Mechanisms by which mercury causes over 30 chronic health conditions

This research paper can be found in numerous places online, but I wanted to clean up the formatting and share it here in a more readable way. It’s very long so you might consider doing a keyword search on it for any of your symptoms – the information contained is astonishing:

Mercury Exposure Levels from Amalgam Dental Fillings; Documentation of Mechanisms by Which Mercury Causes over 30 Chronic Health Conditions; Results of Replacement of Amalgam Fillings; and Occupational Effects on Dental Staff

Bernard Windham, Editor
Chemical Engineer
12164 Whitehouse Road, Tallahassee, FL, 32311,
tel. 850-878-9024

I. Introduction
II. Toxicity and Health Effects of Mercury
III. Systemic Mercury Intake Levels from Amalgam Filling Exposure
IV. Immune System Effects and Autoimmune Disease
V. Medical Studies Finding Health Problems Related to Amalgam Fillings
VI. Documented Results of Removal of Amalgam Fillings
VII. Tests for Mercury Level and Toxicity and Treatments
VIII. Health Effects from Dental Staff Exposure to Mercury
IX. Scientific Panel and Government Bodies That Have Found Amalgam Fillings Unsafe
References

I. Introduction

1. Toxic metals such as mercury, lead, cadmium, etc. have been documented to be neurotoxic, immunotoxic, reproductive/developmental toxins that according to U.S. Government agencies cause adverse health effects and learning disabilities to millions in the U.S. each year, especially children and the elderly (160, 105, 27d). Exposure of humans and animals to toxic metals such as mercury, cadmium, lead, copper, aluminum, arsenic, chromium, manganese, etc. is widespread and in many areas increasing. A 2009 study found that inorganic mercury levels in people have been increasing rapidly in recent years (543b). It 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 percent of women aged 18 to 49 in the 1999-2000 NHANES survey, that level rose to 30 percent of women by 2005-2006. Surveys in all states using hair tests have found dangerous levels of mercury in an average of 22 % of the population, with over 30% in some states like Florida and New York (543c).

The U.S. Center for Disease Control (276) 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 7 toxics having 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 (276). A National Academy of Sciences report of July 2000 and other studies (39, 125, 308, 540) 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. A California clinical study found adverse effects at exposures below 10 ug/l (540). 1 ug/l is the upper level of mercury exposure recommended by the German Commission on Human Biomonitoring in the blood (39). The National Academy of Sciences safety limit is 5 micrograms per liter. But 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. And mercury amalgam dental fillings have been found to be the largest source of both inorganic and methyl mercury in most 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 (405, 342). 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 (342, 369, 375, 382, 595).

While there have been large increases of most neurological and immune conditions among adults over the last 2 decades (574), 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 (2, 409, 441, 476). A recent report by the National Research Council found that 50% of all pregnancies in the U.S. are now resulting in prenatal or postnatal mortality, significant birth defects, developmental neurological or immune conditions, or otherwise chronically unhealthy babies (441). Exposure to toxic chemicals or environmental factors appear to be a factor in as much as 28 percent of the 4 million children born each year (441, 160), with 1 in 6 having one of the neurological conditions previously listed. EPA estimates that over 3 million of these are related to lead or mercury toxicity (2, 125, 276, 409), with approximately 25% of U.S. infants receiving dangerous levels of mercury exposure (276). A recent study found that prenatal Hg exposure is correlated with lower scores in neurodevelopmental screening, but more so in the linguistic pathway (32c). 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 6 months (476), and a followon 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 (476b). Thimerosal has also been found to cause hormonal effects (555, 413). Prenatal exposure to mercury has also been found to predispose animals and infants to seizures and epilepsy (5, 52).

The health effects of toxic metals are synergistic with other toxic exposures such as pesticides, endocrine disrupting substances like organochlorine compounds and PCBs, etc. There are also synergistic effects with the various types of parasites, bacteria, viruses to which people have common exposures and commonly become infected when the immune system is weakened by toxic exposures (485, 469b, 470) While there is considerable commonality to the health effects commonly 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.

II. Toxicity and Health Effects of Mercury

1. Dental amalgam contains about 50 % mercury, as well as other toxic metals such as tin, copper, nickel, palladium, etc. The average filling has 1 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 (182, 192, 276b, 292, 348, 349, 525), resulting in significant exposure for most with amalgam fillings (see Section III). Mercury vapor is transmitted rapidly throughout the body, easily crosses cell membranes, and like organic methyl mercury has significant toxic effects at much lower levels of exposure than other inorganic mercury forms (38, 281, 287, 304, 329). The OSHA level for mercury vapor in air is 50% lower than for organic mercury in air. According to the U.S. EPA & ATSDR, mercury is among the top 3 toxic substances adversely affecting large numbers of people (217), and amalgam is the number one source of exposure for most people (see III).

A large U.S. Centers for Disease Control epidemiological study, NHANES III, found that those with more amalgam fillings (more mercury exposure) have significantly higher levels of chronic health conditions (543). The conditions in which the number of dental amalgam surfaces were most highly correlated with disease incidence were MS, epilepsy, migraines, mental disorders, diseases of the nervous system, disorders of the thyroid gland, cancer, and infectious diseases (543). 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 (543). MS clusters in areas with high metals emissions from facilities such as metal smelters have been documented (184).

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 are due to the death of these 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 (576, 585). Most of these excitotoxins are secreted from microglial immune cells in the central nervous system. This not only destroys these myelin-producing cells 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 resulting in MS are mercury and aspartame, with additional effects from MSG and methanol. Mercury and other toxic metals inhibit astrocyte function in the brain and CNS (119), causing increased glutamate and calcium related neurotoxicity (119, 333, 416, 496) which are factors in neural degeneration in MS and ALS. There is evidence that astrocyte damage/malfunction is a major factor in MS (544). Mercury and increased glutamate activate free radical forming processes like xanthine oxidase which produce oxygen radicals and oxidative neurological damage (142, 13). Nitric oxide related toxicty caused by peroxynitrite formed by the reaction of NO with superoxide anions, which results in nitration of tyrosine residues in neurofilaments and manganese Superoxide Dimustase (SOD) has been found to cause inhibition of the mitochondrial respiratory chain, inhibition of the glutamate transporter, and glutamate-induced neurotoxicity involved in ALS (524, 521).

It is now known the cause for the destruction of the myelin in the lesions is overactivation of the microglia in the region of the myelin (585). 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 calming down inflammation of the microglia.

Mercury and cadmium inhibiting magnesium and zinc levels as well as inhibiting glucose transfer are other mechanisms by which mercury and toxic metals are factors in metabolic syndrome and insulin resistance/diabetes (43, 198, 338, 589). Reduced levels of magnesium and zinc are related to metabolic syndrome, insulin resistance, and brain inflammation and are protective against these conditions (587, 43).

According to neurologist Dr. RL Blaylock (585), 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 (576) . 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 2X a day. They 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 triggers harmful immune reactions.

2. 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:

(a) is cytotoxic (kills cells) (2, 21, 27, 36, 56, 147, 148, 150, 160, 210, 259, 295, 333/333)

(b) penetrates and damages the blood brain barrier (311), resulting in accumulation of mercury and other toxic substances in the brain (14, 20, 21b, 25, 85, 99, 175, 273, 301, 305, /149, 262, 274); also accumulates in the motor function areas of the brain and CNS (48, 119, 175, 291, 327, 329).

(c) is neurotoxic (kills brain and nerve cells): damages brain cells and nerve cells (19, 27, 34, 36, 43, 69, 70, 147, 148, 175, 207, 211, 258, 273, 291, 295, 327, 329, 301, 303, 305, 395/39, 262, 274, 303); 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 (13, 56, 98, 102, 145, 169, 170, 184, 213, 219, 250, 257, 259, 286, 288, 290, 291, 302, 324, 326, 329, 416, 424, 442, 496, 564, 565); kills or inhibits production of brain tubulin cells (66, 67, 161, 166, 207, 258, 300); inhibits production of neurotransmitters by inhibiting: calcium-dependent neurotransmitter release (372, 432), dihydroteridine reductase (27, 122, 257, 333), nitric oxide synthase (259), blocking neurotransmitter amino acids (412), and effecting phenylalanine, serotonin, tyrosine and tryptophan transport to neurons (34, 122, 126, 257, 285, 288, 333, 372, 374, 412/333)

(d) is immunotoxic (damages and inhibits immune T-cells, B-cells, neutrophil function, etc.) (17, 27, 31, 38, 44, 45, 46, 60, 127, 128, 129, 130, 152, 155, 165, 181, 226, 252, 270, 285, 316, 343, 355, 425, 467/272) and induces ANA antibodies and autoimmune disease (38, 43, 45, 59, 60, 118, 181, 234, 269, 270, 313, 314, 334, 342, 343, 425, 405)

(e) is nepthrotoxic (toxic to kidneys) (14, 20, 203, 209c, 223, 254, 260, 268, 334, 438)

(f) is endocrine system-disrupting chemical (accumulates in pituitary gland and damages or inhibits pituitary glands hormonal functions at very low levels (9, 19, 20, 25, 85, 99, 105, 273, 312, 327, 348, 369, 543b/274), adrenal gland function (84, 369, 381), thyroid gland function (50, 212, 369, 382, 459, 508-511, 35), thymus gland function (513a), and disrupts enzyme production processes at very low levels of exposure (9, 13, 33, 35, 56, 111, 194, 258, 348, 355, 410-412)

(g) exposure to mercury vapor (or methyl mercury) causes rapid transmittal through the placenta to the fetus (20, 22-24, 27, 38, 39, 61, 112, 186, 281, 287, 304, 311, 338, 339, 348, 361, 366, 20/ 4, 22, 37, 39, 41, 42) 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 (287, 304, 276e, etc.).

(h) reproductive and developmental toxin (2, 4, 9, 10, 22, 23, 24, 31, 37, 38, 41, 61, 105, 125, 160, 175, 275, 281, 305, 338, 361, 367, 381, 20/4, 39, 55, 149, 162, 255, 308, 339, 357, 540); damages DNA (296, 327, 272, 392, 142, 38, 41, 42, 35) and inhibits DNA & RNA synthesis (114, 175, 35/149); damages sperm, lowers sperm counts and reduces motility. (4, 37, 104.105, 159, 160, 433, 35/4, 55, 162); causes menstrual disturbances (9, 27, 146); reduces bloods ability to transport oxygen to fetus and transport of essential nutrients including amino acids, glucose, magnesium, zinc and Vit B12 (43, 96, 198, 260d, 264, 338, 339, 347, 427); depresses enzyme isocitric dehydrogenase (ICD) in fetus, causes reduced iodine uptake & hypothyroidism (50, 91, 212, 222, 369, 382, 390, 459, 35ab) ; causes learning disabilities and impairment, and reduction in IQ (1, 3, 38, 110, 160, 285c, 264, 338, 509/39), causes infertility (4, 9, 10, 24, 38, 121, 146, 357, 365, 367, 511 /4, 10, 55, 162), causes birth defects (23, 35ab, 37, 38, 50, 110, 142, 241, 338c, 509, 511/241).

(i) prenatal/early postnatal exposure affects level of nerve growth factor in the brain, impairs astrocyte function, and causes imbalances in development of brain (38, 119, 131, 161, 175, 194, 305, 458/149, 255, 39)

(j) 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 (84, 35, 201, 539), and increased risk of acute myocardial infarction (35, 59, 201, 202, 205, 212, 232, 306, 310, 351, 510, 50/201, 308).

(k) causes immune system damage resulting in allergies, asthma, lupus (234, 260e), schleraderma (468), chronic fatigue syndrome (CFS), and multiple sensitivities (MCS) (8, 17, 26, 35, 45, 46, 60, 75, 86, 87, 90, 95, 97, 101, 128, 129, 131, 132, 154, 156, 168, 181, 212, 226, 228, 230, 234, 265, 267, 296, 313, 342, 388, 445, 595, 446/272) and neutrophil functional impairment (285, 404, 467/59, etc.).

(l) causes interruption of the cytochromeC oxidase system/ATP energy function (43, 84, 232, 338c, 35) 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 (34, 35, 69, 70, 73, 210, 212, 226, 232, 258, 260)

(m) inhibition of immune system facilitates increased damage by bacterial, viral, and fungal infections (17, 45, 59, 129, 131, 251, 296, 350, 40), and increased antibiotic resistance (116, 117, 161, 389, 53, 79).

(n) 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 (338, 405, 35, 21c) and adversely alters bacterial populations in the intestines causing leaky gut syndrome with toxic, incompletely digested complexes in the blood (222, 228b, 35) and accumulation of heliobacter pylori, a suspected major factor in stomach ulcers and stomach cancer (256) and candida albicans, as well as poor nutrient absorption.

(o) forming strong bonds with and modification of the-SH groups of proteins causes mitochondrial release of calcium (1, 21, 35, 38, 43, 329, 333, 432), as well as altering molecular function of amino acids and damaging enzymatic process (33, 96, 111, 194, 252, 338, 405, 410-412) resulting in improper cysteine regulation (194), inhibited glucose transfer and uptake (338, 254), damaged sulfur oxidation processes (33, 194, 338), and reduced glutathione availability (necessary for detoxification) (13, 126, 54).

3. 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 (1, 14, 16, 19, 20, 25, 34, 38, 50, 61, 85, 99, 162, 211, 273, 274, 287, 327, 348, 360, 366, 369, 543b).

Thus mercury has a greater effect on the functions of these areas. Studies have documented that mercury causes hypothyroidism (50, 390, 35), damage of thyroid RNA (458), autoimmune thyroiditis (369, 382, 91) and impairment of conversion of thyroid T4 hormone to the active T3 form (369, 382, 459, 35, 50d, 91). An overactive thyroid gland, or hyperthyroidism, can trigger restlessness, hyperactivity, insomnia and irritability – symptoms that could be mistaken for mania (560). 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. “Collectively, reports show that 30-60% of women positive for TPO antibodies in pregnancy develop postpartum thyroiditis, ” the researchers point out (561), calling it “a strong association.” 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 (508). 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 (509).

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 (509). Hypothyroidism is a well documented cause of mental retardation (509). Women with the highest levels of thyroid-stimulating-hormone (TSH) and lowest free levels of thyroxine 17 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 8.

Based on study findings, maternal hypothyroidism appears to play a role in at least 15% of children whose IQs are more than 1 standard deviation below the mean, millions of children. Studies have also established a “clear association” between the presence of thyroid antibodies and spontaneous abortions (511), as well as a connection between maternal thyroid disease and babies born with heart, brain, and kidney defects (509c). Levels of recurrent abortions in a population with positive levels of thyroid antibodies in one study were 40%, 5 times the normal rate (511).

Hypothyroidism is a well documented risk factor in spontaneous abortions and infertility (9). Another study of pregnant women who suffer from hypothyroidism (underactive thyroid) found a four-times greater risk for miscarriage during the second trimester than those who don’t, and women with untreated thyroid deficiency were four-times more likely to have a child with a developmental disabilities and lower I.Q. (509). The American Assoc. 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 (558).

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 (390e). 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 (85), while another (348) found the mean level to be 30ppb- 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 (543b). 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 (99). This may explain why dentists have much higher levels of emotional problems, depression, suicide, etc (Section VIII.). Amalgam fillings, nickel and gold crowns are major factors in reducing pituitary function (35, 50, 369, etc.). Supplementary oxytocin extract has been found to alleviate many of these mood problems (35), along with replacement of metals in the mouth (Section VI.). The normalization of pituitary function also often normalizes menstrual cycle problems, endometriosis, and increases fertility (9, 35).

The thymus gland plays a significant part in the establishment of the immune system and lymphatic system from the 12^th 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 (513a). 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 (513b). 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 (513c). Pyruvate and glycolysis problems are often seen in mercury toxic children being treated for autism (409). L-arginine restored thymulin activity, TEC proliferation, NKT cytotoxicity, cytokine profiles and nitrite and nitrate plasma levels both in vivo and in vitro (513a).

4. Mercury’s biochemical damage at the cellular level include DNA damage, inhibition of DNA and RNA synthesis (4, 38, 41, 42, 114, 142, 175, 197, 272, 296, 305, 392/149); alteration of protein structure (33, 111, 114, 194, 252/114); alteration of the transport of calcium (333, 43, 96, 254, 329, 432); inhibition of glucose transport (338, 254), and of enzyme function and other essential nutrient transport (96, 198, 254, 258, 263, 264, 338, 339, 347, 410-412); induction of free radical formation (13, 54, 496), depletion of cellular glutathione (necessary for detoxification processes) (111, 126), inhibition of glutathione peroxidase enzyme (13, 258, 496), endothelial cell damage (202), abnormal migration of neurons in the cerebral cortex (149), and immune system damage (34, 38, 111, 194, 226, 252, 272, 316, 325, 355).

Part of the toxic effects of mercury, cadmium, lead, etc. are through their replacing essential minerals such as zinc at their sites in enzymes, disabling the necessary enzymatic processes.

