC) has been found to be effective at increasing glutathione levels and chelating methylmercury.

The level of mercury in the tissue of the fetus, newborn, and young children is directly proportional to the number of amalgam surfaces in the mother’s mouth. The level of mercury in umbilical cord blood, meconium, and placenta was higher than that in mother’s blood, with meconium level the most reliable indicator of mercury exposure levels. The saliva and feces of children with amalgams have approximately ten times the level of mercury as children without. A group of German children with amalgam fillings had urine mercury level 4 times that of a control group without amalgams, while a Canadian study found 3.2 times as much exposure in those with amalgam with adverse health effects (low weight and height), and in a Norwegian group with average age 12 there was a significant correlation between urine mercury level and number of amalgam fillings. The level of mercury in maternal hair was significantly correlated to level of mercury in nursing infants. One study found a 60% increase in average cord blood mercury level between 1980 and 1990 in Japan. Amalgam use in dentistry in Europe has been declining rapidly. The routine use of amalgam in pediatric dentistry in the UK, previously 80%, had declined to 35% in favor of glass ionomer cements. A recent study found that glass ionomer cement fillings (ART) were more effective than amalgam in children’s teeth.

The fetal mercury content after maternal inhalation of mercury vapor was found to be higher than in the mother. Mercury from amalgam in the blood of pregnant women crosses the placenta and appears in amniotic fluid and fetal blood, liver, and pituitary gland soon after placement. Dental amalgams are the main source of mercury in breast milk. Milk increases the bioavailability of mercury. Mercury is transferred mainly by binding to amino acids like albumin. The level of mercury in breast milk was found to be significantly correlated with the number of amalgam fillings, with milk from mothers with seven or more fillings having levels in milk approximately ten times that of amalgam-free mothers. The milk sampled ranged from 0.2 to 6.9 ug/L. Several authors suggest use of early mother’s milk as a screen for potential problems since it is correlated both to maternal and infant mercury levels. The highest level is in the pituitary gland of the fetus which affects development of the endocrine system. Levels for exposure to mercury vapor has been found to be approximately ten times that for maternal exposure to an equivalent dose of inorganic mercury, and developmental behavioral effects from vapor have been found at levels considerably below that required for similar effects by methylmercury. The level of total mercury in nursing infants was significantly correlated to total mercury level in maternal hair.

There is a significant correlation between number of amalgam fillings of the mother and the level of the fetus and older infants, and also with the level in mother’s milk. Fertile women should not be exposed to vapor levels above government health guidelines; or have amalgams placed or removed during pregnancy. The U.S. ATSDR mercury health MRL of 0.2 mcg/M3.

Immune System Effects and Autoimmune Disease

Many thousands of people with symptoms of mercury toxicity have been found in tests to have high levels of mercury, and many thousands who have had amalgam fillings removed(most) have had health problems and symptoms alleviated or greatly improved. From clinical experience some of the symptoms of mercury sensitivity/mercury poisoning include chronic fatigue, dizziness, frequent urination, insomnia, amnesia, headaches, irritability, chronic skin problems, metallic taste, gastrointestinal problems, asthma, stuffy nose, dry crusts in nose, rhinitis, plugged ears, ringing ears, chest pain, hyperventilation, diabetes, spacy feeling, chills, chronic skin problems, immune and autoimmune diseases, cardiovascular problems, muscle weakness, and many types of neurological problems. Amalgam results in chronic exposure rather than acute exposure and accumulation in body organs over time, so most health effects are of the chronic rather than acute in nature, but serious health problems have been documented to be related to amalgam and researchers have attributed some deaths as due to amalgam.

Mercury caused adverse effects on both neutrophil and macrophage function and after depletion of thiol reserves, T-cells were susceptible to Hg induced cellular death (apoptosis). Interferon syntheses was reduced in a concentration dependent manner with either mercury or methylmercury as well as other immune functions, and low doses also induce aggregation of cell surface proteins and dramatic tyrosine phosporlation of cellular proteins related to asthma, allergic diseases such as eczema and lupus, and autoimmunity. Porphyrins are precursors to heme, the oxygen carrying component of blood. Mercury inhibits the conversion of specific porphyrins to heme. Mercury and other toxic metals block coproporphyrin and uroporphyrin which is a marker in using the porphyrin test for lupus diagnosis and treatment. One study found that insertion of amalgam fillings or nickel dental materials causes a suppression of the number of T-lymphocytes, and impairs the T-4/T-8 ratio. Low T4/T8 ratio has been found to be a factor in lupus, anemia, MS, eczema, inflammatory bowel disease, and glomerulonephritis. Mercury-induced autoimmunity in animals and humans has been found to be associated with mercury’s expression of major histocompatibility complex (MHC) class II genes. Both mercuric and methylmercury chlorides caused dose dependent reduction in immune B-cell production. B-cell expression of IgE receptors were significantly reduced, with a rapid and sustained elevation in intracellular levels of calcium induced. Mercury also inhibited B-cell and T-cell RNA and DNA synthesis. The inhibition of these functions by 50 % occurred rapidly at very low levels, in the range of 10 to 25 ug/L. All types of cells exhibited a dose dependent reduction in cellular glutathione when exposed to mercury, inhibiting generation of GSH by lymphocytes and monocytes.

Workers occupationally exposed to mercury at levels within guidelines have been found to have impairment of lytic activity of neutrophils and reduced ability of neutrophils to kill invaders such as candida. Immune Th1 cells inhibit candida by cytokine related activation of macrophages and neutrophils. Development of Th2 type immune responses deactivate such defenses. Mercury inhibits macrophage and neutrophil defense against candida by its effects on Th1 and Th2 cytokine effects. Low doses also induced autoimmunity in some species. Candida overgrowth results in production of the highly toxic canditoxin and ethanol, which are known to cause fatigue, toxicity, and depressive symptoms. Another amalgam effect found an increase in the average blood white cell count significantly. The increased white count usually normalizes after amalgam removal.

Mercury also blocks the immune function of magnesium and zinc, whose deficiencies are known to cause significant neurological effects. The low Zn levels result in deficient CuZnSuperoxide dismustase (CuZnSOD), which in turn leads to increased levels of superoxide due to toxic metal exposure. This is in addition to mercury’s effect on metallothionein and copper homeostasis as previously discussed. Copper is an essential trace metal which plays a fundamental role in the biochemistry of the nervous system. Several chronic neurological conditions involving copper metabolic disorders are well documented like Wilson’s disease and Menkes Disease. Mutations in the copper/zinc enzyme superoxide dismutase (SOD) have been shown to be a major factor in the motor neuron degeneration in conditions like familial ALS and similar effects on Cu/Zn SOD to be a factor in other conditions such as autism, Alzheimer’s, Parkinson’s, and non-familial ALS. This condition can result in zinc deficient SOD and oxidative damage involving nitric oxide, peroxynitrite, and lipid peroxidation, which have been found to affect glutamate mediated excitability and apoptosis of nerve cells and effects on mitochondria. These effects can be reduced by zinc supplementation, as well as supplementation with antioxidants and nitric oxide-suppressing agents and peroxynitrite scavengers, such as vitamin C, vitamin E, lipoic acid, Coenzyme Q10, carnosine, gingko biloba, N-acetylcysteine, etc. Some of the antioxidants were also found to have protective effects through increasing catalase and SOD action, while reducing lipid peroxidations. Ceruloplasmin in plasma can be similarly affected by copper metabolism disfunction, like SOD function, and is often a factor in neurodegeneration.

Mercury from amalgam interferes with production of cytokines that activate macrophage and neutrophils, disabling early control of viruses or micoplasma and leading to enhanced infection. Animal studies have confirmed that mercury increases effects of the herpes simplex virus type 2 for example. Both mercuric and methylmercury were equally highly toxic at the cellular level and in causing cell volume reductions. However, methylmercury inhibits macrophage functions such as migration and phagocytosis at lower levels. Large numbers of people undergoing amalgam removal have clinically demonstrated significant improvements in the immune system parameters discussed here and recovery and significant improvement in immune system problems in most cases surveyed. Antigen specific LST-test was performed on a large number of patients with atopic eczema, using T-cells of peripheral blood. 87% showed LST positive reactions to Hg, 87% to Ni, 38% to Au and 40% to Pd. They removed LST positive dental metals from the oral cavities of patients. Improvement of symptoms was obtained in 82% of the patients within 1-10 months. Similar results have been obtained at other clinics. Several studies found adverse health effects at mercury vapor levels of 1 to 5 mcg/M3.

Body mercury burden was found to play a role in resistant infections such as chlamydia trachomatis and herpes family viral infections; it was found many cases can only be effectively treated by antibiotics after removal of body mercury burden (cilantro tablets were used with follow-up antibiotics). Various bacteria have enzymes that convert organic mercury to inorganic mercury in the intestine, facilitating excretion. However, taking antibiotics kills these bacteria and significantly reduces mercury excretion, resulting in more mercury damage. Similar results regarding mercury have been found for treatment of cancer. Studies have found conventional chemotherapy to be no more effective than no treatment and clinical cases have demonstrated that detoxification and nutritional support can be effective in treating multiple myeloma and other cancers.

Mercury by its effect of weakening the immune system contributes to increased chronic diseases and cancer. Exposure to mercury vapor causes decreased zinc and methionine availability, depresses rates of methylation, and increased free radicals-all factors in increased susceptibility to cancer. Amalgam fillings have also been found to be positively associated with mouth cancer. Mercury from amalgam fillings has also been found to cause increase in white blood cells and in some cases to result in leukemia. White cell levels decline after total dental revision (TDR) and some have recovered from leukemia after removal of amalgam fillings in a very short time. Among a group of patients testing positive as allergic to mercury, low level mercury exposure was found to cause adverse immune system response, including effects on vitro production of tumor necrosis factor TNF alfa and reductions in interleukin-1.

Nickel and beryllium are two other metals commonly used in dentistry that are very carcinogenic and toxic and cause DNA malformations. Nickel ceramic crowns, root canals and cavitations have also been found to be a factor in some breast cancer and other cancers and some have recovered after TDR, which includes amalgam replacement, replacement of metal crowns over amalgam, nickel crowns, extraction of root canaled teeth, and treatment of cavitations where necessary. Similarly nickel crowns and gold crowns over amalgam have been found to be a factor in lupus and Belle’s Palsy from which some have recovered after TDR and Felderkrais exercises. Nickel has also been found to accumulate in the prostate and be related to prostate cancer.

A high correlation has been found between patients subjectively diagnosed with CNS; systemic symptoms suggestive of mercury intoxication and immune reactivity to inorganic mercury as well as with MRI positive patients for brain damage. Controls without CNS problems did not have such positive correlations. Mercury, nickel, palladium, and gold induce autoimmunity in genetically predisposed or highly exposed individuals. Tests have found a significant portion of people to be in this category and thus more affected by exposure to amalgam than others.

Mercury also interrupts the cytochrome C oxidase system, blocking the ATP energy function. These effects along with reductions in red blood cells oxygen carrying capability often result in fatigue and reduced energy levels as well as neurological effects. The majority of those with CFS having SPECT scans was found to have five times more areas of regional brain damage and reduced blood flow in the cerebral areas. The majority studied were also found to have increased Th2 inflammatory cytokine activity and a blunted DHEA response curve to I.V. ATCH indicative of hypothalamic deficiency such as relative glucocorticoid deficiency. CFS and Fibromyalgia patients have also been found to commonly have abnormal enzymatic processes that affect among other things the sodium-potassium ATPase energy channels, for which mercury is a known cause. This also results in inflammatory processes that cause muscle tissue damage and result in higher levels of urinary excretion of creatinine, choline, and glycine in CFS and higher levels of excretion of choline, taurine, citrate, and trimethyl amine oxide in FM.

People with chronic and immune reactive problems are increasing finding dental materials are a factor in their problems and getting biocompatiblity tests run to test their immune reactivity to the various dental materials used. A high percentage of such patients test immune reactive to many of the toxic metals. Of the many thousands who have had the Clifford immune reactivity test, the following percentages were immune reactive to the following metals that have very common exposures:

  • mercury (93%)
  • nickel (98%)
  • aluminum (91%)
  • arsenic (86%)
  • chromium (83%)
  • cobalt (78%)
  • beryllium (74%)
  • lead (68%)
  • cadmium (63%)
  • antimony (36%)
  • copper (32%)
  • palladium (32%)
  • tin (32%)
  • zinc (33%)
  • silver (25%).

Toxic/allergic reactions to metals often result in lichen planus lesions in oral mucosa or gums and play a role in pathogenesis of periodontal disease. Removal of amalgam fillings usually results in cure of such lesions. A high percentage of patients with oral mucosal problems along with other autoimmune problems have significant immune reactions to mercury, palladium, gold, and nickel, including to mercury preservatives such as thimerosal. 94% of such patients had significant immune reactions to inorganic mercury and 72% had immune reactions to low concentrations of HgCl2. 61% also had immune reaction to phenylHg, which has been commonly used in root canals and cosmetics. 10% of controls had significant immune reactions to HgCl and 8.3% to palladium. Other studies of patients suffering from chronic fatigue found similar results. Of fifty patients suffering from serious fatigue referred for MELISA test, over 70% had significant immune reaction to inorganic mercury and 50% to nickel, with most patients also reactive to one or more other metals such as palladium, cadmium, lead, and methylmercury.

Mercury has been found to impair conversion of thyroid T4 hormone to the active T3 form as well as causing autoimmune thyroiditis common to such patients. In general immune activation from toxics such as heavy metals resulting in cytokinen release and abnormalities of the hypothalamus-pituitary-adrenal axis can cause changes in the brain, fatigue, and severe psychological symptoms, such as profound fatigue, muscosketal pain, sleep disturbances, gastrointestinal and neurological problems as are seen in CFS, fibromyalgia, and autoimmune thyroidititis. Such symptoms usually improve significantly after amalgam removal. Hypersensitivity has been found most common in those with genetic predisposition to heavy metal sensitivity, such as found more frequently in patients with HLA-DRA antigens. A significant portion of the population appears to fall in this category. Conditions involving allergies, chemical sensitivities, and autoimmunity have been increasing rapidly in recent years.

The enzymatic processes blocked by such toxic substances as mercury also result in chronic formation of metal-protein compounds (HLA antigens or antigen-presenting macrophages) that the body’s immune system (T-lymphocytes) does not recognize, resulting in autoimmune reactions.

The metals bind to SH-groups on proteins which can then be recognized as “foreign” and attacked by immune lymphocytes. Such has been extensively documented by studies such as the documentation of the autoimmune function test MELISA, a sophisticated immune/autoimmune test which was developed to test for such reactions. Very low doses and short-term exposures of inorganic Hg (20-200 mug/kg) exacerbate lupus and accelerate mortality in mice. Low dose Hg exposure increases the severity and prevalence of experimental autoimmune myocarditis induced by other factors. In a study of small-scale gold mining using mercury, there was a positive interaction between Hg autoimmunity and malaria. These results suggest a new model for Hg immunotoxicity, as a co-factor in autoimmune disease, increasing the risks and severity of clinical disease in the presence of other triggering events, either genetic or acquired.

Mercury has been found to accumulate in the pineal gland and reduce melatonin levels, which is thought to be a significant factor in mercury’s toxic effects. Melatonin has found to have a significant protective action against methylmercury toxicity.

There is also evidence that mercury affects neurotransmitter levels which has effects on conditions like depression, mood disorders, ADHD, etc. There is evidence that mercury can block the dopamine-beta-hydroxylase (DBH) enzyme. DBH is used to make the noradrenaline neurotransmitter and low noradrenaline can cause fatigue and depression. Mercury molecules can block all copper catalyzed dithiolane oxidases, such as coproporphyrin oxidase and DBH.

Patients with other systemic neurological or immune symptoms such as arthritis, myalgia, eczema, CFS, MS, lupus, ALS, diabetes, epilepsy, Hashimoto’s thyroiditis, Scleroderma, etc. also often recover or improve significantly after amalgam replacement. Of a group of 86 patients with CFS symptoms, 78% reported significant health improvements after replacement of amalgam fillings within a relatively short period, and MELISA test found significant reduction in lymphocyte reactivity compared to pre-removal tests. The improvement in symptoms and lymphocyte reactivity imply that most of the Hg-induced lymphocyte reactivity is allergenic in nature. Although patch tests for mercury allergy are often given for unresolved oral symptoms, this is not generally recommended as a high percentage of such problems are resolved irrespective of the outcome of a patch test. Also using mercury in a patch test has resulted in some adverse health effects. A group of patients that had amalgams removed because of chronic health problems were able to detect subjectively when a patch test used mercury salts in a double blind study.

Of the over 3,000 patients with chronic conditions tested for lymphocyte reactivity to metals, the following were the percentages testing positive:

  • nickel 34%
  • inorganic mercury 20%
  • phenol mercury 13%
  • gold 14%
  • cadmium 16%
  • palladium 13%
  • lead 11%.

For people with autoimmune conditions, the percentage testing immune reactive to mercury was much higher:

  • 28% percent were immune reactive to palladium
  • 26% to gold, 23% to inorganic mercury
  • 23% to phenyl mercury
  • 12% to methyl mercury, as compared to less than 5% for controls.

Of 98 patients who had amalgam fillings replaced, 76% had long term health improvement and significant improvement in MELISA scores.

Other studies have also found relatively high rates of allergic reactions to inorganic mercury and nickel. For groups with suspected autoimmune diseases such as neurological problems, CFS, and oral lichen planus, most of the patients tested positive to inorganic mercury and most patients’ health improved significantly and immune reactivity declined after amalgam removal. In a group of patients tested by MELISA before and after amalgam removal at a clinic in Uppsala Sweden, the patients’ reactivity to inorganic mercury, palladium, gold and phenyl mercury all had highly significant differences from the control group, with over 20% being highly reactive to each of these metals. Animal studies have found that after sensitization to mercury, patients and animals are also usually reactive to gold. A high percentage was also reactive to nickel in both groups. After amalgam removal, the immune reactivity to all of these metals other than nickel declined significantly, and 76% reported significant long-term health improvements after two years. Only 2% were worse. The study concluded that immune reactivity to mercury and palladium is common and appears to be immune-related in nature since immune reactivity declines when exposure levels are reduced. Such studies have also found that deficiencies in detoxification enzymes, such as glutathione transfereases, cause increased susceptibility to metals and other chemicals. Such deficiencies can be due to genetic predisposition but are also known to be caused by acute or chronic toxic exposures.

For MS and lupus patients, a high percentage tested positive to nickel and/or inorganic Mercury (MELISA). A patch test was given to a large group of medical students to assess factors that lead to sensitization to mercury. 13% tested positive for allergy to mercury. Eating fish was not a significant factor between sensitive and non-sensitized students, but the sensitized group had a significantly higher average number of amalgam fillings and higher hair mercury levels. In a population of dental students tested, 44% were positive for allergy to mercury.

A high correlation has been found between patients subjectively diagnosed with CNS and systemic symptoms suggestive of mercury intoxication and immune reactivity to inorganic mercury as well as with MRI positive patients for brain damage. 81% of the group with health complaints had pathological MRI results including signs of degeneration of the basal ganglia of the brain. 60% of the symptom group tested positive for immune system reaction to mercury. Controls without CNS problems did not have such positive correlations. The authors concluded that immune reactions have an important role in development of brain lesions and tumors, and amalgam fillings induce immune reactions in many patients. Mercury, nickel, palladium, and gold induce autoimmunity in genetically predisposed or highly expose individuals. Tests have found a significant portion of people to be in this category and thus more affected by exposure to amalgam than others.

Low level mercury exposure, including exposure to amalgam fillings, has been found to be associated with increased autoimmune diseases, including lupus, Crohn’s disease, lichen planus, and endometriosis. Silver also is released from amalgam fillings, stored in the body, and has been shown to cause immune complex deposits, immune reactions, and autoimmunity in animal studies.

Mercury exposure through dental fillings appears to be a major factor in chronic fatigue syndrome (CFS) through its effects on ATP and immune system (lymphocyte reactivity, neutrophil activity, effects on T-cells and B-cells) as well as its promotion of growth of candida albicans in the body and the methylation of inorganic mercury by candida and intestinal bacteria to the extremely toxic methylmercury form, which like mercury vapor crosses the blood-brain barrier and also damages and weakens the immune system. Mercury vapor or inorganic mercury has been shown in animal studies to induce autoimmune reactions and disease through effects on immune system T cells. Chronic immune activation is common in CFS, with increase in activated CD8+ cytotoxic T-cells and decreased natural killer (NK) cells. Numbers of suppressor-inducer T cells and NK cells have been found to be inversely correlated with urine mercury levels. CFS patients usually improve and immune reactivity is reduced when amalgam fillings are replaced.

Medical Studies Finding Health Problems Related to Amalgam Fillings (Other Than Immune)

Neurological problems are among the most common and serious; they include memory loss, moodiness, depression, anger and sudden bursts of anger/rage, self-effacement, suicidal thoughts, lack of strength/force to resolve doubts or resist obsessions or compulsions, etc. Many studies of patients with major neurological diseases have found evidence amalgam fillings may play a major role in development of conditions, such as depression, schizophrenia, bipolar disorder, memory problems, and other more serious neurological diseases such as MS, ALS,
Parkinson’s, and Alzheimer’s. A large U.S. Centers for Disease Control study found that those with more amalgam fillings have significantly more chronic health problems, especially neurological problems and cancer.

Some factors that have been documented in depression are low serotonin levels, abnormal glucose tolerance (hypoglycemia), brain inflammation, and low folate levels, which mercury has also been found to cause. Occupational exposure to mercury has been documented to cause depression and anxiety. One mechanism by which mercury has been found to be a factor in aggressiveness and violence is its documented inhibition of the brain neurotransmitter acetylcholinesterase. Low serotonin levels and/or hypoglycemia have also been found in the majority of those with impulsive and violent behavior.

Mercury causes decreased lithium levels, which is a factor in neurological diseases such as depression and Alzheimer’s. Lithium protects brain cells against excess glutamate and calcium, and low levels cause abnormal brain cell balance and neurological disturbances. Medical texts on neurology point out that chronic mercurialism is often not recognized by diagnosticians and misdiagnosed as dementia, neurosis, functional psychosis, or just “nerves.” Diagnosis of mercury toxicity can be made based on exposure history and three or more of such symptoms mercury is known to cause. Very high levels of mercury are found in brain memory areas such as the cerebral cortex and hippocampus of patients with diseases with memory-related symptoms. Mercury has been found to cause memory loss by inactivating enzymes necessary for brain cell energy production and proper assembly of the protein tubulin into microtubules.

Mercury (as well as toxins from root canals and cavitations) interact with brain tubulin and disassembles microtubules that maintain neurite structure. Thus chronic exposure to low level mercury vapor can inhibit polymerzation of brain tubulin and creatinine kinase which are essential to formation of microtubules. The effects of mercury with other toxic metals have also been found to be synergistic, having much more effect than with individual exposure.

Flu shots have mercury and aluminum, both of which are known to accumulate in the brain over time. A study of people who received flu shots regularly found that if an individual had five consecutive flu shots between 1970 and 1980 (the years studied) his/her chances of getting
Alzheimer’s disease is ten times higher than if they had one or no shots.

Animal studies of developmental effects of mercury on the brain have found significant effects at extremely low exposure levels—levels commonly seen in those with amalgam fillings or in dental staff working with amalgam. One study found prenatal mercury vapor exposure decreased NGF concentration in newborn rat’s forebrain at four parts per billion (ppb) tissue concentration. Another study found general toxicity effects at one micromole (uM) levels in immature cell cultures, increased immune-reactivity for glial fibrillary protein at one nanamole (0.2 ppb) concentration. Other studies on rodents and monkeys have found brain cellular migration disturbances and behavioral changes, along with reduced learning and adaption capacity after low levels of mercury vapor exposure. The exposure levels in these studies are seen in the fetus and newborn babies of mothers with amalgam fillings or who had work involving amalgam during pregnancy. Mercury vapor has been found to primarily affect the central nervous system, while methylmercury primarily affects the peripheral nervous system.

Epidemiological studies have found that human embryos are also highly susceptible to brain damage from prenatal exposure to mercury. Studies have confirmed that there are vulnerable periods during brain and CNS development that are especially sensitive to neurotoxic exposures and affect development processes and results. The fetal period is most sensitive, but neural development extends through adolescence. A recent study found that prenatal Hg exposure is correlated with lower scores in neurodevelopmental screening but more so in the linguistic pathway. Maternal hypothyroidism has been found to cause endocrine system abnormalities in the fetus, and mercury is documented to commonly cause hypothyroidism. Some conditions found to be related to such toxic exposures include autism, schizophrenia, ADD, dyslexia, eczema, etc. Prenatal/early postnatal exposure to mercury affects level of nerve growth factor (NGF) in the brain and causes brain damage and imbalances in development of the brain. Exposure of developing neuroblastoma cells to sub-cytotoxic doses of mercuric oxide resulted in lower levels of neurofilament proteins than unexposed cells. Mercury vapor exposure causes impaired cell proliferation in the brain and organs, resulting in reduced volume for cerebellum and organs and subtle deficiencies. Exposure to mercury and four other heavy metals tested for in a study of school children accounted for 23% of the variation in test scores for reading, spelling, and visual motor skills. A Canadian study found that blood levels of five metals were able to predict with a 98% accuracy which children were learning disabled.

Several studies found that mercury causes learning disabilities and impairment and reduction in IQ. Mercury has an effect on the fetal nervous system at levels far below that considered toxic in adults, and background levels of mercury in mothers correlate significantly with incidence of birth defects and still births. The upper level of mercury exposure recommended by the German Commission on Human Bio-monitoring is one microgram per liter in the blood, and adverse effects, such as increases in blood pressure and cognitive effects, have been documented as low as one ug/L, with impacts higher in low birth weight babies.

Calcium plays a major role in the extreme neurotoxicity of mercury and methylmercury. Both inhibit cellular calcium ATPase and calcium uptake by brain microsomes at very low levels of exposure. Protein Kinase C (PKC) regulates intracellular and extra cellular signals across neuronal membranes, and both forms of mercury inhibit PKC at micromolar levels, as well as inhibiting phorbal ester binding. They also block or inhibit calcium L-channel currents in the brain in an irreversible and concentration-dependent manner. Mercury vapor or inorganic mercury exposure affects the posterior cingulate cortex and causes major neurological effects with sufficient exposure. Some of the resulting conditions include stomatitis, tremor, ADD, erythism, etc. Metallic mercury is much more potent than methyl mercury in such actions, with 50% inhabitation in animal studies at 13 ppb. Motor neuron dysfunction and loss in amyotrophic lateral sclerosis (ALS) have been attributed to several different mechanisms, including increased intracellular calcium, glutamate excitotoxicity, oxidative stress and free radical damage, mitochondrial dysfunction, and neurofilament aggregation and dysfunction of transport mechanisms. These alterations are not mutually exclusive, and increased calcium and altered calcium homeostasis appear to be a common denominator.

Spatial and temporal changes in intracellular calcium concentrations are critical for controlling gene expression and neurotransmitter release in neurons. Mercury alters calcium homeostasis and calcium levels in the brain and affects gene expression and neurotransmitter release through its effects on calcium, etc. Mercury inhibits sodium and potassium (N,K)ATPase in dose dependent manner and inhibits dopamine and norepinephrine uptake by synaptosomes and nerve impulse transfer. Mercury also interrupts the cytochrome oxidase system, blocking the ATP energy function, lowering immune growth factor IGF-I levels, and impairing astrocyte function. Astrocytes are common cells in the CNS involved in the feeding and detox of nerve cells. IGF-I protects against brain and neuronal pathologies, like ALS, MS, and fibromyalgia, by protecting the astrocytes from this destructive process.

As far back as 1996, it was shown that the lesions produced in the myelin sheath of axons in cases of multiple sclerosis were related to excitatory receptors on the primary cells involved called oligodendroglia. The loss of myelin sheath on the nerve fibers characteristic of the disease is due to the death of oligodendroglial cells at the site of the lesions (called plaques). Further, these studies have shown that the death of these important cells is as a result of excessive exposure to excitotoxins at the site of the lesions. Most of these excitotoxins are secreted from microglial immune cells in the central nervous system. This not only destroys these myelin-producing cells, but it also breaks down the blood-brain barrier (BBB), allowing excitotoxins in the blood stream to enter the site of damage. Some common exposures that cause such proliferation of such excitotoxins are mercury and aspartame, with additional effects from MSG and methanol. Aspartame and methanol are both in diet drinks.

Mercury and aspartame have been found to be causes of MS, along with other contributing exicitotoxins. It is now known the cause for the destruction of the myelin in the lesions is over-activation of the microglia in the region of the myelin. An enzyme that converts glutamine to glutamate called glutaminase increases tremendously, thereby greatly increasing excitotoxicity. Any dietary excitotoxin can activate the microglia, thereby greatly aggravating the injury. This includes the aspartate in aspartame. The methanol adds to this toxicity as well. Now, the secret to treatment appears to be shutting down, or at least calming down, the microglia.

According to neurologist Dr. RL Blaylock, the good news is that there are supplements and nutrients that calm the microglia. The most potent are silymarin, curcumin, and ibuprophen. Phosphatidylcholine helps re-myelinate the nerve sheaths that are damaged, as does B12, B6, B1, vitamin D, folate, vitamin C, natural vitamin E (mixed tocopherols) and L-carnitine. DHA plays a major role in repairing the myelin sheath. Vitamin D may even prevent MS, but it acts as an immune modulator, preventing further damage. The dose is 2000 IU a day. Magnesium, as magnesium malate, is needed in a dose of 500 mg two times a day. They must avoid all excitotoxins, even natural ones in foods, such as soy, red meats, nuts, mushrooms, and tomatoes. Avoid fluoride and vaccinations since these either inhibit antioxidant enzymes or trigger harmful immune reactions.

Metals like mercury bind to SH-groups (sulfhydryl) in sulfur compounds like amino acids and proteins, changing the structure of the compound that it is attached to. This often results in the immune systems T-cells not recognizing them as appropriate nutrients and attacking them. Such binding and autoimmune damage has been documented in the fat-rich proteins of the myelin sheaths of the CNS and collagen, which are affected in MS. Metals by binding to SH radicals in proteins and other such groups can cause autoimmunity by modifying proteins which via T-cells activate B-cells that target the altered proteins inducing autoimmunity as well as causing aberrant MHC II expression on altered target cells. Studies have also found mercury and lead cause autoantibodies to neuronal proteins, neurofilaments, and myelin basic protein (MBP). Mercury and cadmium also have been found to interfere with zinc binding to MBP, which affects MS symptoms since zinc stabilizes the association of MBP with brain myelin. MS has also been found to commonly be related to inflammatory activity in the CNS such as that caused by the reactive oxygen species and cytokine generation caused by mercury and other toxic metals. Mercury from amalgam has been found to reduce antioxidant enzymes and antioxidant effects in blood plasma. Antioxidants like lipoic acid which counteract such free radical activity have been found to alleviate symptoms and decrease demyalination. A group of metal exposed MS patients with amalgam fillings were found to have lower levels of red blood cells, hemoglobin, hemocrit, thyroxine, T-cells, and CD8+ suppresser immune cells than a group of MS patients with amalgam replaced and more exacerbations of MS than those without. Immune and autoimmune mechanisms are thus seen to be a major factor in neurotoxicity of metals. The immune suppression caused by exposure to mercury or other toxics has also been found to increase susceptibility to other common pathogens such as viruses, mycoplasma, bacteria, candida, and parasites. The majority of those tested with autoimmune conditions, such as ALS, MS, CFS, and FMS, have been found to be infected with mycoplasma and similar for parasites.

Mercury lymphocyte reactivity and effects on glutamate in the CNS induce CFS type symptoms including profound tiredness, musculoskeletal pain, sleep disturbances, gastrointestinal and neurological problems along with other CFS symptoms and fibromyalgia. Mercury has been found to be a common cause of fibromyalgia, which based on a Swedish survey, occurs in about 12% of women over 35 and 5.5% of men. Glutamate is the most abundant amino acid in the body and in the CNS acts as excitory neurotransmitter, which also causes inflow of calcium. Astrocytes, a type of cell in the brain and CNS with the task of keeping clean the area around nerve cells, have a function of neutralizing excess glutamate by transforming it to glutamic acid. If astrocytes are not able to rapidly neutralize excess glutamate, then a buildup of glutamate and calcium occurs, causing swelling and neurotoxic effects. Mercury and other toxic metals inhibit astrocyte function in the brain and CNS, causing increased glutamate and calcium related neurotoxicity, which are responsible for much of the fibromyalgia symptoms and a factor in neural degeneration in MS and ALS. There is some evidence that astrocyte damage/malfunction is a major factor in MS.

This is also a factor in conditions such as CFS, Parkinson’s, and ALS. Animal studies have confirmed that increased glutamate levels cause increased sensitivity to pain, as well as higher body temperature. Mercury and increased glutamate activate free radical forming processes like xanthine oxidase, which produces oxygen radicals and oxidative neurological damage. Nitric oxide related toxicity caused by peroxynitrite formed by the reaction of NO with superoxide anions, which results in nitration of tyrosine residues in neurofilaments, and manganese superoxide dismutase has been found to cause inhibition of the mitochondrial respiratory chain, inhibition of the glutamate transporter, and glutamate-induced neurotoxicity involved in ALS.

Medical studies and doctors treating fibromyalgia have found that supplements which cause a decrease in glutamate or protect against its effects have a positive effect on fibromyalgia and other chronic neurologic conditions. Some that have been found to be effective include ginkgo biloba and pycnogenol, NAC, vitamin B6, methyl cobalamine (B12), L-carnitine, choline, ginseng, vitamins C and E, nicotine, and omega 3 fatty acids (fish and flaxseed oil).

Extremely toxic anaerobic bacteria from root canals or cavitations formed at incompletely healed tooth extraction sites have also been found to be common factors in fibromyalgia and other chronic neurological conditions such as Parkinson’s and ALS, with condensing osteitis which must be removed with a surgical burr along with 1 mm of bone around it. Cavitations have been found in 80% of sites from wisdom tooth extractions tested and 50% of molar extraction sites tested. The incidence is likely somewhat less in the general population.

A recent study assessed the large decrease in ALS incidence in Guam and similar areas to look for possible explanations in the cause of past high incidence and recent declines. One of the study’s conclusions was that a likely major factor for the high ALS rates in Guam and similar areas in the past was chronic dietary deficiency since birth in Ca, Mg and Zn induced excessive absorption of divalent metal cations which accelerates oxidant-mediated neuronal degenerations in a genetically susceptible population.

Numerous studies have found long-term chronic low doses of mercury cause neurological, memory, behavior, sleep, and mood problems. Neurological effects have been documented at very low levels of exposure (urine Hg 4 ug/L). One of the studies at a German University assessed 20,000 people. Substantial occupational mercury exposure can have long-term adverse effects on the peripheral nervous system, which becomes detectable decades after cessation of exposure. Organic tin compounds formed from amalgam are even more neurotoxic than mercury. Studies of groups of patients with amalgam fillings found significantly more neurological, memory, mood, and behavioral problems than the control groups.

Mercury binds to hemoglobin oxygen binding sites in the red blood cells, thus reducing oxygen carrying capacity and adversely affects the vascular response to norepinephrine and potassium. Mercury’s effect on pituitary gland vasopressin is a factor in high blood pressure. Mercury also increases cytosolic free calcium levels in lymphocytes in a concentration-dependent manner, causing influx from the extracellular medium, and blocks entry of calcium ions into the cytoplasm. Amalgam fillings have been found to be related to higher blood pressure, hemoglobin irregularities, tachycardia, chest pains, etc. Mercury also accumulates in the heart and damages myocardial and heart valves. Mercury has been found to be a cause of athersclerosis, hypertension, tachycardia in children and adults, and heart attacks in adults.

Mercury also interrupts the cytochrome oxidase system, blocking the ATP energy function and impairing astrocyte function. These effects often result in fatigue and reduced energy levels. Both mercury and methylmercury have been shown to cause depletion of calcium from the heart muscle and to inhibit myosin ATPase activity by 50% at 30 ppb, as well as reducing NK-cells in the blood and spleen. The interruption of the ATP energy chemistry results in high levels of porphyrins in the urine. Mercury, lead, and other toxics have different patterns of high levels for the 5 types of porphyrins, with pattern indicating likely source and the level extent of damage.

The average for those with amalgams is over three time that of those without. The FDA has approved a test measuring porphyrins as a test for mercury poisoning. However, some other dental problems, such as nickel crowns, cavitations, and root canals also can cause high porphyrins. Cavitations are diseased areas in bone under teeth or extracted teeth usually caused by lack of adequate blood supply to the area. Tests by special equipment (Cavitat) found cavitations in over 80% of areas under root canals or extracted wisdom teeth that have been tested, and toxins, such as anaerobic bacteria, significantly inhibit body enzymatic processes in virtually all cavitations. These toxins have been found to have serious systemic health effects in many cases, and significant health problems to be related such as arthritis, MCS, and CFS. These have been found to be factors along with amalgam in serious chronic conditions such as MS, ALS, Alzheimer’s, MCS, CFS, etc. The problem occurs in extractions that are not cleaned out properly after extraction. Supplements such as glucosamine sulfate and avoidance of orange juice and caffeine have been found to be beneficial in treating arthritic conditions as well.

A study funded by the Adolf Coors Foundation found that toxicity is a significant cause of abnormal cholesterol levels, increasing as a protective measure against metals toxicity. However, lowering cholesterol levels by other means below 160 correlates with much higher rates of depression, suicide, cancer, violent deaths, cerebral hemorrhage, and deaths—all known to be affected by mercury effects. The study also found that mercury has major adverse effects on red and white blood cells, oxygen carrying capacity, and porphyrin levels, with most cases seeing significant increase in oxyhemoglobin level and reduction in porphyrin levels along with 100% experiencing improved energy.

Patch tests for hypersensitivity to mercury have found from 2% to 44% to test positive, much higher for groups with more amalgam fillings and length of exposure than those with less. In studies of medical and dental students, those testing positive had significantly higher average number of amalgam fillings than those not testing positive (and higher levels of mercury in urine). Of the dental students with ten or more fillings at least five years old, 44% tested allergic. Based on these studies and statistics for the number with ten or more fillings, the percent of Americans allergic to mercury just from this group would be about 17 million people especially vulnerable to increased immune system reactions to amalgam fillings. However, the total would be much larger and patch tests do not measure the total population having toxic reactions to mercury. The most sensitive reactions are immune reactions, DNA mutations, developmental, enzyme inhibition, nerve growth inhibition, and systemic effects.

People with amalgam fillings have an increased number of intestinal microorganisms resistant to mercury and many standard antibiotics. Mercury is extremely toxic and kills many beneficial bacterial, but some forms of bacteria can alter their form to avoid being killed by adding a plasmid to their DNA, making the bacteria mercury resistant. This transformation also increases antibiotic resistance. Recent studies have found that drug resistant strains of bacteria causing ear infections, sinusitis, tuberculosis, and pneumonia more than doubled since 1996, and results were similar for strains of bacteria in U.S. rivers. Studies have found a significant correlation between mercury resistance and multiple antibiotic resistances and have found that, after reducing mercury burden, antibiotic resistance declines. The alteration of intestinal bacterial populations necessary for proper digestion along with other damage and membrane permeability effects of mercury are major factors in creating “leaky gut” conditions with poor digestion and absorption of nutrients and toxic, undigested compounds in the bloodstream. Some of the gastrointestional problems caused by mercury include poor mineral absorption, diarrhea, stomatis, bloating, wasting disease, etc.

When intestinal permeability is increased, food and nutrient absorption is impaired. Dysfunction in intestinal permeability can result in leaky gut syndrome, where larger molecules and toxins in the intestines can pass through the membranes and into the blood, triggering an immune response. Progressive damage can occur to the intestinal lining, eventually allowing disease-causing bacteria, undigested food particles, and toxins to pass directly into the blood stream. Dysfunctions in intestinal permeability have been found to be associated with diseases such as ulcerative colitis, irritable bowel syndrome (IBS), Crohn’s disease, CFS, eczema, psoriasis, food allergies, autoimmune disease, and arthritis.

Mercury and toxic metals have been found to be common toxic exposures that have been found to cause increased intestinal permeability and intestinal dysfunction, as well as of the kidney epithelial and brush border cells. Mercury exposure also reduced the mucosal entry of sugars and amino acids to 80-90% of control levels in the small intestine cells within several minutes. Mercury exposure blocks intestinal nutrient transport by interacting directly with brush border membrane transport proteins. Mercury causes significant destruction of stomach and intestine epithelial cells, resulting in damage to stomach lining which along with mercury’s ability to bind to SH hydroxyl radical in cell membranes alters permeability and adversely alters bacterial populations in the intestines. This causes leaky gut syndrome with toxic, incompletely digested complexes in the blood and accumulation of heliobacter pylori.

Dental amalgam has been found to be the largest source of mercury exposure in most people who have several amalgam fillings. Replacement of amalgam fillings and metals detoxification have been found to significantly improve the health of most with conditions related to bowel dysfunction and leaky gut syndrome. Clinical studies have found that diets high in flavanoids, cartenoids, and including nutritional supplements, such as buffered vitamin C and natural E, selenium, omega-3 oils, and probiotics are effective in preventing ear infections and other chronic conditions. These in addition to multiple B vitamins, the flavonoids, curcumin, hesperidin, and quercetin are effective in preventing and treating leaky gut related conditions. Supplements and other treatments that reduce intestinal permeability have also been found to be protective against and to improve these conditions. Glutamine, berberine, probiotics, and vitamin D have been found to decrease intestinal permeability and protect against effects caused by leaky gut syndrome.

Mercury from amalgam binds to the -SH (sulfhydryl) groups, resulting in inactivation of sulfur and blocking of enzyme functions such as cysteine dioxygenase(CDO), gamma-glutamyltraspeptidase(GGC), and sulfite oxidase, producing sulfur metabolites with extreme toxicity that the body is unable to properly detoxify, along with a deficiency in sulfates required for many body functions. Sulfur is essential in enzymes, hormones, nerve tissue, and red blood cells. These exist in almost every enzymatic process in the body. Blocked or inhibited sulfur oxidation at the cellular level has been found in many patients with chronic degenerative diseases, including Parkinson’s, Alzheimer’s, ALS, lupus, rheumatoid arthritis, MCS, autism, etc., and appears to be a major factor in these conditions. Mercury also blocks the metabolic action of manganese and the entry of calcium ions into cytoplasm. Mercury from amalgam thus has the potential to disturb all metabolic processes. Mercury is transported throughout the body in blood and can affect cells in the body and organs in different ways.

Parkinson’s disease involves the aggregation of alpha-synuclein to form fibrils, which are the major constituent of intracellular protein inclusions (Lewy bodies and Lewy neurites) in dopaminergic neurons of the substantia nigra. Occupational exposure to specific metals, especially manganese, copper, lead, iron, mercury, zinc, and aluminum, appears to be a risk factor for Parkinson’s disease based on epidemiological studies. Elevated levels of several of these metals have also been reported in the substantia nigra of Parkinson’s disease subjects. One study found that EDTA chelation was effective at reducing some of the effects. In some cases, Molybdenum, B12 vitamin, P5P vitamin, B1 vitamin, and tetrahydrofolate supplementation has helped to boost the protective sulfite oxidase.

A large study of 20,000 subjects at a German university found a significant relation between the number of amalgam fillings with periodontal problems, neurological problems, and gastrointestinal problems. Allergies and hair loss were found to be two to three times as high in a group with large number of amalgam fillings compared to controls. Levels of mercury in follicular fluid were significantly higher for those with amalgam fillings. Based on this finding, a gynecological clinic that sees a large number of women suffering from alopecia/hair loss that was not responding to treatment suggested amalgams be replaced in 132 women who had not responded to treatment. After amalgam removal, 68% of the women then responded to treatment and alopecia was alleviated. In other studies involving amalgam removal, the majority had significant improvement. Higher levels of hormone disturbances, immune disturbances, infertility, and recurrent fungal infections were also found in the amalgam group. Other clinics have also found alleviation of hair loss/alopecia after amalgam removal and detox. Another study in Japan found significantly higher levels of mercury in gray hair than in dark hair.

Mercury accumulates in the kidneys with increasing levels over time. One study found levels ranging from 21 to 810 ppb. A study of levels in kidney donors found an average of three times higher mercury level in those with amalgams versus those without. Health Canada has estimated that about 20% of the population suffers a subclinical impairment of kidney or CNS function related to amalgam mercury. Inorganic mercury exposure has been found to exert a dose-dependent cytotoxicity by generating extremely high levels of hydrogen peroxide, which is normally quenched by pyruvate and catalase. HgCl2 also has been found to impair function of other organelles, such as lysomomes that maintain transmembrane proton gradient, and to decrease glutathione peroxidase activity in the kidneys while upregulating heme oxidase function. The government’s toxic level for mercury in urine is 30 mcg/L, but adverse effects have been seen at lower levels. Low levels in urine often mean high mercury retention and chronic toxicity problems. For this reason, urine tests are not a reliable measure of mercury toxicity.

Amalgam fillings produce electrical currents, which increase mercury vapor release and may have other harmful effects. These currents are measured in micro amps, with some measured at over 4 micro amps. The central nervous system operates on signals in the range of nano-amps, which is 1000 times less than a micro amp. Negatively charged fillings or crowns push electrons into the oral cavity since saliva is a good electrolyte. Patients with autoimmune conditions like MS, epilepsy, depression, etc. are often found to have a lot of high negative current fillings. The Huggins’ total dental revision (TDR) protocol calls for teeth with the highest negative charge to be replaced first. Other protocols for amalgam removal are available from international dental associations like IAOMT and mercury poisoned patient organizations like DAMS. For these reasons it is important that no new gold dental work be placed in the mouth until at least six months after replacement. Some studies have also found persons with chronic exposure to electromagnetic fields (EMF) to have higher levels of mercury exposure and excretion and higher likelihood of getting chronic conditions.

Mercury from amalgam fillings is transferred to the fetus of pregnant women and children who breast feed at levels usually higher than those of the mother. Mercury has an effect on the fetal nervous system at levels far below that considered toxic in adults, and background levels of mercury in mothers correlate significantly with incidence of birth defects and still births. Mercury vapor exposure causes impaired cell proliferation in the brain and organs, resulting in reduced volume for cerebellum and organs and subtle deficiencies.

Mercury can reduce reproductive function and cause birth defects and developmental problems in children. Clinical evidence indicates that amalgam fillings lead to hormone imbalances that can reduce fertility. Mercury has been found to cause decreased sperm volume and motility, increased sperm abnormalities, spontaneous abortions, increased uterine fibroids/endometritis, and decreased fertility in animals and in humans. In miscarriages or birth defect studies, men were found to typically have low sperm counts and significantly more visually abnormal sperm. It’s now estimated that up to 85% of the sperm produced by a healthy male is DNA-damaged. Abnormal sperm is also being blamed for a global increase in testicular cancer, birth defects, and other reproductive conditions. Studies indicate an increase in the rate of spontaneous abortions with an increasing concentration of mercury in the fathers’ urine before pregnancy. Studies have found that mercury accumulates in the ovaries and testes, inhibits enzymes necessary for sperm production, affects DNA in sperm, causes aberrant numbers of chromosomes in cells, causes chromosome breaks, etc.

Studies in monkeys have found decreased sperm motility, abnormal sperm, increased infertility, and abortions at low levels of methylmercury. Astrocytes play a key role in MeHg-induced excitotoxicity. MeHg preferentially accumulates in astrocytes. MeHg potently and specifically inhibits glutamate uptake in astrocytes. Neuronal dysfunction is secondary to disturbances in astrocytes. Co-application of nontoxic concentrations of MeHg and glutamate leads to the typical appearance of neuronal lesions associated with excitotoxic stimulation. MeHg induces swelling of astrocytes. These observations are fully consistent with MeHg-induced dysregulation of excitatory amino acid homeostasis and indicate that a glutamate-mediated excitotoxic mechanism is involved.

Mercury and other toxic metals such as copper and lead cause breaks in DNA and also have synergistic effects with x-rays. Low non-cytotoxic levels of mercury induce dose-dependent binding of mercury to DNA and significantly increased cell mutations and birth defects. In addition to effects on DNA, mercury also promotes cancer in other ways. Mercury depletes and weakens the immune system in many ways documented throughout this paper. A large U.S. Centers for Disease Control epidemiological study found that those with more amalgam fillings have much higher cancer rates and MS, as well as more chronic health problems.

Mercury has been documented to be an endocrine system-disrupting chemical in animals and people, disrupting function of the pituitary gland, hypothalamus, thyroid gland, enzyme production processes, and many hormonal functions at very low levels of exposure. The pituitary gland controls many of the body’s endocrine system functions and secretes hormones that control most bodily processes, including the immune system and reproductive system. The hypothalamus regulates body temperature and many metabolic processes. Mercury damage results in poor bodily temperature control, in addition to many problems caused by hormonal imbalances. Such hormonal secretions are affected at levels of mercury exposure much lower than the acute toxicity effects normally tested. Mercury also damages the blood brain barrier and facilitates penetration of the brain by other toxic metals and substances. Low levels of mercuric chloride also inhibit ATPase activity in the thyroid, with methylmercury inhibiting ATP function at even lower levels. Both types of mercury were found to cause denaturing of protein, but inorganic mercury was more potent. These effects result commonly in a reduction in thyroid production and an accumulation in the thyroid of radiation. Toxic metal exposure’s adverse influence on thyrocytes can play a major role in thyroid cancer etiology. Among those with chronic immune system problems with related immune antibodies, the types showing the highest level of antibody reductions after amalgam removal include thyroglobulin and microsomal thyroid antigens.

There has been no evidence found that there is any safe level of mercury in the body that does not kill cells and harm body process. This is especially so for the pituitary gland of the developing fetus where mercury has been shown to accumulate and which is the most sensitive to mercury.

Low levels of mercury and toxic metals have been found to inhibit dihydroteridine reductase, which affects the neural system function by inhibiting transmitters through its effect on phenylalanine, tyrosine and tryptophan transport into neurons. This was found to cause severe impaired amine synthesis and hypokinesis. Tetrahydrobiopterin, which is essential in production of neurotransmitters, is significantly decreased in patients with Alzheimer’s, Parkinson’s, MS, ALS, and autism. Such patients have abnormal inhibition of neurotransmitter production. Such symptoms improved for most patients after administration of R-tetrahydrobiopterin, and some after 5-formyltetrahydrofolate, tyrosine, and 5-HTP. The level of mercury released by amalgam fillings is often more than the levels documented in medical studies to produce adverse effects and above the U.S. government health guidelines for mercury exposure.

Many studies of patients with major neurological or degenerative diseases have found evidence amalgam fillings may play a major role in development of conditions such as Alzheimer’s, ALS, MS, Parkinson’s, ADD, etc. Mercury exposure causes high levels of oxidative stress/reactive oxygen species (ROS). Mercury and quinones form conjugates with thiol compounds such as glutathione and cysteine and cause depletion of glutathione, which is necessary to mitigate reactive damage. Such conjugates are found to be highest in the brain substantia nigra with similar conjugates formed with L-Dopa and dopamine in Parkinson’s disease. Mercury depletion of GSH and damage to cellular mitochondria and the increased lipid peroxidation in protein and DNA oxidation in the brain appear to be a major factor in Parkinson’s disease.

One study found higher than average levels of mercury in the blood, urine, and hair of Parkinson’s disease patients. Another study found blood and urine mercury levels to be very strongly related to Parkinson’s with odds ratios of approximately twenty at high levels of Hg exposure. Increased formation of reactive oxygen species (ROS) has also been found to increase formation of advanced glycation end products (AGEs). They can be considered part of a vicious cycle, which finally leads to neuronal cell death in the substantia nigra in PD. Another study that reviewed occupational exposure data found that occupational exposure to manganese and copper have high rations for relation to PD.

Mercury has been found to accumulate preferentially in the primary motor function related areas such as the brain stem, cerebellum, rhombencephalon, dorsal root ganglia, and anterior horn motor neurons, which enervate the skeletal muscles. Mercury, with exposure either to vapor or organic mercury tends to accumulate in the glial cells in a similar pattern, and the pattern of deposition is the same as that seen from morphological changes. Though mercury vapor and organic mercury readily cross the blood-brain barrier, mercury has been found to be taken up into neurons of the brain and CNS without having to cross the blood-brain barrier, since mercury has been found to be taken up and transported along nerve axons as well through calcium and sodium channels and along the olfactory path. In addition to the documentation showing the mechanisms by which mercury causes the conditions and symptoms seen in ALS and other neurodegenerative diseases, many studies of patients with major neurological or degenerative diseases have found direct evidence mercury and amalgam fillings play a major role in development of neurological conditions such as such as ALS. Mercury penetrates and damages the blood brain barrier allowing penetration of the barrier by other substances that are neurotoxic. Damage to the blood brain barrier’s function has been found to be a major factor in chronic neurological diseases. MS patients have been found to have much higher levels of mercury in cerebrospinal fluid compared to controls.

Low levels of toxic metals have been found to inhibit dihydroteridine reductase, which affects the neural system function by inhibiting brain transmitters through its effect on phenylalanine, tyrosine, and tryptophan transport into neurons. This was found to cause severely impaired amine synthesis and hypokinesis. Tetrahydro-biopterin, which is essential in production of nerurotransmitters, is significantly decreased in patients with Alzheimer’s, Parkinson’s, and MS. Such patients have abnormal inhibition of neurotransmitter production.

Clinical tests of patients with MND, ALS, Parkinson’s, Alzheimer’s, Lupus, rheumatoid arthritis, and autism have found that the patients generally have elevated plasma cysteine to sulphate ratios, with the average being 500% higher than controls. This means that these patients have insufficient sulfates available to carry out necessary bodily processes. Mercury has been shown to diminish and block sulfur oxidation and thus reduces glutathione levels, which is the part of this process involved in detoxifying and excretion of toxins. Glutathione is produced through the sulfur oxidation side of this process. Low levels of available glutathione have been shown to increase mercury retention and increase toxic effects, while high levels of free cysteine have been demonstrated to make toxicity due to inorganic mercury more severe. Mercury has also been found to play a part in inducing intolerance and neuronal problems through blockage of the P-450 enzymatic process.

Mercury has been shown to be a factor that can cause rheumatoid arthritis by activating localized CD4+ T-cells which trigger production of immune macrophages and immunoglobulin (Ig) producing cells in joints. This has been found to produce inflammatory cytokines such as IL-1 and TNF that contribute to cartilage and bone destruction. Also, it is documented that the process thus involves free radical/reactive oxygen species effects, and antioxidants have been found to have benefits in treatment.

In one subtype of ALS, damaged, blocked, or faulty enzymatic superoxide dismutase (SOD) processes appear to be a major factor in cell apoptosis involved in the condition. Mercury is known to damage or inhibit SOD activity. Mercury at extremely low levels also interferes with formation of tubulin producing neurofibrillary tangles in the brain similar to those observed in Alzheimer’s patients, with high levels of mercury in the brain, and low levels of zinc. Mercury and the induced neurofibrillary tangles also appear to produce a functional zinc deficiency in AD sufferers, as well as cause reduced lithium levels which is another factor in such diseases.
Lithium protects brain cells against excess glutamate induced excitability and calcium influx.

It has been documented that conditions like depression and other chronic neurological conditions often involve damage and nerve cell death in areas of the brain like the hippocampus, and lithium has been found to not only prevent such damage but also promote cell gray matter cell growth in such areas and to be effective in treating not only depressive conditions but degenerative conditions like Huntington’s Disease.

Also mercury binds with cell membranes interfering with sodium and potassium enzyme functions, causing excess membrane permeability, especially in terms of the blood-brain barrier. Less than one ppm mercury in the blood stream can impair the blood-brain barrier. Mercury was also found to accumulate in the mitochondria and interfere with their vital functions and to inhibit cytochrome C enzymes, which affect energy supply to the brain. Persons with the Apo-E4 gene form of apolipoprotein E, which transports cholesterol in the blood, are especially susceptible to this damage, while those with Apo-E2, which has extra cysteine and is a better mercury scavenger, have less damage. The majority have an intermediate form Apo-E3. This appears to be a factor in susceptibility to Alzheimer’s disease, Parkinson’s disease, and MS. One’s susceptibility can be estimated by testing for this condition. In many cases, removal of amalgam fillings and treatment for metal toxicity led to significant improvement in health. Mercury causes an increase in white blood cells, with more created to try to react to a foreign toxic substance in the body. There is evidence that some forms of leukemia are abnormal response to antigenic stimulation by mercury or other such toxics, and removal of amalgam has led to remission very rapidly in some cases.