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. (13, 35c, 56, 84, 98, 145, 169, 207b, 258, 424, 442-444, 453, 462, 496). Mercury induced lipid peroxidation has been found to be a major factor in mercury’s neurotoxicity, along with leading to decreased levels of glutathione peroxidation and superoxide dismustase (SOD) (13, 254, 489, 494-496, 577). Metalloprotein (MT) are involved in metals transport and detoxification (442, 464). Mercury inhibits sulfur ligands in MT and in the case of intestinal cell membranes inactivates MT that normally bind cuprous ions (477), 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 (114, 241, 296, 442, 464, 477, 495). 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 (114, 60, 313, 342, 369, 442, 464). Of a population of over 3000 tested by the immune lymphocyte reactivity test (MELISA, 60, 342), 22% tested positive for inorganic mercury and 8% for methyl mercury .

Programmed cell death (apoptosis) is documented to the 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 inflamatory cytokine Tumor Necrosis Factor-alpha (TNFa) (126), reactive oxygen species and oxidative stress (13, 43b, 56a, 296b), reduced glutathione levels (56, 126a, 111a), inhibition of protein kinase C (43), nitric oxide and peroxynitrite toxicity (43a), excitotoxicity and idation (490, 496, 521, 524), excess free cysteine levels (56d, 111a), excess glutamate toxicity (13b, 416e), excess dopamine toxicity (56d, 13a), beta-amyloid generation (462), increased calcium influx toxicity (416e, 296b, 333, 432, 462c, 507)and DNA fragmentation (296) and mitochondrial membrane dysfunction (56d, 416e, 51a).

TNFa (tumor necrosis factor-alpha) is a cytokine that controls a wide range of immune cell response in mammals, including cell death (apoptosis). This process is involved in inflamatory and degenerative neurological conditions like ALS, MS, Parkinson’s, rheumatoid arthritis, etc. Cell signaling mechanisms like sphingolipids are part of the control mechansim for the TNFa apoptosis mechanism (126a). 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 mechinsisms 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 inflamatory effects and cellular apoptosis in neuronal and immune cells (126b, 126c).

(11) 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 (408-414, 439, 464, 468, 476, 33, 160, 251c), schizophrenia (409, 410), lupus (234, 330, 331, 468, 260e), scleroderma (468), eczema and psoriasis (323, 342, 385, 419, 455, 33), and allergies (26, 46, 60, 95, 132, 152, 156, 271, 313, 330, 331, 445, 446, 468).

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 (411, 412) as well as of xanthine oxidase (439). 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 (410).

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 (413, 60, 313). 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 (33, 114, 194, 412), enzymatic processes involving vitamins B6 and B12 (418), effects on the cytochrome-C energy processes (43, 84, 232, 338c, 35), along with mercury’s adverse effects on cellular mineral levels of calcium, magnesium, zinc, and lithium (43, 96, 119, 198, 333, 386, 427, 432, 38).

And 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 (60, 203d, 313, 314, 21). Most doctors treating such conditions also usually recommend supplementing the deficient essential minerals previously noted that mercury affects, often obtaining a hair element test to determine imbalances and needs (386, 484).

But 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 (413, 313, 415).

Much mercury in saliva and the brain is also organic (220, 272, 506), since mouth bacteria and other organisms in the body methylate inorganic mercury to organic mercury (51, 81, 225, 503b, 506, 512). Studies and clinical tests have found amalgam to be the largest source of methyl mercury in most people (506, 220, 79, 386, etc.). Bacteria also oxidize mercury vapor to the water soluble, ionic form Hg (II) (431).

A clinical study found that methyl mercury in saliva is significantly higher in those with amalgam fillings than those without, and correlated with the number of amalgam fillings (506). The average level of methyl mercury in the blood of a group with amalgam was more than 4 times that of groups without amalgam or that had amalgam replced. Total mercury in those with amalgams was over 10 times that of those without amalgam. Other studies have found similar results (512, 79, etc.).

5. Because of the extreme toxicity of mercury, only ½ gram is required to contaminate a 10 acre lake to the extent that a health warning would be issued by the government to not eat the fish (151, 160). Over half the rivers and lakes in Florida have such health warnings banning or limiting eating of fish, and most other states and 4 Canadian provinces have similar health warnings (2). 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 (2)

Over 30 % of all U.S. lakes have mercury health warnings and 15% of all U.S. river miles. 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 1part per million) have died from chronic mercury poisoning (104, 160, 2). Since mercury is an estrogenic chemical and reproductive toxin, themajority of the rest cannot reproduce. The average male Florida panther has higher estrogen levels than females, due to the estrogenic properties of mercury (105, 160). Similar is true of some other animals at the top of the food chain like alligators, polar bears, minks, seals, beluga and orca whales, etc. , which are affected by mercury and other hormone disrupting chemicals. (105, 533)

7. An average amalgam filling contains over ½ gram of mercury, and the average adult had at least 5 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 (182, 192, 292, 348, 349, 525), so that within 10 years up to half has been found to have been transferred to the body of the host (18, 34, 35, 182, 86c, & section III). In patients with galvanic cell in their oral cavity we found decreased levels of antiinflamatory markers, such as secretory IgA, IgA 1, IgA 2, and lysozyme, and increased levels of the proinflammatory marker albumin (192i).

The amount of mercury released by a gold alloy bridge over amalgam over a 10 year period was measured to be approx. 101 milligrams (mg) (60% of total) or 30 micrograms (ug) per day (18).

8. 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 (38, 82, 183, 287, 360, 376e, 21a, section III).

Mercury vapor rapidly crosses the blood-brain barrier (14, 85, 311) and placenta of pregnant women (20, 22-24, 27, 38, 105, 162, 186, 231, 281, 287, 304, 308, 311, 361) Developmental, learning, and behavioral effects have been found from mercury vapor at much lower levels than for exposure to methyl mercury (287, 304). Similarly for inhibition of some essential cellular processes (333, 338, 329).

9. 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 (548, 549), 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 (548, 549), 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 (231), amounting to several hundred grams per year per office. This is in addition to air emissions. In Canada the annual amount discharged is about 2 tons per year (28), with portions ending up in waters/fish, some in landfills and cropland, and 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 (547b).

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 (547).

Mercury excreted into sewers by those with amalgam fillings was found by government agencies to be the second largest source of mercury in sewers (548, 549, 553). 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 (553). The percentage exceeding the standard doubled for each additional 10 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 that small country, cremation released over 65 kilograms of mercury per year as emissions, often exceeding site air mercury standards (420), 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 5 ten acre lakes to the extent there would be dangerous levels in fish (151). A Japanese study estimated mercury emissions from a small crematorium there as 26 grams per day (421). 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% (422).

10. 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 (3, 160).

Studies have found that both genetic susceptibility and environmental exposures are a factor in xenobiotic related effects and disease propagation (21d, 7e, 11a, 230b, etc.). Large numbers of animal studies have documented that genetically susceptible strains are more affected by xenobiotic exposures than less susceptible strains (234, 336, 425, 526, etc.).

Some genetic types are susceptible to mercury induced autoimmunity and some are resistant and thus much less affected (234, 336, 425, 383, 21d). 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 of autoimmunity.

Also when a condition has been initiated and exposure levels decline, autoimmune antibodies also decline in animals or humans (342, 369, 405, 233, 234d). 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 (425c). Mercury has been found to affect both Th1 and Th2 cytokines causing an increase in inflammatory Th2 cytokines (152, 181, 285, 404b).

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 (501). Mercury inhibits production of insulin and is a factor in diabetes and hypoglycemia, with significant reductions in insulin need after replacement of amalgam filings and normalizing of blood sugar (35).

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 (501d). 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) (501e).

Another genetic difference found in animals and humans is cellular retention differences for metals related to the ability to excrete mercury (426). For example it has been found that individuals with genetic blood factor type APOE-4 do not excrete mercury readily and bioaccumulate mercury, resulting in susceptibility to chronic autoimmune conditions such as Alzheimer’s, Parkinson’s, etc. as early as age 40 (437cd, 577, 35), whereas those with type APOE-2, which contains 2 cysteine molocules, readily excrete mercury and are less susceptible. Those with type APOE-3 are intermediate to the other 2 types. The incidence of autoimmune conditions have increased to the extent this is now one of the leading causes of death among women (450).

Another study found that many of the symptoms and signs of chronic candidiasis, multiple chemical sensitivity and chronic fatigue syndromes 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 (404).

Other studies (285c) 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 (128), as well as maternal exposure being linked to mental retardation (110) and birth defects (23, 35, 37, 38, 50, 142, 241, 361, 338c/241).

III. Systemic Mercury Intake Level from Amalgam Fillings

1. The tolerable daily exposure level for mercury developed in a report for Health Canada is .014 micrograms/kilogram body weight (ug/kg) or approximately 1 ug/day for average adult (209). The U.S. EPA Health Standard for elemental mercury exposure (vapor) is 0.3 micrograms per cubic meter of air (2). The U.S. ATSDR health standard (MRL) for mercury vapor is 0.2 ug/ M ³ of air, and the MRL for methyl mercury is 0.3 ug/kg body weight/day (217).

For the average adult breathing 20 M ³ of air per day, this amounts to an exposure of 4 or 6 ug/day for the 2 elemental mercury standards. The EPA health guideline for methyl mercury is 0.1 ug/kg body weight per day or 7 ug for the average adult (2), or approx. 14 ug for the ATSDR acute oral toxicicity standard. Since mercury is methylized in the body, some of both types are present in the body. The older World Health Organization (183) mercury health guideline (PTWI) is 300 ug per week total exposure or approx. 42 ug/day.

The EPA drinking water standard for mercury is 2ppb (125). The upper level of mercury exposure recommended by the German Commission on Human Biomonitoring is 1 micrograms per liter in the blood (39), since adverse effects such as increases in blood pressure and cognitive effects have been documented as low as 1 ug/L cord blood, with impacts higher in low birth weight babies (308) and commonly in adults with levels below 10 ug/l (540).

The FDA limit for mercury in seafood is 1 ppm, with a warning at ½ ppm (125). The Japanese government’s limit for mercury contamination, 0.4 micrograms per gram (533) and studies have found adverse health effects eating fish at levels below 0.5 ppm (20, 540).

EPA and several medical labs suggest health safety guideline of 1 ppm (438). The EPA safety standard for mercury in blood is 5.8 ppb (218b) and 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.

2. 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 (174, 182, 192, 436, 525, 179, 199, 86c). 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 (15-19, 26, 31, 36, 79, 83, 211, 182, 183, 199, 276b, 298, 299, 303, 332, 335, 371). 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 (183, 199, 209, 18, 19, 77, 83, 85, 100, 335, 352, 371, etc.). (see further details continued)

A large study was carried out at the Univ. Of Tubingen Health Clinic in which the level of mercury in saliva of 20, 000 persons with amalgam fillings was measured (199). The level of mercury in unstimulated saliva was found to average 11.6 ug Hg/L, with the average after chewing being 3 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. The following table gives the average daily mercury exposure from saliva alone for those tested, based on the average levels found per number of fillings and using daily saliva volumes of 890 ml for unstimulated saliva flow and 80 ml for stimulated flow (estimated from measurements made in the study and comparisons to other studies). It also gives the 84th percentile mercury exposure from saliva for the 20, 000 tested by number of fillings.

Note that 16% of all of those tested with 4 amalgam fillings had daily exposure from their amalgam fillings of over 17 ug per day, and even more so for those with more than 4 fillings.

Table: Average daily mercury exposure in saliva by number of amalgam fillings (199)

Number of fillings: 4 5 6 7 8 9 10 11 12 13 14 15 16

Av. Daily Hg (ug) 6.5 8 9.5 11 12.4 14 15.4 16.9 18.3 19.8 21.3 22.8 24.3

84th percentile (ug) 17 23.5 26 30.5 35 41.5 43.8 48.6 50.3 46.7 56.6 61.4 64.5

Saliva tests for mercury are commonly performed in Europe, and many other studies have been carried out with generally comparable results (292, 315, 79, 9b, 335, 179, 317, 352). Another large German study (352) 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 (199, 352). 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 12 fillings found generally higher levels than this study, with average mercury level in unstimulated saliva of 29 ug/L (18), 32.7 ug/L (292c), and 175 ug/day (352).

The average for those with 4 or less fillings was 8 ug/L (18). 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 tooth paste 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 (15, 35, 136, 258).

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 (191), while a Norwegian study found the average level in oral air to be 0.8 ug/M3 (176).

Another study at a Swedish University (335) 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 (83, 95), and some individuals have been found to have intraoral air mercury levels above 400 ug/ M3 (319). Most of those whose intraoral air mercury levels were measured exceeded U.S. Gov’t health guidelines for workplace exposure (2). The German workplace mercury limit is even lower than the U.S. guideline, at 1 ug/M³ (258).

3. 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. (6, 17, 18, 31, 34, 77, 79, 83, 94, 133, 174, 182, 209, 211, 216, 222, 319, 335, 348, 364, 436) 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 (34) based on the high levels of mercury vapor and methyl mercury found in saliva and oral cavity of those with amalgam.

A study at Stockholm Univ. (335) 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. Daily excretion through feces amounted to from 30 to 190 ug of mercury, being more variable than other paths.

Other studies had similar findings (6, 15, 16, 18, 19, 25, 31, 36, 77, 79, 80, 83, 115, 196, 386.) 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 (528). (13 times that of the population w/o amalgam). Other labs found similar results (386). This level of mercury gives a daily excretion of over 30 micrograms per day.

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 (335, 348, 349, 363).

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 approx. 20 % of swallowed mercury sulfhydryl compounds are absorbed in the digestive tract, but approx 60% of swallowed mercury vapor is absorbed (292, 335, 348). At least 80% of particle mercury is excreted.

Approx. 80% of swallowed methyl mercury is absorbed (335, 199, etc.)e, 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 (111, 252, 538), 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 (538).

The range of mercury excreted in urine per day by those with amalgams is usually less than 15 ug (6, 49, 83, 138, 174, 335, etc.), but some patients are much higher (93). A large NIDH study of the U.S. military population (49) 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, with 93% being inorganic mercury.

The average in those with amalgam was 4.5 times that of controls and more than the U.S. EPA maximum limit for mercury in drinking water (218). The average level of those with over 49 surfaces was over 8 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 10 amalgam surfaces increased urine mercury by approx. 1 ug/L. A study of mercury species found blood mercury was 89% organic and urine mercury was 87% inorganic (349b), while another study (363) found on average 77% of the mercury in the occipital cortex was inorganic.

In a population of women tested In the Middle East (254, 223e), 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 (506, 79, 386, 220, etc.). Nutrient transport and renal function were also found to be adversely affected by higher levels of mercury in the urine.

As is known from autopsy studies for those with chronic exposure such as amalgam fillings (1, 14, 17, 20, 31, 34, 85, 94), mercury also bioaccumulates in the kidneys (85, 273, 14), liver, brain/CNS (301, 273, 274, 327, 329, 348, 18, 19, 85), heart (59, 205, 348)), hormonal glands (85, 99, 348), and oral mucosa (174, 192, 436, etc.) with the half life in the brain being over 20 years.

Studies have found dental amalgam, chewing on amalgam, and fish consumption were positively associated with Urinary-HgC (85d). 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 (38, 61, 287, 311, 361), 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 though relatively fast is slower than the time required by pumped blood to reach these organs (290, 370).

Thus the level in the brain and heart is higher after exposure to Hg vapor than for other forms (360, 370). 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 (85, 273, 274, 503b, etc.).

Thyroid imbalances, which are documented to be commonly caused by mercury (369, 382, 459, 35, 50, 91), have been found to play a major role in chronic heart conditions such as clogged arteries, mycardial infarction, and chronic heart failure (510). 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 (510c).

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 (510a). These are also known factors in developing arteriosclerotic vascular disease. Homocysteine levels are significantly increased in hypothtyroid patients and normalize with treatment (510efg, 597).

4. 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 5 years and 80% by 20 years (182, 204). 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 (14, 16, 17, 19, 36, 57, 61, 77-83, 94, 129, 130, 138, 161, 167, 183, 191, 196, 211, 216, 273, 292, 303, 332, ), averaging about 80% of total systemic intake.

After filling replacement levels of mercury in the blood, urine, and feces typically temporarily are increased for a few days, but levels usually decline in blood and urine within 6 months to from 60 to 85% of the original levels (57, 79, 82, 89, 196, 303). Mercury levels in saliva and feces usually decline between 80 to 95% (79, 196, 335, 386)

Concentrations of mercury in oral mucosa for a population of patients with 6 or more amalgam fillings taken during oral surgery were 20 times the level of controls (174). Studies have shown mercury travels from amalgam into dentin, root tips, and the gums, with levels in roots tips as high as 41 ppm (192, 47). 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 (200, 47, 86c, 35).

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 intracellularly within macrophages, multinucleated giant cells, endothelial cells, and fibroblasts.

There is in most cases chronic inflammatory response or macrophagic reaction to the metals (47), usually in the form of a foreign body granuloma with multinucleated giant cells of the foreign body and Langhans types (192). 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 (192).

Such metals are documented to cause local and systemic lesions and health effects, which usually recover after removal of the amalgam tattoo by surgery (47fghi). 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 inflamation, bleeding, and bone loss (29, 21ab, 47, 7d etc.).