Mercury and methylmercury impair or inhibit all cell functions and deplete calcium stores. This can be a major factor in bone loss of calcium (osteoporosis). Mercury (like copper) also accumulates in areas of the eyes, such as the endothelial layer of the cornea and macula, and is a major factor in chronic and degenerative eye conditions, such as iritis, astigmatism, myopia, black streaks on retina, cataracts, macular degeneration, retinitis pigmentosa, color vision loss,
etc. Most of these conditions have been found to improve after amalgam replacement.

Results of Removal of Amalgam Fillings

For the week following amalgam removal, body mercury levels increase significantly, depending on protective measures taken, but within two weeks levels fall significantly. Chronic conditions can worsen temporarily, but they usually improve if adequate precautions are taken to reduce exposure during removal. In a study comparing replacement protocols, only the non-rubber dam group showed significant increases in the mercury levels found in plasma and urine after replacement. Compared to the pre-removal mercury levels in plasma and urine, the levels found one year after removal of all amalgam restorations were on average 52% lower in plasma and 76% lower in urine.

Removal of amalgam fillings resulted in a significant reduction in body burden and body waste product load of mercury. Total reduction in mercury levels in blood and urine is often over 80% within a few months. On average, those with 29 amalgam surfaces excreted over three times more mercury in urine after DMPS challenge than those with three amalgam surfaces.

For the following case studies of amalgam replacement, some clinics primarily replaced amalgam fillings using patient protective measures and supportive supplements, whereas some clinics do something comparable to Hal Huggins’ total dental revision where in addition to amalgam replacement, patients’ gold or nickel crowns over amalgam are replaced by biocompatible alternatives, root canals are extracted, and cavitations are checked for and cleaned. A Jerome meter was used to measure mercury vapor level in the mouth, and the average was 54.6 micrograms mercury per cubic meter of air, far above the government health guideline for mercury.

Some of the above cases used chemical or natural chelation to reduce accumulated mercury body burden in addition to amalgam replacement. Some clinics using DMPS for chelation reported over 80% with chronic health problems were cured or significantly improved. Other clinics reported similar success. The recovery rate of those using dentists with special equipment and training in protecting the patient reported much higher success rates than those with standard training and equipment. The Huggins’ TDR protocol includes testing teeth with metal for level of galvanic current caused by the mixed metals, and removal of the teeth with highest negative galvanic current first. This has been found to improve recovery rate for chronic conditions like epilepsy and autoimmune conditions. Metals are being pushed into the body from negatively charged metal dental work with saliva as electrolyte, and the highest charged teeth lose the most metal to the body.

Clinical studies have found that patch testing is not a good predictor of success of amalgam removal, as a high percentage of those testing negative also recovered from chronic conditions after replacement of fillings. The Huggins Clinic using TDR has successfully treated over a thousand patients with chronic autoimmune conditions. In a large German study of MS patients after amalgam revision, extraction resulted in 85% recovery rate versus only 16% for filling replacement alone. Other cases have found that recovery from serious autoimmune diseases, dementia, or cancer may require more aggressive mercury removal techniques than simple filling replacement due to body burden. This appears to be due to migration of mercury into roots and gums that is not eliminated by simple filling replacement.

Among those with chronic immune system problems with related immune antibodies, the types showing the highest level of antibody reductions after amalgam removal include glomerular basal membrane, thyroglobulin, and microsomal thyroid antigens. TDR and other measures used in metals detox have been found to increase T-cells and immune function in AIDS patients. Swedish researchers have developed a sophisticated test for immune/autoimmune reactions that has proved successful in diagnosing and treating environmentally caused diseases related to mercury and other immune-toxics, such as lichen planus, CFS, MS, etc..

Interviews of a large population of Swedish patients that had amalgams removed due to health problems found that virtually all reported significant health improvements and that the health improvements were permanent. A compilation of an even larger population found similar results.
For example 89% of those reporting allergies had significant improvements or total elimination; extrapolated to U.S. population, this would represent over 17 million people who would benefit regarding allergies alone.

Fecal matter is the major path of excretion of mercury from the body, having a higher correlation to systemic body burden than urine or blood. For this reason many researchers consider feces to be the most reliable indicator of daily exposure level to mercury or other toxics. The average level of mercury in feces of populations with amalgam fillings is as much as one ppm and approximately ten times that of a similar group without fillings, with significant numbers of those with several filings having over ten ppm and 170 times those without fillings. For those with several fillings, daily fecal mercury excretion levels range between 20 to 200 ug/day. The saliva test is another good test for daily mercury exposure, done commonly in Europe and representing one of the largest sources of mercury exposure. There is only a weak correlation between blood or urine mercury levels and body burden or level in a target organ. Mercury vapor passes through the blood rapidly (half-life in blood is 10 seconds and accumulates in other parts of the body, such as the brain, kidneys, liver, thyroid gland, pituitary gland, etc. Thus blood test measures mostly recent exposure. Kidneys have a lot of hydroxyl (SH) groups, which mercury binds to, causing accumulation in the kidneys and inhibiting excretion. As damage occurs to kidneys over time, mercury is less efficiently eliminated, so urine tests are not reliable for body burden after long term exposure. Some researchers suggest hair offers a better indicator of mercury body burden than blood or urine, although still not totally reliable and may be a better indicator for organic mercury than inorganic. In the early stages of mercury exposure, before major systemic damage other than slight fatigue results, you usually see high hemoglobin, hemocrit, alkaline phosphatase, and lactic dehydroganese; in later states you usually see marginal hemoglobin, hemocrit, plus low oxyhemoglobin. Hair was found to be significantly correlated with fish consumption, as well as with occupational dental exposure and to be a good medium for monitoring internal mercury exposure, except that external occupational exposure can also affect hair levels. Mercury hair level in a population sampled in Madrid Spain ranged from 1.3 to 92.5 ppm. This study found a significant positive correlation between maternal hair mercury and mercury level in nursing infants. Hair mercury levels did not have a significant correlation with urine mercury in one study and did not have a significant correlation to number of fillings. One researcher suggests that mercury levels in hair of greater than five ppm are indicative of mercury intoxication.

A new test approved by the FDA for diagnosing damage that has been caused by toxic metals like mercury is the fractionated porphyrin test, which measures the amount of damage as well as likely source. Mercury blocks enzymes needed to convert some types of porphyrins to hemoglobin and adenosine triphosphate (ATP). The pattern of which porphyrins are high gives an indication of likely toxic exposure, with high precoproporphyrin almost always high with mercury toxicity and often coproporphyrin.

Provocation challenge tests after use of chemical chelators such as DMPS or DMSA also are effective at measuring body burden, but high levels of DMPS can be dangerous to some people, especially those still having amalgam fillings or those allergic to sulfur drugs or sulfites. Many studies using chemical chelators such as DMPS or DMSA have found post-chelation levels to be poorly correlated with pre-chelation blood or urine levels, but one study found a significant correlation between pre and post chelation values when using DMPS. Challenge tests using DMPS or DMSA appear to have a better correlation with body burden and toxicity symptoms such as concentration, memory, and motor deficits. On average those with 29 amalgam surfaces excreted over three times more mercury in urine after DMPS challenge than those with three amalgam surfaces, and those with 45 amalgam surfaces more than six times as much mercury. Several doctors use 16 ug/L as the upper bound for mercury after DMPS challenge and consider anyone with higher levels to have excess body burden. However, one study found significant effects at lower levels. Some researchers believe DMSA has less adverse side effects than DMPS and prefer to use DMSA for chelation for this reason. Some studies have also found DMSA as more effective at removing mercury from the brain. A common protocol for DMSA (developed to avoid redistribution effects) is 50 mg orally every four hours for three days and then off eleven days.

Another chelator used for clogged arteries, EDTA, forms toxic compounds with mercury and can damage brain function. Use of EDTA may need to be restricted in those with high Hg levels. N-acetylcysteine (NAC) has been found to be effective at increasing cellular glutathione levels and chelating mercury. Experienced doctors have also found additional zinc to be useful when chelating mercury as well as counteracting mercury’s oxidative damage. Zinc induces metallothionein which protects against oxidative damage and increases protective enzyme activities and glutathione which tend to inhibit lipid peroxidation and suppress mercury toxicity.
Also lipoic acid has been found to dramatically increase excretion of inorganic mercury (over 12 fold) and to cause decreased excretion of organic mercury and copper. Lipoic acid has a protective effect regarding lead or inorganic mercury toxicity through its antioxidant properties, but it should not be used with high copper. Lipoic acid and N-acetylcysteine (NAC) also increase glutathione levels and protect against superoxide radical/peroxynitrite damage. Zinc is a mercury and copper antagonist and can be used to lower copper levels and protect against mercury damage. Lipoic acid has been found to have protective effects against cerebral ischemic-reperfusion, excitotoxic amino acid (glutamate) brain injury, mitochondrial dysfunction, diabetic neuropathy. Other antioxidants such as carnosine, co-enzyme Q10,vitamins C and E, gingko biloba, pycnogenol and selenium have also been found protective against degenerative neurological conditions.

Tests suggested by Huggins/Levy for evaluation and treatment of mercury toxicity:

  • hair element test (low hair mercury level does not indicate low body level)(more than 3 essential minerals out of normal range indicates likely metals toxicity)
  • CBC blood test with differential and platelet count
  • blood serum profile
  • urinary mercury (for person with average exposure with amalgam fillings, average mercury level is 3 to 4 ppm;
  • lower test level than this likely means person is poor excreter and accumulating mercury, often mercury toxic
    fractionated porphyrin (note test results sensitive to light, temperature, shaking)
  • individual tooth electric currents(replace high negative current teeth first)
  • patient questionnaire on exposure and symptom
  • specific gravity of urine

Note: During initial exposure to mercury, the body marshals immune system and other measures to try to deal with the challenge, so many test indicators will be high; after prolonged exposure the body and immune system inevitably lose the battle and measures to combat the challenge decrease. Some test indicator scores decline then. Chronic conditions are common during this phase. Also, high mercury exposures with low hair mercury or urine mercury level usually indicate body is retaining mercury and likely toxicity problem.

Huggins Total Dental Revision Protocol

The steps of the Huggins’ Total Dental Revision Protocol include:

  • conduct history questionnaire and panel of tests.
  • replace amalgam fillings starting with filling with highest negative current or highest negative quadrant, with supportive vitamin/mineral supplements.
  • extract all root canaled teeth using proper finish protocol.
  • test and treat cavitations and amalgam tattoos where relevant provide supportive supplementation and periodic monitoring tests evaluate need for further treatment (not usually needed).
  • avoid acute exposures/challenge to the immune system on a weekly 7/14/21 day pattern.

Note: After treatment of many cases of chronic autoimmune conditions, it has been observed that often mercury along with root canal toxicity or cavitation toxicity are major factors in these conditions, and most with these conditions improve after TDR if protocol is followed carefully. Also, it is documented that the process is inflammatory involving free radical/reactive oxygen species effects, and antioxidants have been found to have benefits in treatment. Other measures in addition to TDR that have been found to help in treatment of MS in clinical experience are avoidance of milk products, get lots of sunlight, supplementation of calcium AEP and alpha lipoic acid. Progesterone creme has been found to promote regrowth of myelin sheaths in animals.

Health Effects from Dental Personnel Exposure to Mercury Vapor

Dental offices are known to be one of the largest users of inorganic mercury. It is well documented that dentists and dental personnel who work with amalgam are chronically exposed to mercury vapor, which accumulates in their bodies to much higher levels than for most non-occupationally exposed. Adverse health effects of this exposure including subtle neurological effects have also been well documented that affect most dentists and dental assistants, with measurable effects among those in the lowest levels of exposure. Mercury levels of dental personnel average at least two times that of controls for hair, urine, toenails, and for blood.

A U.S. national sample of dentists provided by the American Dental Association (ADA) had an average of 5.2 ug/L. In that large sample of dentists, 10% of dentists had urine mercury levels over 10.4 ug/L and 1% had levels over 33.4ug/L, indicating daily exposure levels of over 100 ug/day. Researchers from the University of Washington School of Dentistry and Deptartment of Chemistry tested a sample of dentists at an annual ADA meeting. The study found that the dentists had a significant body burden of mercury, and the group with higher levels of mercury had significantly more adverse health conditions than the group with lower exposure. The increased effects in the group with more mercury exposure included mood disturbances, memory deficits, fatigue, confusion, anxiety, and delay in simple reaction time.

Mercury excretion levels were found to have a positive correlation with the number of amalgams placed or replaced per week, the number of amalgams polished each week, and with the number of fillings in the dentist. In one study, each filling was found to increase mercury in the urine approximately 3%, although the relationship was nonlinear and increased more with larger number of fillings. Much higher accumulated body burden levels in dental personnel were found based on challenge tests than for controls, with excretion levels after a dose of a chelator as high as ten times the corresponding levels for controls. Autopsy studies have found similar high body accumulation in dental workers. Autopsies of former dental staff found levels of mercury in the pituitary gland averaged as high as 4,040 ppb. They also found much higher levels in the brain occipital cortex (as high as 300 ppb), renal cortex (as high as 2110 ppb) and thyroid (as high as 28,000 ppb). In general, dental assistants and women dental workers showed higher levels of mercury than male dentists.

Mercury levels in blood of dental professionals ranged from 0.6 to 57 ug/L, with study averages ranging from 1.34 to 9.8 ug/L. A review of several studies of mercury level in hair or nails of dentists and dental workers found median levels were 50 to 300% more than those of controls. Dentists have been found to have elevated skeletal mercury levels, which has been found to be a factor in osteoporosis, as well as mercury retention and kidney effects that tend to cause lower measured levels of mercury in urine tests. A group of dental students taking a course involving work with amalgam had their urine tested before and after the course was over. The average urine level increased by 500% during the course. Allergy tests given to another group of dental students found 44% of them were allergic to mercury. Studies have found that the longer time exposed, the more likely to be allergic and the more effects. One study found that over a four year period of dental school, the sensitivity rate increased to over 10%. Another group of dental students had similar results, while another group of dental student showed compromised immune systems compared to medical students. The total lymphocyte count, total T cell numbers (CD3), T helper/ inducer (CD4+CD8-), and T suppressor/cytotoxic (CD4-CD8+) numbers were significantly elevated in the dental students compared to the matched control group. Similar results have been seen in other studies as well.

More than 10,000 dental assistants were exposed to extremely high concentrations of mercury fumes, while working with amalgam in dental offices during the 60s, 80s, and early 90s. 25% of them report they often or very often have neurological problems. They have been compared with a group of nurses of the same age. Dental assistants scored much higher than nurses on four health problems: tremor/shaking; heart and lung problems, depression, and lack of memory/memory failure.

Urinary porphyrin profiles were found to be an excellent biomarker of level of body mercury level and mercury damage neurological effects, with coproporphyrin significantly higher in those with higher mercury exposure and urine levels. Coproporphyrin levels have a higher correlation with symptoms and body mercury levels as tested by challenge test, but care should be taken regarding challenge tests as the high levels of mercury released can cause serious health effects in some, especially those who still have amalgam fillings or high accumulations of mercury.

Use of high speed drill in removal or replacement has been found to create a high volume of mercury vapor and breathable particles, and dental masks only filter out about 40 % of such particles. Amalgam dust generated by high speed drilling is absorbed rapidly into the blood through the lungs and major organs receive a high dose within minutes. This produces high levels of exposure to patient and dental staff and common adverse health effects. Use of water spray, high velocity evacuation, and rubber dams reduce exposure to patient and dental staff significantly. In addition to these measures, researchers also advise all dental staff to wear face masks and patients be supplied with outside air. Some studies note that carpeting and rugs in dental offices should be avoided as it is a major repository of mercury.

Dentists were found to score significantly worse than a comparable control group on neurobehavioral tests of motor speed, visual scanning, and visuomotor coordination, concentration, verbal memory, visual memory, and emotional/mood tests. Test performance was found to be proportional to exposure/body levels of mercury. Significant adverse neurobehavioral effects were found even for dental personnel receiving low exposure levels(less than 4 ug/l Hg in urine). This study was for dental personnel having mercury excretion levels below the 10th percentile of the overall dental population. Such levels are also common among the general population of non-dental personnel with several fillings. This study used a new methodology which used standard urine mercury levels as a measure of recent exposure, and urine levels after chelation with a chemical, DMPS, to measure body burden mercury levels.

30% of dentists with more than average exposure were found to have neuropathies and visuographic dysfunction. Mercury exposure has been found to often cause disability in dental workers.

Chelators like DMPS have been found to release mercury from cells. This method was found to give enhanced precision and power to the results of the tests and correlations. Even at the low levels of exposure of the subjects of this study, there were clearly demonstrated differences in test scores involving memory, mood, and motor skills related to the level of exposure pre and post chelation. Those with higher levels of mercury had deficits in memory, mood, and motor function compared to those with lower exposure levels. Mood scores, including anger, were found to correlate more strongly with pre-chelation urine mercury levels; while toxicity symptoms, concentration, memory (vocabulary, word), and motor function correlated more strongly with post-chelation mercury levels. Another study using DMPS challenge test found over 20 times higher mercury excretion in dentists than in controls, indicating high body burden of mercury compared to controls.
Many dentists have been documented to suffer from mercury poisoning other than the documented neurological effects, such as chronic fatigue, muscle pains, stomach problems, tremors, motor effects, immune reactivity, etc. One of the common effects of chronic mercury exposure is chronic fatigue due to immune system overload and activation. Many studies have found this occurs frequently in dentists and dental staff along with other related symptoms. In a group of dentists and dental workers suffering from extreme fatigue and tested by the immune test MELISA, 50% had autoimmune reaction to inorganic mercury and immune reactions to other metals used in dentistry were also common. Tests of controls did not find such immune reactions common. In another study, nearly 50 % of dental staff in a group tested had positive autoimmune ANA titers compared to less than 1 % of the general population.

One dentist with severe symptoms similar to ALS improved after treatment for mercury poisoning, and another with Parkinson’s disease recovered after reduction of exposure and chelation. Similar cases among those with other occupational exposure have been seen. A survey of over 60,000 U.S. dentists and dental assistants with chronic exposure to mercury vapor and anesthetics found increased health problems compared to controls, including significantly higher liver, kidney, and neurological diseases. A study in Scotland found similar results. Other studies reviewed found increased rates of brain cancer and allergies. Swedish male dentists were found to have an elevated standardized mortality ratio compared to other male academic groups. Dentists were also found to have a high incidence of radicular muscular neuralgia and peripheral sensory degradation. In one study of dentists and dental assistants, 50% reported significant irritability, 46% arthritic pains, and 45% headaches, while another study found selective atrophy of muscle fibre in women dental workers. In a study in Brazil, 62% of dental workers had urine mercury levels over 10 mg/L, and indications of mild to moderate mercury poisoning in 62% of workers. The most common problems were related to the central nervous system.

Both dental hygienists and patients get high doses of mercury vapor when dental hygienists polish or use ultrasonic scalers on amalgam surfaces. Pregnant women or pregnant hygienist especially should avoid these practices during pregnancy or while nursing since maternal mercury exposure has been shown to affect the fetus and to be related to birth defects, SIDS, etc. Amalgam has been shown to be the main source of mercury in most infants and breast milk, which often contain higher mercury levels than in the mother’s blood. Because of high documented exposure levels when amalgam fillings are brushed, dental hygienists are advised not to polish dental amalgams when cleaning teeth. Face masks worn by dental workers filter out only about 40% of small dislodged amalgam particles from drilling or polishing, and very little mercury vapor. Korean dental technicians have a high incidence of contact dermatitis, with dental metals the most common sensitizers. Over 25% had contact dermatitis with over 10% sensitive to 5 metals, cromium, mercury, nickel, cobalt, and palladium. Another study found a high prevalence of extrapyramidal signs and symptoms (tremor) in a group of male dental technicians working in a state technical high school in Rome.

An epidemiological survey conducted in Lithuania on women working in dental offices (where Hg concentrations were 80 ug/M3) had increased incidence of spontaneous abortions and breast pathologies that were directly related to the length of time on the job. A large U.S. survey also found higher spontaneous abortion rates among dental assistants and wives of dentists, and another study found an increased risk of spontaneous abortions and other pregnancy complications among women working in dental surgeries. A study of dentist and dental assistants in the Netherlands found 50% higher rates of spontaneous abortions, stillbirths, and congenital defects than for the control group, with unusually high occurrence of spina bifida. A study in Poland also found a significant positive association between mercury levels and occurrence of reproductive failures and menstrual cycle disorders and concluded dental work to be an occupational hazard with respect to reproductive processes.

Body burden increases with time and older dentists have median mercury urine levels about four times those of controls, as well as higher brain and body burdens, and poor performance on memory tests. Some older dentists have mercury levels in some parts of the brain as much as 80 times higher than normal levels. Dentists and dental personnel experience significantly higher levels of neurological, memory, musculoskeletal, visiomotor, mood, and behavioral problems, which increase with years of exposure. Most studies find dentists have increased levels of irritability and tension, high rates of drug dependency and disability due to psychological problems, and higher suicide rates than the general white population, but one study found rates in same range as doctors.

Female dental technicians who work with amalgam tend to have increased menstrual disturbances, significantly reduced fertility and lowered probability of conception, increased spontaneous abortions, and their children have significantly lower average IQ compared to the general population. Populations with only slightly increased levels of mercury in hair had decreases in academic ability. Effects are directly related to length of time on the job. The level of mercury excreted in urine is significantly higher for female dental assistants than dentists due to biological factors. Several dental assistants have been diagnosed with mercury toxicity and some have died of related health effects. From the medical register of births since 1967 in Norway, it can be seen that dental nurse/assistants have a clearly increased risk of having a deformed child or spontaneous abortion. Female dentists have increased rates of spontaneous abortion and perinatal mortality, compared to controls. A study in Poland found a much higher incidence of birth defects among female dentist and dental assistants than normal. A chronically ill dental nurse diagnosed with mercury sensitivity recovered after replacement of fillings and changing jobs, and a female dentist recovered from Parkinson’s after mercury detox. Some studies have found increased risk of lung, kidney, brain, and CNS system cancers among dental workers.

References

Denton S. The mercury cover-up: Controversies in dentistry. Townsend Letter For Doctors. 1990: 488-491.

Marlowe M, et al. Main and interactive effects of metallic toxins on classroom behavior. J Abnormal Child Psychol. 1985; 13(2): 185-98.

Moon C, et al. Main and interactive effect of metallic pollutants on cognitive functioning. Journal of Learning Disabilities. 1985.

Pihl RO, et al. Hair element content in learning disabled children. Science. 1977; 198: 204-6.

Gowdy JM, et al. Whole blood mercury in mental hospital patients. Am J Psychiatry. 1978; 135(1): 115-7.

Lee IP. Effects of mercury on spermatogenesis. J Pharmacol Exp Thera. 1975; 194(1): 171-181.

Ben-Ozer EY, Rosenspire AJ, et al. Mercuric chloride damages cellular DNA by a non-apoptotic mechanism. Mutat Res. 2000; 470(1):19-27.

Ogura H, Takeuchi T, Morimoto K. A comparison of chromosome aberrations and micronucleus techniques for the assessment of the genotoxicity of mercury compounds in human blood lymphocytes. Mutat Res. 1996; 340(2-3):175-82.

Klinghardt D. Migraines, seizures, and mercury toxicity. Future Medicine Publishing. 1997.

Klinghardt D. Migraines, seizures, and mercury toxicity. Alternative Medicine Magazine. 1997; 21.

Klinghardt D. A series of fibromyalgia cases treated for heavy metal toxicity: Case report and hypothesis. Journal of Orthopaedic Medicine. 2001; 23: 58-59.

Schulein TM, et al. Survey of Des Moines area dental offices for mercury vapor. Iowa Dent. J. 1984; 70(1): 35-36.

Jones DW, et al. Survey of mercury vapor in dental offices in Atlantic Canada. Can. Dent. Assoc. J. 1983; 4906: 378-395.

Miller RW, et al. Report on independent survey taken of Austin dental offices for mercury contamination. Texas Dent. J. 1983; 100(1): 6-9.

Skuba A. Survey for mercury vapor in Manitoba dental offices. J Can. Dent. Assoc. 1984; 50(7): 517-522.

Roydhouse RH, et al. Mercury in dental offices. J Can Dent Assoc. 1985; 51(2): 156-158.

McNerney RT, et al. Mercury contamination in the dental office: A Review. NYS Dental Journal. 1979: 457-458.

Kantor L, et al. Mercury vapor in the dental office: Does carpeting make a difference? JADA. 1981; 103(9): 402-407.

Chop GF, et al. Mercury vapor related to manipulation of amalgam and to floor surfaces. Oper. Dent. 1983; 8(1): 23-27.

Battistone GC, et al. Mercury as occupational hazard in dentistry. Clinical Chemistry and Chemical Toxicity of Metals. 1977; 219: 205-8.

Gerhard I, Monga B, Waldbrenner A, Runnebaum B. Heavy metals and fertility. J of Toxicology and Environmental Health, Part A. 1998; 54(8): 593-611.

Gerhard I, Waibel S, Daniel V, Runnebaum B. Impact of heavy metals on hormonal and immunological factors in women with repeated miscarriages. Hum Reprod Update. 1998; 4(3): 301-309.

Gerhard I, Waldbrenner P, Thuro H, Runnebaum B. Diagnosis of heavy metal loading by the oral DMPS and chewing gum tests. Klinisches Labor. 1992; 38: 404-411.

Gordon HP, Cordon LD. Reduction in mercury vapor levels in Seattle dental offices. J Dent Res Abstract. 1981; 1092, 57A: 347.

Lamm O, et al. Subclinical effects of exposure to inorganic mercury revealed by somatosensory-evoked potentials. Eur Neurol. 1985; 24: 237-243.

Altmann L, Sveinsson K. Visual evoked potentials in 6 year old children in relation to mercury and lead levels. Neurotoxicol Teratol. 1998; 20(1): 9-17.

Chang YC, Yeh CY, Wang JD. Subclinical neurotoxicity of mercury vapor revealed by a multimodality potential study of chloralkali workers. Immunol. 1995; 117(3): 482-8.

Hussain S, et al. Mercuric chloride-induced reactive oxygen species and its effect on antioxidant enzymes in different regions of rat brain. J Environ Sci Health B. 1997; 32(3): 395-409.

Bulat P. Activity of Gpx and SOD in workers occupationally exposed to mercury. Arch Occup Environ Health. 1998; 71: S37-9.

Stohs SJ, Bagchi D. Oxidative mechanisms in the toxicity of metal ions. Free Radic Biol Med. 1995; 18(2): 321-36.

Jay D. Glutathione inhibits SOD activity of Hg. Arch Inst cardiol Mex. 1998; 68(6): 457-61.

Tan S, et al. Oxidative stress induces programmed cell death in neuronal cells. J Neurochem. 1998; 71(1): 95-105.

Matsuda T, Takuma K, Lee E, et al. Apoptosis of astroglial cells. Nippon Yakurigaku Zasshi. 1998; 112(1): 24.

Lee YW, Ha MS, Kim YK. Role of reactive oxygen species and glutathione in inorganic mercury-induced injury in human glioma cells. Neurochem Res. 2001; 26(11): 1187-93.

Ho PI, Ortiz D, Rogers E, Shea TB. Multiple aspects of homocysteine neurotoxicity: Glutamate excitotoxicity, kinase hyperactivation and DNA damage. J Neurosci Res. 2002; 70(5): 694-702.

Pizzichini M, et al. Influence of amalgam fillings on Hg levels and total antioxidant activity in plasma of healthy donars. Sci Total Environ. 2003; 301(1-3): 43-50.

Valko M, Morris H, Cronin MT. Metals, toxicity and oxidative stress. Curr Med Chem. 2005; 12(10): 1161-208.

Nylander M, et al. Mercury concentrations in the human brain and kidneys and exposure from amalgam fillings. Swed Dent J. 1987; 11: 179-187.

Barregard L, Svalander C, Schutz A, et al. Cadmium, mercury, and lead in kidney cortex of the general Swedish population: A study of biopsies from living kidney donors. Environ Health Perspect. 1999; 107(11): 867-871.

Eggleston DW, et al. Correlation of dental amalgam with mercury in brain tissue. J Prosthet Dent. 1987; 58(6): 704-7.

Grandi M. Dental amalgam and mercury levels in autopsy tissues. Am J Forensic Med Pathol. 2006; 27(1): 42-5.

Svare CW, et al. The effects of dental amalgam on mercury levels in expired air. J. Dent. Res. 1981; 60(9):1668-1671.

Patterson JE. Mercury in human breath from dental amalgams. Bull Env Contam Toxicol. 1985; 34: 459.

Ott K, et al. Mercury burden due to amalgam fillings. Dtsch. Zahnarztl Z. 1984; 39(9): 199-205.

Lichtenberg H. Mercury vapor in the oral cavity in relation to number of amalgam surfaces and the classic symptoms of chronic mercury poisoning. J Orthomol Med. 1996; 11(2): 87-94.

Abraham J, Svare C, et al. The effects of dental amalgam restorations on blood mercury levels. J. Dent. Res. 1984; 63(1): 71-73.

Snapp KR, Boyer DB, Peterson LC, Svare CW. The contribution of dental amalgam to mercury in blood. J Dent Res. 1989; 68(5): 780-5.

Vimy MJ, Lorscheider FL. Intra oral mercury released from dental amalgams and estimation of daily dose. J. Dent Res. 1985; 64(8): 1069-1075.

Lorscheider FL, et al. Evaluation of the safety issue of mercury release from amalgam fillings. FASEB J. 1993; 7: 1432-33.

Holland RI. Galvanic currents between gold and amalgam. Scand J Dent Res. 1980; 88: 269-72.

Wang Chen CP, Greener EH. A galvanic study of different amalgams. Journal of Oral Rehabilitation. 1977; 4: 23-7.

Lemons JE, et al. Intraoral corrosion resulting from coupling dental implants and restorative metallic systems. Implant Dent. 1992; 1(2): 107-112.

Vimy MJ, Takahashi Y, Lorscheider FL. Maternal-fetal distribution of mercury released from dental amalgam fillings. Amer. J. Physiol. 1990; 258: R939-945.

Boyd ND, Vimy J, et al. Mercury from dental “silver” tooth fillings impairs sheep kidney function. Am. J. Physiol. 1991; 261: R1010-R1014.

Hahn L, et al. Distribution of mercury released from amalgam fillings into monkey tissues. FASEB J. 1990; 4: 5536.

Takahashi Y, Tsuruta S, Hasegawa J, Kameyama Y, Yoshida M. Release of mercury from dental amalgam fillings in pregnant rats and distribution of mercury in maternal and fetal tissues. Toxicology. 2001; 163(2-3): 115-26.

Galic N, Ferencic Z, et al. Dental amalgam mercury exposure in rats. Biometals. 1999; 12(3): 227-31.

Arvidson B, Arvidsson J, Johansson K. Mercury deposits in neurons of the trigeminal ganglia after insertion of dental amalgam in rats. Biometals. 1994; 7(3): 261-3.

Danscher G, Horsted-Bindslev P, Rungby J. Traces of mercury in organs from primates with amalgam fillings. Exp Mol Pathol. 1990; 52(3): 291-9.

Kuhnert P, et al. Comparison of mercury levels in maternal blood fetal cord blood and placental tissue. Am. J. Obstet and Gynecol. 1981; 139: 209-212.

Vahter M, Akesson A, Lind B, Bjors U, Schutz A, Berglund M. Longitudinal study of methylmercury and inorganic mercury in blood and urine of pregnant and lactating women, as well as in umbilical cord blood. Environ Res. 2000; 84(2): 186-94.

Kuntz WD. Maternal and cord blood mercury background levels: Longitudinal surveillance. Am J Obstet and Gynecol. 1982; 143(4): 440-443.

Ramirez GB, Cruz MC, Pagulayan O, Ostrea E, Dalisay C. The Tagum study I: Analysis and clinical correlates of mercury in maternal and cord blood, breast milk, meconium, and infants’ hair. Pediatrics. 2000; 106(4): 774-81.

Ramirez GB, Pagulayan O, Akagi H, Francisco Rivera A, Lee LV, Berroya A, Vince Cruz MC, Casintahan D. Tagum study II: Follow-up study at two years of age after prenatal exposure to mercury. Pediatrics. 2003; 111(3): e289-95.

Roshan D, Curzon ME, Fairpo CG. Changes in dentists’ attitudes and practice in paediatric dentistry. Eur J Paediatr Dent. 2003; 4(1): 21-7.

Taifour D, Frencken JE, Beiruti N, et al. Effectiveness of glass-ionomer (ART) and amalgam restorations in the deciduous dentition: results after 3 years. Caries Res. 2002; 36(6): 437-44.

Brodsky JB. Occupational exposure to mercury in dentistry and pregnancy outcome. JADA. 1985; 111(11): 779-780.

Malmstrom C. Amalgam derived mercury in feces. Journal of Trace Elements in Experimental Medicine. 1992; 5.

Zamm AF. Removal of dental mercury: often an effective treatment for very sensitive patients. J Orthomolecular Med. 1990; 5(53): 138-142.

Hartman DE. Missed diagnoses and misdiagnoses of environmental toxicant exposure, MCS. Psychiatr Clin North Am. 1998; 21(3): 659-70.

Schmidt F, et al. Mercury in urine of employees exposed to magnetic fields. Tidsskr Nor Laegeforen. 1997; 117(2): 199-202.

Granlund-Lind R, Lans M, Rennerfelt J. Computers and amalgam are the most common causes of hypersensitivity to electricity according to sufferers’ reports. Läkartidningen. 2002; 99: 682-683.

Ortendahl T W, Hogstedt P, Holland RP. Mercury vapor release from dental amalgam in vitro caused by magnetic fields generated by CRT’s. Swed Dent J. 1991: 31.

Bergdahl J, Anneroth G, Stenman E. Description of persons with symptoms presumed to be caused by electricity or visual display units—oral aspects. Scand J Dent Res. 1994; 102(1): 41-5.

Mortazavi SM, Daiee E, Yazdi A, et al. Mercury release from dental amalgam restorations after magnetic resonance imaging and following mobile phone use. Pak J Biol Sci. 2008; 11(8): 1142-6.

Goldschmidt, et al. Effects of amalgam corrosion products on human cells. J. Perio. Res., 1976; 11: 108-115.

Trivedi, Talim. The response of human gingiva to restorative materials. J. Prosth. Dentistry. 1973; 29: 73-81.

Mareck, Hockman. Simulated crevice corrosion experiment for ph and solution chemistry determinations. Corrosion. 1974; 23: 1000-1006.

Till T, et al. Mercury release from amalgam fillings and oral dysbacteriosis as a cause of resorption phenomena. ZWR. 1978; 87: 1130-1134.

Olsson S, et al. Release of elements due to electrochemical corrosion of dental amalgam. J of Dental Research. 1994; 73: 33-43.

Freden H, et al. Mercury in gingival tissues adjacent to amalgam fillings. Odontal Revy. 1974; 25(2): 207-210.

Horsted-Binslev P, Danscher G. Dentinal and pulpal uptake of mercury from lined and unlined amalgam restorations. Eur J Oral Sci. 1997; 105: 338-43.

Cook TA, et al. Fatal mercury intoxication in a dental surgery assistant. British Dent Journal. 1969; 127: 533-555.

Markovich, et al. Heavy metals (Hg, Cd) inhibit the activity of the liver and kidney sulfate transporter Sat-1. Toxicol Appl Pharmacol. 1999; 154(2): 181-7.

McFadden SA. Xenobiotic metabolism and adverse environmental response: sulfur-dependent detox pathways. Toxicology. 1996; 111(1-3): 43-65.

Alberti A, Pirrone P, Elia M, Waring RH, Romano C. Sulphation deficit in low-functioning autistic children. Biol Psychiatry. 1999; 46(3): 420-4.

Henriksson J, Tjalve H. Uptake of inorganic mercury in the olfactory bulbs via olfactory pathways in rats. Environ Res. 1998; 77(2): 130-40.

Anttila, et al. Effects of paternal occupation exposure to lead or mercury on spontaneous abortion. J of Occup & Environ Med. 1995; 37(8): 915-21.

Cordier S, Deplan F, Mandereau L. Hemon D. Paternal exposure to mercury and spontaneous abortions. Br J Ind Med. 1991; 48(6): 375-81.

Savitz DA, Sonnenfeld NL. Olshan AF. Review of epidemiologic studies of paternal occupational exposure and spontaneous abortion. Am J Ind Med. 1994; 25(3): 361-83.

Mohamed, et al. Laser light scattering study of the toxic effects of methylmercury on sperm motility. J Androl. 1986; 7(1): 11-15.

Podzimek S, Prochazkova J, Bultasova L, et al. Sensitization to inorganic mercury could be a risk factor for infertility. Neuro Endocrinol Lett. 2005; 26(4): 277-82.

Inouye M, et al. Behavioral and neuropathological effects of prenatal methyl mercury exposure in mice. Neurobehav Toxicol Teratol. 1985; 7: 227-232.

Annau Z, et al. Mechanisms of neurotoxicity and their relationships to behavioral changes. Toxicology. 1988; 49(2): 219-25.

Vinay SD, Sood PP. Inability of thiol compounds to restore CNS arylsulfatases inhibited by methyl mercury. Pharmacol Toxicol. 1991; 69(1): 71-4.

Grandjean P, et al. MeHg and neurotoxicity in children. Am J Epidemiol. 1999; 150(3): 301-5.

Budtz-Jorgensen E, Grandjean P, Keiding N, White RF, Weihe P. Benchmark dose calculations of methylmercury-associated neurobehavioral deficits. Toxicol Lett. 2000; 15(112-113): 193.

Crump KS, Kjellstrom T, Shipp AM, Silvers A, Stewart A. Influence of prenatal mercury exposure upon scholastic and psychological test performance: Benchmark analysis of a New Zealand cohort. Risk Anal. 1998; 18(6): 701-13.

Grandjean P, Weihe P, Murata K, Sorensen N, Dahl R, Jorgensen PJ. Cognitive deficit in 7-year-old children with prenatal exposure to methylmercury. Neurotoxicol Teratol. 1997; 19(6): 417-28.

Prati M, Gornati R, Boracchi P, et al. A comparative study of the toxicity of mercury dichloride and methylmercury, assayed by the Frog Embryo Teratogenesis Assay–Xenopus (FETAX). Altern Lab Anim. 2002; 30(1): 23-32.

Babich, et al. The mediation of mutagenicity and clastogenicity of heavy metals by physiochemical factors. Environ Res. 1985; 37: 253-286.

Hansen K, et al. A survey of metal induced mutagenicity in vitro and in vivo. J Amer Coll Toxicol. 1984; 3: 381-430.

Rodgers JS, Hocker JR, et al. Mercuric ion inhibition of eukaryotic transcription factor binding to DNA. Biochem Pharmacol. 2001; 61(12): 1543-50.

Knapp LT, Klann E. Superoxide-induced stimulation of protein kinase C via thiol modification and modulation of zinc content. J Biol Chem. 2000.

Jenner P. Oxidative mechanisms in PD. Mov Disord. 1998; 13(1): 24-34.

Offen D, et al. Antibodies from ALS patients inhibit dopamine release mediated by L-type calcium channels. Neurology. 1998; 51(4): 1100-3.

Rajanna B, et al. Modulation of protein kinase C by heavy metals. Toxicol Lett. 1995; 81(2-3): 197-203.

Badou A, et al. HgCl2-induced IL-4 gene expression in T cells involves a protein kinase C-dependent calcium influx through L-type calcium channels. J Biol Chem. 1997; 272(51): 32411-8.

Veprintsev DB. Pb2+ and Hg2+ binding to alpha-lactalbumin. Biochem Mol Biol Int. 1996; 39(6): 1255-65.

Verchaeve L, et al. Comparative in vitro cytogenetic studies in mercury exposed human lymphocytes. Mutation Res. 1985; 157: 221-226.

Pelletier L, et al. In vivo self-reactivity of mononuclear cells to T cells and macrophages exposed to Hg Cl2. Eur. J Immun. 1985: 460-465.

Pelletier, et al. Autoreactive T cells in mercury induced autoimmune disease. J Immunol. 1986; 137(8): 2548-54.

Kubicka M, et al. Autoimmune disease induced by mercuric chloride. Int Arch Allergy. Immunol. 1996; 109(1): 11-20.

Buchner A, et al. Amalgam tattoo of the oral mucosa: A clinicopatholigic study of 268 cases. Surg Oral Med Oral Pathol. 1980; 49(2): 139-47.

Forsell M, et al. Mercury content in amalgam tattoos of human oral mucosa and its relation to local tissue reactions. Euro J Oral Sci. 1998; 106(1): 582-7.

Weaver T, Auclair PL. Amalgam tattoo as a cause of local and systemic disease? Oral Surg. Oral Med. Oral Pathol. 1987; 63: 137-40.

Staines KS, Wray D. Amalgam-tattoo-associated oral lichenoid lesion. Contact Dermatitis. 2007 Apr; 56(4): 240-1.

Arvidson K. Corrosion studies of dental gold alloy in contact with amalgam. Swed. Dent. J. 1984; 68: 135-139.

Kingman A, Albertini T, Brown LJ. Mercury concentrations in urine and blood associated with amalgam exposure in the U.S. military population. J Dent Res. 1998; 77(3): 461-71.

Sin YM, Teh WF, Wong MK, Reddy PK. Effect of mercury on glutathione and thyroid hormones. Bulletin of Environmental Contamination and Toxicology. 1990; 44(4): 616-622.

Kawada J, et al. Effects of inorganic and methylmercury on thyroidal function. J Pharmacobiodyn. 1980; 3(3): 149-59.

Kabuto M. Chronic effects of methylmercury on the urinary excretion of catecholamines and their responses to hypoglycemic stress. Arch Toxicol. 1991; 65(2): 164-7.

Heintze, et al. Methylation of Mercury from dental amalgam and mercuric chloride by oral streptococci. Scan. J. Dent. Res. 1983; 91: 150-152.

Rowland, Grasso, Davies. The methylation of mercuric chloride by human intestinal bacteria. Experientia. Basel. 1975; 31: 1064-1065.

Hamdy MK, et al. Formation of methyl mercury by bacteria. App Microbiol. 1975.

Brun A, Abdulla M, Ihse I, Samuelsson B. Uptake and localization of mercury in the brain of rats after prolonged oral feeding with mercuric chloride. Histochemistry. 1976; 47(1): 23-9.

Ludwicki JK. Studies on the role of gastrointestinal tract contents in the methylation of inorganic mercury compounds. Bull Env Contam Toxicol. 1989; 42: 283-288.

Choi SC, Bartha R. Cobalamin-mediated mercury methylation by desulfovibrio desulfuricans LS. Appl Environ Microbiol. 1993; 59(1): 290-5.

Guzzi G, Minoia C, Pigatto PD, Severi G. Methylmercury, amalgams, and children’s health. Environ Health Perspect. 2006; 114: 149.

Szasz A, Barna B, Gajda Z, Galbacs G, Kirsch-Volders M, Szente M. Effects of continuous low-dose exposure to organic and inorganic mercury during development on epileptogenicity in rats.
Neurotoxicology. 2002; 23(2): 197-206.

Lund ME, et al. Treatment of acute MeHg poisoning by NAC. J Toxicol Clin Toxicol. 1984; 22(1): 31-49.

Livardjani F, Ledig M, Kopp P, Dahlet M, Leroy M, Jaeger A. Lung and blood superoxide dismutase activity in mercury vapor exposed rats: Effect of N-acetylcysteine treatment. Toxicology. 1991; 66(3): 289-95.

Dickman MD, Leung KM. Hong Kong subfertility links to mercury in human hair and fish. Sci Total Environ. 1998; 214: 165-74.

Gerhar I, Wallis E. Individualized homeopathic therapy for male infertility. Homeopathy. 2002; 91(3): 133-44.

Nicole A, et al. Direct evidence for glutathione as mediator of apoptosis in neuronal cells. Biomed Pharmacother. 1998; 52(9): 349-55.

Spencer JP, et al. Cysteine & GSH in PD mechanisms involving ROS. J Neurochem. 1998; 71(5): 2112-22.

Bains JS, et al. Neurodegenerative disorders in humans and role of glutathione in oxidative stress mediated neuronal death. Brain Res Rev. 1997; 25(3): 335-58.

Medina S, Martinez M, Hernanz A. Antioxidants inhibit the human cortical neuron apoptosis induced by hydrogen peroxide, tumor necrosis factor alpha, dopamine and beta-amyloid peptide 1-42. Free Radic Res. 2002; 36(11): 1179-84.

Offen D, et al. Use of thiols in treatment of PD. Exp Neurol. 1996; 141(1): 32-9.

Pocernich CB, et al. Glutathione elevation and its protective role in acrolein-induced protein damage in synaptosomal membranes: relevance to brain lipid peroxidation in neurodegenerative disease. Neurochem Int. 2001; 39(2): 141-9.

Pearce RK, Owen A, Daniel S, Jenner P, Marsden CD. Alterations in the distribution of glutathione in the substantia nigra in Parkinson’s disease. J Neural Transm. 1997; 104(6-7): 661-77.

Shen XM, et al. Neurobehavioral effects of NAC conjugates of dopamine: Possible relevance for Parkinson’s disease. Chem Res Toxicol. 1996; 9(7): 1117-26.

Li H, Shen XM, Dryhurst G. Brain mitochondria catalyze the oxidation of 7-(2-aminoethyl)-3,4-dihydro-5-hydroxy-2H-1,4-benzothiazine-3-carboxyli c acid (DHBT-1) to intermediates that irreversibly inhibit complex I and scavenge glutathione: potential relevance to the pathogenesis of Parkinson’s disease. J Neurochem. 1998; 71(5): 2049-62.

Araragi S, Sato M, et al. Mercuric chloride induces apoptosis via a mitochondrial-dependent pathway in human leukemia cells. Toxicology. 2003; 184(1): 1-9.

Campbell N, Godfrey M. Confirmation of mercury retention and toxicity using DMPS provocation. J of Advancement in Medicine. 1994; 7(1).

Kostial K, et al. Decreased Hg retention with DMSA. J Appl Toxicol. 1993; 13(5): 321-5.

Frustaci A, et al. Marked elevation of myocardial trace elements in idiopathic dilated cardiomyopathy. J of American College of Cardiology. 1999; 33(6): 1578-83.

Husten L. Trace elements linked to cardiomyopathy. Lancet. 1999; 353(9164): 1594.

Vassalo DV. Effects of mercury on the isolated heart muscle are prevented by DTT and cysteine. Toxicol Appl Pharmacol. 1999; 156(2): 113-8.

Ilblack NG, et al. New aspects of murine coxsackie B3 mycocarditis: Focus on heavy metals. European Heart J. 1995; 16: 20-4.

Lorscheider F, Vimy M. Mercury and idiopathic dilated cardiomyopathy. J Am Coll Cardiol. 2000; 35(3): 819-20.

Souza de Assis GP, et al. Effects of small concentrations of mercury on the contractile activity of the rat ventricular myocardium. Comp Biochem Physiol C Toxicol Pharmacol. 2003; 134(3): 375-83.

VDM Stejskal, et al. MELISA: Tool for the study of metal allergy. Toxicology in Vitro. 1994; 8(5): 991-1000.

Stejskal VD, Danersund A, Lindvall A, et al. Metal-specific lymphocytes: Biomarkers of sensitivity in man. Neuroendocrinology Letters. 1998.

Lutz E, et al. Concentrations of mercury in brain and kidney of fetuses and infants. Journal of Trace Elements in Medicine and Biology. 1996; 10: 61-67.

Drasch G, et al. Mercury burden of human fetal and infant tissues. Eur J Pediatr. 1994; 153: 607-610.

Peiper K, et al. Study of mercury uptake in dental students. Dtsch Zahnarzt Z. 1989; 44(9): 714.

Steinberg D, Grauer F, Niv Y, Perlyte M, Kopolivic K. Mercury among dental personnel in Israel. Med Sci. 1995; 31(7): 428-32.

Fung YK, et al. In vivo mercury and methylmercury levels in patients at different intervals after amalgam restorations. Northwest Dent. 1991; 70(3): 23-6.

Thompson CM, Markesbery WR, et al. Regional brain trace-element studies in Alzheimer’s disease. Neurotoxicology. 1988; 9(1): 1-7.

Hock, et al. Increased blood mercury levels in Alzheimer’s patients. Neural. Transm. 1998; 105: 59-68.

Cornett, et al. Imbalances of trace elements related to oxidative damage in Alzheimer’s diseased brain. Neurotoxicolgy. 1998; 19: 339-345.

Vance DE, Ehmann WD, Markesbery WR. A search for longitudinal variations in trace element levels in nails of Alzheimer’s disease patients. Biol Trace Elem Res. 1990; 26-27: 461-70.

Gonzalez-Ramirez D, et al. Urinary mercury, porphyrins, and neurobehavioral changes of dental workers in Monterrey, Mexico. J Pharmocology and Experimental Therapeutics. 1995; 272(1):
264-274.

Echeverria D, et al. Behavioral effects of low level exposure to Hg vapor among dentists. Neurotoxicology & Teratology. 1995; 17(2): 161-168.

Foo SC, et al. Neurobehavioral effects in occupational chemical exposure. Environmental Research. 1993; 60(2): 267-273.

Mantyla DG, et al. Mercury toxicity in the dental office: a neglected problem. JADA. 1976; 92: 1189-1194.

Symington D. Mercury poisoning in dentists. J Soc Occup Med. 1980; 30: 37-39.

Smith DL. Mental effects of mercury poisoning. South Med J. 1978; 71: 904-5.

Cianciola ME, et al. Epidemiologic assessment of measures used to indicate exposure to mercury vapor. Toxicol Eniviron Health. 1997; 52(1): 19-33.

Bittner AC, et al. Behavior effects of low level mercury exposure among dental professionals. Neurotoxicology & Teratology. 1998; 20(4): 429-39.

Katsunuma, et al. Anaphylaxis improvement after removal of amalgam fillings. Annals of Allergy. 1990; 64(5): 472-75.

Yoshida S, Mikami H, Nakagawa H, Amayasu H. Amalgam allergy associated with exacerbation of aspirin-intolerant asthma. Clin Exp Allergy. 1999; 29(10): 1412-4.

Drouet M, et al. Is mercury a respiratory tract allergen? Allerg Immunol(Paris). 1990; 22(3): 81.

Schulte A, et al. Mercury concentrations in children with and without amalgam restorations. J. Dent Res. 1980; 73(4): A-334.

Becker K, Seifert B. German environmental survey 1998 (GerES III): Environmental pollutants in blood of the German population. Int J Hyg Environ Health. 2002; 205(4): 297-308.

Levy M, Schwartz S, Dijak M, Weber JP, Tardif R, Rouah F. Childhood urine mercury excretion: dental amalgam and fish consumption as exposure factors. Environ Res. 2004; 94(3): 283-90.

Pesch A, et al. Mercury concentrations in urine, scalp hair, and saliva in children from Germany. J Expo Anal Environ Epidemiol. 2002; 12(4): 252-258.

Skare I. Mass balance and systemic uptake of mercury released from dental fillings. Water, Air, and Soil Pollution. 1995; 80(1-4): 59-67.

Drasch G, et al. Silver concentrations in human tissues: The dependence on dental amalgam. J Trace Elements in Medicine and Biology. 1995; 9(2): 82-7.

Calsakis LJ, et al. Allergy to silver amalgams. Oral Surg. 1978; 46: 371-5.

Bjorkman L, et al. Mercury in saliva and feces after removal of amalgam fillings. Toxicology and Applied Pharmacology. 1997; 144(1): 156-62.

Osterblad M, et al. Antimicrobial and mercury resistance among persons with and without amalgam fillings. Antimicrobial Agents and Chem. 1995; 39(11): 2499.

Begerow J, et al. Long-term mercury excretion in urine after removal of amalgam fillings. Int Arch Occup Health. 1994; 66: 209-212.

Skare I, et al. Human exposure to Hg and Ag released from dental amalgam restorations. Archives of Health. 1994; 49(5): 384-394.

Veltman JC, et al. Alterations of heme, cytochrome P-450, and steroid metabolism by mercury in rat adrenal gland. Arch Biochem Biophys. 1986; 248(2): 467-78.

Riedl AG, et al. P450 and hemeoxygenase enzymes in the basal ganglia and their roles in Parkinson’s disease. Adv Neurol. 1999; 80: 271-86.

Zamm AV. Dental mercury: A factor that aggravates and induces xenobiotic intolerance. J. Orthmol. Med. 1991; 6(2): 67-77.

Weiner JA, et al. The relationship between mercury concentration in human organs and n-predictor variables. Sci Tot Environ. 1993; 138(1-3): 101-115.

Falnoga I, Tusek-Znidaric M, Horvat M, Stegnar P. Mercury, selenium, and cadmium in human autopsy samples from Idrija residents and mercury mine workers. Environ Res. 2000; 84(3): 211-8.

Franko A, Budihna MV. Long-term effects of elemental mercury on renal function in miners of the Idrija mercury mine. Ann Occup Hyg. 2005; 49(6): 521-7.

Jarosiska D, Horvat M, Barregård L, et al. Urinary mercury and biomarkers of early renal dysfunction in environmentally and occupationally exposed adults: a three-country study. Environ Res. 2008; 108(2): 224-32.

Dunsche A, et al. Oral lichenoid reactions associated with amalgam: improvement after amalgam removal. British Journal of Dermatology. 2003; 148(1): 70-6.

Smart ER, et al. Resolution of lichen planus following removal of amalgam restorations. Br Dent J. 1995; 178(3): 108-112.

Markow H. Regression from orticaria following dental filling removal. New York State J Med. 1943: 1648-1652.

Sasaki G, et al. Three cases of oral lichenosis caused by metallic fillings. J. Dermatol. 1996; 12: 890-892.

Bratel J, et al. Effect of replacement of dental amalgam on OLR. Journal of Dentistry. 1996; 24(1-2): 41-45.

Wong L, Freeman S. Oral lichenoid lesions (OLL) and mercury in amalgam fillings. Contact Dermatitis. 2003; 48(2): 74.

Ibbotson SH, et al. The relevance of amalgam replacement on oral lichenoid reactions. British Journal of Dermatology. 1996; 134(3): 420-3.

Godfrey ME. Chronic ailments related to amalgams. J. Adv. Med. 1990; 3: 247.

Godfrey ME, Feek C. Dental amalgam. New Zealand Medical Journal. 1998; 111: 326.

Berglund A, Molin M. Mercury levels in plasma and urine after removal of all amalgam restorations: The effect of using rubber dams. Dent Mater. 1997; 13(5): 297-304.

Molin M, et al. Mercury, selenium, and GPX before & after amalgam removal. Acta Odontol Scand. 1990; 48: 189-202.

Koch P, et al. Oral lesions and symptoms related to metals. Dermatol. 1999; 41(3): 422-430.

Jolly M, et al. Amalgam related chronic ulceration of oral mucosa. Br Dent J. 1986; 160: 434-437.

Camisa C, et al. Contact hypersensitivity to mercury. Cutis. 1999; 63(3): 189.

Lindqvist B, et al. Effects of removing amalgam fillings from patients with diseases affecting the immune system. Med Sci Res. 1996; 24(5): 355-356.

Tandon L, et al. Elemental imbalance studies by INAA on ALS patients. J Radioanal Nuclear Chem. 1995; 195(1): 13-19.

Mano Y, et al. Mercury in the hair of ALS patients. Rinsho Shinkeigaku. 1989; 29(7): 844-848.

Khare, et al. Trace element imbalances in ALS. Neurotoxicology. 1990; 11: 521-532.

Carpenter DO. Effects of metals on the nervous system of humans and animals. Int J Occup Med Environ Health. 2001; 14(3): 209-18.

Barregard L, et al. People with high mercury uptake from their own dental amalgam fillings. Occup Envir Med. 1995; 52: 124-128.

Langworth S, et al. A case of high mercury exposure from dental amalgam. European J Oral Sci. 1996; 104(3): 320-321.

Stromberg R, et al. A case of unusually high mercury exposure from amalgam fillings. Tandlakartidningen. 1996; 88(10): 570-572.

Tuthill JY. Mercurial neurosis resulting from amalgam fillings. Brooklyn Medical Journal. 1898; 12(12): 725-742.

Lichtenberg HJ. Elimination of symptoms by removal of dental amalgam from mercury poisoned patients. J Orthomol Med. 1993; 8: 145-148.