Mercury also accumulates in the trigeminal ganglia (325, 329ab) and can cause trigeminal neuralgia from which patients recover after amalgam replacement (525a, 192a, 35d, 222). Cavitations from improperly healed tooth extractions also commonly cause trigeminal neuralgia and most such recover after cavitation surgery (437b, 35a).

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 (35, 437ab).

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 50 times that of low copper amalgams (191). 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 (35, 258, 298, 299).

Clinics have found the increased toxicity and higher exposures to be factors in increased incidence of chronic degenerative diseases (35, etc). 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: they form droplets of mercury on the surface of the amalgams (182, 297).

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” (95, 199, 238, 258). Numerous other studies also support this finding (Section IV).

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 (51, 222, 262). 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 (297). 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 (228a).

6. The number of amalgam surfaces has a statistically significant correlation to :

(b) urine mercury level (38, 49, 57, 76, 77, 79, 82, 83, 134, 138, 167, 176, 254, 303, 332, 335)

(c) oral air (16, 18, 100, 176, 335)

(d) saliva and oral mucosa (18, 30, 77, 79, 117, 179, 174, 199, 211, 222, 292, 315, 317)

(e) feces mercury (25, 79, 80, 83, 115, 117, 182, 335, 386)

(f) pituitary gland (19, 20, 25, 85, 99, 273, 543b, 572c/274)

(g) brain occipital cortex (14, 16, 19, 25, 34, 85, 211, 273, 348, 366/274) and frontal lobe (572c)

(h) renal (kidney) cortex (14, 16, 19, 20, 85, 254, 273, 348, 366)

(I) liver (14, 19, 85, 366)

(j) motor function areas of the brain & CNS: brain stem, cerebellum, rhombencephalon, dorsal root ganglia, and anterior horn motor neurons (48, 291, 327, 329, 442, 35.)

(k) fetal and infant liver/brain levels (61, 112, 186, 231, 22) related to maternal fillings.

 7. A person with amalgam fillings has daily systemic intake from mercury vapor of between 3 and 70 micrograms of mercury, with the average being at least 7 micrograms (ug) per day (18, 77, 83, 85, 93, 138, 183, 199, 211, 292, 315, 335). In a large German study, the median daily exposure for those with fillings through saliva was approx. 10 ug/day, 4% of those with fillings had daily exposure through saliva of over 80 ug/day, and 1% had over 160 ug/day (199). The methods and results of the Tubingen study (199) were similar to those of other German studies (292, 315, 9, 138, 317, 335).

Total intake is proportional to the number and extent of amalgam surfaces, but other factors such as chewing gum, drinking hot liquids, brushing or polishing or bleaching, and using fluoride toothpaste significantly increase the intake (15, 18, 28, 31, 100, 134-137, 182, 183, 199, 209, 211, 292, 317, 319, 348, 349, 350). Vapor emissions range up to 200 ug/M3 (35) and are much higher after chewing (15, 137, 319).

After chewing, those with amalgams had levels over 50 times higher than those without, and the average level of exposure was 29 ug/day for those with at least 12 occlusal surfaces (18). At least 30% of those having amalgam fillings tested in a large German study had ingested mercury levels exceeding the WHO PTWI mercury standard of 43 ug/day (199, 183), and over 50% of those with 6 or more fillings had daily exposures more than the U.S. EPA health guideline level (199) of 0.1 ug/kg body weight/day (199).

The median daily exposure through saliva for those with 10 or more fillings was over 10 times that of those with no fillings (199, 292, 315, 318). Mercury level in saliva has been found to give much better indication of body levels than blood or urine levels (36). Most people with fillings have daily exposure levels exceeding the U.S. ATSDR and EPA health guideline levels (2, 36, 83, 89, 183, 199, 209, 217, 261, 292, 335, 93). Note that the WHO standard assumes exposure for a 40 hour week with no other exposure, which gives large differences with standards or guidelines based on assuming continuous exposure.

8. The blood and urine mercury load of a person with amalgam fillings is often 5 times that of a similar person without. (14, 16, 17, 79, 80, 82, 93, 136, 138, 303, 315, 317, 318) The average blood level for one large population was 5 ug/l (176). 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 10 micrograms per day (177), and a large German study (199) found median exposure through saliva alone for those with fillings to be about 10 ug/day, with many having several fillings with over 10 times that level. Other studies have found similar amounts (18, 83, 211, 183, 209).

9. 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 ) have paths to the rest of the body. (34, etc.) German studies of mercury loss from vapor in unstimulated saliva found the saliva of those with amalgams had at least 5 times as much mercury as for controls (138, 199, 292, 315).

10. Mercury (especially mercury vapor) rapidly crosses the blood brain barrier and is stored preferentially in the pituitary gland (14, 85, 327, 543b), hypothalamus (348c), thyroid gland (99), adrenal gland (84, 369, 381), and occipital cortex in direct proportion to the number and extent of amalgam surfaces (14, 19, 20, 25, 34, 38, 85, 99, 273, 274, 287, 348, 366).

Thus mercury has a greater effect on the functions of these areas. The range in one study was 2.4 to 28.7 ppb (85), and one study found on average that 77% of the mercury in the occipital cortex was inorganic (363). 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 (14d). Infants of mothers who had dental work involving amalgam during pregnancy had significantly higher levels of mercury in hair tests (541a).

11. Some mercury entering nasal passages is absorbed directly into the olfactory lobe and brain without coming from blood (34, 35, 182, 222, 348, 364). Mercury also is transported along the axons of nerve fibers (5, 25, 34, 35, 327, 329).

12. Mercury has a long half life in the body and over 20 years in the brain, and chronic low level intake results in a slow accumulation in body tissues. (20, 34, 35, 38, 85, etc.)

13. Methyl mercury is more toxic to some body processes than inorganic mercury. Mercury from amalgam is methylated by bacteria, galvanic electric currents (35), and candida albicans in the mouth and intestines (51, 81, 98, 182, 225, 503b, 506). The level of organic mercury in saliva is significantly related to the number of amalgam fillings (506). Oral bacteria streptococommus mitior, S.mutans, and S.sanguis were all found to methylate mercury (81).

High levels of Vit B12 in the system also have been found to result in increased methyl mercury concentrations in the liver and brain (51). Methyl mercury is 10 times more potent in causing genetic damage than any other known chemical (Ramel, in (35)), and also crosses the blood-brain barrier readily. Once mercury vapor or methyl mercury 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 methyl mercury (54, 126).

14. The level of mercury in the tissue of the fetus, new born, and young children is directly proportional to the number of amalgam surfaces in the mother’s mouth (20, 23, 61, 112, 210, 361). The level of mercury in umbilical cord blood, meconium, and placenta was higher than that in mother’s blood (22, 23b, 186), with meconium level the most reliable indicator of mercury exposure levels.

The saliva and feces of children with amalgams have approximately 10 times the level of mercury as children without (25, 315, 386, 528), and much higher levels in saliva after chewing. A group of German children with amalgam fillings had urine mercury level 4 times that of a control group without amalgams (76), while a Canadian study found 3.2 times as much exposure in those with amalgam with adverse health effects (low weight and height) (76c), and in a Norwegian group with average age 12 there was a significant correlation between urine mercury level and number of amalgam fillings (167).

The level of mercury in maternal hair was significantly correlated to level of mercury in nursing infants (541). One study found a 60% increase in average cord blood mercury level between 1980 and 1990 in Japan (186).

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 favour of glass ionomer cements (23d). A recent study found that glass ionomer cement fillings (ART) were more effective than amalgam in children’s teeth (23e).

16. The fetal mercury content after maternal inhalation of mercury vapor was found to be higher than in the mother (4, etc). 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 (20, 22, 23, 31, 36, 61, 162, 186, 281, 348, 366). Dental amalgams are the main source of mercury in breast milk (112, 186, 304, 339, 20).

Milk increases the bioavailability of mercury (112, 304, 391) and mercury is often stored in breast milk and the fetus at much higher levels than that in the mother’s tissues (19, 20, 22, 23, 61, 112, 186, 210, 287, 304). Mercury is transferred mainly by binding to amino acids like albumin (339). The level of mercury in breast milk was found to be significantly correlated with the number of amalgam fillings (61, 339), with milk from mothers with 7 or more fillings having levels in milk approx. 10 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 approx 10 times that for maternal exposure to an equivalent dose of inorganic mercury (281, 287), and developmental behavioral effects from vapor have been found at levels considerably below that required for similar effects by methyl mercury (20, 49, 119c, 264, 287, 304, 338). The level of total mercury in nursing infants was significantly correlated to total mercury level in maternal hair (22, 541).

17. There is a significant correlation between number of amalgam fillings of the mother and the level of the fetus and older infants (20, 22, 23, 61, 304), and also with the level in mother’s milk (19, 20, 38, 112, 304, 339). Fertile women should not be exposed to vapor levels above government health guidelines (38, 61, 182, 282);or have amalgams placed or removed during pregnancy (20, 182, 231, 304, 339). The U.S. ATSDR mercury health MRL of 0.2 mcg/M3 (2, 217).

IV. Immune System Effects and Autoimmune Disease

1. 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 (see Section VI).

From clinical experience some of the symptoms of mercury sensitivity/mercury poisoning include chronic fatigue, dizziness, frequent urination, insomnia (199d), amnesia (119d), headaches, irritability, chronic skin problems, metallic taste, gastrointestinal problems (21c), asthma (8, 97), stuffy nose, dry crusts in nose, rhinitis, plugged ears, ringing ears, chest pain, hyperventilation, diabetes (35, 501, 369), spacy feeling, chills, chronic skin problems, immune and autoimmune diseases, cardiovascular problems, muscle weakness, and many types of neurological problems (21, 26, 34, 35, 36, 38, 45, 59, 60, 69, 70, 71, 75, 91, 109, 148, 165, 199, 204, 212, 246, 255, 268-270, 290, 291, 294, 313, 343, 503, 504, 508-510, 539, 595).

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 (356, 32, 245).

2. Mercury vapor exposure at very low levels adversely affects the immune system (17, 27, 31, 38, 45, 60, 84, 118, 129, 131, 165, 226, 270, 285, 296, 313, 314, 355, 342, 369). From animal studies it has been determined that mercury damages T-cells by generating reactive oxygen species (ROS); depleting the thiol reserves of cells; binding with mitochondria, damaging and decreasing the dimension of mitochondria, impairing cellular respiration and cellular energy; causing destruction of cytoplasmic organelles with loss of cell membrane integrity, inhibiting ability to secrete interleukin IL-1 and IL-2R, causing activation of glial cells to produce superoxide and nitric oxide, and inactivating or inhibiting enzyme or coenzyme systems or hormones involving the sulfhydryl protein (SH)groups (181, 226, 338, 405, 424, 442), along with OH, NH2, and Cl groups in proteins.

HgCl2 also inhibits aquaporin‑mediated water transport in red blood cells (479) as well as oxygen transport by hemoglobin (232). Thus some of the main mechanisms of toxic effects of metals include cytotoxicity; changes in cellular membrane permeability; inhibition of enzymes, coenzymes, and hormones; and generation of lipid peroxides or free radicals- which result in neurotoxicity, immuno toxicity, impaired cellular respiration, gastrointestinal/metabolic effects, hormonal effects, and immune reactivity or autoimmunity.

Occupational studies have found that the number of suppressor-inducer immune cells and natural killer cells are significantly negatively correlated with urine mercury level (270ad). 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) (226, 272, 355).

Interferon syntheses was reduced in a concentration dependent manner with either mercury or methyl mercury as well as other immune functions (131), 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 (234, 260e, 323, 35), and autoimmunity (181, 314, 405).

Porphyrins are precursors to heme, the oxygen carrying component of blood. Mercury inhibits the conversion of specific porphyrins to heme. (84, 35, 201, 260, 539) Mercury and other toxic metals block coproporphyrin and uroporphyrin which is a marker in using the porphyrin test for lupus diagnosis and treatment (260e).

One study found that insertion of amalgam fillings or nickel dental materials causes a suppression of the number of T-lymphocytes (270), 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 (314, 181, 226, 425c). Both mercuric and methyl mercury chlorides caused dose dependent reduction in immune B-cell production (316). B-cell expression of IgE receptors were significantly reduced (316, 165), with a rapid and sustained elevation in intracellular levels of calcium induced (316, 333). Both forms are immunotoxic and cytotoxic at very low levels seen in individuals.

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 (252).

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 (285, 404). Immune Th1 cells inhibit candida by cytokine related activation of macrophages and neutrophils.

Development of Th2 type immune responses deactivate such defenses (404b). Mercury inhibits macrophage and neutrophil defense against candida by its affects on Th1 and Th2 cytokine effects (181, 285). Low doses also induced autoimmunity in some species (181, 314, 369, 404, 405, 129, 43). Candida overgrowth results in production of the highly toxic canditoxin and ethanol which are known to cause fatigue, toxicity, and depressive symptoms (460). Another amalgam effect found is increase in the average blood white cell count significantly (35). The increased white count usually normalizes after amalgam removal.

Mercury also blocks the immune function of magnesium and zinc (198, 427, 43, 38), whose deficiencies are known to cause significant neurological effects (461, 463). 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 (477).

Copper is an essential trace metal which plays a fundamental role in the biochemistry of the nervous system (489, 495, 464). 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 dismustase (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 (489, 495, 464, 111).

This condition can result in zinc deficient SOD and oxidative damage involving nitric oxide, peroxynitrite, and lipid peroxidation (495, 496, 489, 524), which have been found to affect glutamate mediated excitability and apoptosis of nerve cells and effects on mitochondria (495, 496, 524, 119).

These effects can be reduced by zinc supplementation (464, 495), as well as supplementation with antioxidants and nitric oxide-suppressing agents and peroxynitrite scavengers such as Vit C, Vit E , lipoic acid, Coenzyme Q10, carnosine, gingko biloba, N-acetylcysteine, etc. (237, 444, 464, 494, 495, 469, 521, 524, 572, 597). Some of the antioxidants were also found to have protective effects through increasing catalase and SOD action, while reducing lipid peroxidations (494a). Ceruloplasmin in plasma can be similarly affected by copper metabolism disfunction, like SOD function, and is often a factor in neurodegeneration (489).

3. 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 (131, 251, 470). Animal studies have confirmed that mercury increases effects of the herpes simplex veris type 2 for example (131). Both mercuric and methyl mercury were equally highly toxic at the cellular level and in causing cell volume reductions (131).

However methyl mercury 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 (Section VI). Antigen specific LST-test was performed on a large number of patients with atopic eczema (323), 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% (160/196) of the patients within 1-10 months. Similar results have been obtained at other clinics (455). Several studies found adverse health effects at mercury vapor levels of 1 to 5 mcg/M3 (35).

4. 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 followup antibiotics) (251, 131).

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 (35, 228a, 530, 543b, 597). 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 (550) and other cancers (486, 597).

5. Mercury by its effect of weakening the immune system contributes to increased chronic diseases and cancer (91, 180, 228a, 237, 239, 222, 234, 355, 530, 543, 35, 38, 40, etc). 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 (14, 34, 38, 43, 143, 144, 180, 237, 239, 251, 256, 283, 530).

Amalgam fillings have also been found to be positively associated with mouth cancer (206, 251, 403, 543b). Mercury from amalgam fillings has also been found to cause increase in white blood cells and in some cases to result in leukemia (35, 180). 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 (35, 180). 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. (126, 131, 152)

Nickel and beryllium are 2 other metals commonly used in dentistry that are very carcinogenic, toxic, and cause DNA malformations (35, 456). 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 (35, 200, 228a, 486, 530). Similarly nickel crowns and gold crowns over amalgam have been found to be a factor in lupus (456, 35, 229) and Belle’s Palsy from which some have recovered after TDR and Felderkrais exercises (35). Nickel has also been found to accumulate in the prostate and be related to prostate cancer (581).

 6. A high correlation has been found between patients subjectively diagnosed with CNS & systemic symptoms suggestive of mercury intoxication and immune reactivity to inorganic mercury (MELISA test, 118, 160) 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 (314, 234, 130, 342, 375, 468). Tests have found a significant portion of people to be in this category and thus more affected by exposure to amalgam than others (see section V).

Mercury also interrupts the cytochrome C oxidase system, blocking the ATP energy function (35, 43, 84, 232, 338c). 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 (35, 60, 119, 140, 141, 182, 202, 212, 232, 235, 313).

The majority of those with CFS having SPECT scans were found to have 5 times more areas of regional brain damage and reduced blood flow in the cerebral areas (471). 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 (472).

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 (473), for which mercury is a known cause (43, 288, 527). 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 (474).

7. 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 (445), 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 such as mercury often result in lichen planus lesions in oral mucosa or gums and play a roll in pathogenesis of periodontal disease. Removal of amalgam fillings usually results in cure of such lesions (60, 75, 78, 82, 86, 87, 90, 94, 101, 118, 133, 168, 192bcf, 313).

A high percentage of patients with oral mucosal problems along with other autoimmune problems such as CFS have significant immune reactions to mercury, palladium, gold, and nickel (46, 60, 118, 313, 81, 90, 212, 313, 342, 369, 375, 456, 468), including to mercury preservatives such as thimerosal. 94% of such patients had significant immune reactions to inorganic mercury (MELISA test) and 72% had immune reactions to low concentrations of HgCl2 (<0.5 ug/ml). 61% also had immune reaction to phenylHg, which has been commonly used in root canals and cosmetics (313, 468). 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 (369, 468, 342). Of 50 patients suffering from serious fatigue referred for MELISA test (369), 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 methyl mercury.

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 (369, 382, 459, 35, 50d). In general immune activation from toxics such as heavy metals resulting in cytokine release and abnormalities of the hypothalamus-pituitary-adrenal axis can cause changes in the brain, fatigue, and severe psychological symptoms (369, 342, 379-382, 385, 453, 118, 60) 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. Such hypersensitivity has been found most common in those with genetic predisposition to heavy metal sensitivity (342, 369, 382, 60), such as found more frequently in patients with HLA-DRA antigens (342, 383). 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 (405).

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 (114, 342, 405).

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 (60, 405). Very low doses and short term exposures of inorganic Hg (20-200 mug/kg) exacerbates lupus and accelerates 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 (234f). 

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 (569). Melatonin has found to have a significant protective action against methyl mercury toxicity, likely from antioxidative effect of melatonin on the MMC induced neurotoxicity (567).

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 (571). 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 (260) and DBH.

8. Patients with other systemic neurological or immune symptoms such as arthritis, myalgia, eczema, CFS (60, 342, 369), MS (369, 170, 35c), lupus (369, 405), ALS, diabetes (501, 35), epilepsy (5, 35, 229, 309), Hashimoto’s thyroiditis (369, 382), scleroderma (353), etc. also often recover or improve significantly after amalgam replacement (thousands of cases- see section VI).

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 (342, 369). 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 (87, 86, 90, 101, 168, etc.) 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 (373).

Other studies have also found relatively high rates of allergic reactions to inorganic mercury and nickel (81, 35, 445, 456). For groups with suspected autoimmune diseases such as neurological problems, CFS, and oral lichen planus (313); most of the patients tested positive to inorganic mercury and most of such 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 (342).

Animal studies have found that after sensitiztion to mercury, patients and animals are also usually reactive to gold (375). A high percentage were 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 2 years. Only 2% were worse.

The study concluded that immune reactivity to mercury and palladium is common and appears to be allergenic/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 (384). 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 (132). 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 (156).

9. A high correlation has been found between patients subjectively diagnosed with CNS & systemic symptoms suggestive of mercury intoxication and immune reactivity to inorganic mercury (MELISA test, 118) 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, but none in the controls. 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 (91, 118) (270, 286, 328). Mercury, nickel, palladium, and gold induce autoimmunity in genetically predisposed or highly exposed individuals (60, 314, 234, 130, 342, 35). Tests have found a significant portion of people to be in this category and thus more affected by exposure to amalgam than others.

10. Low level mercury exposure (as well as other toxic metals) including exposure to amalgam fillings has been found to be associated with increased autoimmune diseases (19, 27, 34, 35, 44, 45, 60, 215, 234, 268, 269, 270, 313, 314), including lupus (12, 35, 60, 113, 229, 233, 234, 270, 323, 330, 331, 456), Chrons Disease, lichen planus (86, 87, 90, 168, 313), endometriosis (1, 9, 38, 229). Silver also is released from amalgam fillings and stored in the body and has been shown to cause immune complex deposits, immune reactions and autoimmunity in animal studies (77, 78, 129, 314).

 11. 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 intensional bacteria to the extremely toxic methyl mercury form, which like mercury vapor crosses the blood‑brain barrier, and also damages and weakens the immune system (222, 225, 226, 234, 235, 281, 293, 60, 313, 314, 342, 369, 404).

Mercury vapor or Inorganic mercury have been shown in animal studies to induce autoimmune reactions and disease through effects on immune system T cells (226, 234, 268, 269, 270, 314, 425, 426, 21c/272.) . Chronic immune activation is common in CFS, with increase in activated CD8+ cytotoxic T-cells and decreased natural killer (NK) cells (518). Numbers of suppressor-inducer T cells and NK cells have been found to be inversely correlated with urine mercury levels (270ad). CFS patients usually improve and immune reactivity is reduced when amalgam fillings are replaced (342, 383, 405).

V. Medical Studies Finding Health Problems Related to Amalgam Fillings (other than immune)

1. Neurological problems are among the most common and serious and include memory loss (119ef, 481c), moodiness, depression (119dfg, 285c, 481c, 595), anger and sudden bursts of anger/rage (119d, 285c, 290, 465, 480-483, 487, 534), self-effacement, suicidal thoughts (119g), 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 (94, 107, 109, 212, 222, 271, 294, 212, 229, 233, 285ce, 317, 320, 322, 372, 374, 453, 595), schizophrenia (34, 35, 295, 465), bipolar disorder (294), memory problems (212, 222), and other more serious neurological diseases such as MS, ALS, Parkinson’s, and Alzheimer’s (see # 25). 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 (543).

Some factors that have been documented in depression are low serotonin levels, abnormal glucose tolerance (hypoglycemia), brain inflammation (584, 585), and low folate levels (480-83), which mercury has also been found to be a cause of. Occupational exposure to mercury has been documented to cause depression and anxiety (534, 285c, 119df).

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 (175, 251c, 305, 451, 465, 254). Low serotonin levels and/or hypoglycemia have also been found in the majority of those with impulsive and violent behavior (481, 482).

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 (280, 294, 333, 33, 56 ).

Medical texts on neurology (21, 27, 295, 503b) point out that chronic mercurialism is often not recognized by diagnosticians and misdiagnosed as dementia or neurosis or functional psychosis or just “nerves”. “Early manifestations are likely to be subtle and diagnosis difficult: Insomnia, nervousness, mild tremor, impaired judgment and coordination, decreased mental efficiency, emotional lability, headache, fatigue, loss of sexual drive, excitability, depression, etc. are often mistakenly ascribed to psychogenic causes”.

Diagnois of mercury toxicity can be made based on exposure history and 3 or more of such symptoms mercury is known to cause (21, 27, 295). 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 (158, 34, 207, etc.} 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 (258).

Mercury (as well as toxins from root canals and cavitations) interact with brain tubulin and disassembles microtubules that maintain neurite structure (207b, 258, 35, 200, 437). Thus chronic exposure to low level mercury vapor can inhibit polymerzation of brain tubulin and creatinine kinase which are essential to formation of microtubules. Studies of mercury studies on animals give results similar to that found the Alzheimer brain. The effects of mercury with other toxic metals have also been found to be synergistic, having much more effect than with individual exposure (35).

Flu shots have mercury and aluminum which both 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 (475).

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 (429).

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 (32c). Maternal hypothyroidism has been found to cause endocrine system abnormalities in the fetus (458, 508, 509, 511), and mercury is documented to commonly cause hypothyroidism, both chronically or as a transient condition.

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 (38, 119, 181, 305, 259, 210, 175, 305, 24/ 39, 255, 149).

Exposure of developing neuroblastoma cells to sub-cytotoxic doses of mercuric oxide resulted in lower levels of neurofilament proteins than unexposed cells (305). Mercury vapor exposure causes impaired cell proliferation in the brain and organs, resulting in reduced volume for cerebellum and organs and subtle deficiencies (38, 175, 305, 328).

Exposure to mercury and 4 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 (3). A Canadian study found that blood levels of five metals were able to predict with a 98% accuracy which children were learning disabled (3).

Several studies found that mercury causes learning disabilities and impairment, and reduction in IQ (3, 21, 38, 110, 264, 285c, 279, 541b). 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 (23, 38, 50, 287, 338c, 10).

The upper level of mercury exposure recommended by the German Commission on Human Biomonitoring is 1 micrograms per liter in the blood (39), and adverse effects such as increases in blood pressure and cognitive effects have been documented as low as 1 ug/L, with impacts higher in low birth weight babies (39).

2. Calcium plays a major role in the extreme neurotoxicity of mercury and methyl mercury. Both inhibit cellular calcium ATPase and calcium uptake by brain microsomes at very low levels of exposure (270, 288, 329, 333, 432, 56, ). 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 (43, 432).

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 (428, 453). 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 % inhibitation in animal studies at 13 ppb (333, 329). 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 (507). These alterations are not mutually exclusive, and increased calcium and altered calcium homeostatis 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 (432, 412). 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 noreprenephrine uptake by synaptosomes and nerve impulse transfer (288, 50, 270, 35).

Mercury also interrupts the cytochrome oxidase system, blocking the ATP energy function (35, 43, 84, 232, 338c), lowering immune growth factor IGF-I levels and impairing astrocyte function (119, 497). Astrocytes are common cells in the CNS involved in the feeding and detox of nerve cells. Increases in inflammatory cytokines such as caused by toxic metals trigger increased free radical activity and damage to astrocyte and astrocyte function (152). 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 are due to the death of these 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 (576). Most of these excitotoxins are secreted from microglial immune cells in the central nervous system. This not only destroys these myelin-producing cells 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 and many may drink diet drinks with Chinese food that has MSG.

Mercury and aspartame have been found to be causes of MS, along with other contributing exicitotoixns. It is now known the cause for the destruction of the myelin in the lesions is overactivation 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.

A Canadian study found those with 15 or more amalgam fillings to have more than 250% greater risk of MS than controls, and likewise higher risk for those who have had amalgam fillings more than 15 years (324). A retrospective study conducted in England found that the odds of being an MS case multiplied for every additional unit of dental fillings. Overall this represents a 21% increase in risk of MS in relation to dental caries restorations (324c).

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 (576) .

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 2X a day. They 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 triggers harmful immune reactions.

It has also been found that the antibiotic minocycline powerfully shuts down the microglia. Dr. Blaylock, tried this treatment on a friend of mine who just came down with fulmanant MS. He was confined to a wheelchair. I had him placed on minocycline and now, just a few weeks later, he is walking.

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 (226).

Such binding and autoimmune damage has been documented in the fat-rich proteins of the myelin sheaths of the CNS (478, 39b, 35c) and collagen (405), 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 (425de, 343).

Studies have also found mercury and lead cause autoantibodies to neuronal proteins, neurofilaments, and myelin basic protein (MBP) (39b, 269ag, 405, 478, 515, 516). Mercury and cadmium also have been found to interfere with zinc binding to MBP (517b) which affects MS symptoms since zinc stabilizes the association of MBP with brain myelin (517a).

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 (405, 478, 515, 126, 516, 35c, 369). Mercury from amalgam has been found to reduce antioxidant enzymes and antioxidant effects in blood plasma (13ad). Antioxidants like lipoic acid which counteract such free radical activity have been found to alleviate symptoms and decrease demyalination (572b, 597).

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 (102a). 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 be found to increase susceptibility to other common pathogens such as viruses, mycoplasma, bacteria, candida, and parasites (469b, 470, 485). The majority of those tested with autoimmune conditions such as ALS, MS, CFS, FMS have been found to be infected with mycoplasma (470) and similar for parasites (485).

Mercury lymphocyte reactivity and effects on glutamate in the CNS induce CFS type symptoms including profound tiredness, musculoskeletal pain, sleep disturbances, gastrointestinal (21c) and neurological problems along with other CFS symptoms and Fibromyalgia (342, 346, 369, 496). Mercury has been found to be a common cause of Fibromyalgia (293, 346, 369, 527) , which based on a Swedish survey occurs in about 12% of women over 35 and 5.5% of men (368).

Glutamate is the most abundant amino acid in the body and in the CNS acts as excitory neurotransmitter (346, 386, 412, 496, 119), 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 (119, 152, 333, 416, 496). Mercury and other toxic metals inhibit astrocyte function in the brain and CNS (119, 131), causing increased glutamate and calcium related neurotoxicity (119, 152, 333, 226a, 416, 496, 527) 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 (544). This is also a factor in conditions such as CFS, Parkinson’s, and ALS (346, 416, 496). Animal studies have confirmed that increased levels of glutamate (or aspartate, another amino acid excitory neurotransmitter) cause increased sensitivity to pain, as well as higher body temperature- both found in CFS/Fibromyalgia.

Mercury and increased glutamate activate free radical forming processes like xanthine oxidase which produce oxygen radicals and oxidative neurological damage (346, 142, 13). Nitric oxide related toxicty caused by peroxynitrite formed by the reaction of NO with superoxide anions, which results in nitration of tyrosine residues in neurofilaments and manganese Superoxide Dimustase (SOD) has been found to cause inhibition of the mitochondrial respiratory chain, inhibition of the glutamate transporter, and glutamate-induced neurotoxicity involved in ALS (524, 521).

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 CoQ10 (444), ginkgo biloba and pycnogenol (494ab), NAC (54, 56, 494a), Vit B6, methylcobalamin (B12), L-carnitine, choline, ginseng, vitamins C and E (444, 494c), nicotine, and omega 3 fatty acids (fish and flaxseed oil) (417, 495e).

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 (35, 200, 437ab). Cavitations have been found in 80% of sites from wisdom tooth extractions tested and 50% of molar extraction sites tested (35, 200, 437ab). 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 studies 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 (466).

3. Numerous studies have found long term chronic low doses of mercury cause neurological, memory, behavior, sleep, and mood problems (3, 34, 60, 69, 70, 71, 74, 107-109, 119, 140, 141, 160, 199, 212, 222, 246, 255, 257, 282, 285, 290, 453). Neurological effects have been documented at very low levels of exposure (urine Hg< 4 ug/L), levels commonly received by those with amalgam fillings (290). One of the studies at a German University (199) assessed 20, 000 people.

There is also evidence that fetal or infant exposure causes delayed neurotoxicity evidenced in serious effect at middle age (255, 306). Substantial occupational mercury exposure can have long-term adverse effects on the peripheral nervous system detectable decades after cessation of exposure (255c).

Organic tin compounds formed from amalgam are even more neurotoxic than mercury (222, 262). Studies of groups of patients with amalgam fillings found significantly more neurological, memory, mood, and behavioral problems than the control groups. (3, 34, 107, 108, 109, 140, 141, 160, 199, 212, 222, 290, 453).

 4.Mercury binds to hemoglobin oxygen binding sites in the red blood cells thus reducing oxygen carrying capacity (232, 35) and adversely affects the vascular response to norepinephrine and potassium. Mercury’s effect on pituitary gland vasopressin is a factor in high blood pressure (35, 201).

Mercury also increases cytosolic free calcium levels in lymphocytes in a concentration-dependant manner causing influx from the extracellular medium (270c), and blocks entry of calcium ions into the cytoplasm (1, 16, 17, 21, 33, 35, 333), and at 100 ppb can destroy the membrane of red blood cells (35, 22, 17, 270c) and damage blood vessels- reducing blood supply to the tissues (34, 202, 306)

Amalgam fillings have been found to be related to higher blood pressure, hemoglobin irregularities, tachycardia, chest pains, etc. (201, 202, 205, 212, 222, 306, 310, 539, 35, 59). Mercury also accumulates in the heart and damages myocardial and heart valves (Turpayev, in (35) & 59, 201, 205, 306, 351, 370).

Mercury has been found to be a cause of athersclerosis, hypertension, and tachycardia in children and adults (539, 59, 201, 205, 306, 308, 35) and heart attacks in adults (59, 201, 310).

Mercury also interrupts the cytochrome oxidase system, blocking the ATP energy function (35, 43, 84, 232, 338c) and impairing astrocyte function (119). These effects often result in fatigue and reduced energy levels (35, 60, 119, 140, 141, 182, 202, 212, 232, 235, 313). Both mercury and methyl mercury have been shown to cause depletion of calcium from the heart muscle and to inhibit myosin ATPase activity by 50% at 30 ppb (59), 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 (260). 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 3 time that of those without, and is over 20 times normal for some severely poisoned people (232, 260).

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 and other toxics which significantly inhibit body enzymatic processes in virtually all cavitations (200, 437ab). 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. (35, 200, 204, 222, 292, 437). 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 (35).

A study funded by the Adolf Coors Foundation (232) found that toxicity such as mercury is a significant cause of abnormal cholesterol levels, increasing as a protective measure against metals toxicity, and that cholesterol levels usually normalize after amalgam replacement.

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 (35, 228a, 530). The study also found that mercury has major adverse effects on red and white blood cells, oxygen carrying capacity, and porphyrin levels (232), with most cases seeing significant increase in oxyhemoglobin level and reduction in porphyrin levels along with 100% experiencing improved energy.

5. Patch tests for hypersensitivity to mercury have found from 2% to 44% to test positive (87, 154, 156, 178, 267), 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 (132, 156).

Of the dental students with 10 or more fillings at least 5 years old, 44% tested allergic. Based on these studies and statistics for the number with 10 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 getting toxic reactions from mercury. The most sensitive reactions are immune reactions, DNA mutations, developmental, enzyme inhibition, nerve growth inhibition, and systemic effects (34, 38, 61, 149, 175, 186, 226, 263, 264, 270, 272, 296, 305, 410-412/149, 357).

6. People with amalgam fillings have an increased number of intestinal microorganisms resistant to mercury and many standard antibiotics (35, 116, 117, 161, 389, 79). 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. But this transformation also increases antibiotic resistance and results in adversely altered populations of bacteria in the intestines.