Lichtenberg HJ. Symptoms before and after proper amalgam removal in relation to serum-globulin reaction to metals. Journal of Orthomolecular Medicine. 1996; 11(4): 195-203.

Goyer RA. Toxic and essential metal interactions. Annu Rev Nutr. 1997; 17: 37-50.

Goyer RA, et al. Environmental risk factors for osteoporosis. Envir Health Perspectives. 1994; 102(4): 390-394.

Lindh U, Carlmark B, Gronquist SO, Lindvall A. Metal exposure from amalgam alters the distribution of trace elements in blood cells and plasma. Clin Chem Lab Med. 2001; 39(2): 134-142.

Goldberg AF, et al. Effect of amalgam restorations on whole body potassium and bone mineral content in older men. Gen Dent. 1996; 44(3): 246-8.

Schirrmacher K. Effects of lead, mercury, and methylmercury on gap junctions and [Ca2+]I in bone cells. Calcif Tissue Int. 1998; 63(2): 134-9.

Redhe O, Pleva J. Recovery from ALS and from asthma after removal of dental amalgam fillings. Int J Risk & Safety in Med. 1994; 4: 229-236.

Adams CR, Ziegler DK, Lin JT. Mercury intoxication simulating ALS. JAMA. 1983; 250(5): 642-5.

Seidler A, et al. Possible environmental factors for Parkinson’s disease. Neurology. 1996; 46(5): 1275-1284.

Ohlson, et al, Parkinson’s disease and occupational exposure to mercury. Scand J. of Work Environment Health. 1981; 7(4): 252-256.

Golota LG. Therapeutic properties of unitihiol. Farm. Zh. 1980, 1: 18-22.

Nylander M, et al. Mercury accumulation in tissues from dental staff and controls. Swedish Dental Journal. 1989; 13: 235-243.

Nylander M, et al. Mercury and selenium concentrations and their interrelations in organs from dental staff and the general population. Br J Ind Med. 1991; 48(11): 729-34.

Hanson M, et al. The dental amalgam issue: A review. Experientia. 1991; 47: 9-22.

Weiner JA, et al. Does mercury from amalgam restorations constitute a health hazard? Sci Total Environ. 1990; 99(1-2): 1-22.

Henriksson E, et al. Healing of lichenoid reactions following removal of amalgam. J Clinical Periodontol. 1995; 22(4): 287-94.

Larsson A, et al. The histopathology of oral mucosal lesions associated with amalgam. Oral Dis. 1995; 1(3): 152-8.

Siblerud RL, et al. Evidence that mercury from silver fillings may be an etiological factor in multiple sclerosis. Sci Total Environ. 1994; 142(3): 191-205.

Tanchyk AP. Amalgam removal for treatment of arthritis. Gen Dent. 1994; 42(4): 354.

Facemire CF, et al. Reproductive impairment in the Florida panther. Health Perspect. 1995; 103 (4): 79-86.

Yang JM, et al. The distribution of HgCl2 in rat body and its effect on fetus. Environ Sci. 1996; 9(4): 437-42.

Rao MV, Sharma PS. Protective effect of vitamin E against mercuric chloride reproductive toxicity in male mice. Reprod Toxicol. 2001; 15(6): 705-12.

Monsees TK, Franz M, Gebhardt S, Winterstein U, Schill WB, Hayatpour J. Sertoli cells as a target for reproductive hazards. Andrologia. 2000; 32(4-5): 239-46.

Maretta M, et al. Effect of mercury on the epithelium of the fowl testis. Vet Hung. 1995; 43(1): 153-6.

Orisakwe OE, Afonne OJ. Low-dose mercury induces testicular damage in mice that is protected against by zinc. Eur J Obstet Gynecol Reprod Biol. 2001; 95(1): 92-6.

Giwercman A, Carlsen E, Keiding N, Skakkabaek NE. Evidence for increasing incidence of abnormalities of the human testis: A review. Environ Health Perspect. 1993; 101(2): 65-71.

Bruce GR. Cytotoxicity of retrofil materials. J Endodont. 1993; 19(6): 288-92.

Henningsson M, et al. Defensive characteristics in individuals with amalgam illness. Acta Odont Scand. 1996; 54(3): 176-181.

Liang YX, et al. Psychological effects of low exposure to mercury vapor. Environmental Med Research. 1993; 60(2): 320-327.

Kampe T, et al. Personality traits of adolescents with intact and repaired dentitions. Acta Odont Scand. 1986; 44: 95.

Kishi R, et al. Residual neurobehavioral effects of chronic exposure to mercury vapor. Occupat. Envir. Med. 1994; 51: 35-41.

Sikora A, et al. Evaluation of mental functions in workers exposed to metallic mercury. Med Pr. 1992; 43(2): 109-21.

Quig D. Cysteine metabolism and metal toxicity. Altern Med Rev. 1998; 3(4): 262-270.

de Ceaurriz J, et al. Role of gamma-glutamyltraspeptidase(GGC) and extracellular glutathione in dissipation of inorganic mercury. J Appl Toxicol. 1994; 14(3): 201.

Berndt WO, et al. Renal glutathione and mercury uptake. Fundam Appl Toxicol. 1985; 5(5): 832-9.

Zalups RK, Barfuss DW. Accumulation and handling of inorganic mercury in the kidney after co-administration with glutathione. J Toxicol Environ Health. 1995; 44(4): 385-99.

Clarkson TW, et al. Billiary secretion of glutathione-metal complexes. Fundam Appl Toxicol. 1985; 5(5): 816-31.

Oskarsson A, et al. Mercury in breast milk in relation to fish consumption and amalgam. Arch Environ Health. 1996; 51(3): 234-41.

Drasch, et al. Mercury in human colostrum and early breast milk. J. Trace Elem. Med. Biol. 1998; 12: 23-27.

Grandjean P, Jurgensen PJ, Weihe P. Milk as a source of methylmercury exposure in infants. Environ Health Perspect. 1994; 102(1): 74-7.

Glavinskiaia TA, et al. Complexons in the treatment of lupus erghematousus. Dermatol Venerol. 1980; 12: 24-28.

Aschner M, et al. Metallothionein induction in fetal rat brain by in utero exposure to elemental mercury vapor. Brain Research. 1997; 778(1): 222-32.

Aschner M, Rising L, Mullaney KJ. Differential sensitivity of neonatal rat astrocyte cultures to mercuric chloride (MC) and methylmercury (MeHg): Studies on K+ and amino acid transport and metallothionein (MT) induction. Neurotoxicology. 1996; 17(1): 107-16.

O’Halloran TV. Transition metals in control of gene expression. Science. 1993; 261(5122): 715-25.

Matts RL, Schatz JR, Hurst R, Kagen R. Toxic heavy metal ions inhibit reduction of disulfide bonds. J Biol Chem. 1991; 266(19): 12695-702.

Boot JH. Effects of SH-blocking compounds on the energy metabolism in isolated rat hepatocytes. Cell Struct Funct. 1995; 20(3): 233-8.

Baauweegers HG, Troost D. Localization of metallothionein in the mammilian central nervous system. Biol Signals. 1994; 3: 181-7.

Liebert CA, Wireman J, Smith T, Summers AO. The impact of mercury released from dental “silver” fillings on antibiotic resistance in the primate oral and intestinal bacterial flora. Met Ions Biol Syst. 1997; 34: 441-60.

Grewal JS, Tiwari RP. Resistance to antibiotics, metals, hydrophobicity and klebocinogeny of Klebsiella pneumoniae isolated from foods. Cytobios. 1999; 98(388): 113-23.

Aguiar JM, et al. Heavy metals and antibiotic resistance in Escherichia coli isolates from ambulatory patients. Chemother. 1990; 2(4): 238-40.

Tibbling L, Stejskal VDM, et al. Immunological and brain MRI changes in patients with suspected metal intoxication. Int J Occup Med Toxicol. 1995; 4(2): 285-294.

Ronnback L, et al. Chronic encephalopaties induced by low doses of mercury or lead. Br J Ind Med. 1992; 49: 233-240.

Langauer-Lewowicka H. Changes in the nervous system due to occupational metallic mercury poisoning. Neurol Neurochir Pol. 1997; 31(5): 905-13.

Langauer-Lewowicka H. Chronic toxic encephalopathies. Med Pr. 1982; 33(1-3): 113-7.

Pohl L. The dentist’s exposure to elemental mercury during clinical work. Acta Odontol Scand. 1995; 53(1): 44-48.

Harakeh S, Sabra N, Kassak K, Doughan B. Factors influencing total mercury levels among Lebanese dentists. Sci. Total Environ. 2002; 297(1-3): 153-60.

Rowland AS, et al. The effect of occupational exposure to mercury vapor on the fertility of female dental assistants. Occupational & Environmental Medicine. 1994; 55(1).

Ono B, et al. Reduced tyrosine uptake in strains sensitive to inorganic mercury. Genet. 1987; 11(5): 399.

Skare I, et al. Mercury exposure of different origins among dentists and dental nurses. Scand J Work Environ Health. 1990; 16: 340-347.

Akesson I, et al. Status of mercury and selenium in dental personnel. Arch Environ Health. 1991; 46(2): 102-109.

Chang SB, et al. Factors affecting blood mercury concentrations in practicing dentists. Dent Res. 1992; 71(1): 66-74.

Singh I, Pahan K, Khan M, Singh AK. Cytokine-mediated induction of ceramide production is redox-sensitive. Implications to pro-inflammatory cytokine-mediated apoptosis in demyelinating diseases. J Biol Chem. 1998; 273(32): 20354-62.

Pahan K, Raymond JR, Singh I. Inhibition of phosphatidylinositol 3-kinase induces nitric-oxide synthase in lipopolysaccharide-or cytokine-stimulated C6 glial cells. J. Biol. Chem. 1999; 274: 7528-7536.

Xu J, Yeh CH, et al. Involvement of de novo ceramide biosynthesis in tumor necrosis factor-alpha/cycloheximide-induced cerebral endothelial cell death. J Biol Chem. 1998; 273(26): 16521-6.

Dbaibo GS, El-Assaad W, et al. Ceramide generation by two distinct pathways in tumor necrosis factor alpha-induced cell death. FEBS Lett. 2001; 503(1): 7-12.

Liu B, Hannun YA, et al. Glutathione regulation of neutral sphingomyelinase in tumor necrosis factor-alpha-induced cell death. J Biol Chem. 1998; 273(18): 11313-20.

Noda M, Wataha JC, et al. Sublethal, 2-week exposures of dental material components alter TNF-alpha secretion of THP-1 monocytes. Dent Mater. 2003; 19(2): 101-5.

Kim SH, Johnson VJ, Sharma RP. Mercury inhibits nitric oxide production but activates pro-inflammatory cytokine expression in murine macrophage: Differential modulation of NF-kappaB and p38 MAPK signaling pathways. Nitric Oxide. 2002; 7(1): 67-74.

Dastych J, Metcalfe DD, et al. Murine mast cells exposed to mercuric chloride release granule-associated N-acetyl-beta-D-hexosaminidase and secrete IL-4 and TNF-alpha. J Allergy Clin Immunol. 1999; 103(6): 1108-14.

Tortarolo M, Veglianese P, et al. Persistent activation of p38 mitogen-activated protein kinase in a mouse model of familial amyotrophic lateral sclerosis correlates with disease progression. Mol Cell Neurosci. 2003; 23(2): 180-92.

Moszczynski, et al. The behavior of T-Cells in the blood of workers exposed to mercury. Med Lav. 1994; 85(3): 239-241.

Queiroz MLS, et al. Immunoglobulin levels in workers exposed to inorganic mercury. Pharmacol Toxicol. 1994; 74: 72-75.

Hultman P, et al. Adverse immunological effects and immunity induced by dental amalgam. FASEB J. 1994; 8: 1183-1190.

Enestrom S, et al. Does amalgam affect the Immune System? Int Arch Allergy Immunol. 1995; 106: 180-203.

Christensen MM, Ellermann-Eriksen S, Mogensen SC. Influence of mercury chloride on resistance to generalized infection with herpes simplex virus type 2 in mice. Toxicology. 1996; 114(1): 57-66.

Ellermann-Eriksen S, et al. Effect of mercuric chloride on macrophage-mediated resistance mechanisms against infection. Toxicology. 1994; 93: 269-297.

Christensen MM, et al. Comparison of interaction of meHgCl2 and HgCl2 with murine macrophages. Arch Toxicol. 1993; 67(3): 205-11.
Sato K, et al. An epidemiological study of factors relating to mercury sensitization. Arerugi. 1995; 44(2): 86-92.

Mori T, et al. Mercury sensitization caused by environmental factors. Nippon Eiseigaku Zasshi. 1998; 52(4): 661-6.

Molin M, et al. Mercury in plasma in patients allegedly subject to oral galvanism. Scand J Dent Res. 1987; 95: 328-334.

Bjorkman L, et al. Factors influencing mercury evaporation rate from dental amalgam fillings. Scand J Dent Res. 1992; 100(6): 354-360.

Sallsten G, et al. Long term use of nicotine chewing gum and mercury exposure from dental amalgam. J Dent Res. 1996; 75(1): 598.

Gebel T, et al. Influence of chewing gum on urine mercury content. Zentralbl Hyg Umweltmed. 1996; 199(1): 69-75.

Sallsten G, et al. Mercury in cerebrospinal fluid in subjects exposed to mercury vapor. Environmental Research. 1994; 65: 195-206.

Ariza ME, Bijur GN, Williams MV. Lead and mercury mutagenesis: role of H2O2, superoxide, dismutase, and xanthine oxidase. Environ Mol Mutagen. 1998; 31(4): 352-61.

Boffetta P, et al. Carciagenocity of mercury. Scand J Work Environ Health. 1993; 19(1): 1-7.

Zaichick Y, et al. Trace elements and thyroid cancer. Analyst. 1995; 120(3).

Carpenter DO. Effects of metals on the nervous system of humans and animals. Int J Occup Med Environ Health. 2001; 14(3): 209-18.

Gorell JM, et al. Occupational exposure to mercury, manganese, copper, lead, and the risk of Parkinson’s. Neurotoxicology. 1999; 20(2-3): 239-47.

Gorell JM, et al. Occupational exposures to metals as risk factors for Parkinson’s disease. Neurology. 1997; 48(3): 650-8.

Discalzi G, Meliga F, et al. Occupational Mn parkinsonism: magnetic resonance imaging and clinical patterns following CaNa2-EDTA chelation. Neurotoxicology. 2000; 21(5): 863-6.

Yang JM, Chen QY, Jiang XZ. Effects of metallic mercury on the perimenstrual symptoms and menstrual outcomes of exposed workers. Am J Ind Med. 2002; 42(5): 403-9.

Choi B, et al. Abnormal neuronal migration of human fetal brain. Journal of Neurophalogy. 1978; 37: 719-733.

Larkfors L, et al. Methylmercury induced alterations in the nerve growth factor level in the developing brain. Res Dev Res. 1991; 62(2): 287.

Belletti S, Gatti R. Time course assessment of methylmercury effects on C6 glioma cells: submicromolar concentrations induce oxidative DNA damage and apoptosis. J Neurosci Res. 2002; 70(5): 703-11.

Langworth, et al. Effects of low exposure to inorganic mercury on the human immune system. Scand J Work Environ Health. 1993; 19(6): 405-413.

Walum E, et al. Use of primary cultures to study astrocytic regulatory functions. Clin Exp Pharmoacol Physiol. 1995; 22: 284-7.

Kerkhoff H, Troost D, Louwerse ES. Infammatory cells in the peripheral nervous system in motor neuron disease. Acta Neuropathol. 1993; 85: 560-5.

Appel Sh, Smith RG. Autoimmunity as an etiological factor in amyotrophic lateral sclerosis. Adv Neurol. 1995; 68: 47-57.

Nordlind K, et al. Patch test reactions to metal salts in patients with oral mucosal lesions associated with amalgam fillings. Contact Dermatitis. 1992; 27(3): 157-160.

White RR, et al. Mercury hypersensitivity among dental students. JADA. 1976; 92: 124-7.

Goldwater LG. Toxicology of inorganic mercury. Annals: NY Acad Sci. 1957; 65: 498-503.

Nielsen JB, et al. Evaluation of mercury in hair & blood as biomarkers for methylmercury exposure. Arch of Toxicology. 1994; 65(5): 317-321.

Wenstrup, et al. Trace element imbalances in the brains of Alzheimer’s patients. Research. 1990; 533: 125-131.

Lorscheider FL, Haley B, et al. Mercury vapor inhibits tubulin binding. FASEB J. 1995; 9(4): A-3485.

de Saint-Georges, et al. Inhibition by mercuric chloride of the in vitro polymerization of microtubules. CR Seances Soc Biol Fil. 1984; 178(5): 562-6.

Mohamed MK, et al, Effects of methyl mercury on testicular functions in monkey. Toxicol. 1987; 60(1): 29-36.

Ivanitskaia NF. Evaluation of effect of mercury on reproductive function of animals. Gig Sanit. 1991; 12: 48-51.

Aschner M, Yao CP, Allen JW, Tan KH. Methylmercury alters glutamate transport in astrocytes. Neurochem Int. 2000; 37(2-3): 199-206.

Anneroth G, Ericson T, Johansson I, Mornstad H, Skoglund A. Comprehensive medical examination of patients with alleged adverse effects from dental amalgams. Acta Odontal Scand. 1992; 50(2): 101-11.

Olsted ML, et al. Correlation between amalgam restorations and mercury in urine. J Dent Res. 1987; 66(6): 1179-1182.

Laine J, et al. Immunocompetent cells in amalgam-associated oral licheinoid contact lesions. Oral Pathol Med. 1999; 28(3): 117-21.

Adachi A, Horikawa T. Efficacy of dental metal elimination in the management of atopic dermatitis. J Dermatology. 1997; 24(1): 12-19.

Ngim CH, et al. Epidemiologic study on the association between body burden mercury level and idiopathic Parkinson’s disease. Neuroepidemiology. 1989; 8(3): 128-41.

Jokstad A. Mercury excretion and occupational exposure of dental personnel. Community Dent Oral Epidemiology. 1990; 18(3): 143-8.

Nilsson B, et al. Urinary mercury excretion in dental personnel. Swed Dent J. 1986; 10(6): 221-32.

Zander D, et al. Mercury exposure of male dentists, female dentists, and dental aides. Zentralbl Hyg Umweltmed. 1992; 193(4): 318-28.

Willershausen B, et al. Mercury in the mouth mucosa of patients with amalgam fillings. Dtsch Med Wochenschr. 1992; 117(46): 1743-7.

Monnet-Tschudi F, et al. Comparison of the developmental effects of 2 mercury compounds on glial cells and neurons in the rat telencephalon. Brain Research. 1996; 741: 52-59.

Chang LW, Hartmann HA. Quantitative cytochemical studies of RNA in experimental mercury poisoning. Acta Neruopathol(Berlin). 1973; 23(1): 77-83.

Sorensen FW, Larsen JO, Eide R, Schionning JD. Neuron loss in cerebellar cortex of rats exposed to mercury vapor: A stereological study. Acta Neuropathol (Berlin). 2000; 100(1): 95-100.

Olsson S, et al. Daily dose calculations from measurements of intra-oral mercury vapor. J Dent Res. 1992; 71(2): 414-23.

Lenihan J, et al. Mercury hazards in dental practice. Br Dent J. 1973; 135: 363-376.

Lussi A. Mercury release from amalgam into saliva. Schweiz Monatsschr Zahnmed. 1993; 103(6): 722-29.

Schimpff SC, Young WH, Greene WH. Origin of infections in acute nonlymphocytic leukemia. Annals of International Medicine. 1972; 77: 707-711.

Kinjo Y, et al. Cancer mortality in patients exposed to methyl mercury through fish diet. J Epidemiol. 1996; 6(3): 134-8.

Murdoch RD, Pepys J. Enhancement of antibody and IgE production by mercury and platinum salts. Int Arch Allergy Appl Immunol. 1986; 80: 405-11.

Parronchi P, Brugnolo F, Sampognaro S, Maggi E. Genetic and environmental factors contributing to the onset of allergic disorders. Int Arch Allergy Immunol. 2000; 121(1): 2-9.

Jones L. Health outcomes following amalgam removal. New Zealand Psychology Journal. 1999.

Yang J, Wang Yl. Maternal-fetal transfer of metallic mercury via the placenta and milk. Annals of Clin & Lab Sci. 1997; 27(2): 135-41.

Ong CN, et al. Concentrations of heavy metal in maternal and umbilical cord blood. Biometals. 1993; 6(1): 61-66.

Suzuki T, et al. Mercury in human amniotic fluid. Scand J Work Environ & Health. 1977; 3: 32-35.

Spencer DA, et al. Mercury concentration in cord Blood. Arch Dis Child. 1988; 63(2): 202-3.

Sikorski R, et al. The intrapartum content of toxic metals in maternal and umbilical cord blood. Ginekol Pol. 1989; 60(3): 151.

Ask K, Akesson A, Berglund M, Vahter M. Inorganic mercury and methylmercury in placentas of Swedish women. Environ Health Perspect. 2002; 110(5): 523-6.

Klobusch J, Rabe T, Gerhard I, Runnebaum B. Alopecia and environmental pollution. Klinisches Labor. 1992; 38: 469-476.

Urban P, et al. Neurological examination on 3 groups of workers exposed to mercury vapor. Eur J Neurology. 1999; 6(5): 571-7.

Polakowska B. Neurological assessment of health status in dentists. Med Pr. 1994; 45(3): 221-5.

Ekenvall L, et al. Sensory perception in the hands of dentists. J Work Environ Health. 1990; 16(5): 334-9.

Brune D, et al. Gastrointestinal and in vitro release of metals from conventional and copper-rich amalgams. Scand J Dent Res. 1983; 91: 66-71.

Nogi N. Electric current around dental metals as a factor producing allergic metal ions in the oral cavity. Nippon Hifuka Gakkai Zasshi. 1989; 99(12): 1243-54.

Bergdahl J, Certosimo AJ, et al. Oral electricity. Gen Dent. 1996; 44(4): 324-6.

Rose MD, et al. The tarnished history of a posteria restoration. Br Dent J. 1998; 185(9): 436.

Meyer RD, et al. Intraoral galvanic corrosion. Prosthet Dent. 1993; 69(2): 141-3.

Ogletree RH, et al. Effect of mercury on corrosion of eta’ Cu-Sn phase in dental amalgams. Dent Mater. 1995; 11(5): 332-6.

Cohen EN, et al. Occupational disease in dentistry. Amer. Dent Assoc. 1980; 101(1): 21-31.

Bjorklund G. Risk evaluation of the occupational environment in dental care. Tidsski Nor Laegeforen. 1991; 111(8): 948-50.

Ahlbom A, et al. Dentists, dental nurses, and brain tumors. Br Med J. 1986; 202(6521): 662.

Zalups RK, et al. Nephrotoxicity of inorganic mercury co-administered with L-cysteine. Toxicology. 1996; 109(1): 15-29.

Moller-Madsen B, et al. Mercury concentrations in blood of Danish dentists. Scand J Dent Res. 1988; 96(1): 56-9.

Sandborgh-Englund G, et al. Mercury in biological fluids after amalgam removal. J Dental Res. 1998; 77(4): 615-24.

Ekstrand J, Bjorkman L, Edlund C, Sandborgh-Englund G. Toxicological aspects on the release and systemic uptake of mercury from dental amalgam. Eur J Oral Sci. 1998; 106(2.2): 678-86.

Fabbri E, Caselli F, Piano A, Sartor G, Capuzzo A.Cd2+ and Hg2+ affect glucose release and cAMP-dependent transduction pathway in isolated eel hepatocytes. Aquat Toxicol. 2003; 62(1): 55-65.

Danielsson BRG, et al. Ferotoxicity of inorganic mercury: Distribution and effects of nutrient uptake by placenta and fetus. Biol Res Preg Perinatal. 1984; 5(3): 102-109.

Nadarajah V, et al. Localized cellular inflammatory response to subcutaneously implanted dental mercury. J Toxicol Environ Health. 1996; 49(2): 113-25.

Salonen JT, et al. Intake of mercury from fish and the risk of myocardial infarction and cardiovascular disease in eastern Finnish men. Circulation. 1995; 91(3): 645-55.

Salonen JT, Seppanen K, Lakka TA, Salonen R, Kaplan GA. Mercury accumulation and accelerated progression of carotid atherosclerosis: a population-based prospective 4-year follow-up study in men in eastern Finland. Atherosclerosis. 2000; 148(2): 265-73.

Gualler E, et al. Mercury, fish oils, and the risk of myocardial infarction. New England J of Medicine. 2002; 347.

Kishimoto T, et al. Methyl mercury injury of cultured human vascular endothelial cells. Journal of Trace Elements in Experimental Medicine. 1993; 6(4): 155-163.

Vimy MJ, et al. Renal function and amalgam mercury. Amer J Physiol. 1997; 273: 1199.

Miller DM, Lund BO, Woods JS. Reactivity of Hg(II) with superoxide: Evidence for the catalytic dismutation of superoxide by Hg(II). J Biochem Toxicol. 1991; 6(4): 293-8.

Nath KA, et al. Renal oxidant injury induced by mercury. Kidney Int. 1996; 50(3): 1032-43.

Ware RA, et al. Ultrastructural changes in renal proximal tubules after chronic organic and inorganic mercury intoxication. Environ Res. 1975; 10(1): 121-40.

Bigazzi PE. Metals and kidney autoimmunity. Environ Health Perspect. 1999; 107(5): 753-765.

Nuyts GD, et al. New occupational risk factors for chronic renal failure. Lancet. 1995; 346(8966): 7-11.

Ma R, et al. Association between dental restorations and carcinoma of the tongue. European Journal of Cancer. Part B, Oral Oncology. 1995; 31B(4): 232-4.

Siblerud RL. Health effects after dental amalgam removal. J. Orthomol. Med. 1990; 5: 95-106.

Sehnert KW. Autoimmune disorders. Advance. 1995: 47-48.

Cutright DE, et al. Systemic mercury levels caused by inhaling mist during high-speed amalgam grinding. J Oral Med. 1973; 28(4): 100-104.

Nimmo A, et al. Inhalation during removal of amalgam restorations. J Prosthet Dent. 1990; 3(2): 228-33.

Stonehouse CA, Newman AP. Mercury vapour release from a dental aspirator. Br Dent J. 2001; 190(10): 558-60.

Taskinen H, Kinnunen E, Riihimaki V. A possible case of mercury-related toxicity resulting from the grinding of old amalgam restorations. Scand J Work Environ Health. 1989; 15(4): 302-4.

Sellars WA, Sellars R. Methyl mercury in dental amalgams in the human mouth. Journal of Nutritional & Environmental Medicine. 1996; 6(1): 33-37.

Golden R, et al. Dementia and Alzheimer’s disease. Minnesota Medicine. 1995; 78: 25-29.

Schofield P. Dementia associated with toxic causes and autoimmune disease. Int Psychogeriatr. 2005; 17: S129-47.

Nicholson, et al. Mercury nephrotoxicity. Nature. 1983; 304: 633.

Friberg, et al. Kidney injury after chronic exposure to inorganic mercury. Archives of Environ Health. 1967; 15: 64.

Kazantis, et al. Nephrotic syndrome following exposure to mercury. Quarterly J. Of Medicine. 1962; 31: 403-418.

Mortada WL, Sobh MA. Mercury in dental restoration: Is there a risk of nephrotoxicity? J Nephrol. 2002; 15(2): 171-6.

Yannai S, et al. Transformations of inorganic mercury by candida albicans and Saccharomyces cerevisiae. Applied Envir Microbiology. 1991; 7: 245-247.

Zorn NE, et al. A relationship between Vit B-12, mercury uptake, and methylation. Life Sci. 1990; 47(2): 167-73.

Ridley WP, Dizikes L, Cheh A, Wood JM. Recent studies on biomethylation and demethylation of toxic elements. Environ Health Perspect. 1977; 19: 43-6.

Shenker BJ, et al. Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes: Alterations in cell viability. Immunopharmacologicol Immunotoxical. 1992; 14(3): 555-77.

Miller, et al. Mercuric chloride induces apoptosis in human T lymphocytes. Toxicol Appl Pharmacol. 1998; 153(2): 250-7.

Rossi AD,Viviani B, Vahter M. Inorganic mercury modifies Ca2+ signals, triggers apoptosis, and potentiates NMDA toxicity in cerebral granule neurons. Cell Death and Differentiation. 1997; 4(4): 317-24.