Recent studies have found that drug resistant strains of bacteria causing ear infections, sinusitis, tuberculosis, and pneumonia more than doubled since 1996, and similar for strains of bacteria in U.S. rivers (53). Studies have found a significant correlation between mercury resistance and multiple antibiotic resistance (116, 117, 161, 369), and have found that after reducing mercury burden antibiotic resistance declines (251, 389, 40).

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 incompletely digested compounds in the bloodstream (338, 21c, 222, 228b35, etc.). Some of the gastrointestional problems caused by mercury include poor mineral absorption, diarrhea, stomatis, bloating, wasting disease, etc. (21c, 338, 35, 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 immune response (598). 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 (591 abcdefgh, 592b, 598).

Mercury and toxic metals have been found to be common toxic exposures that have been found to cause increased intestinal permeability and intestinal dysfunction (592, 338), 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 (593a). Mercury exposure blocks intestinal nutrient transport by interacting directly with brush border membrane transport proteins (593b).

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 (338, 405, 35, 21c, 592) and adversely alters bacterial populations in the intestines causing leaky gut syndrome with toxic, incompletely digested complexes in the blood (116, 228b, 35, 598) and accumulation of heliobacter pylori, a suspected major factor in stomach ulcers and stomach cancer (256, 6bc) and Candida albicans, as well as poor nutrient absorption (338, 593).

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.

Other common causes or factors in leaky gut and the related conditions include food allergies and intolerances; drugs (NSAIDs, aspirin, stomach h2 blockers, steroids, etc.); Dysbiosis ( overgrowth of harmful organisms due to antibiotic use and/or low probiotic levels); chronic alcohol consumption; toxic exposures and chemical sensitivity; chronic infections; inadequate digestive enzymes (598b). 

Clinical studies have found that diets high in flavanoids, cartenoids, and including nutritional supplements such as buffered Vit C and natural E, selenium, omega-3 oils, probiotics are effective in preventing ear infections and other chronic conditions (598b). These in addition to multiple B vitamins, the flavanoids curcumin, hesperidin, and quercetin are effective in preventing and treating leaky gut related conditions (598).

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 (594, 586, 597).

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 (564). Occupational exposure to specific metals, especially manganese, copper, lead, iron, mercury, zinc, aluminum, appears to be a risk factor for Parkinson’s disease based on epidemiological studies (98, 145, 564, 565).

Elevated levels of several of these metals have also been reported in the substantia nigra of Parkinson’s disease subjects (564). One study found that EDTA chelation was effective at reducing some of the effects (145). In some cases, Molybdenum, B12‑vitamin, P5P‑vitamin, B1‑vitamin, and tetrahydrofolate supplementation has helped to boost the protective sulfite oxidase.

8. 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 (199). Allergies and hair-loss were found to be 2-3 times as high in a group with large number of amalgam fillings compared to controls (199, 9).

Levels of mercury in follicular fluid was significantly higher for those with amalgam fillings (9, 146). 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 had amalgams replaced in 132 women who had not responded to treatment. 68 % of the women then responded to treatment and alopecia was alleviated (187).

In other studies involving amalgam removal, the majority had significant improvement (40, 317). Higher levels of hormone disturbances, immune disturbances, infertility, and recurrent fungal infections were also found in the amalgam group. The results of hormone tests, cell culture studies, an intervention studies agree (9, 146). Other clinics have also found alleviation of hair loss/alopecia after amalgam removal and detox (40, 317). Another study in Japan found significantly higher levels of mercury in gray hair than in dark hair (402).

9. 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 3 times higher mercury level in those with amalgams versus those without (14c). Mercury exposure has been shown to adversely affect kidney function in occupational and animal studies (20, 203, 211, 223, 260, 438), and also in those with more than average number of amalgam fillings (254, 223).

Richardson (Health Canada) has estimated that about 20% of the population suffers a subclinical impairment of kidney or CNS function related to amalgam mercury (209c). 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 (203). 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 (189), but adverse effects have been seen at lower levels and low levels in urine often mean high mercury retention and chronic toxicity problems (258). For this reason urine tests are not a reliable measure of mercury toxicity (11, 36, 57, 183, 216, 258, 260, 503).

10. Amalgam fillings produce electrical currents which increase mercury vapor release and may have other harmful effects (19, 27, 28, 29, 30, 35, 100, 192, 194). 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 (28).

Negatively charged fillings or crowns push electrons into the oral cavity since saliva is a good electrolyte and cause higher mercury vapor losses (35, 192). Patients with autoimmune conditions like MS, or epilepsy, depression, etc. are often found to have a lot of high negative current fillings (35).

The Huggins total dental revision (TDR) protocol calls for teeth with the highest negative charge to be replaced first (35). Other protocols for amalgam removal are available from international dental associations like IAOMT (153) and mercury poisoned patients organizations like DAMS (447).

For these reasons it is important that no new gold dental work be placed in the mouth until at least 6 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 (28, 251c) and higher likelihood of getting chronic conditions like ALS (526) and Alzheimer’s (251c) and cancer (546).

11. 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 (18, 19, 20, 23, 31, 38, 61, 112, 186, 281). 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 (10, 23, 38, 50, 197, 210, 287, 338c, 361). Mercury vapor exposure causes impaired cell proliferation in the brain and organs, resulting in reduced volume for cerebellum and organs and subtle deficiencies (38, 305).

12. Since mercury (all forms) is documented from studies of humans and animals to be a reproductive and developmental toxin (23, 38, 61, 105, 186, 224, 255, 287.305, 381, etc.), mercury can reduce reproductive function and cause birth defects and developmental problems in children (2, 4, 9, 10, 20, 23, 24, 31, 37, 38, 39, 41, 50, 55, 61, 104, 146, 159, 162, 224, 255, 458). Clinical evidence indicates that amalgam fillings lead to hormone imbalances that can reduce fertility (9, 38, 55, 4, 105, 146, 367).

Mercury has been found to cause decreased sperm volume and motility , increased sperm abnormalities and spontaneous abortions, increased uterine fibroids/endometritis, and decreased fertility in animals (4, 104, 105, 162) and in humans (9, 10, 23, 31, 37, 105, 146, 159, 395, 433, 27, 35, 38). In studies of women having miscarriages or birth defects, husbands were found to typically have low sperm counts and significantly more visually abnormal sperm (393).

It’s now estimated that up to 85 per cent of the sperm produced by a healthy male is DNA-damaged (433). 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 (37).

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.- all of which can cause infertility, spontaneous abortions, or birth defects (10, 31, 35, 296). Subfertile males in Hong Kong were found to have 40% more mercury in their hair than fertile controls . ‘Infertile males with abnormal semen’ and ‘infertile females with unexplained infertility’ also had higher blood mercury concentrations than their fertile counterparts. (55). The number of amalgam fillings was found to be an important factor in success of treating male infertility (55c).

Studies in monkeys have found decreased sperm motility, abnormal sperm, increased infertility and abortions at low levels of methyl mercury (162, 365). Astrocytes play a key role in MeHg-induced excitotoxicity (162c). 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 (162c). Researcher’s advise pregnant women should not be exposed to mercury vapor levels above government health standards (2, 19, 25, 227, 61, 100, 182, 282, 366); currently U.S. ATSDR mercury health MRL of 0.2 mcg/M3 which is exceeded by any dental work involving amalgam (Section III). Many governments have bans or restrictions on use of amalgam by women of child-bearing age.

13. Mercury and other toxic metals such as copper and lead cause breaks in DNA (4, 38, 41, 42, 197, 272, 296) and also have synergistic effects with x-rays (296) . Low non-cytotoxic levels of mercury induce dose dependent binding of mercury to DNA and significantly increased cell mutations (142, 4) and birth defects (197, 38, 105).

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 (543) and MS , as well as more chronic health problems.

15. 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 processes (WHO, 183, 189, etc.). 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 (2-4, 19-24, 30, 31, 36-44, 61, 186).

16. 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 (27, 98, 122, 257, 372, 342, 372, 412). 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 (412), and some after 5-formyltetrahydrofolate, tyrosine (257), and 5-HTP (412).

17. 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 (see previous text).

18. 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 such as Alzheimers (66, 67, 158, 166, 204, 221, 238, 242, 244, 257, 258, 295, 300, 462, 577, 35), ALS (92, 97, 325, 346, 416, 423, 35), MS (102, 163, 170, 183, 184, 212, 229, 285, 291, 302, 324, 326, 537, 35c), Parkinson’s (98, 117c, 169, 248, 250, 363, 469, 56, 84, 35), ADD (285e, 461, 160, 504b), etc.

Mercury exposure causes high levels of oxidative stress/reactive oxygen species (ROS) (13, 442), which has been found to be a major factor in neurological disease (56, 442). 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 (56). 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 (33, 346).

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 (48, 291, 327, 329, 442). 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 (327g, 287a).

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 (329, 288, 333, 34).

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 (92, 97, 207, 229b, 305, 325, 327, 416, 423, 442, 468, 470, 520, 35).

Mercury penetrates and damages the blood brain barrier allowing penetration of the barrier by other substances that are neurotoxic (20, 38, 85, 105, 162, 301, 311/262). Such damage to the blood brain barrier’s function has been found to be a major factor in chronic neurological diseases such as MS (286, 289, 291, 302, 324, 326, 369, 478).

MS patients have been found to have much higher levels of mercury in cerebrospinal fluid compared to controls (163, 35c, 139). Large German studies including studies at German universities have found that MS patients usually have high levels of mercury body burden, with one study finding 300% higher than controls (271). Most recovered after mercury detox, with some requiring additional treatment for viruses and intestinal dysbiosis. Studies have found mercury related mental effects to be indistinguishable from those of MS (207, 212, 222, 244, 271, 289, 291, 302, 183, 184, 324, 326, 369, 35c).

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 (122, 257, 372). This was found to cause severe 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. (supplements which inhibit breach of the blood brain barrier such as bioflavonoids have been found to slow such neurological damage).

In one subtype of ALS, damaged, blocked, or faulty enzymatic superoxide Dismustase (SOD) processes appear to be a major factor in cell apoptosis involved in the condition (443). Mercury is known to damage or inhibit SOD activity (13, 33, 111, 254).

19. 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 (207, 305), and low levels of zinc (363, 43). Mercury and the induced neurofibrillary tangles also appear to produce a functional zinc deficiency in the of AD sufferers (242), as well as causing reduced lithium levels which is another factor in such diseases. Lithium protects brain cells against excess glutamate induced excitability and calcium influx (280, 56).

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 (280), and to be effective in treating not only depressive conditions but degenerative conditions like Huntington’s Disease which are related to such damage.

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 (155, 207, 311). Less than 1ppm 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 (43, 84, 232, 338c, 35). Persons with the Apo-E4 gene form of apolipoprotein E which transports cholesterol in the blood, are especially susceptible to this damage (207, 221, 346), 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 multiple sclerosis. Ones susceptibility can be estimated by testing for this condition.

In many cases (many thousand documented) removal of amalgam fillings and treatment for metal toxicity led to “cure’ or significant improvement in health (see Section V). 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 (35, 38, 180, 239).

20. Mercury and methyl mercury impair or inhibit all cell functions and deplete calcium stores (96, 258). 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. (529) Most of these conditions have been found to improve after amalgam replacement (35, 212, 271, 322, 529, etc.)

VI. Results of Removal of Amalgam Fillings

1. For the week following amalgam removal, body mercury levels increase significantly, depending on protective measures taken, but within 2 weeks levels fall significantly. (82, 89) Chronic conditions can worsen temporarily, but 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 (89a).

Compared to the pre-removal mercury levels in plasma and urine, the levels found 1 year after removal of all amalgam restorations were on average 52 %) lower in plasma and 76 %) lower in urine. (89a)

2. Removal of amalgam fillings resulted in a significant reduction in body burden and body waste product load of mercury (75, 82, 88, 89, 93, 95, 115). Total reduction in mercury levels in blood and urine is often over 80% within a few months (79, 82, 89, 93, 115, 57). On average those with 29 amalgam surfaces excreted over 3 times more mercury in urine after DMPS challenge than those with 3 amalgam surfaces, and those with 45 amalgam surfaces more than 6 times as much mercury (12b).

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 extracted and cavitations checked for and cleaned.

There are extensive documented cases (many thousands) where removal of amalgam fillings led to cure or significant improvement of serious health problems such as periodontal diseases (tissue inflamation, metal mouth, mouth sores, bone loss, burning mouth, etc.) (8, 35, 40, 46, 57, 60, 62, 75, 78, 82, 94, 95, 100, 115, 133, 192bcf, 212, 222, 233abcdefgh, 271, 313, 317, 321, 322, 341, 376, 525, 532, 538, 551, 552, 572, 583), oral lichen planus/leukaplakia (56, 86, 87, 90, 101, 168, 313a) (oral keratosis (pre cancer) (87, 251, 543b), immune system/ autoimmune problems (8, 35, 60, 62, 222, 270, 271, 313, 323, 322, 342, 91, 212, 229, 291, 452, 470, 485, 523, 532, 552), multiple chemical sensitivities (26, 35, 60, 62, 95, 222, 229, 232, 233, 115, 313, 342, 537, 583), allergies (8, 26, 35, 40, 46, 62, 94, 95, 97, 165, 212, 222, 228, 229, 233, 271, 317, 322, 349, 376, 469, 525c, 532, 557, 583), asthma (8, 75, 97, 222, 228, 271, 322, 552, 556, 557), chronic headaches/migraines (5, 8, 34, 35, 47f, 62, 95, 185, 212ab, 222, 229, 233abdefgh, 271, 317, 322, 349, 354, 115, 376, 440, 453, 523, 525, 532, 537, 538, 552, 556, 583, 595), epilepsy (5, 35, 309, 229, 386e, 557), tachycardia and heart problems (8, 35, 59, 94, 115, 205, 212, 222 , 232, 233bcdg, 271, 306, 310, 322, 525c, 554, 556, 557), blood conditions (8, 212, 222, 232, 233, 271, 322, 523, 551, 35, 95), Chron’s disease (60, 222, 229, 469, 485), stomach (gastrointestinal) problems (8, 35, 62, 95, 212ab, 222, 228, 229, 233bdg, 271, 317, 322, 440, 469, 525c, 532) , lupus (12, 35, 60, 113, 222, 233, 323, 537), dizzyness/vertigo (8, 40, 95, 212, 222, 229, 233bcdgh, 271, 322, 376, 453, 525c, 551, 552), joint pain/ arthritis (8, 35, 62, 95, 103, 212ab, 222, 229, 233abcg, 271, 313, 322, 358, 386de, 469, 523, 525c, 538, 551, 552, 556, 557, 583), insomnia (35, 62, 94, 212, 222, 233ag, 271, 317, 322, 376, 525c, 583), MS (62, 94, 95, 102, 163, 170, 212, 222, 229, 271, 291, 302, 322, 369, 469, 485, 34, 35c, 229, 523, 532), ALS (97, 246, 423, 405, 469, 470, 485, 535, 35), Alzheimer’s (62, 204, 251c, 386e, 535, 35), Parkinson’s/ muscle tremor (222, 248, 228a, 229, 233f, 271, 322, 469, 557, 212, 62, 94, 98, 35), Chronic Fatigue Syndrome (8, 35, 47f, 60, 62, 88, 185, 212, 293, 229, 222, 232, 233abcdfgh, 271, 313, 317, 322, 323, 342, 346, 369, 376, 386de, 440, 469, 470, 523, 532, 537, 538, 551, 552, 556, 557, 595), nausea (525c), neuropathy/paresthesia (8, 35, 62, 94, 163, 212, 222, 322, 556, 557), muscular/jointpain/Fibromyalgia (5, 8, 35, 60, 62, 185, 222, 233bcfg, 293, 317, 322, 346, 369, 440, 469, 470, 523, 527, 532, 538, 552, 94), infertility (9, 35, 38, 229, 367), endometriosis (229, 35, 38, 9), autism (601) schizophrenia and bipolar disorder (294, 465, 34, 35), memory disorders (8, 35, 94, 212, 222, 322, 437, 440, 453, 552, 557, 595), depression (62, 94, 107, 163, 185, 212, 222, 229, 233bcfh, 271, 294, 285e, 317, 322, 376, 386de, 437, 453, 465, 485, 523, 525c, 532, 538, 551, 556, 557, 583, 595, 35, 40), anger (212, 233, 102, 557, 35, 62), anxiety & mental confusion (62, 94, 212, 222, 229, 233abcfgh, 271, 317, 322, 440, 453, 525c, 532, 551, 557, 583, 35, 57), susceptibility to infections (35, 40, 62, 222, 233cd, 251, 317, 322, 349, 350, 469, 470, 532), antibiotic resistant infection (251), cancer (breast, etc./leukemia/oral) (35, 38, 94, 180, 228a, 469, 486, 530, 543b), neuropathy/paresthesia (8, 35, 62, 94, 163, 212, 222, 322, 556, 557), alopecia/hair loss (40, 187, 271, 317, 322, 349, 583), sinus problems (35, 40, 47f, 94, 222, 271, 322, 532, 583), tinnitus (8, 35, 62, 94, 222, 233cdg, 271, 322, 349, 376, 525c), chronic eye conditions: inflamation/ iritis/ astigmatism/myopia /cataracts/macula degeneration/retinitis pigmentosa, color vision loss, etc. (35, 222, 233abcg, 271, 322, 440, 529), vision disturbances (8, 35, 62, 212, 233abcg, 271, 322, 525c), eczema and psoriasis (62, 168b, 212b, 233c, 322, 323, 385, 342, 375, 408, 459, 525c, 557), autoimmune thyroiditis (369, 382, 91), skin conditions (8, 62, 212, 222, 233bc, 322, 525c, 583), urinary/prostrate problems (212, 222), hearing loss (102, 322, 35), candida (26, 35, 404, 537, etc.), PMS (35, 6, 322, etc.), diabetes (35, 369, etc.), etc.

The above over 60,000 cases of cure or significant improvements were not isolated cases of cures; the clinical studies indicated a large majority of most such type cases treated showed significant improvement. Details are available and case histories. For example, one of the clinics (95) replacing amalgams in a large number of patients with chronic conditions had full recovery or significant improvement:

• in over 90% of cases for: metallic taste, tender teeth, bad breath, and mouth sores;
• in over 80% of cases for: depression, irrational fear, head aches/migraines, irritability, dizziness,
• insomnia, bleeding gums, throat irritation, nasal congestion or discharge, muscle tremor, and leg cramps;
• in over 70% of cases for: bloating or intestinal cramps, skin reactions, sciatic pain, chest pain, poor memory, urinary disorders, fatigue, poor concentration/ADD, watery eyes;
• in over 60% of cases for: allergies, constipation, muscle fatigue, cold hands/feet, heart problems.

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 (217).

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 (222, 271, 359).

Other clinics reported similar success. But 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, 97% versus 37 to 88% (435). 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 (35, 228a). 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 (35).

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 (86, 87, 168, etc.).

The Huggins Clinic using TDR has successfully treated over a thousand patients with chronic autoimmune conditions like MS, Lupus, ALS, AD, diabetes, etc. (35), including himself with the population of over 600 (approx. 85%) who experienced significant improvement in MS.

In a large German study of MS patients after amalgam revision, extraction resulted in 85% recovery rate versus only 16% for filling replacement alone (222, 302). 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 & gums that is not eliminated by simple filling replacement. That such mercury (and similarly bacteria) in the teeth and gums have direct routes to the brain and CNS has been documented by several medical studies (34, 325, etc.).

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 (91). TDR and other measures used in metals detox have been found to increase T-cells and immune function in AIDS patients (35).

Swedish researchers have developed a sophisticated test for immune/autoimmune reactions that has proved successful in diagnosing and treating environmentally caused diseases such as lichen planus, CFS, MS, etc. related to mercury and other immunotoxics (60, 313, 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 (233). (study period 17 years) A compilation of an even larger population found similar results (212, 282). 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.

VII. Tests for Mercury Level or Toxicity and Treatment

A new test approved by the FDA for diagnosing damage that has been caused by toxic metals like mercury is the fractionated porphyrin test (260, 35), that measures amount of damage as well as likely source. Mercury blocks enzymes needed to convert some types of porphyrins to hemoglobin and adenosine tri phosphate (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 (57, 58), 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 prechelation blood or urine levels (57, 115, 303), but one study (340) 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 (290)- with many studies finding a significant correlation between post chelation mercury level and the number of amalgam surfaces (57, 172, 173, 222, 290, 292, 273, 303). On average those with 29 amalgam surfaces excreted over 3 times more mercury in urine after DMPS challenge than those with 3 amalgam surfaces, and those with 45 amalgam surfaces more than 6 times as much mercury (12b).

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 (222, 352). However one study (290) 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 (58). A common protocol for DMSA (developed to avoid redistribution effects) is 50 mg orally every 4 hours for 3 days and then off 11 days.

Another chelator used for clogged arteries, EDTA, forms toxic compounds with mercury and can damage brain function (307). 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 (54).

Experienced doctors have also found additional zinc to be useful when chelating mercury (222) as well as counteracting mercury’s oxidative damage (43). 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 (430, 464).

Also lipoic acid, LA, has been found to dramatically increase excretion of inorganic mercury (over 12 fold), but to cause decreased excretion of organic mercury (572d) and copper. Lipoic acid has a protective effect regarding lead or inorganic mercury toxicity through its antioxidant properties (572), but should not be used with high copper.

Lipoic acid and N-acetylcysteine (NAC) also increase glutathione levels and protect against superoxide radical/peroxynitrite damage, so thus have an additional neuroprotective effect (494a, 521, 524, 572b, 54, 56).

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 (572).

Other antioxidants such as carnosine (495a), Coenzyme Q10, Vitamins C & E, gingko biloba, pycnogenol and selenium have also been found protective against degenerative neurological conditions (494, 495e, 444, 237, 597).

2. Tests suggested by Huggins/Levy (35) for evaluation and treatment of mercury toxicity:

(a) hair element test (386) (low hair mercury level does not indicate low body level) (more than 3 essential minerals out of normal range indicates likely metals toxicity)

(b) CBC blood test with differential and platelet count

(c) blood serum profile

(d) 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 (35)

(e) fractionated porphyrin (note test results sensitive to light, temperature, shaking)

(f) individual tooth electric currents (replace high negative current teeth first)

(g) patient questionnaire on exposure and symptom history

(h) specific gravity of urine (test for pituitary function, s.g>1.022 normal; s.g.< 1.008 consistent with depression and suicidal tendencies (35)}

3. 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- so some test indicator scores decline.

Chronic conditions are common during this phase. Also high mercury exposures with low hair mercury or urine mercury level usually indicates body is retaining mercury and likely toxicity problem (35). In such cases where (calcium> 1100 or < 300 ppm) and low test mercury, manganese, zinc, potassium; mercury toxicity likely and hard to treat since retaining mercury.

Test results indicating mercury/metals toxicity (35):

(a) white blood cell count >7500 or < 4500

(b) hemocrit > 50% or < 40%

(c) lymphocyte count > 2800 or < 1800

(d) blood protein level > 7.5 gm/100 ml

(e) triglycerides > 150 mg %ml

(f) BUN > 18 or < 12

(g) hair mercury > 1.5 ppm or < .4 ppm

(h) oxyhemoglobin level < 55% saturated

(I) carboxyhemoglubin > 2.5% saturated

(j) T lymphocyte count < 2000

(k) DNA damage/cancer

(l) TSH > 1 ug

(m) hair aluminum > 10 ppm

(n) hair nickel > 1.5 ppm

(o) hair manganese > 0.3 ppm

(p) immune reactive to mercury, nickel, aluminum, etc.

(q) high hemoglobin and hemocrit and high alkaline phosphatase (alk phos) and lactic dehydrogenese (LDA) during initial phases of exposure; with low/marginal hemoglobin and hemocrit plus low oxyhemoglobin during long term chronic fatigue phase.

4. Huggins Total Dental Revision Protocol (35):

(a) history questionnaire and panel of tests.

(b) replace amalgam fillings starting with filling with highest negative current or highest negative quadrant, with supportive vitamin/mineral supplements.

(c) extract all root canaled teeth using proper finish protocol.

(d) test and treat cavitations and amalgam tattoos where relevant

(e) supportive supplementation, periodic monitoring tests, evaluate need for further treatment (not usually needed).

(f) 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 such as MS, ALS, Parkinson’s, Alzheimer’s, CFS, Lupus, Rheumatoid Arthritis, etc., 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 (35).

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 (514, 597). 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 (448) and alpha lipoic acid (572). Progesterone creme has been found to promote regrowth of myelin sheaths in animals (448c).

VIII. Health Effects from Dental Personnel Exposure to Mercury Vapor

1. Dental offices are known to be one of the largest users of inorganic mercury (71b, etc.). 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 2 times that of controls for hair (397-401), urine (25d, 57, 64, 69, 99, 123, 124, 138, 171, 173, 222, 249, 290, 362, 397-399), toenails (562), and for blood (124, 195, 253, 249, 397, 563). A Lebonese study (398b) found 25 % of dentists had hair mercury levels over 5ppm and 8% had level over 10 ppm.

Sweden, which voted to phase out use of mercury in fillings, is the country with the most exposure and health effects studies regarding amalgam, and urine levels in dental professionals from Swedish and European studies ranged from 0.8 to 30.1 ug/L with study averages from 3.7 to 6.2 ug/L (124, 172, 253, 64, 68). The Swedish safety guideline for mercury in urine is 5.6 nmol Hg/nmol (11.6 ug/L).

Study averages for other countries ranged from 3.3 to 36 microgram/liter (ug/L) (69, 70, 171, 290, 397). A large survey of dentists at the Norwegian Dental Assoc. meeting (171) found that the mean mercury level in 1986 was 7.8 ug/L with approx. 16% above 13.6ug/L, and for 1987 found an average of 8.6 ug/L with approx. 15% above 15.8 ug/L, with women having higher levels than men in general.

A U.S. national sample of dentists provided by the American Dental Association had an average of 5.2 ug/L (70, 290). 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 (290, 25c), indicating daily exposure levels of over 100 ug/day. Researchers from the Univ. of Washington School of Dentistry and Dept. of Chemistry tested a sample of dentists at an annual ADA meeting (230).

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.

A Norwegian study compared the occurrence of neurological symptoms among dental assistants likely to be exposed to mercury from work with dental filling material, compared to similar health personnel with no such exposure (596). The dental assistants reported significant higher occurrence of neurological symptoms; psychosomatic symptoms, problems with memory, concentration, fatigue and sleep disturbance.

Another study of a group of 194 U.S. male dentists with mean urine mercury level of 3.3 ug/L and 233 female dental assistants with mean urine mercury level of 2.0 ug/L considered effects of polymorphism in brain-derived neurotrophic factor (BDNF) as well as mercury level (290b). The study found significant effects of mercury level on 9 measures of neurologicial deficits for the dentists and on 8 measures of neurological deficits for dental assistants (290b), as well as a significant difference relating to BDNF.

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 (171, 172, 173). In one study, each filling was found to increase mercury in the urine approx. 3%, though the relationship was nonlinear and increased more with larger number of fillings (124).

Much higher accumulated body burden levels in dental personnel were found based on challenge tests than for controls (303), with excretion levels after a dose of a chelator as high as 10 times the corresponding levels for controls (57, 69, 290a, 303). Autopsy studies have found similar high body accumulation in dental workers, with levels in pituitary gland and thyroid over 10 times controls and levels in renal cortex 7 times controls (99, 363, 38).

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 (171, 172, 173, 253, 303, 362).

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 (124, 195, 253, 249, 531). 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 (38, p287-288, & 10, 16, 178, 531). 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 (258).

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 (63). Allergy tests given to another group of dental students found 44% of them were allergic to mercury (156). Studies have found that the longer time exposed, the more likely to be allergic and the more effects (6b, 154c, 156, 503a).

One study found that over a 4 year period of dental school, the sensitivity rate increased 5 fold to over 10% (154c). Another group of dental students had similar results (362), 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 (408). Similar results have been seen in other studies as well (408).

More than 10, 000 dental assistants were exposed to extremely high concentrations of mercury fumes while working with amalgam in dental offices during the 60’s, 70’s, 80’s, and early 90’s (575). 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 4 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 (70, 260). Coproporphyrin levels have a higher correlation with symptoms and body mercury levels as tested by challenge test (69, 303), 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. Screening test that are less burdensome and less expensive are now available as first morning void urine samples have been found to be highly correlations to 24 hour urine test for mercury level or porphyrins (73).

2. The average dental office exposure affects the body mercury level at least as much as the workers on fillings (57, 64, 69, 123, 138, 171, 173, 303), with several studies finding levels approximately the same as having 19 amalgam fillings (123, 124, 173). Many surveys have been made of office exposure levels (1, 6, 7, 10, etc.) The level of mercury at breathing point in offices measured ranged form 0.7 to over 300 micrograms per cubic meter (ug/M3) (120, 172, 253, 249).

The average levels in offices with reasonable controls ranged from 1.5 to 3.6 ug/M3, but even in Sweden which has had more office environmental controls than others spot levels of over 150 ug/M3 were found in 8 offices (172) . Another study found spot readings as high as 200 ug/M3 in offices with few controls that only used saliva extractor (120). OSHA surveys find 6-16% of U.S. dental offices exceed the OSHA dental office standard of 50 ug/M³, and residual levels in equipment sterilizers often exceed this level (454a).

Note that the OSHA standard of 50 ug/M3 assumes a 40 hour work week exposure period with no other exposures, assumptions which are never met but the standard hasn’t been revised based on new toxicity information like those of other agencies. The German workplace mercury standard of 1 ug/M³ is almost always exceeded (258).

Hursh and coworkers (454b), in a study of five male volunteers, measured absorption of mercury vapor through the forearm skin. On the basis of their measurements, and exposure assumptions comparable to the OSHA air concentration of 50 μg/m³, (and a skin area of 18, 000 cm²), these investigators calculated a mean uptake of 10.4 µμg/day mercury by this route during an 8-hour period

The U.S. ATSDR mercury vapor exposure MRL for chronic exposure is much lower, 0.2 ug/M3 (217) (giving approx. 4 ug/day exposure), similar to U.S. EPA and Health Canada guidelines (2, 209). Thus most office mercury levels were found to far exceed the U.S. guidelines for chronic mercury exposure.

Use of high speed drill in removal or replacement has been found to create high volume of mercury vapor and respirable particles, and dental masks to only filter out about 40 % of such particles (219, 247). Amalgam dust generated by high speed drilling is absorbed rapidly into the blood through the lungs and major organs such as the heart receive a high dose within minutes (219a, 395c, 503c). This produces high levels of exposure to patient and dental staff and common adverse health efffects.

Use of water spray, high velocity evacuation and rubber dam reduce exposure to patient and dental staff significantly, as seen in previous discussion. In addition to these measures researchers also advise all dental staff should wear face masks and patients be supplied with outside air (120, 153).

Some studies note that carpeting and rugs in dental offices should be avoided as it is a major repository of mercury (6, 7, 21d, 71b, 188, 395c, 503) For office’s using an aspirator, at the dentist’s breathing zone, mercury vapor concentrations of ten times the current occupational exposure limit of 25 microg/m3 were recorded after 20 minutes of continuous aspirator operation (219). A build up of amalgam contamination within the internal corrugated tubing of the aspirator was found to be the main source of mercury vapor emissions followed by particulate amalgam trapped within the vacuum motor.

As the vacuum motor heated up with run time, mercury vapor emissions increased. It was found that the bacterial air exhaust filter (designed to clean the contaminated waste air entering the surgery) offered no protection to mercury vapor. Use of such measures along with a Clean-Up^TM aspirator tip was found to reduce exposure to patient and staff approximately 90% (397).

3. Dentists were found to score significantly worse than a comparable control group on neurobehavioral tests of motor speed, visual scanning, and visuomotor coordination (69, 70, 123, 249, 290ab, 395, 531, 563, 1b), concentration , verbal memory, visual memory (68, 69, 70, 249, 290ab, 395, 531, 1b), and emotional/mood tests (70, 249, 290a, 395, 563, 1b). Test performance was found to be proportional to exposure/body levels of mercury (68, 70, 249, 290ab, 395, 1b). Significant adverse neurobehavioral effects were found even for dental personnel receiving low exposure levels (less than 4 ug/l Hg in urine) (70).

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.

Thirty percent of dentists with more than average exposure were found to have neuropathies and visuographic dysfunction (395). Mercury exposure has been found to often cause disability in dental workers (230b, 395c, 503, 504a, etc.)

Chelators like DMPS have been found after a fast to release mercury from cells in tissue to be available for excretion. 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 clear demonstrated differences in test scores involving memory, mood, and motor skills related to the level of exposure pre and post chelation (70).

Those with higher levels of mercury had deficits in both memory, mood, and motor function compared to those with lower exposure levels. And the plotted test results gave no indication of there existing a threshold below effects were not measurable. 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 (491).

Many dentists have been documented to suffer from mercury poisoning (6f, 71, 72, 74, 193, 246, 247, 248, 369, 531) 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- lack of ability to concentrate, chronic muscular pain, burnout, etc. (249, 369, 377, 378, 490, 531, 1b). 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 (369). 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 (35).

One dentist with severe symptoms similar to ALS improved after treatment for mercury poisoning (246), and another with Parkinson’s disease recovered after reduction of exposure and chelation (248). 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 (99, 193).

A recent study in Scotland found similar results (531). Other studies reviewed found increased rates of brain cancer and allergies (99, 193, 328). Swedish male dentists were found to have an elevated standardized mortality ratio compared to other male academic groups (284). Dental workers and other workers exposed to mercury vapor were found to have a shortening of visual evoked potential latency and a decrease in amplitude, with magnitudes correlated with urine excretion levels (190).

Dentists were also found to have a high incidence of radicular muscular neuralgia and peripheral sensory degradation (190, 395, 490). In one study of dentists and dental assistants, 50% reported significant irritability, 46% arthritic pains, and 45% headaches (490a), while another study found selective atrophy of muscle fibre in women dental workers (490b). In a study in Brazil (492a), 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. A recent study in Turkey (492b) found the dental staff group had higher whole blood (B-Hg) and urine (U-Hg) Hg levels than the control group. The mean B-Hg value was 2.18 nmol/l and U-Hg was 1.17 nmol/mmol creatinine. U-Hg had an inverse relationship with logical memory (in WMS-R test) and total retention score (in VTMP test), and a positive relationship with increased scores of Anxiety and Psychoticism (in SCL-90-R).