Goering PL, Thomas D, Rojko JL, Lucas AD. Mercuric chloride-induced apoptosis is dependent on protein synthesis. Toxicol Lett. 1999; 105(3): 183-95.

Shenker BJ, et al. Immune suppression of human T-cell activation. Immunopharmacologicol Immunotoxical. 1992; 14(3): 555-77.

Zamm AF. Removal of dental mercury: Often an effective treatment for very sensitive patients. J Orthomolecular Med. 1990; 5(53): 138-142.

Nechipurenko N, Griboedova T, Vlasyuk P. Experimental study on brain oxygenation in relation to tissue water redistribution and brain oedema. Acta Neurochir Suppl. 2000; 76: 279-81.

Cooper GS, Dooley MA., et al. Occupational risk factors for the development of systemic lupus erythematosus. J Rheumatol. 2004; 31(10): 1928-33.

Bigazzi PE, Autoimmunity and heavy metals. Lupus. 1994; 3: 449-453.

Pollard KM, Pearson Dl, Hultman P. Lupus-prone mice as model to study xenobiotic-induced autoimmunity. Environ Health Perspect. 1999; 107(5): 729-735.

Nielsen JB, Hultman P. Experimental studies on genetically determined susceptibility to mercury-induced autoimmune response. Ren Fail. 1999; 21(3-4): 343-8.

Hultman P, Enestrom S. Mercury induced antinuclear antibodies in mice. Clinical and Exper Immunology. 1988; 71(2): 269-274.

Robbins SM, Quintrell NA, Bishop JM. Mercuric chloride activates the Src-family protein tyrosine kinase, Hck in myelomonocytic cells. Eur J Biochem. 2000; 267(24): 7201-8.

Via CS, Nguyen P, Silbergeld EK, et al. Low-dose exposure to inorganic mercury accelerates disease and mortality in acquired murine lupus. Environ Health Perspect. 2003; 111(10): 1273-7.

Silbergeld EK, Silva IA, Nyland JF. Mercury and autoimmunity: Implications for occupational and environmental health. Toxicol Appl Pharmacol. 2005; 207(2): 282-92.

Hamre HJ. Mercury from dental amalgam and chronic fatigue syndrome. The CFIDS Chronicle. 1994: 44-47.

Foster HD. The calcium-selenium-mercury connection in cancer and heart disease. Hypotheses. 1997; 48(4): 335-60.

Whanger PD. Selenium in the treatment of heavy metal poisoning and chemical carcinogenesis. J Trace Elem Electrolytes Health Dis. 1992; 6(4): 209-21.

Varga J, et al. High incidence of cross stimulation by natural allergens of rat basophilic leukemia cells sensitized with IgE antibodies. Int Arch Allergy Immunol. 1995; 108(2): 196-9.

Gainer JH. Activation of Rauscher leukemia virus by metals. J Natl Cancer Inst. 1973; 51(2): 609-13.

Haikel Y, Gasser P, Salek P, Voegel JC. Exposure to mercury vapor during setting, removing, and polishing amalgam restorations. J Biomed Mater Res. 1990; 24(11): 1551-8.

Schoeny R. Use of genetic toxicology data in U.S. EPA risk assessment: the mercury study. Environ Health Perspect. 1996; 104(3): 663-73.

Constantinidis J. Hypothesis regarding amyloid and zinc in the pathogenisis of Alzheimer’s disease. Alzheimer’s Dis Assoc Disord. 1991; 5(1): 31-35.

Walker PR, et al. Effects of aluminum and mercury on the structure of chromatin. Biochemistry. 1989; 28(9): 3911-3915.

Basun H, et al. Trace metals in plasma and cerebrospinal fluid in Alzheimer’s disease. J Neural Transm Park Dis Dement Sect. 1991; 3(4): 231.

Lokken P. Lethal mercury poisoning in a dental assistant. Nor Tannlaegeforen Tid. 1971; 81(4): 275-288.

Wronski R, et al. A case of panarteritis nodoa associated with chronic mercury poisoning. Dtsch Med Wohenschr. 1977; 102(9): 323-325.

Iyer K, et al. Mercury poisoning in a dentist. Arch Neurol. 1976; 33: 788-790.

Lonnroth EC, et al. Adverse health reactions in skin, eyes, and respiratory tract among dental personnel in Sweden. Swed Dent J. 1998; 22(1-2): 33-45.

Kanerva L, et al. Occupational contact urticarial. Contact Dermatitis. 1996; 35(4): 229-33.

Lee JY, Yoo JM, Cho BK, Kim HO. Contact dermatitis in Korean dental technicians. Contact Dermatitis. 2001; 45(1): 13-6.

Fabrizio E, Vanacore N, Valente M, Rubino A, Meco G. High prevalence of extrapyramidal signs and symptoms in a group of Italian dental technicians. BMC Neurol. 2007; 7: 24.

Finkelstein Y. The enigma of parkinsonism in chronic borderline mercury intoxication resolved by challenge with penicillamine. Neurotoxicology. 1996; 17(1): 291-5.

Hryhorczuk E, et al. Treatment of mercury intoxication in a dentist with penicilamine. J Toxicol Clin Toxicol. 1982; 19(4): 401.

Ngim CH, et al. Chronic neurobehavioral effects of elemental mercury in dentists. British Journal of Industrial Medicine. 1992; 49(11): 782-790.

Rybicki BA, et al. Parkinson’s disease mortality and the industrial use of heavy metals in Michigan. Mov Disord. 1993; 8(1): 87-92.

Yamanaga H. Quantitative analysis of tremor in Minamata disease. Tokhoku J Exp Med. 1983; 141(1): 13-22.

Omura Y, et al. Role of mercury in resistant infections and recovery after Hg detox with cilantro. Acupuncture & Electro-Therapeutics Research. 1995; 20(3): 195-229.

Omura Y. Abnormal deposits of Al, Pb, and Hg in the brain, particularly in the hippocampus, as one of the main causes of decreased cerebral acetylcholine, electromagnetic field hypersensitivity, Pre-Alzheimer’s disease, and autism in children. Acupuncture & Electro-Therapeutics Research. 2000; 25(3/4): 230.

Shenker BJ, et al. Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes: Alterations in cellular glutathione content. Immunopharmacol Immunotoxicol. 1993; 15(2-3): 273-90.

Langworth S, et al. Exposure to mercury vapor and impact on health in the dental profession in Sweden. J Dent Res. 1997; 76(7): 1397-404.

al-Saleh I, Shinwari N. Urinary mercury levels in females: Influence of dental amalgam fillings. Biometals. 1997; 10(4): 315-23.

Mortada WL, Sobh MA, El-Defrawy MM, Farahat SE. Mercury in dental restoration: is there a risk of nephrotoxicity? J Nephrol. 2002; 15(2): 171-6.

Zabinski Z, Dabrowski Z, Moszczynski P, Rutowski J. The activity of erythrocyte enzymes and basic indices of peripheral blood erythrocytes from workers chronically exposed to mercury vapors. Toxicol Ind Health. 2000; 16(2): 58-64.

Rice DC. Evidence of delayed neurotoxicity produced by methyl mercury developmental exposure. Neurotoxicology. 1996; 17(3-4): 583-96.

Weiss B, Clarkson TW, Simon W. Silent latency periods in methylmercury poisoning and in neurodegenerative disease. Environ Health Perspect. 2002; 110(5): 851-4.

Letz R, Gerr F, Cragle D, et al. Residual neurologic deficits 30 years after occupational exposure to elemental mercury. Neurotoxicology. 2000; 21(4): 459-74.

Smith I, et al. Pteridines and mono-amines: Relevance to neurological damage. Postgrad Med J. 1986; 62(724): 113-123.

Kay AD, et al. Cerebrospinal fluid biopterin is decreased in Alzheimer’s disease. Arch Neurol. 1986; 43(10): 996-9.

Yamiguchi T, et al. Effects of tyrosine administration on serum bipterin in patients with Parkinson’s disease and normal control. Science. 1983; 219(4580): 75-77.

Nagatsu T, et al. Catecholoamine-related enzymes and the biopterin cofactor in Parkinson’s. Neurol. 1984; 40: 467-73.

Ely JTA, Mercury induced Alzheimer’s disease: Accelerating Incidence? Bull Environ Contam Toxicol. 2001; 67: 800-6.

Mittal CK, et al. Interaction of heavy metals with the nitric oxide synthase. Mol Cell Biochem. 1995; 149-150: 263-5.

Woods JS, et al. Urinary porphyrin profiles as biomarker of mercury exposure: Studies on dentists. J Toxicol Environ Health. 1993; 40(2-3): 235.

Martin MC, et al. Validity of urine samples for low-level mercury exposure assessment and relationship to porphyrin and creatinine excretion rates. J Pharmacol Exp Ther. 1996.

Woods JS, et al. Effects of porphyrinogenic metals on coproporphrinogen oxidase in liver and kidney. Toxicology and Applied Pharmacology. 1989; 97: 183-190.

Strubelt O, Kremer J, et al. Comparative studies on the toxicity of mercury, cadmium, and copper toward the isolated perfused rat liver. J Toxicol Environ Health. 1996; 47(3): 267-83.

Kaliman PA, Nikitchenko IV, Sokol OA, Strel’chenko EV. Regulation of heme oxygenase activity in rat liver during oxidative stress induced by cobalt chloride and mercury chloride. Biochemistry (Mosc). 2001; 66(1): 77-82.

Kumar SV, Maitra S, Bhattacharya S. In vitro binding of inorganic mercury to the plasma membrane of rat platelet affects Na+-K+-Atpase activity and platelet aggregation. Biometals. 2002; 15(1): 51-7.

Heyer NJ, Bittner AC, Echeverria D, Woods JS. A cascade analysis of the interaction of mercury and coproporphyrinogen oxidase (CPOX) polymorphism on the heme biosynthetic pathway and porphyrin production. Toxicol Lett. 2006; 161(2): 159-66.

Chang LW. The Neurotoxicology and pathology of organomercury, organolead, and organotin. J Toxicol Sci. 1990; 15(4): 125-51.

Kumar AR, Kurup PA. Inhibition of membrane Na+-K+ ATPase activity: A common pathway in central nervous system disorders. J Assoc Physicians India. 2002; 50: 400-6.

Danielsson BR, et al. Behavioral effects of prenatal metallic mercury inhalation exposure in rats. Neurotoxicol Teratol. 1993; 15(6): 391-6.

Fredriksson A, et al. Prenatal exposure to metallic mercury vapor and methyl mercury produce interactive behavioral changes in adult rats. Neurotoxicol Teratol. 1996; 18(2): 129-34.

Matsuo N, et al. Mercury concentration in organs of contemporary Japanese. Environ Health. 1989; 44(5): 298-303.

Suzuki T, et al. The hair-organ relationship in mercury concentration in contemporary Japan. Arch Environ Health. 1993; 48(4): 221-9.

Duuet P, et al. Glomerulonephritis induced by heavy metals. Arch Toxicol. 1982; 50:187-194.

Robinson CJG, et al. Mercuric chloride induced anti-nuclear antibodies in mice. Toxic Appl Pharmacology. 1986; 86: 159-169.

Andres P. IgA-IgG disease in the intestines of rats ingesting HgCl. Clin Immun Immunopath. 1984; 30: 488-494.

Cossi, et al. Beneficial effect of human therapeutic IV-Ig in mercury induced autoimmune disease. Clin Exp Immunol. 1991.

El-Fawai HA, Waterman SJ, De Feo A, Shamy MY. Neuroimmunotoxicology: Humoral assessment of neurotoxicity and autoimmune mechanisms. Contact Dermatitis. 1999; 41(1): 60-1.

Eggleston DW. Effect of dental amalgam and nickel alloys on T-lymphocytes. J Prosthet Dent. 1984; 51(5): 617-623.

Strauss FG, Eggleston DW. IgA nephropathy associated with dental nickel alloy sensitization. Am J Nephrol. 1985; 5(5): 395-7.

Tan XX, Tang C, Castoldi AF, Costa LG. Effects of inorganic and organic mercury on intracellular calcium levels in rat T lymphocytes. J Toxicol Environ Health. 1993; 38(2):159-70.

Park SH, et al. Effects of occupational metallic mercury vapor exposure on suppressor-inducer (CD4+CD45RA+) T lymphocytes and CD57+CD16+ natural killer cells. Int Arch Occup Environ Health. 2000; 73(8): 537-42.

Shenker BJ. Induction of apoptosis in human T-cells by methyl mercury. Toxicol Appl Pharmacol. 1999; 157(1): 23-35.

Shenker BJ, Pankoski L, Zekavat A, Shapiro IM. Mercury-induced apoptosis in human lymphocytes: caspase activation is linked to redox status. Antioxid Redox Signal. 2002; 4(3): 379-89.

Insug O, et al. Mercuric compounds inhibit human monocyte function by inducing apoptosis: evidence for formation of reactive oxygen species(ROS), development of mitochondrial membrane permeability, and loss of reductive reserve. Toxicology. 1997; 124(3): 211-24.

Elghany NA, Stopford W, Bunn WB, Fleming LE. Occupational exposure to inorganic mercury vapour and reproductive outcomes. Occup Med (Lond). 1997; 47(6): 333-6.

Wiksztrajtis, B. Baranski. Epidemiological survey of Lithunia dental offices. Med. Pr. 1973; 24: 248.

Gonzalez MJ, et al. Mercury in human hair: Residents of Madrid, Spain. Arch Environ Health. 1985; 40(4): 225-8.

Katz SA, et al. Use of hair analysis for evaluating mercury intoxication of the human body. J Appl Toxicol. 1992; 12(2): 79-84.

Wilhelm M, Muller F, Idel H. Biological monitoring of mercury vapor exposure by scalp hair analysis in comparison to blood and urine. Toxicol Lett. 1996; 88(1-3): 221-6.

Nonaka S, et al. Lithium treatment protects neurons in CNS from glutamate induced excitability and calcium influx. Neurobiology. 1998; 95(5): 2642-2647.

Endo T, Sakata M, Shaikh ZA. Mercury uptake by primary cultures of rat renal cortical epithelial cells. II. Effects of pH, halide ions, and alkali metal ions. Toxicol Appl Pharmacol. 1995; 134(2): 321-325.

Greenwood MR, et al. Transfer of metallic mercury into the fetus. Experientia. 1972; 28:1455-1456.

Ahlbom A, et al. Dentists, dental nurses, and brain tumors. British Medical Journal. 1986; 292: 262.

Simpson R, et al. Suicide rates of Iowa dentists. J. Of Amer. Dental Assoc. 1983; 107: 441.

Arnetz BB, et al. Suicide among Swedish dentists. Scand J Soc Med. 1987; 15(4): 243-6.

Perlingeiro RC, et al. Polymorphonuclear phagentosis in workers exposed to mercury vapor. Int J Immounopharmacology. 1994; 16(12): 1011-7.

Albers JW, et al. Neurological abnormalities associated with remote occupational elemental mercury exposure. Ann Neurol. 1988; 24(5): 651-9.

Soleo L, et al. Effects of low exposure to inorganic mercury on psychological performance. Br J Ind Med. 1990; 47(2):105-9.

Smith PJ, et al. Effect of exposure to elemental mercury on short term memory. Br J Ind Med. 1983; 40(4): 413-9.

Hua MS, et al. Chronic elemental mercury intoxication. Brain Inj. 1996; 10(5): 377-84.

Gunther W, et al. Repeated neurobehavioral investigations in workers. Neurotoxicology. 1996; 17(3-4): 605-14.

Lai M, et al. Sensitivity of MS detections by MRI. Journal of Neurology, Neurosurgery, and Psychiatry. 1996; 60(3): 339-341.

Newland MC, et al. Behavioral consequences of in utero exposure to mercury vapor in squirrel monkeys. Toxicology & Applied Pharmacology. 1996; 139: 374-386.

Warfvinge K, et al. Mercury distribution in neonatal cortical areas after exposure to mercury vapor. Environmental Research. 1994; 67: 196-208.

Hisatome I, Kurata Y, et al. Block of sodium channels by divalent mercury: role of specific cysteinyl residues in the P-loop region. Biophys J. 2000; 79(3): 1336-45.

Bhattacharya S, Sen S, et al. Specific binding of inorganic mercury to Na(+)-K(+)-ATPase in rat liver plasma membrane and signal transduction. Biometals. 1997; 10(3): 157-62.

Anner BM, Moosmayer M, Imesch E. Mercury blocks Na-K-ATPase by a ligand-dependent and reversible mechanism. Am J Physiol. 1992; 262(5.2): F830-6.

Anner BM, Moosmayer M. Mercury inhibits Na-K-ATPase primarily at the cytoplasmic side. Am J Physiol. 1992; 262(5.2): F84308.

Wagner CA, Waldegger S, et al. Heavy metals inhibit Pi-induced currents through human brush-border NaPi-3 cotransporter in Xenopus oocytes. Am J Physiol. 1996; 271(4.2): F926-30.

Lewis RN, Bowler K. Rat brain (Na+-K+)ATPase: modulation of its ouabain-sensitive K+-PNPPase activity by thimerosal. Int J Biochem. 1983; 15(1): 5-7.

Rajanna B, Hobson M, Harris L, Ware L, Chetty CS. Effects of cadmium and mercury on Na(+)-K(+) ATPase and uptake of 3H-dopamine in rat brain synaptosomes. Arch Int Physiol Biochem. 1990, 98(5): 291-6.

Hobson M, Rajanna B. Influence of mercury on uptake of dopamine and norepinephrine. Toxicol Letters. 1985; 27(2-3): 7-14.

McKay SJ, Reynolds JN, Racz WJ. Effects of mercury compounds on the spontaneous and potassium-evoked release of [3H]dopamine from mouse striatial slices. Can J Physiol Pharmacol. 1986; 64(12):1507-14.

Scheuhammer AM, Cherian MG. Effects of heavy metal cations, sulfhydryl reagents and other chemical agents on striatal D2 dopamine receptors. Biochem Pharmacol. 1985; 34(19): 3405-13.

Hoyt KR, et al. Mechanisms of dopamine-induced cell death and differences from glutamate induced cell death. Exp Neurol. 1997; 143(2): 269-81.

Offen D, et al. Antibodies from ALS patients inhibit dopamine release mediated by L-type calcium channels. Neurology. 1998; 51(4): 1100-3.

Mai J, Sorensen PS, Hansen JC. High dose antioxidant supplementation to MS patients. Effects on glutathione peroxidase, clinical safety, and absorption of selenium. Biol Trace Elem Res. 1990; 24(2): 109-17.

Echeverria, Woods JS, Heyer NJ, et al. Chronic low-level mercury exposure, BDNF polymorphism, and associations with cognitive and motor function. Neurotoxicol Teratol. 2005; 27(6): 781-96.

Bucio L, et al. Uptake, cellular distribution and DNA damage produced by mercuric chloride in a human fetal hepatic cell line. Mutat Res. 1999; 423(1-2): 65-72.

Ho PI, Ortiz D, Rogers E, Shea TB. Multiple aspects of homocysteine neurotoxicity: Glutamate excitotoxicity, kinase hyperactivation and DNA damage. J Neurosci Res. 2002; 70(5): 694-702.

Snyder RD, Lachmann PJ. Thiol involvement in the inhibition of DNA repair by metals in mammalian cells. Source Mol Toxicol. 1989; 2(2): 117-28.

Verschaeve L, et al. Comparative in vitro cytogenetic studies in mercury-exposed human lymphocytes. Muta Res. 1985; 157(2-3): 221-6.

Verschaeve L. Genetic damage induced by low level mercury exposure. Envir Res. 1976; 12: 306-10.

Berglund A. A study of the release of mercury vapor from different types of amalgam alloys. J Dent Res. 1993; 72: 939-946.

Boyer DB. Mercury vaporization from corroded dental amalgam. Dental Materials. 1988; 4: 89-93.

Psarras V, et al. Effect of selenium on mercury vapor released from dental amalgams. Swed Dent J. 1994; 18: 15-23.

Moberg LE. Long term corrosion studies of amalgams and casting alloys in contact. Acta Odontal Scand. 1985; 43:163-177.

Lichtenberg H. Mercury vapor in the oral cavity in relation to the number of amalgam fillings and chronic mercury poisoning. Journal of Orthomolecular Medicine. 1996; 11(2): 87-94.

Hock C, et al. Increased blood mercury levels in patients with Alzheimer’s disease. J. Neural Transm. 1998; 105(1): 59-68.

Chang LW. Neurotoxic effects of mercury. Environ. Res. 1977; 14(3): 329-73.

Soderstrom S, Fredriksson A, Dencker L, Ebendal T. The effect of mercury vapor on cholinergic neurons in the fetal brain. Brain Research & Developmental Brain Res. 1995; 85: 96-108.

Abdulla EM, et al. Comparison of neurite outgrowth with neurofilament protein levels in neuroblastoma cells following mercuric oxide exposure. Clin Exp Pharmocol Physiol. 1995; 22(5): 362-3.

Leong CC, Syed NI, Lorscheider FL. Retrograde degeneration of neurite membrane structural integrity of nerve growth cones following in vitro exposure to mercury. Neuroreport. 2001; 12(4): 733-7.

Oliveira EM, et al. Mercury effects on the contractile activity of the heart muscle. Toxicol Appl Pharmacol. 1994; 1: 86-91.

Duhr EF, Pendergrass JC, Slevin JT, Haley BE. HgEDTA complex inhibits GTP interactions with the E-site of brain beta-tubulin. Toxicology & Applied Pharmacology. 1993; 122 (2): 273-80.

Sorensen N, Murata K, Budtz-Jorgensen E, Weihe P, Grandjean P. Prenatal methylmercury exposure as a cardiovascular risk factor at seven years of age. Epidemiology. 1999; 10(4): 370-5.

Marsh DO, et al. Fetal methyl mercury poisoning. Ann Neurol. 1980; 7: 348-55.

Siblerud RL. The relationship between mercury from dental amalgam and the cardiovascular system. Science of the Total Envir. 1990; 99(1-2): 23-35.

Chang LW, Hartmann HA. Blood-brain barrier dysfunction in experimental mercury intoxication. Acta Neuropathol (Berl). 1972; 21(3): 179-84.

Ware RA, Chang LW, Burkholder PM. An Ultrastructural study on the blood-brain barrier dysfunction following mercury intoxication. Acta Neurolpathol(Berlin). 1974; 30(3): 211-214.

Stejskal VDM, et al. Mercury-specific lymphocytes: an indication of mercury allergy in man. J. Of Clinical Immunology. 1996; 16(1): 31-40.

Kubicka-Muranyi M, et al. Systemic autoimmune disease induced by mercuric chloride. Int Arch Allergy Immunol. 1996; 109(1): 11-20.

Shenker BJ, et al. Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes: Alterations in B-cell function and viability. Immunopharmacol Immunotoxicol. 1993; 15(1): 87-112.

Daum JR. Immunotoxicology of mercury and cadmium on B-lymphocytes. Int J Immunopharmacol. 1993; 15(3): 383-94.

Johansson U, et al. The genotype determines the B cell response in mercury-treated mice. Int Arch Allergy Immunol. 1998; 116(4): 295-305.

Motorkina AV, Barer GM, Volozhin AI. Hg release from amalgam fillings into oral cavity. Stomatologiiia(Mosk). 1997; 76(4): 9-11.

Navas-Acien A, Pollan M, Gustavsson P, Plato N. Occupation, exposure to chemicals and risk of gliomas and meningiomas in Sweden. Am J Ind Med. 2002; 42(3): 214-27.

Arvidson B, Arvidsson J, Johansson K. Mercury deposits in neurons of the trigeminal ganglia after insertion of dental amalgam in rats. Biometals. 1994; 7 (3): 261-263.

Arvidson B. Inorganic mercury is transported from muscular nerve terminasl to spinal and brainstem motorneurons. Muscle Nerve. 1992; 15: 1089-94.

Arvidson B, et al. Retograde axonal transport of mercury in primary sensory neurons. Acta Neurol Scand. 1990; 82: 324-237.

Arvidson B, Arvidsson J. Retrograde axonal transport of mercury in primary sensory neurons innervating the tooth pulp in the rat. Neurosci Lett. 1990; 115(1): 29-32.

Candura SM, et al. Effects of mercuryic chloride and methyly mercury on cholinergic neuromusular transmission. Pharmacol Toxicol. 1997; 80(5): 218-24.

Castoldi AF, et al. Interaction of mercury compounds with muscarinic receptor subtypes in the rat brain. Neurotoxicology. 1996; 17(3-4): 735-41.

Wilkinson LJ, Waring RH. Cysteine dioxygenase: modulation of expression in human cell lines by cytokines and control of sulphate production. Toxicol In Vitro. 2002; 16(4): 481-3.

Tanner CM, et al. Abnormal liver enzyme metabolism in Parkinson’s. Neurology. 1991; 41(5): 89-92.

Heafield MT, et al. Plasma cysteine and sulphate levels in patients with motor neurone disease, Parkinson’s disease, and Alzheimer’s disease. Neurosci Lett. 1990; 110(1-2): 216-20.

Pean A, et al. Pathways of cysteine metabolism in MND/ALS. J Neurol Sci. 1994; 124: 59-61.

Steventon GB, et al. Xenobiotic metabolism in motor neuron disease. Lancet. 1988: 644-47.

Gordon C, et al. Abnormal sulphur oxidation in systemic lupus erythrmatosus (SLE). Lancet. 1992; 339: 8784.

Emory P, et al. Poor sulphoxidation in patients with rheumatoid arthritis. Ann Rheum Dis. 1992; 51(3): 318-20.

Bradley H, et al. Sulfate metabolism is abnormal in patients with rheumatoid arthritis. J Rheumatol. 1994; 21(7): 1192-6.

Perry TL, et al. Hallevorden-Spatz disease: Cysteine accumulation and cysteine dioxygenase defieciency. Ann Neural. 1985; 18(4): 482-489.

Trepka MJ, et al. Factors affecting mercury burdens among German children. Arch Environ Health. 1997; 52(2): 134-8.

Soleo L, et al. Influence of amalgam fillings on urinary mercury excretion. G Ital Med Lav Ergon. 1998; 20(2): 75-81.

Freitas AJ, et al. Effects of Hg2+ and CH3Hg+ on Ca2+ fluxes in the rat brain. Brain Research. 1996; 738(2): 257-64.

Yallapragoda PR, et al. Inhibition of calcium transport by Hg salts in rat cerebellum and cerebral cortex. J Appl Toxicol. 1996; 164(4): 325-30.

Chavez E, et al. Mitochondrial calcium release by Hg+2. J Biol Chem. 1988; 263(8): 3582.

Szucs A, et al. Effects of inorganic mercury and methylmercury on the ionic currents of cultured rat hippocampal neurons. Cell Mol Neurobiol. 1997; 17(3): 273-8.

Busselberg D. Calcium channels as target sites of heavy metals. Toxicol Lett. 1995; 82-83: 255-61.

Rossi AD, et al. Modifications of Ca2+ signaling by inorganic mercury in PC12 cells. FASEB J. 1993; 7: 1507-14.

Eggleton P, et al. Pathophysicological roles of calreticulin in autoimmune disease. Scand J Immunol. 1999; 49(5): 466-73.

Engqvist A, et al. Speciation of mercury excreted in feces from individuals with amalgam fillings. Arch Environ Health. 1998; 53(3): 205-13.

Hill GS. Drug associated glomerulopathies. Toxicol Pathol. 1986; 14(1): 37-44.

Adler SG, et al. Hypersensitivity phenomena and the kidney: Role of drugs and environmental agents. Am J Kidney Dis. 1985.

Abadin HG, et al. Breast-feeding exposure of infants to mercury, lead, and cadmium: A public health perspective. Toxicol Ind Health. 1997; 13(4): 495-517.

Boadi WY, et al. In vitro effect of mercury on enzyme activities and its accumulation in the first-trimester human placenta. Environ Res. 1992; 57(1): 96-106.

Caron GA, et al. Lymphocytes transformation induced by inorganic and organic mercury. Int Arch Allergy. 1970; 37: 76-87.

Nielsen NH, et al. The relationship between IgE-mediated and cell-mediated hyper-sensitives. British J of Dermatol. 1996; 134: 669-72.

Clauw DJ. The pathogenesis of chronic pain and fatigue syndromes. Fibromyalgia Med Hypothesis. 1995; 44: 369-78.

Hanson S. Fibromyalgia, glutamate, and mercury. Heavy Metal Bulletin. 1999; 4: 5-6.