4. Both dental hygienists and patients get high doses of mercury vapor when dental hygienists polish or use ultrasonic scalers on amalgam surfaces (240, 400, 503c). 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. (10, 23, 31c, 37, 38, 110, 142, 146, 401, 19, 31, 50).

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 (20, 61, 112, 186, 287). Because of high documented exposure levels when amalgam fillings are brushed (182, 222, 348) dental hygienist 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 (247). Dental staff have been found to have significantly higher prevalence of eye problems, conjunctivitis, atopic dermatitis, and contact urticaria (247, 156, 74). Finnish dental staff have the highest occupational risk of contact dermatitis with 71% affected over time (247b) with plastics, rubber, and mercury the most common causes of sensitization.

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 (247c). 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 (247d).

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 (277a). A large U.S. survey also found higher spontaneous abortion rate among dental assistants and wives of dentists (193), and another study found an increased risk of spontaneous abortions and other pregnancy complications among women working in dental surgeries (277b).

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 (394), 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 (401).

5. Body burden increases with time and older dentists have median mercury urine levels about 4 times those of controls, as well as higher brain and body burdens (1, 34, 68-74, 99), and poor performance on memory tests (68, 69, 70, 249, 290) Some older dentists have mercury levels in some parts of the brain as much as 80 times higher than normal levels (14, 34, 99).

Dentists and dental personnel experience significantly higher levels of neurological, memory, musculoskeletal, visiomotor, mood, and behavioral problems, which increase with years of exposure (1, 34, 68-73, 88, 123, 188, 246, 247, 248, 249, 290, , 395). Even dental personnel with relatively low exposure (urine Hg<4 ug/l) were found to have significant neurological effects (290) and was found to be correlated with body burden of mercury.

Most studies find dentists have increased levels of irritability and tension (1, 490, 504b), high rates of drug dependancy and disability due to psychological problems (15, 1b), and higher suicide rates than the general white population (284, 493, 1b), but one study found rates in same range as doctors.

6. Female dental technicians who work with amalgam tend to have increased menstrual disturbances (275, 401, 10, 38), significantly reduced fertility and lowered probability of conception (10, 24, 38, 121), increased spontaneous abortions (10, 31, 38, 277, 433), and their children have significantly lower average IQ compared to the general population (1, 279, 541, 38, 110). Populations with only slightly increased levels of mercury in hair had decreases in academic ability (3).

Effects are directly related to length of time on the job (277). The level of mercury excreted in urine is significantly higher for female dental assistants than dentists due to biological factors (171, 172, 173, 247, 124a). Several dental assistants have been diagnosed with mercury toxicity and some have died of related health effects (32, 245, 246, 247, 248). 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 (433).

Female dentists have increased rates of spontaneous abortion and perinatal mortality (193, 38, 10, 433)), compared to controls. A study in Poland found a much higher incidence of birth defects among female dentist and dental assistants than normal (10). A chronically ill dental nurse diagnosed with mercury sensitivity recovered after replacement of fillings and changing jobs (60), and a female dentist recovered from Parkinson’s after mercury detox (248). Some studies have found increased risk of lung, kidney, brain, and CNS system cancers among dental workers (14, 34, 99, 143, 283).

7. Many homes of dentists have been found to have high levels of mercury contamination used by dentists bringing mercury home on shoes and clothes (188).

IX. Scientists and Government Panels or Bodies That Have Found Amalgam Fillings to be Unsafe.

1. A World Health Organization Scientific Panel concluded that there is no safe level of mercury exposure (183, 189, 208). The Chairman of the panel, Lars Friberg stated that “dental amalgam is not safe for everyone to use (208, 238). A study of dental personnel having very low levels of mercury excretion found measurable neurological effects including memory, mood, and motor function related to mercury exposure level as measured by excretion levels (290). and found no threshold level below which effects were not measurable.

Other studies have found measurable effects to the immune, cardiovascular, hormonal, and reproductive systems from common levels of exposure (Section IV). Studies have found significant measurable adverse health effects at levels far below current government regulatory levels for mercury (290).

2. In 1987 the Federal Dept. of Health in Germany issued an advisory warning against use of dental amalgam in pregnant women (61). Most major countries other than the U.S. have similar or more extensive bans or health warnings regarding the use of amalgam, including Canada (209), Great Britain, France, Austria, Norway (435), Sweden (164), Switzerland (536), Italy (434), Japan (536), Australia (573), New Zealand, etc.

Mercury fillings for youth are already banned or restricted in a host of first-world countries, including Germany, Sweden Denmark and Austria. In Japan and Switzerland, dental schools have stopped teaching amalgam use as the primary source of dental care (536). A Swedish National Mercury Amalgam Review Panel and a similar Norwegian panel found that “from a toxicological point of view, mercury is too toxic to use as a filling material” (164, 435). A Swedish medical panel unanimously recommended to the government “discontinuing the use of amalgam as a dental material” (282). A futher review also recommended banning amalgam use (282b). Both countries have banned use of amalgam in dentistry (435).

Amalgam has been found to be the largest source of mercury in sewers and most sewer systems have dangerous levels of mercury. Thus installation of an approved amalgam-separating apparatus in dental clinics is now mandatory in most countries with advanced medical systems- for example, Switzerland, Germany, Sweden, Denmark, and Canada ().

 A major amalgam manufacturer, Caulk Inc., advises that amalgam should not be used as a base for crowns or for retrograde root fillings as is commonly done in some countries (387). Other manufacturers have similar warnings. U.S. EPA found that removed amalgam fillings are hazardous and must be sealed airtight and exposed of as hazardous waste (214).

Most European countries require controls on dental waste amalgam emissions to sewers or air. A Canadian Government study for Health Canada concluded that any person with any number of amalgam fillings receives exposure beyond that recommended by the USPHS Standard (209). Many of those researching amalgam related health effects including several very prominent scientists have concluded that the health effects are widespread and serious so that mercury should not be used as a filling material (1, 18, 19, 20, 36, 38, 57, 60, 61, 88, 94, 99, 115, 148, 153, 164, 170, 183, 208, 209, 210, 212, 222, 227, 236, 238, 282, 541, etc.).

3. The Legislature of the State of California passed a law, Proposition 65, that requires all dentists in the state to discuss the safety of dental materials with all patients and to post the following warning about use of amalgam on the wall of their office: “This office uses amalgam filling materials which contain and expose you to a chemical known to the State of California to cause birth defects and other reproductive harm”. Maine and New Hampshire also require such warnings (542).

4. The use of mercury amalgams has been banned for children and women of child-bearing age or put on a schedule for phase out by several European countries. The use of amalgam is declining in Europe and Germany’s largest producer of amalgam has ceased production, The director of the U.S. Federal program overseeing dental safety advises against using mercury amalgam for new fillings.

References

(1) Denton S (MD), Butler J, Dept. Of Psychology, Univ. Of North Texas, ; Proceedings of the First International Conference on Biocompatibility, Life Sciences Press, Oct 1990, p133-145; & Denton, Sandra, M.D., The Mercury Cover-Up: Controversies in Dentistry, Townsend Letter For Doctors, July 1990;488-491

(2) U.S. Environmental Protection Agency (EPA), 1999, “Integrated Risk Information System, National Center for Environmental Assessment, Cincinnati, Ohio, http://www.epa.gov/ncea/iris.htm; & United States Environmental Protection Agency, Office of Water, June 2003, The National Listing of Fish and Wildlife Advisories: Summary of 2002 Data, www.epa.gov/waterscience/fish/; & U.S. EPA, Office of Water, Mercury Update: Impact on Fish Advisories-Fact Sheet, www.epa.gov/ost/fish/mercury.html & Environmental Effects of Mercury from Amalgam, www.flcv.com/damspr2f.html

(3) 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, April, 1985; & Pihl RO et al, “Hair element content in Learning Disabled Children”, Science, Vol 198, 1977, 204-6; & Gowdy JM et al, “Whole blood mercury in mental hospital patients”, Am J Psychiatry, 1978, 135 (1):115-7.

(4) Lee IP, ”Effects of Mercury on Spermatogenisis”, 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 Oct 10;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 Jun;340 (2‑3):175‑82

(5) D.Klinghardt (MD), “Migraines, Seizures, and Mercury Toxicity”, Future Medicine Publishing, 1997; & Migraines, Seizures, and Mercury Toxicity; Klinghardt D. Alternative Medicine Magazine, Issue 21 Dec, 1997 / Jan, 1998. http://www.healingartscenter.com/Library/articles/art10.htm & (b) Klinghardt D; A series of fibromyalgia cases treated for heavy metal toxicity: case report and hypothesis; Journal of Orthopaedic Medicine 2001 23 58-59

(6) T.M.Schulein et al, ”Survey of Des Moines area dental offices for Mercury vapor”, Iowa Dent. J. 70 (1):35‑36 1984; & D.W. Jones et al, “Survey of Mercury vapor in dental offices in Atlantic Canada”, Can. Dent. Assoc. J. 4906:378‑395, 1983; & R.W. Miller et al, ”Report on Independent survey taken of Austin dental offices for mercury contamination”, Texas Dent. J. 100 (1): 6‑9, 1983; & A.Skuba, “Survey for Mercury vapor in Manitoba dental offices”, J Can. Dent. Assoc. 50 (7):517‑522, 1984; & R.H. Roydhouse et al, ”Mercury in dental offices” J Can Dent Assoc., 51 (2):156‑158, 1985; & RT McNerney et al, “Mercury Contamination in the Dental Office: A Review”, NYS Dental Journal, Nov 1979, p457-458; Button, Mercury poisoning, Virginia Dental J, 1980, 57 (2):19-21; &

Mercury in the Office, ADA News, Nov 21, 1983.

(7) L.Kantor et al, “Mercury vapor in the dental office‑does carpeting make a difference?”, JADA 103 (9):402‑407, 1981; & (b) G.F.Chop et al, “Mercury vapor related to manipulation of amalgam and to floor surfaces” .Oper. Dent. 8 (1):23‑27, 1983; & (c) G.C.Battistone et al, “Mercury as Occupational Hazard in Dentistry”, Clinical Chemistry and Chemical Toxicity of Metals, 1977, 219:205-8; & (d)Recommendations in dental mercury hygiene, JADA, 1984, Oct, p617; & National Inst of Dental Research, Workshop: Biocompatibility of metals in dentistry, JADA Sept 1984.

(8) Redhe, O. Sick From Amalgam R-Dental Ab, Frejavagen 33, S-79133 Falun, Sweden (100 cases).Olle Redhe ; [olle.redhe@telia.com]

(9) (a) Dr.I.Gerhard, Dr. E.Roller, et al, Tubingen Univ. Gynecological Clinic, Heidelberg, 1996; & (b)Gerhard I, Monga B, Waldbrenner A, Runnebaum B “Heavy Metals and Fertility”, J of Toxicology and Environmental Health, Part A, 54 (8):593-611, 1998; & (c) 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 May;4 (3):301‑309; & (d) Gerhard I, “Ganzheitiche Diagnostik un Therapie bie Infertilitat”, Erfahrungsheilkunde, 1993, 42 (3): 100-106; & (e)“Hormonal conditions affecting women caused by environmental poisons” in Pravention, Diagnose und Therapie von Umwelterkrankungen, JD Kruse-Jarres (Ed.), 1993, p51-68; & (f) 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.

(10) Proceedings of Intl Conference on Mercury Hazards in Dental Practice, Sept 2‑4, 1981 , Glasgow Scot, Dept. Of Clinical Physics and Bio-Engineering, (Gordon – Pregnancy in Female Dentists‑ a Mercury Hazard)& (several survey studies comparing level of mercury in hair of dental staff vs controls); & Gordon HP, Cordon LD, Reduction in mercury vapor levels in Seattle dental offices. J Dent Res Abstract 1092, 57A:347, 1981.

(11) Lamm O et al, “Subclinical effects of exposure to inorganic mercury revealed by somatosensory‑evoked potentials. Eur Neurol, 1985, 24:237-243; & (b)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.

(12) Dimaval Scientific monograph, sixth Ed., Jan 1997, Dr Johann Ruprecht, Heyl Corporation; & (b) Dr. Johann Ruprecht, Dimaval (DMPS), Wissenschaftliche Produktmonographie, 1997, page 119

(13) (a) S.Hussain 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 May;32 (3):395‑409; & P.Bulat, “Activity of Gpx and SOD in workers occupationally exposed to mercury”, Arch Occup Environ Health, 1998, Sept, 71 Suppl:S37-9; & Stohs SJ, Bagchi D. Oxidative mechanisms in the toxicity of metal ions. Free Radic Biol Med 1995; 18 (2): 321-36 ; & D.Jay, “Glutathione inhibits SOD activity of Hg”, Arch Inst cardiol Mex, 1998, 68 (6):457-61 & (b) S.Tan 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 [Article in Japanese] Nippon Yakurigaku Zasshi. 1998 Oct;112 Suppl 1:24P-; & 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 Nov;26 (11):1187-93. & (c)Ho PI, Ortiz D, Rogers E, Shea TB. Multiple aspects of homocysteine neurotoxicity: glutamate excitotoxicity, kinase hyperactivation and DNA damage. J Neurosci Res. 2002 Dec 1;70 (5):694-702; & (d) 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; & (e) Metals, toxicity and oxidative stress. Valko M, Morris H, Cronin MT. Curr Med Chem. 2005;12 (10):1161-208.

(14) (a) M.Nylander et al, “Mercury concentrations in the human brain and kidneys and exposure from amalgam fillings”, Swed Dent J 1987; 11:179-187, & (b) Schupp, Riedel et al, “ the mercury concentration in humans from amalgam fillings”, Organen.Dt.Zahnarztl.Z. 1992; 47:490-496; & (c)Barregard L, Svalander C, Schutz A, Sallsten G, Blohm, Molne J, Attman PO, Haglind P, “Cadmium, Mercury, and Lead in Kidney Cortex of the General Swedish Population: A Study of Biopsies from Living Kidney Donors”, Environ Health Perspect 1999 Nov;107 (11):867-871; & (d) D.W.Eggleston et al, Correlation of dental amalgam with mercury in brain tissue. J Prosthet Dent, 1987, 58 (6), 704-7; http://home.swipnet.se/misac/research6.html; & (e) Dental amalgam and mercury levels in autopsy tissues, Guzzi G, Grandi M, Severi G et al. Am J Forensic Med Pathol. 2006 Mar;27 (1):42-5

(15) Svare CW et.al, Univ. of Iowa, “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 34 1985 459

(16) K. Ott et. al. “Mercury burden due to amalgam fillings” Dtsch. Zahnarztl Z 39 (9):199‑205, 1984; & 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), v11, n.2, 87-94 http://www.lichtenberg.dk/mercury_vapour_in_the_oral_cavit.htm

(17) J.Abraham, C.Svare, 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 May;68 (5):780-5

(18) M.J.Vimy, F.L.Lorscheider, ”Intra oral Mercury released from dental amalgams and estimation of daily dose” J. Dent Res., 1985, 64 (8):1069‑1075; & Res, 1985, 64 (8):1072-5; & (b) Jackson GH, Safety and Review Board of North Carolina, Quantitative analysis of Hg, Ag, Sn , Cu, Zn and trace elements in amalgam removed from an abutment tooth underneath a gold alloy bridge that had been in vivo for nine plus years, www.ibiblio.org/amalgam/

(20) (a)M.J.Vimy, Takahashi, Y, Lorscheider, FL Maternal ‑Fetal Distribution of Mercury Released From Dental Amalgam Fillings. Dept of Medicine and Medical Physiology , faculty of Medicine, Univ. of Calgary, Calgary Alberta Canada, 1990 & Amer.J.Physiol., 1990, 258:R939-945; & (b) N.D. Boyd, J.Vimy, et al, ” Mercury from dental “Silver tooth fillings impairs sheep kidney function”, Am.J. Physiol. 261 (Regulatory Integrative Comp Physiol. 30):R1010‑R1014, 1991.‑ & (c) L.Hahn et al, Distribution of mercury released from amalgam fillings into monkey tissues”, FASEB J., 1990, 4:5536; & (d)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 Jun 21;163 (2-3):115-26; & Galic N, Ferencic Z et al, Dental amalgam mercury exposure in rats. Biometals. 1999 Sep;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 Jul;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 Jun;52 (3):291-9.

(21) R.A.Goyer, ”Toxic effects of metals”in: Caserett and Doull’s Toxicology- TheBasic Science of Poisons, McGraw-Hill Inc., N.Y., 1993; & (b) Goodman, Gillman, The Pharmacological Basis of Therapeutics, Mac Millan Publishing Company, N.Y. 1985; & (c) Encyclopedia of Occumpational Health and Safety, International Labour Office, Geneva, Vol 2, 3rd Edition.;& (d) Arena, Drew, Poisoning. Fifth Edition. Toxicology-Symptoms-Treatment, Charles C. Thomas-Publisher, Springfield, Il 1986.