Benga G. Water exchange through erythrocyte membranes. Neurol Neurochir Pol. 1997; 31(5): 905-13.

Villegas J, Martinez R, Andres A, Crespo D. Accumulation of mercury in neurosecretory neurons of mice after long-term exposure to oral mercuric chloride. Neurosci Lett. 1999; 271: 93-96.

Kozik MB, Gramza G. Histochemical changes in the neurosecretory hypothalic nuclei as a result of intoxication with mercury compounds. Acta Histochem. 1980; 22: 367-80.

Nixon DE, Mussmann GV, Moyer TP. Inorganic, organic, and total mercury in blood and urine. J Anal Toxicol. 1996; 10(1): 17-22.

Schweinsberg F. Risk estimation of mercury intake from different sources. Toxicol. Lett. 1994, 72: 45-51.

Pzheusskaia LD. Disintoxication therapy of patients with nonspecific inflammatory diseases of the female genital organs. Akush. Ginekol. 1977; (4): 30-34.

Halbach S, et al. Thiol chelators and mercury effects on isolated heart muscle. Plzen. Lek. Sborn. 1990; 62: 39-41.

Klykov NV. Treatment of patients with myocardial infarction. Vrach. Delo. 1979; 12: 50-3.

Monaci F, et al. Concentrations of major elements and mercury in unstimulated human saliva. Biol Trace Elem Res. 2002; 89(3): 193-203.

Guida PP. Therputic efficacy of unithiol in Buschke’s Scleroderma. Vrach. Delo. 1983; 8: 36-38.

Dubinskii AA, et al. Morpholcial changes in the skin in Scleroderma after treatment with unithiol. Vrach. Delo. 1978; (10): 112-114.

Elhassani SB. The many faces of methyl mercury poisoning. J Toxicol Clin Toxicol. 1982(8): 875-9

Shtelmakh NI, et al. Comparative treatments of rheumatoid arthritis. Vrasch. Delo. 1982; 1: 49-52.

Buchet JP, Lauwerys RR. Influence of DMPS on the mobilization of mercury from tissues of rats pretreated with mercuric chloride, phenylmercury acetate, or mercury vapor. Toxicology. 1989; 54(3): 323-33.

Reinhardt JW. Side effects: Mercury contribution to body burden from dental amalgam. Adv Dent Res. 1992; 6: 110-3.

Gerhard I. Amalgam from gynacological view. Der Frauenarzt. 1995; 36(6): 627-28.

Sterzl I, Prochazkova J, Stejskal VDM, et al. Mercury and nickel allergy: Risk factors in fatigue and autoimmunity. Neuroendocrinology Letters. 1999; 20: 221-228.

Prochazkova J, Sterzl I, Kucerova H, Bartova J, Stejskal VD. The beneficial effect of amalgam replacement on health in patients with autoimmunity. Neuroendocrinology Letters. 2004; 25(3): 211-8.

Kosuda LL, Greiner DL, Bigazzi PE. Effects of HgCl2 on the expression of autoimmune responses and disease in diabetes-prone (DP) BB rats. Autoimmunity. 1997; 26(3): 173-87.

Magos L, Clarkson TW, Hudson AR. The effects of dose of elemental mercury and first pass circulation time on organ distribution of inorganic mercury in rats. Biochem Biophys Acta. 1989; 1991(1): 85-9.

Halbach S. Estimation of mercury dose by a novel quantification of elemental and inorganic species released from amalgam. Int Arch Occup Environ Health. 1995; 67(5): 295-300.

Atchison WD. Effects of neurotoxicants on synaptic transmission. Neurotoxicol Teratol. 1998, 10(5): 393-416.

Sidransky H, Verney E. Influence of lead acetate and selected metal salts on tryptophan binding to rat hepatic nuclei. Toxicol Pathol. 1999; 27(4): 441-7.

Shukla GS, Chandra SV. Effect of interaction of Mn2+withZn2+, Hg2+, and Cd2+ on some neurochemicals in rats. Toxicol Lett. 1982; 10(2-3): 163-8.

Brouwer M, et al. Functional changes induced by heavy metal ions. Biochemistry. 1982; 21(20): 2529-38.

Marcusson JA. Psychological and somatic subjective symptoms as a result of dermatological patch testing with metallic mercury and PHA. Toxicol Lett. 1996; 84(2): 113-22.

Benkelfat C, et al. Mood lowering effect of tryptophan depletion. Arch Gen Psychiatry. 1994; 51(9): 687-97.

Young SN, et al. Tryptophan depletion causes a rapid lowering of mood in normal males. Psychopharmacology. 1985; 87(2): 173-77.

Smith KA, et al. Relapse of depression after depletion of tryptophan. Lancet. 1997; 349(9056): 915-19.

Delgado PL, et al. Serotonin function, depletion of plasma tryptophan, and the mechanism of antidepressant action. Arch Gen Psychiatry. 1990; 47(5): 411-18.

Räsänen L, Kalimo K, Laine J, et al. Contact allergy to gold in dental patients. Br J Dermatol. 1996; 134(4): 673-7.

Osawa J, Kitamura K, Ikezawa Z, Hariya T, Nakajima H. Gold dermatitis due to ear piercing: correlations between gold and mercury hypersensitivities. Contact Dermatitis. 1994; 31(2): 89-91.

Björkner B; Bruze M; Möller H. High frequency of contact allergy to gold sodium thiosulfate. An indication of gold allergy? Contact Dermatitis. 1994; 30(3): 144-51.

Melchart D, Wuhr E, Weidenhammer W, Kremers L. A multicenter survey of amalgam fillings and subjective complaints in non-selected patients in the dental practice. Eur J Oral Sci. 1998; 106: 770-77.

Murtomaa H, Haavio-Manila, Kandolin I. Burnout and its causes in Finnish dentists. Community Dental Oral Epidemiol. 1990; 18: 208-12.

Cheraskin E, Ringsdorf Wm, Medford FH. Daily vitamin C consumption and fatigability. J Am Gerialr Soc. 1976; 24:136-37.

MacDonald EM, Mann AH, Thomas HC. Interferons as mediators of psychiatric morbidity. Lancet. 1978: 1175-78.

Hickie I, Lloyd A. Are cytokines associated with neuropsychiatric syndrome in humans? Int J Immunopharm. 1995; 4: 285-294.

Komaroff AL, Buchwald DS. Chronic fatigue syndrom: an update. Ann Rev Med. 1998; 49: 1-13.

Buchwald DS, Wener MH, Kith P. Markers of inflammation and immune activation in CFS. J Rheumatol. 1997; 24: 372-76.

Demitrack MA, Dale JK. Evidence for impaired activation of the hypothalamic-pituitary-adrenal axis in patients with chronic fatigue syndrome. J Clin Endocrinol Metabol. 1991; 73: 1224-1234.

Turnbull AV, Rivier C. Regulation of the HPA axis by cytokines. Brain Behav Immun. 1995; 20: 253-75.

Ng TB, Liu WK. Toxic effect of heavy metals on cells isolated from the rat adrenal and testis. In Vitro Cell Dev Biol. 1990; 26(1): 24-8.

Sterzl I, Fucikova T, Zamrazil V. The fatigue syndrome in autoimmune thyroiditis with polyglandular activation of autoimmunity. Vnitrni Lekarstvi. 1998; 44: 456-60.

Sterzl I, Hrda P, Prochazkova J, Bartova J. Reactions to metals in patients with chronic fatigue and autoimmune endocrinopathy. Vnitr Lek. 1999; 45(9): 527-31.

Kolenic J, Palcakova D, Benicky L, Kolenicova M. The frequency of auto-antibody occurrence in occupational risk (mercury). Prac Lek. 1993; 45(2): 75-77.

Saito K. Analysis of a genetic factor of metal allergy-polymorphism of HLA-DR-DO gene. Kokubyo Gakkai Zasschi. 1996; 63: 53-69.

Prochazkova J, Ivaskova E, Bartova J, Stejskal VDM. Immunogentic findings in patients with altered tolerance to heavy metals. Eur J Human Genet. 1998; 6: 175.

Ionescu G. Heavy metal load with atopic dermatitis and psoriasis. Biol Med. 1996; 2: 65-68.

Ellingsen DG, Nordhagen HP, Thomassen Y. Uninary selenium excretion in workers with low exposure to mercury vapor. J Appl Toxicol. 1995; 15(1): 33-6.

Ellingsen DG, Efskind J, Haug E, Thomassen Y, Martinsen I, Gaarder PI. Effects of low mercury vapour exposure on the thyroid function in chloralkali workers. J Appl Toxicol. 2000; 20(6): 483-9.

Barregard L, Lindstedt G, Schutz A, Sallsten G. Endocrine function in mercury exposed chloralkali workers. Occup Environ Med. 1994; 51(8): 536-40.

Watanabe C. Selenium deficiency and brain functions: the significance for methylmercury toxicity. Nippon Eiseigaku Zasshi. 2001; 55(4): 581-9.

Watanabe C, Yoshida K, Kasanuma Y, Kun Y, Satoh H. In utero methylmercury exposure differentially affects the activities of selenoenzymes in the fetal mouse brain. Environ Res. 1999; 80(3): 208-14.

Schumann K. The toxicological estimation of heavy metal content (Hg, Cd, Pb) in food for infants and small children. Z Ernahrungswiss. 1990; 29(1): 54-73.

Gebbart E. Chromosone Damage in Individuals exposed to heavy metals. Curr Top Environ Toxicol Chem. 1985; 8: 213-25.

Baranski B. Effect of mercury on the sexual cycle and prenatal and postnatal development of progeny. Med Pr. 1981; 32(4): 271-6.

Shapiro IM, Cornblath DR, Sumner AJ. Neurophysiological and neuropsychological function in mercury-exposed dentists. Lancet. 1982; 1: 1147-1150.

Uzzell BP, Oler J. Chronic low-level mercury exposure and neuropsychological functioning. J of Clin and Exper Neuropsych. 1986; 8: 581-93.

Saengsirinavin C, Pringsulaka P. Mercury levels in urine and head hair of dental personnel. J Dent Assoc Thai. 1988; 38(4): 170-9.

Eid F, Harakeh S. Ban or regulate? Costs of dental occupational safety from mercury. J Health Care Finance. 2003; 30(2): 65-83.

Herber RF, Wibowo AA. Exposure of dentists and assistants to mercury: Levels in urine and hair related to conditions of practice. Community Dent Oral Epidemiol. 1988; 16(3): 153-8.

Sikorski R, Juszkiewicz T. Women in dental surgeries: reproductive hazards in occupational exposure to mercury. Int Arch Occup Environ Health. 1987; 59(6): 551-7.

Lewczuk E, Affelska-Jercha A, Tomczyk J. Occupational health problems in dental practice. Med Pr. 2002; 53(2): 161-5.

Ando T, Wakisaka I, Hatano H. Mercury concentration in gray hair. Nippon Eiseigaku Zasshi. 1989; 43(6): 1063-8.

Mayall FG; Hickman J; Knight LC; Singharo S. An amalgam tattoo of the soft palate: A case report with energy dispersive X-ray analysis. J Laryngol Otol. 1992; 106(9): 834-5.

Godfrey ME. Candida, dysbiosis and amalgam. J. Adv. Med. 1996; 9(2).

Romani L. Immunity to candida albicans: Th1,Th2 cells and beyond. Curr Opin Microbiol. 1999; 2(4): 363-7.

Zamm AV. Candida albicans theraphy: Dental mercury removal, an effective adjunct. J. Orthmol. Med. 1986; 1(4): 261-5.

Stejskal J, Stejskal V. The role of metals in autoimmune diseases and the link to neuroendocrinology. Neuroendocrinology Letters. 1999; 20: 345-358.

Goering Pl, Rowland AS. Toxicity assessment of mercury vapor from dental amalgams. Fundam. Appl Toxicol. 1992; 19: 319-329.

Wehner-Caroli J, Scherwitz C, Schweinsberg F, Fierlbeck G. Exacerbation of pustular psoriasis in mercury poisoning. Hautarzt. 1994; 45(10): 708-10.

Eedy DJ, Burrows D, Dlifford T, Fay A. Elevated T cell subpopulations in dental students. J Prosthet Dent. 1990; 63(5): 593-6.

Yonk LJ, et al. CD+4 helper T-cell depression in autism. Immunol Lett. 1990; 25(4): 341-5.

Jaffe JS, Strober W, Sneller MC. Functional abnormalities of CD8+ T cells define a unique subset of patients with common variable immunodeficiency. Blood. 1993; 82(1): 192-20.

Bernard S, Enayati A, Redwood L, Roger H, Binstock T. Autism: A novel form of mercury poisoning. Med Hypotheses. 2001; 56(4): 462-71.

Cade JR, et al. Autism and schizophrenia linked to malfunctioning enzyme for milk protein digestion. Autism. 1999.

Puschel G, Mentlein R, Heymann E. Isolation and characterization of dipeptyl peptidase IV from human placenta. Eur J Biochem. 1982; 126(2): 359-65.

Kar NC, Pearson CM. Dipeptyl Peptidases in human muscle disease. Clin Chim Acta. 1978; 82(1-2): 185-92.

Shibuya-Saruta H, Kasahara Y, Hashimoto Y. Human serum dipeptidyl peptidase IV (DPPIV) and its unique properties. J Clin Lab Anal. 1996; 10(6): 435-40.

Blais A, Morvan-Baleynaud J, Friedlander G, Le Grimellec C. Primary culture of rabbit proximal tubules as a cellular model to study nephrotoxicity of xenobiotics. Kidney Int. 1993; 44(1): 13-8.

Moreno-Fuenmayor H, Borjas L, Arrieta A, Valera V. Plasma excitatory amino acids in autism. Invest Clin. 1996; 37(2): 113-28.

Carlsson ML. Is infantile autism a hypoglutamatergic disorder? J Neural Transm. 1998; 105(4-5): 525-35.

Rolf LH, Haarman FY, Grotemeyer KH, Kehrer H. Serotonin and amino acid content in platelets of autistic children. Acta Psychiatr Scand. 1993; 87(5): 312-6.

Naruse H, Hayashi T, Takesada M, Yamazaki K. Metabolic changes in aromatic amino acids and monoamines in infantile autism and a new related treatment. No To Hattatsu. 1989; 21(2): 181-9.

Wecker L, Miller SB, Cochran SR, Dugger DL, Johnson WD. Trace element concentrations in hair from autistic children. Defic Res. 1985; 29(1): 15-22.

Reichrtova E, et al. Cord serum Immunoglobulin E related to environmental contamination of human placentas with oganochlorine compounds. Envir Health Perspect. 1999; 107(11): 895-99.

Gavett SH, et al. Residual oil fly ash amplifies allergic cytokines, airway responsiveness, and inflammation in mice. Am J Respir Crit Care Med. 1999; 160(6): 1897-1904

Kramer U, et al. Traffic-related air pollution is associated with atopy in children living in urban areas. Epidemiology. 2000; 11(1): 64-70.

Plaitakis A, Constantakakis E. Altered metabolism of excitatory amino acids, N-acetyl-aspartate and acetyl-aspartyl-glutamate in amyotrophic lateral sclerosis. Brain Res Bull. 1993; 30(3-4): 381-6.

Rothstein JD, Martin LJ, Kuncl RW. Decreased glutamate transport by the brain and spinal cord in ALS. New Engl J Med. 1992; 326: 1464-8.

Froissard P, et al. Role of glutathione metabolism in the glutamate-induced programmed cell death of neuronal cells. Eur J Pharmacol. 1997; 236(1): 93-99.

Kim P, Choi BH. Selective inhibition of glutamate uptake by mercury in cultured mouse astrocytes. Yonsei Med J. 1995; 36(3): 299-305.

Brookes N. In vitro evidence for the role of glutatmate in the CNS toxicity of mercury. Toxicology. 1992; 76(3): 245-56.

Albrecht J, Matyja E. Glutamate: A potential mediator of inorganic mercury toxicity. Metab Brain Dis. 1996; 11: 175-84.

Tirosh O, Sen CK, Roy S, Packer L. Cellular and mitochondrial changes in glutamate-induced HT4 neuronal cell death. Neuroscience. 2000; 97(3): 531-41.

Folkers K, et al. Biochemical evidence for a deficiency of vitamin B6 in subjects reacting to MSL-Glutamate. Biochem Biophys Res Comm. 1981; 100: 972.

Felipo V, et al. L-carnatine increases the affinity of glutamate for quisqualate receptors and prevents glutamate neurotoxicity. Neurochemical Research. 1994; 19(3): 373-377.

Akaike A, et al. Protective effects of a vitamin-B12 analog (methylcobalamin, against glutamate cytotoxicity in cultured cortical neurons. European J of Pharmacology. 1993; 241(1): 1-6.

Srikantaiah MV, Radhakrishnan AN. Studies on the metabolism of vitamin B6 in the small intestine. Purification and properties of monkey intestinal pyridoxal kinase. Indian J Biochem.
1970; 7(3): 151-6.

Lipozencic J, Milavec-Puretic V. Contact allergy and psoriasis. Arh Hig Rada Toksikol. 1992; 43(3): 249-54.

Roujeau JC, et al. Acute generalized exanthematous pustulosis. Analysis of 63 cases. Arch Dermatol. 1991; 127(9): 1333-8.

Yiannias JA, Winkelmann RK, Connolly SM. Contact sensitivities in palmar plantar pustulosis (acropustulosis). Contact Dermatitis. 1998; 39(3): 108-11.

Rivola J, Krejci I, Imfeld T, Lutz F. Cremation and the environmental mercury burden. Schweiz
Monatsschr Zahnmed.
1990; 100(11): 1299-303.

Matter-Grutter C, Baillod R, Imfeld T, Lutz F. Mercury emission measurements in a crematorium: The dentistry aspects. Schweiz Monatsschr Zahnmed. 1995; 105(8): 1023-8.

Yoshida M, Kishimoto T, Yamamura Y, et al. Amount of mercury from dental amalgam filling released into the atmosphere by cremation. Nippon Koshu Eisei Zasshi. 1994; 41(7): 618-24.

Barber T. Inorganic mercury intoxification similar to ALS. J of Occup Med. 1978; 20: 667-9.

Brown IA. Chronic mercurialism-a cause of the clinical syndrome of ALS. Arch Neurol Psychiatry. 1954; 72: 674-9.

Schwarz S, Husstedt I. ALS after accidental injection of mercury. J Neurol Neurosurg Psychiatry. 1996; 60: 698.

Felmus MT, Patten BM, Swanke L. Antecedent events in amyotrophic lateral sclerosis. Neurology. 1976; 26(2): 167-72.

Patten BM, Mallette LE. Motor neuron disease: retrospective study of associated abnormalities. Dis Nerv Syst. 1976; 37(6): 318-21.

Kantarjian A. A syndrome clinically resembling amyotrophic lateral sclerosis following chronic mercurialism. Neurology. 1961; 11: 639-644.

Munch G, Gerlach M, Sian J, Wong A, Riederer P. Advanced glycation end products in neurodegeneration: More than early markers of oxidative stress? Ann Neurol. 1998; 44(3): S85-8.

Hu H, Abedi-Valugerdi M, Moller G. Pretreatment of lymphocytes with mercury in vitro induces a response in T cells from genetically determined low-responders and a shift of the interleukin profile. Immunology. 1997; 90(2): 198-204.

Moller G, Abedi-Valugerdi M. Major histocompatibility complex class II antigens are required for both cytokine production and proliferation induced by mercuric chloride in vitro. J Autoimmun. 1997; 10(5): 441-6.

Hu H, Moller G, Abedi-Valugerdi M. Mechanism of mercury-induced autoimmunity: Both T helper 1- and T helper 2-type responses are involved. Immunology. 1999; 96(3): 348-57.

HultmanP, Johansson U, Turley SJ. Adverse immunological effects and autoimmunity induced by dental amalgam in mice. FASEB J. 1994; 8: 1183-90.

Pollard KM, Lee DK, Casiano CA. The autoimmunity-inducing xenobiotic mercury interacts with the autoantigen fibrillarin and modifies its molecular structure and antigenic properties. J Immunol. 1997; 158: 3421-8.

Abedi-Valugerdi M, Hansson M, Moller G. Genetic control of resistance to mercury-induced immune/autoimmune activation. Scand J Immunol. 2001; 54(1-2): 190-7.

Hultman P, Nielsen JB. The effect of toxicokinetics on murine mercury-induced autoimmunity. Environ Res. 1998; 77(2): 141-8.

Hultman, et al. Activation of the immune system and systemic immune-complex deposits in Brown Norway rats with dental amalgam restorations. J Dent Res. 1998; 77(6): 1415-25.

Chetty CS, McBride V, Sands S, Rajanna B. Effects in vitro on rat brain Mg(++)-ATPase. Arch Int Physiol Biochem. 1990; 98(5): 261-7.

Bara M, Guiet-Bara A, Durlach J. Comparison of the effects of taurine and magnesium on electrical characteristics of artificial and natural membranes. Magnesium. 1985; 4(5-6): 325-32.

Rodier PM. Developing brain as a target of toxicity. Environ Health Perspect. 1995; 103(6): 73-76.

Rice DC. Issues in developmental neurotoxicology: interpretation and implications of the data. Can J Public Health. 1998; 89(1): S31-40.

Rice DC, Barone S. Critical periods of vulnerability for the developing nervous system: Evidence from human and animal models. Environ Health Perspect. 2000; 108(3): 511-533.

Crinnion WJ. Environmental toxins and their common health effects. Altern Med Rev. 2000; 5(1): 52-63.

Fukino H, Hirai M, Hsueh YM, Yamane Y. Effect of zinc pretreatment on mercuric chloride-induced lipid. Toxicol Appl Pharmacol. 1984; 73(3): 395-401.

Smith T, Pitts K, Mc Garvey JA, Summers AO. Bacterial oxidation of mercury metal vapor. Appl Environ Microbiol. 1998; 64(4): 1328-32.

Sutton KG, McRory JE, Guthrie H, Snutch TP. P/Q-type calcium channels mediate the activity-dependent feedback of syntaxin-1A. Nature. 1999; 401(6755): 800-4.

Sheiner EK, Sheiner E, Hammel RD, Potashnik G, Carel R. Effect of occupational exposures on male fertility: literature review. Ind Health. 2003; 41(2): 55-62.

Leung TY, Choy CM, Yim SF, Lam CW, Haines CJ. Whole blood mercury concentrations in sub-fertile men in Hong Kong. Aust N Z J Obstet Gynaecol. 2001; 41(1): 75-7.

Godfrey ME, Wojcik DP, Krone CA. Apolipoprotein E genotyping as a potential biomarker for mercury neurotoxicity. J Alzheimers Dis. 2003; 5(3): 189-95.

Stefanovic V, et al. Kidney ectopeptidases in mercuric chloride-induced renal failure. Cell Physiol Biochem. 1998; 8(5): 278-84.

Mondal MS, Mitra S. Inhibition of bovine xanthine oxidase activity by Hg2+ and other metal ions. J Inorg Biochem. 1996; 62(4): 271-9.

Sastry KV, Gupta PK. In vitro inhibition of digestive enzymes by heavy metals and their reversal by chelating agents. Bull Environ Contam Toxicol. 1978; 20(6): 729-35.

Gupta PK, Sastry KV. Effect of mercuric chloride on enzyme activities in the digestive system and chemical composition of liver and muscles of the catfish. Ecotoxicol Environ Saf. 1981; 5(4): 389-400.

Kidd RF. Results of dental amalgam removal and mercury detoxification. Altern Ther Health Med. 2000; 6(4): 49-55.

Olanow CW, Arendash GW. Metals and free radicals in neurodegeneration. Curr Opin Neurol. 1994; 7(6): 548-58.

Troy CM, Shelanski ML. Down-regulation of copper/zinc superoxide dismutase causes apoptotic death in PC12 neuronal cells. Proc. National Acad Sci, USA. 1994; 91(14): 6384-7.

Rothstein JD, Dristol LA, Hosier B, Brown RH, Kunci RW. Chronic inhibition of superoxide dismustase produces apoptotic death of spinal neurons. Proc Nat Acad Sci, USA. 1994; 91(10): 4155-9.

Beal MF. Coenzyme Q10 administration and its potential for treatment of neurodegenerative diseases. Biofactors. 1999; 9(2-4): 262-6.

DiMauro S, Moses LG. CoQ10 use leads to dramatic improvements in patients with muscular disorder. Neurology. 2001.

Schultz C, et al. CoQ10 slows progression of Parkinson’s Disease. Archives of Neurology. 2002.

Schulz JB, Matthews RT, Henshaw DR, Beal MF. Neuroprotective strategies for treatment of lesions produced by mitochondrial toxins: implications for neurodegenerative diseases. Neuroscience. 1996; 71(4): 1043-8.

Nagano S, Ogawa Y, Yanaghara T, Sakoda S. Benefit of a combined treatment with trientine and ascorbate in familial amyotrophic lateral sclerosis model mice. Neurosci Lett. 1999; 265(3): 159-62.
Kidd PM. Neurodegeneration from mitochondrial insufficiency: Nutrients, stem cells, growth factors, and prospects for brain rebuilding using integrative management. Altern Med Rev. 2005; 10(4): 268-293.

Langolf GD, Albers JW. Elemental mercury exposure: peripheral neurotoxicity. Br J Ind Med 1982; 39(2): 136-9.

Walsh SJ, Rau LM. Autoimmune disease overlooked as a leading cause of death in women. Am J Public Health. 2000; 90: 1463-1466.

Miszta H; Dabrowski Z. Effect of mercury and combined effect of mercury on the activity of acetylcholinesterase of rat lymphocytes during in vitro incubation. Folia Haematol Int Mag Klin Morphol Blutforsch. 1989; 116(1): 151-5.

Bear D, Rosenbaum J, Norman R. Aggression in cat and human precipitated by a cholinesterase inhibitor. The Journal Psychosomatics. 1986; 27: 7.

Blumer W. Mercury toxicity and dental amalgam fillings. Journal of Advancement in Medicine. 1998; 11(3): 219.

Cooley RL, Stilley JS, Lubow RM. Mercury vapor produced during sterilization of amalgam-contaminated instruments. The Journal of Prosthetic Dentistry. 1985; 53(3): 304- 308.

Panasiuk J. Peripheral blood lymphocyte transformation test in various skin diseases of allergic origin. Przegl Dermatol. 1980; 67(6): 823-9.

Barnett JH. Discoid lupus erythematosus exacerbated by contact dermatitis. Cutis. 1990; 46(5): 430-2.

Dowling AL, Iannacone EA, Zoeller RT. Maternal hypothyroidism selectively affects the expression of neuroendocrine-specific protein A messenger ribonucleic acid in the proliferative zone of the fetal rat brain cortex. Endocrinology. 2001; 142(1): 390-399.

Edwards AE. Depression and candida. JAMA. 1985; 253(23): 3400.

Crook WG. Depression associated with Candida albicans infections. JAMA. 1984; 251: 22.

Rasmussen HH, Mortensen PB, Jensen IW. Depression and magnesium deficiency. Int J Psychiatry Med. 1989; 19(1): 57-63.

Bekaroglu M, Aslan Y, Gedik Y, Karahan C. Relationships between serum free acids and zinc with ADHD. J Child Psychol Psychiatry. 1996; 37(2): 225-7.

Vandoolaeghe E, Neels H, Demedts P, et al. Lower serum zinc in major depression is a sensitive marker of treatment resistance and of the immune/inflammatory response in that illness. Biol Psychiatry. 1997; 42(5): 349-358.

Olivieri G, et al. Mercury induces cell cytotoxicity and oxidative stress and increases beta-amyloid secretion and tau phosphorylation in SHSY5Y neuroblastoma cells. J Neurochem. 2000; 74(1): 231-6.

Tabner BJ, Turnbull S, El-Agnaf OM, Allsop D. Formation of hydrogen peroxide and hydroxyl radicals from A(beta) and alpha-synuclein as a possible mechanism of cell death in Alzheimer’s disease and Parkinson’s disease. Free Radic Biol Med. 2002; 32(11): 1076-83.

Ho PI, Collins SC, et al. Homocysteine potentiates beta-amyloid neurotoxicity: Role of oxidative stress. J Neurochem. 2001; 78(2): 249-53.

Overzet K, Gensler TJ, Kim SJ, et al. Small nucleolar RNP Scleroderma autoantigens associate with phosphorylated serine/arginine splicing factors during apoptosis. Arthritis Rheum. 2000; 43(6): 1327-36.

van Benschoten MM. Acupoint energetics of mercury toxicity and amalgam removal with case studies. American Journal of Acupuncture. 1994; 22(3): 251-262.

Schwartz RB, Garada BM, Komaroff AL, Gleit M, Holman BL. Detection of intracranial abnormalities in patients with chronic fatigue syndrome: comparison of MRI and SPECT. Am J Roentgenol. 1994; 162(4): 935-41.

Ichiso M, Salit IE, Abbey SE. Assessment of regional cerebral perfusion by SPECT in CFS. Nucl Med Commun. 1992; 13: 767-72.

Patarca-Monero R, Klimas NG, Fletcher MA. Immunotherapy of chronic fatigue syndrome. Chronic Fatigue Syndrome. 2001; 8(1): 3-37.

DeBecker P, De Meirleir K, Joos E, Velkeniers B. DHEA I.V. ACTH in patients with CFS. Horm Metab Res. 1999; 31(1): 18-21.

De Meirleir K, Bisbal C, Campine I, De Becker, et al. A 37 kDa 1-5A binding protein as a potential biochemical marker for CFS. Am J Med. 2000; 108(2): 99-105.

Suhadolnik RJ, Peterson DL, Obrien K, et al. Biochemical evidence for a novel low molecular weight 2-5A-dependent Rnase L in CFS. J Interferon Cytokine Res. 1997; 17(7): 377-85.

Geier MR, Geier DA. Timerosal in childhood vaccines, neurodevelopmental disorders, and heart disease in the U.S. J of Amer Physicians and Surgeons. 2003; 8(1).

Ganser AL, Kirschner DA. The interaction of mercurials with myelin: Comparison of in vitro and in vivo effects. Neurotoxicol. 1985; 6(1): 63-77.

Windebank AJ. Specific inhibition of myelination by lead in vitro: Comparison with arsenic, thallium, and mercury. Exp Neurol. 1986; 94(1): 203-12.

Savage DF, Stroud RM. Structural basis of aquaporin inhibition by mercury. J Mol Biol. 2007; 368(3): 607-17.

Yukutake Y, Tsuji S, Hirano Y, Adachi T, et al. Mercury chloride decreases the water permeability of aquaporin-4-reconstituted proteoliposomes. Biol Cell. 2008.

Salzer HM. Relative hypoglycemia as a cause of neuropsychiatric illness. J National Med Assoc. 1996; 58(1): 12-17.

Heninger GR, et al. Depressive symptoms, glucose tolerance, and insulin tolerance. J Nervous and Mental Dis. 1975; 161(6): 421-32.

Winokur A, et al. Insulin resistance in patients with major depression. Am J Psychiatry, 1988, 145(3): 325-30.

Virkkunen M, Huttunen MO. Evidence for abnormal glucose tolerance among violent offenders. Neuropsychiobilogy. 1982; 8: 30-40.

Markku I, Virkkunen L. Aggression, suicidality, and serotonin. J Clinical Psy. 1992; 53(10): 46-51.

Pranjic N, Sinanovic O, et al. Assessment of chronic neuropsychological effects of mercury vapour poisoning in chloral-alkali plant workers. Bosn J Basic Med Sci. 2002; 2(1-2): 29-34.

Linnoila M, et al. Low serotonin metabolite differentiates impulsive from non-impulsive violent behavior. Life Sciences. 1983; 33(26): 2609-2614.

Lopez-Ibor JJ. Serotonin and psychiatric disorders. Int Clinical Psychopharm. 1992; 7(2): 5-11.

Thomas DE, et al. Tryptophan and nutritional status in patients with senile dementia. Psychological Med. 1986; 16: 297-305.

Urberg M, Zemel MB. Evidence for synergism between chromium and nicotinic acid in the control of glucose tolerance in elderly humans. Metabolism. 1987; 36(9): 896-899.

Anderson RA, et al. Effects of supplemental chromium on patients with reactive hypoglycemia. Metabolism. 1987; 36(4): 351-355.

Haut MW, Morrow LA, Pool D, Callahan TS, Haut JS, Franzen MD. Neurobehavioral effects of acute exposure to inorganic mercury vapor. Appl Neuropsychol. 1999; 6(4): 193-200.

Huang X, Cuajungco MP, et al. Cu(II) potentiation of Alzheimer’s abeta neurotoxicity: Correlation with cell-free hydrogen peroxide production and metal reduction. J Biol Chem. 1999; 274(52): 37111-6.

Waggoner DJ, Bartnikas TB, Gitlin JD. The role of copper in neurodegenerative disease. Neurobiol Dis. 1999; 6(4): 221-30.

Torsdottir G, Kristinsson J, Gudmundsson G, Snaedal J, Johannesson T. Copper, ceruloplasmin and superoxide dismustase (SOD) in amyotrophic lateral sclerosis. Pharmacol Oxicol. 2000; 87(3): 126-30.

Estevez AG, Beckman JS, et al. Induction of nitric oxide-dependent apoptosis in motor neurons by zinc-deficient superoxide dismutase. Science. 1999; 286(5449): 2498-500.

Cookson MR, Shaw PJ. Oxidative stress and motor neurons disease. Brain Pathol. 1999; 9(1): 165-86.

Rojas M, Olivet C. Occupational exposure and health effects of metallic mercury among dentists and dental assistants: A preliminary study. Acta Cient Venez. 2000; 51(1): 32-8.

Nadorfy-Lopez E, Bello B. Skeletal muscle abnormalities associated with occupational exposure to mercury vapors. Histol Histopathol. 2000; 15(3): 673-82.

Nerudova J, Cabelkova Z, Cikrt M. Mobilization of mercury by DMPS in occupationally exposed workers. Int J Occup Med Environ Health. 2000; 13(2): 131-46.

Glina DM, Satut BT, Andrade EM. Occupational exposure to metallic mercury in the dentist’s office of a public primary health care clinic in the city of Sao Paulo. Cad Saude Publica. 1997; 13(2): 257-267.

Aydin N, Yigit A, Keles MS, Kirpinar I, Seven N. Neuropsychological effects of low mercury exposure in dental staff in Erzurum, Turkey. Int Dent J. 2003; 53(2): 85-91.

Karahalil B, Rahravi H, Ertas N. Examination of urinary mercury levels in dentists in Turkey. Hum Exp Toxicol. 2005; 24(8): 383-8.

Moller AT, Spangenberg JJ. Stress and coping amongst South African dentists in private practice. J Dent Assoc S Afr. 1996; 51(6): 347-57.

Stefansson CG, Wicks S. Health care occupations and suicide in Sweden 1961-1985. Soc Psychiatry Psychiatr Epidemiol. 1991; 26(6): 259-64.

Kobayashi MS, Han D, Packer L. Antioxidants and herbal extracts protect HT-4 neuronal cells against glutamate-induced cytotoxicity. Free Radic Res. 2000; 32(2): 115-24.

Ferrante RJ, Klein AM, Dedeoglu A, Beal MF. Therapeutic efficacy of EGb761 (Gingko biloba extract) in a transgenic mouse model of amyotrophic lateral sclerosis. J Mol Neurosci. 2001; 17(1): 89-96.

Bridi R, Crossetti FP, Steffen VM, Henriques AT. The antioxidant activity of standardized extract of Ginkgo biloba (EGb 761) in rats. Phytother Res. 2001;15(5): 449-51.

Li Y, Liu L, Barger SW, Mrak RE, Griffin WS. Vitamin E suppression of microglial activation is neuroprotective. J Neurosci Res. 2001; 66(2): 163-70.

Kang JH, Eum WS. Enhanced oxidative damage by the familial amyotrophic lateral sclerosis-associated Cu, Zn-superoxide dismutase mutants. Biochem Biophys Acta. 2000; 1524 (2-3): 162-70.

Eum WS. Enhanced oxidative damage by the familial amyotrophic lateral sclerosis-associated Cu, Zn-superoxide dismutase mutants. Biochem Biophys Acta. 2000; 1524 (2-3): 162-70.

Liu H, Zhu H, Eggers DK, et al. Copper(2+) binding to the surface residue cysteine 111 of His46Arg human copper-zinc superoxide dismutase, a familial amyotrophic lateral sclerosis mutant. Biochemistry. 2000; 39(28): 8125-32.

Kruman II, Pedersen WA, Springer JE, Mattson MP. ALS-linked Cu/Zn-SOD mutation increases vulnerability of motor neurons to excitotoxicity by a mechanism involving increased oxidative stress and perturbed calcium homeostasis. Exp Neurol. 1999; 160(1): 28-39.

Doble A. The role of excitotoxicity in neurodegenerative disease: Implications for therapy. Pharmacol Ther. 1999; 81(3): 163-221.

Urushitani M, Shimohama S. N-methyl-D-aspartate receptor-mediated mitochondrial Ca(2+) overload in acute excitotoxic motor neuron death: a mechanism distinct from chronic neurotoxicity after Ca(2+) influx. J Neurosci Res. 2001; 63(5): 377-87.

Cookson MR, Shaw PJ. Oxidative stress and motor neurons disease. Brain Pathol. 1999; 9(1): 165-86.

Torres-Aleman I, Barrios V, Berciano J. The peripheral insulin-like growth factor system in amyotrophic lateral sclerosis and in multiple sclerosis. Neurology. 1998; 50(3): 772-6.

Dall R, Sonksen PH, et al. The effect of four weeks of supraphysiological growth hormone administration on the insulin-like growth factor axis in women and men. GH-2000 Study Group. J Clin Endocrinol Metab. 2000; 85(11): 4193-200.

Pons S, Torres-Aleman I. Insulin-like growth factor-I stimulates dephosphorylation of ikappa B through the serine phosphatase calcineurin. J Biol Chem. 2000; 275(49): 38620-5.

Lai EC, Rudnicki SA. Effect of recombinant human insulin-like growth factor-I on progression of ALS. A placebo-controlled study. Neurology. 1997; 49(6): 1621-30.

Yuen EC, Mobley WC. Therapeutic applications of neurotrophic factors in disorders of motor neurons and peripheral nerves. Mol Med Today. 1995; 1(6): 278-86.

Dore S, Kar S, Quirion R. Rediscovering an old friend, IGF-I: potential use in the treatment of neurodegenerative diseases. Trends Neurosci. 1997; 20(8): 326-31.

Couratier P, Vallat JM. Therapeutic effects of neurotrophic factors in ALS. Rev Neurol (Paris). 2000; 156(12): 1075-7.

Van den Berghe G, Bowers C, et al. Neuroendocrinology of prolonged critical illness: Effects of exogenous thyrotropin-releasing hormone and its combination with growth hormone secretagogues. J Clin Endocrinol Metab. 1998; 83(2): 309-19.

Rupp, Paffenberger. Significance to health of mercury used in dental practice: Reports of councils and bureaus. JADA. 1971; 182.

Kong J, Xu Z. Mitochondrial degeneration in motor neurons triggers the onset of ALS in mice expressing a mutant SOD1 gene. J Neurosci. 1998; 18: 3241-50.

Cassarino DS, Bennett JPJ, Mitochrondrial mutations and oxidative pathology, protective nuclear responses, and cell death in neurodegeneration. Brain Res Brain Res Rev. 1999; 29:1-25.

Mitchell JD. Heavy metals and trace elements in amyotrophic lateral sclerosis. Neurol Clin. 1987; 5(1): 43-60.

Sienko DG, Davis JP, Taylor JA. ALS: A case-control study following detection of a cluster in a small Wisconsin community. Arch Neurol. 1990; 9: 255-62.

Provinciali L, Giovagnoli A. Antecedent events in ALS: Do they influence clinical onset and progression? Neuroepidemiology. 1990; 9: 255-62.

Roelofs-Iverson RA, Elveback LR. ALS and heavy metals. Neurology. 1984; 34: 393-5.

Armon C, O’Brien PC. Epidemiologic correlates of sporadic ALS. Neurology. 1991; 41: 1077-84.

Vanacore N, Corsi L, Fabrizio E, Bonifati V, Meco G. Relationship between exposure to environmental toxins and motor neuron disease: a case report. Med Lav. 1995;
86(6): 522-33.

Guermonprez L, Ducrocq C, Gaudry-Talarmain YM. Inhibition of acetylcholine synthesis and tyrosine nitration induced by peroxynitrite are differentially prevented by antioxidants.
Mol Pharmacol. 2001; 60(4): 838-46.

Mahboob M, Shireen KF, Atkinson A, Khan AT. Lipid peroxidation and antioxidant enzyme activity in different organs of mice exposed to low level of mercury. J Environ Sci Health B. 2001; 36(5):687-97.

Kawashima T, Doh-ura K, Kikuchi H, Iwaki T. Cognitive dysfunction in patients with amyotrophic lateral sclerosis is associated with spherical or crescent-shaped ubiquitinated intraneuronal inclusions in the parahippocampal gyrus and amygdala, but not in the neostriatum. Acta Neuropathol (Berl). 2001; 102(5): 467-72.

Urushitani M, Shimohama S. The role of nitric oxide in amyotrophic lateral sclerosis. Amyotroph Lateral Scler Other Motor Neuron Disord. 2001; 2(2): 71-81.

Torreilles F, Salman-Tabcheh S, Guerin M. Torreilles J. Neurodegenerative disorders: the role of peroxynitrite. Brain Res Brain Res Rev. 1999; 30(2): 153-63.

Aoyama K, Matsubara K, Kobayashi S. Nitration of manganese superoxide dismutase in cerebrospinal fluids is a marker for peroxynitrite-mediated oxidative stress in neurodegenerative diseases. Ann Neurol. 2000; 47(4): 524-7.

Guermonprez L, Ducrocq C, Gaudry-Talarmain YM. Inhibition of acetylcholine synthesis and tyrosine nitration induced by peroxynitrite are differentially prevented by antioxidants. Mol Pharmacol 2001 Oct; 60(4): 838-46.

Cheshire WP. The shocking tooth about trigeminal neuralgia. New England Journal of Medicine. 2000; 342: 2003.

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

Hugoson A. Results obtained from patients referred for the investigation of complaints related to oral galvanism. Swed Dent J. 1986; 10: 15-28.

Muller AW, Van Loon LA, Davidson CL. Electrical potentials of restorations in subjects without oral complaints. J Oral Rehabil. 1990; 17: 419-24.

Raue H. Resistance to therapy: Think of tooth fillings. Medical Practice. 1980; 32(72): 2303-2309.

Olynyk F, Sharpe DH. Mercury poisoning in paper pica. N Engl J Med. 1982; 306(17): 1056-1057.

Uchino M, Tanaka Y, Ando Y, Yonehara T, Hara A, Mishima I, Okajima T, Ando M. Neurologic features of chronic minamata disease (organic and mercury poisoning) and incidence of complications with aging. J Environ Sci Health B. 1995; 30(5): 699-715.

Cavalleri A, Belotti L, Gobba FM, Luzzana G, Rosa P, Seghizzi P. Colour vision loss in workers exposed to elemental mercury vapour. Toxicology Letters. 1995; 77(1-3): 351-356.

Urban P, Gobba F, Nerudova J, Lukas E, Cabelkova Z, Cikrt M. Color discrimination impairment in workers exposed to mercury vapor. Neurotoxicology. 2003; 24(4-5): 711-716.

Wesnes K. A pilot study of the effect of low level exposure to mercury on the health of dental surgeons. Occupational & Environmental Medicine. 1995; 52(12): 813-7.

Tirado V, Garcia MA, Franco A. Pneuropsychological disorders after occupational exposure to mercury vapors. Rev Neurol. 2000; 31(8): 712-6.

Powell TJ. Chronic neurobehavioural effects of mercury poisoning on a group of chemical workers. Brain Inj. 2000; 14(9): 797-814.

Wossmann W, Kohl M, Gruning G, Bucsky P. Mercury intoxication presenting with hypertension and tachycardia. Arch Dis Child. 1999; 80(6): 556-7.

Cloarec S, Deschenes G, Sagnier M, Rolland JC, Nivet H. Arterial hypertension due to mercury poisoning: diagnostic value of captopril. Arch Pediatr. 1995; 2(1): 43-6.

Henningsson C, Hoffmann S, McGonigle L, Winter JS. Acute mercury poisoning (acrodynia) mimicking pheochromocytoma in an adolescent. J Pediatr. 1993; 122(2): 252-3.

Hightower J. Methylmercury contamination in fish: Human exposures and case reports. Environmental Health Perspectives. 2002.

Razagui IB, Haswell SJ. Mercury and selenium concentrations in maternal and neonatal scalp hair: relationship to amalgam-based dental treatment received during pregnancy. Biol Trace Elem Res. 2001; 81(1): 1-19.

Cernichiari E, Brewer R, Myers GJ, Marsh DO, Berlin M, Clarkson TW. Monitoring methyl mercury during pregnancy: maternal hair predicts fetal brain exposure. Neurotoxicology. 1995; 16(4): 729005-10.

Behan P, Chaudhuri A. Astrocyte malfunction as cause of MS. Journal of the Royal College of Physicians of Edinburgh. 2002.

Ritchie KA, Gilmour WH, Macdonald EB, et al. Health and neuropsychological functioning of dentists exposed to mercury. Occup Environ Med. 2002; 59(5): 287-93.

Ritchie KA, Burke FJ, et al. Mercury vapour levels in dental practices and body mercury levels of dentists and controls. Br Dent J. 2004; 197(10): 625-32.

London SJ, Bowman JD, Sobel E, et al. Exposure to magnetic fields among electrical workers in relation to leukemia risk in Los Angeles County. Am J Ind Med. 1994; 26(1): 47-60.

Caplan LS, Schoenfeld ER, O’Leary ES, Leske MC. Breast cancer and electromagnetic fields—a review. Ann Epidemiol. 2000; 10(1): 31-44.

Adegbembo AO, Watson PA, Lugowski SJ. The weight of wastes generated by removal of dental amalgam restorations and the concentration of mercury in dental wastewater. J. Canadian Dental Assoc. 2002; 68(9): 553-8.

Lindh U, Hudecek R, Danersund A, Eriksson S, Lindvall A. Removal of dental amalgam and other metal alloys supported by antioxidant therapy alleviates symptoms and improves quality of life in patients with amalgam-associated ill health. Neuroendocrinol Lett. 2002; 23(5-6): 459-82.

Leistevuo J, Leistevuo T, Tenovuo J. Mercury in saliva and the risk of exceeding limits for sewage in relation to exposure to amalgam fillings. Arch Environ Health. 2002; 57(4): 366-70.

Lewis RN, Bowler K. Rat brain (Na-K+)ATPase: Modulation of its ouabain-sensitive K-PNPPase activity by thimerosal. Int J Biochem. 1983; 15(1): 5-7.

Hokkfen B, Kodding R, Hesch RD. Regulation of thyroid hormone metabolism in rat liver fractions. Biochim Biophys Acta. 1978; 539(1): 114-24.

Choy CM, Lam CW, et al. Infertility, blood mercury concentrations, and dietary seafood consumption: a case control study. BJOG. 2002; 109: 1121-1125.

Nath J, Safar R. Late-onset bipolar disorder due to hyperthyroidism. Acta Psychiatr Scand. 2001; 104: 72-75.

Muller AF, Drexhage HA, Berghout A. Postpartum thyroiditis and autoimmune thyroiditis in women of childbearing age: recent insights and consequences for antenatal and postnatal care. Endocrine Reviews. 2001; 22(5): 605-30.

Joshi A, Douglass CW, et al. The relationship between amalgam restorations and mercury levels in male dentists and nondental health professionals. J. Public Health Dent. 2003; 63(1): 52-60.

Aydin N, Karaoglanoglu S, Yigit A, et al. Neuropsychological effects of low mercury exposure in dental-staff in Erzurum, Turkey. Int. Dent. J. 2003; 53(2): 85-91.

Uversky VN, Li J, Fink AL. Metal-triggered structural transformations, aggregation, and fibrillation of human alpha-synuclein: A possible molecular NK between Parkinson’s disease and heavy metal exposure. J Biol Chem. 2001; 276(47): 44284-96.

Beuter A, de Geoffroy A, Edwards R. Quantitative analysis of rapid pointing movements in Cree subjects exposed to mercury and in subjects with neurological deficits. Environ Res. 1999; 80(1): 50-63.

Singh I, Pahan K, Khan M, Singh AK. Cytokine-mediated induction of ceramide production is redox-sensitive. Implications to proinflammatory cytokine-mediated apoptosis in demyelinating diseases. J. Biol. Chem. 1998; 273: 20354-20362.

Kim CY, Satoh H, et al. Protective effect of melatonin on methylmercury-induced mortality in mice. Tohoku J Exp Med. 2000; 191(4): 241-6.

Olivieri G, Hock C, et al. Mercury induces cell cytotoxicity and oxidative stress and increases beta-amyloid secretion and tau phosphorylation in SHSY5Y neuroblastoma cells. J Neurochem. 2000; 74(1): 231-6.

Baccarelli A, Pesatori AC, Bertazzi PA. Occupational and environmental agents as endocrine disruptors: experimental and human evidence. J Endocrinol Invest. 2000; 23(11): 771-81.

Libe R, Baccarelli A, et al. Long-term follow-up study of patients with adrenal incidentalomas. Eur J Endocrinol. 2002; 147(4): 489-94.

Manzo L, Candura SM, Costa LG, et al. Biochemical markers of neurotoxicity: A review of mechanistic studies and applications. Hum Exp Toxicol. 1996; 15(1): S20-35.

Femiano F, Scully C. Burning mouth syndrome (BMS): Double blind controlled study of Alpha-lipoic acid therapy. J Oral Pathol Med. 2002; 31: 267-9.

Packer L, Tritschler HJ, Wessel K. Neuroprotection by the metabolic antioxidant alpha-lipoic acid. Free Radic Biol Med. 1997; 22(1-2): 359-78.

McCarty MF. Versatile cytoprotective activity of lipoic acid may reflect its ability to activate signaling intermediates that trigger the heat-shock and phase II responses. Med Hypotheses. 2001; 57(3): 313-7.

Whiteman M, Tritschler H, Halliwell B. Protection against peroxynitrite-dependent tyrosine nitration and alpha 1-antiproteinase inactivation by oxidized and reduced lipoic acid. FEBS Lett. 1996; 379(1): 74-6.

Patrick L. Mercury toxicity and antioxidants: Part 1: Role of glutathione and alpha-lipoic acid in the treatment of mercury toxicity. Altern Med Rev. 2002; 7(6): 456-71.

Pigatto PD, Guzzi G, et al. Recovery from mercury-induced burning mouth syndrome due to mercury allergy. Dermatitis. 2004: 15: 75-7

Gregus Z, et al. Effect of lipoic acid on biliary excretion of glutathione and metals. Toxicol APPl Pharmacol. 1992; 114(1): 88-96.

Asposhian HV, Morgan DL, et al. Vitamin C, glutathione, or lipoic acid did not decrease brain or kidney mercury in rats exposed to mercury vapor. J Toxicol Clin Toxicol. 2003; 41(4): 339-47.

Pritchard C, et al. Pollutants appear to be the cause of the huge rise in degenerative neurological conditions. Public Health. 2004.

Sannchez-Gomez MV, Malute C. AMPA and kainate receptors each mediate excitotoxicity in oligodendroglial cultures. Neurobiology of Disease. 1999; 6: 475-485.

Yoshika A, et al. Pathophysiology of oligodendroglial excitotoxicity. Neuroscience Research. 1996; 46: 427-437.

Singh P, et al. Prolonged glutamate excitotoxicity: Effects on mitochondrial antioxidants and antioxidant enzymes. Molecular Cell Biochemistry. 2003; 243: 139-145.

Leuchtmann EA, et al. AMPA receptors are the major mediators of excitotoxin death in mature oligodendrocytes. Neurobiology of Disease. 2003; 14: 336-348.

Takahashi JL, et al. Interleukin1 beta promotes oligodendrocyte death through glutamate excitotoxicity. Annal Neurology. 2003; 53: 588-595.

Kong J, Zhang Z, Musch MW, et al. ovel role of the vitamin D receptor in maintaining the integrity of the intestinal mucosal barrier. Am J Physiol Gastrointest Liver Physiol. 2008; 294(1): G208-16.

Rayssiguier Y, Gueux E, et al. High fructose consumption combined with low dietary magnesium intake may increase the incidence of the metabolic syndrome by inducing inflammation. Magnes Res. 2006; 19(4): 237-43.

Bo S, Durazzo M, Pagano G, et al. Dietary magnesium and fiber intakes and inflammatory and metabolic indicators in middle-aged subjects from a population-based cohort. Am J Clin Nutr. 2006; 84(5): 1062-9.

Guerrero-Romero F, Rodríguez-Morán. Hypomagnesemia, oxidative stress, inflammation, and metabolic syndrome. Diabetes Metab Res Rev. 2006; 22(6): 471-6.

Dandona P. Effects of antidiabetic and antihyperlipidemic agents on C-reactive protein. Mayo Clin Proc. 2008; 83(3): 333-42.

Vasdev S, Gill V, Singal P. Role of advanced glycation end products in hypertension and atherosclerosis: therapeutic implications. Cell Biochem Biophys. 2007; 49(1): 48-63.

Barnes DM, Kircher EA. Effects of mercuric chloride on glucose transport in 3T3-L1 adipocytes. Toxicol In Vitro. 2005; 19(2): 207-14.

Iturri SJ, Peña A. Heavy metal-induced inhibition of active transport in the rat small intestine in vitro: Interaction with other ions. Comp Biochem Physiol C. 1986; 84(2): 363-8.

Klip A, Grinstein S, Biber J, Semenza G. Interaction of the sugar carrier of intestinal brush-border membranes with HgCl2. Biochim Biophys Acta. 1980; 598(1): 100-14.

Mankertz J, Schulzke JD. Altered permeability in inflammatory bowel disease: Pathophysiology and clinical implications. Curr Opin Gastroenterol. 2007; 23(4): 379-83.

Welcker K, Martin A, Kölle P, Siebeck M, Gross M. Increased intestinal permeability in patients with inflammatory bowel disease. Eur J Med Res. 2004; 9(10): 456-60.

Soeters PB, Luyer MD, Greve JW, Buurman WA. The significance of bowel permeability. Curr Opin Clin Nutr Metab Care. 2007; 10(5): 632-8.

Cereijido M, Contreras RG, Flores-Benítez D, et al. New diseases derived or associated with the tight junction. Arch Med Res. 2007; 38(5): 465-78.

Weber P, Brune T, Ganser G, Zimmer KP. Gastrointestinal symptoms and permeability in patients with juvenile idiopathic arthritis. Clin Exp Rheumatol. 2003; 21(5): 657-62.

Fasano A, Shea-Donohue T. Mechanisms of disease: The role of intestinal barrier function in the pathogenesis of gastrointestinal autoimmune diseases. Nat Clin Pract Gastroenterol Hepatol. 2005; 2(9): 416-22.

Böhme M, Diener M, Mestres P, Rummel W. Direct and indirect actions of HgCl2 and methyl mercury chloride on permeability and chloride secretion across the rat colonic mucosa. Toxicol Appl Pharmacol. 1992; 114(2): 285-94.

Watzl B, Abrahamse SL, Lishaut S, Neudecker C, Pool-Zobel BL. Enhancement of ovalbumin-induced antibody production and mucosal mast cell response by mercury. Food Chem Toxicol. 1999; 37(6): 627-37.

Aduayom I, Denizeau F, Jumarie C. Multiple effects of mercury on cell volume regulation, plasma membrane permeability, and thiol content in the human intestinal cell line Caco-2. Cell Biol Toxicol. 2005; 21(3-4): 163-79.

van Hoek AN, de Jong MD, van Os CH. Effects of dimethylsulfoxide and mercurial sulfhydryl reagents on water and solute permeability of rat kidney brush border membranes. Biochim Biophys Acta. 1990; 1030(2): 203-10.

Stirling CE. Mercurial perturbation of brush border membrane permeability in rabbit ileum. J Membr Biol. 1975; 23(1): 33-56.

Miller DS. HgCl2 inhibition of nutrient transport in teleost fish small intestine. J Pharmacol Exp Ther. 1981; 216(1): 70-6.

Jiang H P, Liu CA. Protective effect of glutamine on intestinal barrier function in patients receiving chemotherapy. 2006; 9(1): 59-61.

Moen B, Hollund B, Riise T. Neurological symptoms among dental assistants: a cross-sectional study. J Occup Med Toxicol. 2008; 3: 10.

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