(22) P.Kuhnert et al, “Comparison of mercury levels in maternal blood fetal cord blood and placental tissue”. Am. J. Obstet and Gynecol., 139:209‑212., 1981; & Vahter M, Akesson A, Lind B, Bjors U, Schutz A, Berglund M, “Longitudinal study of methyl mercury and inorganic mercury in blood and urine of pregnant and lactating women, as well as in umbilical cord blood”, Environ Res 2000 Oct;84 (2):186-94.

(23) W.D.Kuntz “Maternal and chord blood mercury background levels; Longitudinal surveillance”. Am J Obstet and Gynecol. 143 (4): 440‑443., 1982; & (b) 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 Oct;106 (4):774‑81; & (c) 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 Mar;111 (3):e289-95;& (d)Roshan D, Curzon ME, Fairpo CG. Changes in dentists’ attitudes and practice in paediatric dentistry. Eur J Paediatr Dent. 2003 Mar;4 (1):21-7; & (e)Taifour D, Frencken JE, Beiruti N, van ‘t Hof MA, Truin GJ. Effectiveness of glass-ionomer (ART) and amalgam restorations in the deciduous dentition: results after 3 years. Caries Res. 2002 Nov-Dec;36 (6):437-44.

(24) J.B. Brodsky, “Occupational exposure to Mercury in dentistry and pregnancy outcome”, JADA111 (11):779‑780., 1985 & Review, occupational effects of mercury on dental workers, www.flcv.com/dental.html

(25) C.Malmström, M.Hansson, M. Nylander, Conference on Trace Elements in Health and Disease. Stockholm May 25‑1992; & C. Malmstrom et al., “Silver amalgam: an unstable material”, Swedish paper translated in Bio-Probe Newsletter, Vol 9 (1):5-6, Jan. 1993, http://home.swipnet.se/misac/research1.html & C.Malmstrom, “Amalgam derived mercury in feces”, Journal of Trace Elements in Experimental Medicine, 5, (Abs 122), 1992, http://home.swipnet.se/misac/research7.html ; Nylander et al. Fourth international symposium Epidemiology in Occupational Health. Como Italy Sept 1985, http://home.swipnet.se/misac/infpatient.html & Tidsskrift for Tandlaeger , Oct 1989, 5:85-87, http://home.swipnet.se/misac/research1.html

(27) Matts Hanson.” Why is Mercury toxic?: Basic chemical and biochemical properties of Mercury/amalgam in relation to biological effects”. ICBM conference Colorado Springs, Co, 1988, Proceedings; & (b) Hartman DE. Missed diagnoses and misdiagnoses of environmental toxicant exposure, MCS. Psychiatr Clin North Am 1998, 21 (3):659-70. & (c) Merritt’s Textbook of Neurology, 9th Ed., Williams and Wilkins, Baltimore, 1995, p668-, & Clinical Management of Poisoning, 3rd Ed., (p753) Haddad, Shannon, and Winchester, W.B. Saunders and Company, Philadelphia, 1998; & (d) National Human Adipose Tissue Survey FY82, EPA-560/5-86-039, Dec.1986; *EPA Report: 100% Of Human Adipose Fat Samples Studied Are Laced With Chlorinated Solvents and Heavy Metals www.health‑doc.com/healtharticles/bftoxicityreport.html

(28) F.Schmidt 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 mostcommon causes of hypersensitivity to electricity according to sufferers’ reports”, Läkartidningen 2002; 99: 682-683 (Swedish); & Sheppard AR and EisenbudM., Biological Effects of electric and magnetic fields of extremely low frequency. New York university press. 1977; & 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 p 31 Abstract 22; & 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; & Mercury release from dental amalgam restorations after magnetic resonance imaging and following mobile phone use. Pak J Biol Sci. 2008 Apr 15;11 (8): 1142-6, Mortazavi SM, Daiee E, Yazdi A, Khiabani K, Mood MB, et al

(29) Goldschmidt et al, Effects of amalgam corrosion products on human cells. J. Perio. Res., 11:108-115, 1976 ; & Zander JADA, 55:11-15, 1957; & App , J Prosth Dent 11:522-532, 1961; & Trott and Sherkat, J CDA, 30:766-770, 1964; & Sanches Sotres et al , J. Periodo. l40: 543-546, 1969; & Turgeon et al., J CDA 37:255-256, 1972; & Trivedi and Talim, The response of human gingiva to restorative materials. J. Prosth. Dentistry, 29:73-81, 1973; & Mareck and Hockman. “Simulated crevice corrosion experiment for ph and solution chemistry determinations”, Corrosion, 1974:23;1000‑1006.

(30) T.Till et al, “Mercury Release from Amalgam Fillings and Oral Dysbacteriosis as a Cause of Resorption Phenomena” Zahnarztl Welt/Reform (ZWR), 1978:87;1130‑1134. & S. Olsson et al, “Release of elements due to electrochemical corrosion of dental amalgam” J of Dental Research, 1994, 73:33-43; & T.Fusayama et al, J Dental Res, 1963, 42:1183-1197; & H.Freden et al, “Mercury in gingival tissues adjacent to amalgam fillings”, Odontal Revy, 1974, 25 (2): 207-210;& H Reden, Odontal Revy, 25, 1971, 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.

(31) Langan, Fan, Hoos. The use of Mercury in dentistry: a critical review of the literature. JADA Vol 115 December 1987, 867 Donated by The ADA; & Health damage due to exposure to mercury vapor (Mercury) Szkody zdrowotne wywolane narazeniem na pary rteci (Mercury). Moszczynski‑P Jr; Moszczynski‑P Czas‑Stomatol. 1989 Apr; 42 (4): 233‑81989, POLISH; & I Mandel, Assoc Dean for Research, School of Dental and Oral Surgery, Columbia Univ., N.Y., JADA, Vol 122, Aug 1991.

(32) T.A.Cook et al, “Fatal mercury intoxication in a dental surgery assistant”, British Dent Journal, 1969, 127:533-555.

(33) (a) 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; & (b)2S.A.McFadden, “Xenobiotic metabolism and adverse environmental response: sulfur-dependent detox pathways”, Toxicology, 1996, 111 (1-3):43-65; & (c) S.C. Langley-Evans et al, “SO2: a potent glutathion depleting agent”, Comp Biochem Physiol Pharmocol Toxicol Endocrinol, 114 (2):89-98; & (d)Alberti A, Pirrone P, Elia M, Waring RH, Romano C. Sulphation deficit in “low-functioning” autistic children. Biol Psychiatry 1999, 46 (3):420-4.

(34) PatrickStörtebecker, Associate Professor of Neurology, Karolinska Institute, Stockholm. Mercury Poisoning from Dental amalgam-A Hazard to the Human Brains, ISBN: 0-941011001-1 & Dental Caries as a Cause of Nervous Disorders, Bioprobe.Inc., http://www.bioprobe.com; & Neurology for Barefoot Doctors, Stortebecker Foundation for Research, 1988: & J Canadian Dental Assoc, 33 (6): 300-;& (b) Henriksson J, Tjalve H. Uptake of inorganic mercury in the olfactory bulbs via olfactory pathways in rats. Environ Res. 1998 May;77 (2):130-40..

(36) Sam Queen; Chronic Mercury Toxicity– New Hope Against an Endemic Disease. http://www.bioprobe.com; & F.L.Lorscheider et al, “Mercury exposure from silver tooth fillings: emerging evidence questions a paradigm”, FASEB J 9:504-508, 1995.

(37) A. Anttila et al, Finnish Inst. Of Occupational Health, “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 Jun;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 Mar;25 (3):361‑83; & Mohamed et al. “Lazer Light Scattering Study of the Toxic Effects of Methyl mercury on sperm motility”. J Androl., 7 (1):11‑15., 1986;

(38) Sensitization to inorganic mercury could be a risk factor for infertility; Podzimek S, Prochazkova J, Bultasova L, Bartova J, Ulcova-Gallova Z, Mrklas L, Stejskal VD., Neuro Endocrinol Lett. 2005 Aug;26 (4):277-82; & S.Ziff and M.Ziff, Infertility and Birth Defects: Is Mercury from Dental Fillings a Hidden Cause?, Bio-Probe, Inc. ISBN: 0-941011-03-8.1987

(39) M.Inouye et al, Behavioral and neuropathological effects of prenatal methyl mercury exposure in mice”. Neurobehav.Toxicol Teratol., 1985:7;227‑232; & (b) Z.Annau et al, Johns Hopkins Univ., School of Public Health, “Mechanisms of neurotoxicity and their relationships to behavioral changes”, Toxicology, 1988, 49 (2): 219-25; & (c) Vinay SD, Sood PP. Inability of thiol compounds to restore CNS arylsulfatases inhibited by methyl mercury. Pharmacol Toxicol 1991 Jul;69 (1):71-4;& (d) P.Grandjean et al, “MeHg and neurotoxicity in children”, Am J Epidemiol, 1999, 150 (3):301-5: & (e) Budtz-Jorgensen E, Grandjean P, Keiding N, White RF, Weihe P. Benchmark dose calculations of methylmercury-associated neurobehavioral deficits. Toxicol Lett 2000 Mar 15;112-113:193- ; & (f) 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 Dec;18 (6):701-13; & (g) 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 Nov-Dec;19 (6):417-28; & (h) More evidence of mercury effects in children; Environ Health Perspect. 1999 Nov;107 (11):A554-5; & Epidemiology July 1999;10:370-375; & (i) [Environmental epidemiology research leads to a decrease of the exposure limit for mercury] [Article in Danish] Weihe P, Debes F, White RF, Sorensen N, Budtz-Jorgensen E, Keiding N, Grandjean P. Ugeskr Laeger. 2003 Jan 6;165 (2):107-11; & (j) Revised and new reference values for arsenic, cadmium, lead, and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Wilhelm M, Schulz C, Schwenk M. Int J Hyg Environ Health. 2006 May;209 (3):301-5.

(40) F.Perger, Amalgamtherape, in Kompendiu der Regulationspathologie und Therapie, Sonntag-Verlag, 1990; & “Belastungen durch toxische Schwermetalle”, 1993, 87 (2): 157-63; & K.H.Friese, ”Homoopathische Behandlung der Amalgamvergiftung”, Allg. Homoopathische Z, 241 (5); 184-187, &Erfahrungsheikunde, 1996, (4): 251- 253; & “Amalgamvergiftung_moglicher”Der Naturazt, 1995, 135 (8):13-15; & “Schnupfen-Was tun?”, Therapeutikon, 1994, 8 (3): 62-68;& Homoopathische Behandlung de Amalgamvergiftung & “Polemik und Wirklichkeit”, Allgemeine Homoopathische zeitschrift, 1994, 239 (6): 225-233 ; & “Amalgamtherapie fur Arzte und Zahnarzte”, Panta 3, 1992, Haug-Verlag.; & Natura Med 1992, 7 (4): 295-306; & M.Strassburg et al, “Generalized allergic reaction from silver amalgam fillings”, Dtsche Zahnarztliche Zeit, 22:3-9, 1967. (total:over 1200 cases)

(41) Khera et al., Teratogenic and genetic effects of Mercury toxicity. The biochemistry of Mercury in the environment Nriagu, J.O.Ed, Amsterdam, Elsevier, 503‑18, 1979; & Teratology, 8: 293-304; & Prati M, Gornati R, Boracchi P, Biganzoli E, Fortaner S, Pietra R, Sabbioni E, Bernardini G. A comparative study of the toxicity of mercury dichloride and methylmercury, assayed by the Frog Embryo Teratogenesis Assay–Xenopus (FETAX). Altern Lab Anim. 2002 Jan-Feb;30 (1):23-32.

(42) Babich et al ., The mediation of mutagenicity and clastogenicity of heavy metals by physiochemical factors. Environ Res., 1985:37;253‑286; & K.Hansen 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 Jun 15;61 (12):1543-50.

(44) L.Verchaeve et al., Comparative in vitro cytogenetic studies in Mercury exposed human lymphocytes, Mutation Res., 1985:157; 221‑226; & G.A.Caron et al, “Lymphocyte transformation induced …”, Int Arch Allergy, 37:76-87, 1970.

(45) L.Pelletier 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 & Scand J of Immunology, 1990, 31:65-74 & M. Kubicka et al, “Autoimmune disease induced by mercuric chloride”, Int Arch Allergy Immunol, Jan 1996, 109 (1):11-20 .

(46) Veron et al, “Amalgam Dentaires et Allergies”, J Biol Buccale., 1986 : 14; 83‑100 (41 cases); & D.E. Swartzendruber, Med Hypotheses, 1993, v41, n1, p31-34.

(47) (a) A. Buchner et al, “Amalgam tattoo of the oral mucosa: a clinicopatholigic study of 268 cases”, Surg Oral Med Oral Pathol, 1980, 49 (2):139-47; & (b) M. Forsell 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; & (c) Weaver T, Auclair, PL; Amalgam tattoo as a cause of local and systemic disease?Oral Surg. Oral Med. Oral Pathol. 1987;63:137-40; & (d) Amalgam-tattoo-associated oral lichenoid lesion. Staines KS, Wray D. Contact Dermatitis. 2007 Apr;56 (4):240-1

(48) K.Arvidson, ”Corrosion studies of dental gold alloy in contact with amalgam”, Swed. Dent. J 68: 135-139, 1984; & Skinner, EW, The Science of Dental Materials, 4th Ed.revised, W.B.Saunders Co., Philadelphia, p284-285, 1957; & Schoonover IC, Souder W. Corrosion of dental alloys. JADA, 1941, 28: 1278-91.

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

(50) (a)Sin YM, Teh WF, Wong MK, Reddy PK – “Effect of Mercury on Glutathione and Thyroid Hormones” Bulletin of Environmental Contamination and Toxicology 44 (4):616-622 (1990); & (b)J.Kawada et al, “Effects of inorganic and methyl mercury on thyroidal function”, J Pharmacobiodyn, 1980, 3 (3):149-59; & (c) Ghosh N. Thyrotoxicity of cadmium and mercury. Biomed Environ Sci 1992, 5 (3): 236-40; & (d)Goldman, Blackburn, The Effect of Mercuric Chloride on Thyroid Function of the Rat, Toxicol and Applied Pharm 1979, 48: 49-55; & (e)Kabuto M – “Chronic effects of methylmercury on the urinary excretion of catecholamines and their responses to hypoglycemic stress” Arch Toxicol 65 (2):164-7 (1991) ;& Assoc. for Birth Defect Children, Birth Defect News, March 2001;

(51) 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; & M.K.Hamdy et al, “Formation of methyl mercury by bacteria”, App Microbiol, 1975, Sept.; & W.Forth, “Toxikologie von Quecksilberverbindungen”, in Quecksilber in der Umwelt-Hearing zur Amalgamprolematik, Niedersachsisches Umweltministerium, 1991; & 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 Apr 21;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 42 1989 283-288; & Choi SC, Bartha R.. Cobalamin-mediated mercury methylation by Desulfovibrio desulfuricans LS. Appl Environ Microbiol. 1993 Jan;59 (1):290-5; & Wang J, Liu Z; [.In vitro Study of Strepcoccus Mutans in the Plaque on the Surface of Amalgam Fillings on the Convertion of Inorganic Mercury to Organic Mercury][Article in Chinese], Shanghai Kou Qiang Yi Xue. 2000 Jun;9 (2):70-2; & Guzzi G, Minoia C, Pigatto PD, Severi G. Methylmercury, amalgams, and children’s health. Environ Health Perspect. 2006; 114:149;

(52) 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 Jul;23 (2):197-206. szente@bio.u-szeged.hu

(54) M.E. Lund 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 dismustase activity in mercury vapor exposed rats: effect of N‑acetylcysteine treatment. Toxicology 1991 Mar 11;66 (3):289‑95. & G.Ferrari et al, Dept. Of Pathology, Columbia Univ., J Neurosci, 1995, 15 (4):2857-66; & RR. Ratan et al, Dept. of Neurology, Johns Hopkins Univ., J Neurosci, 1994, 14 (7): 4385-92; & J.F. Balch et al, Prescription for Nutritional Healing”, 2nd Ed., 1997;

(55) Dickman MD; Leung KM, “Hong Kong subfertility links to mercury in human hair and fish”, Sci Total Environ, 1998, 214:165-74; & Mercury and organochlorine exposure from fish consumption in Hong Kong. Chemosphere 1998 Aug;37 (5):991‑1015; & (b) Choy CM, Lam CW, Cheung LT, Briton-Jones CM, Cheung LP, Haines CJ. Infertility, blood mercury concentrations and dietary seafood consumption: a case-control study. BJOG. 2002 Oct;109 (10):1121-5; & (c) Gerhar I, Wallis E. Individualized homeopathic therapy for male infertility. Homeopathy. 2002 Jul;91 (3):133-44.

(56) (a) A.Nicole et al, “Direct evidence for glutathione as mediator of apoptosis in neuronal cells”, Biomed Pharmacother, 1998; 52 (9):349-55; & J.P.Spencer et al, “Cysteine & GSH in PD”, mechanisms involving ROS”, J Neurochem, 1998, 71 (5):2112-22: & & J.S. Bains 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 Nov;36 (11):1179-84. & (b) D. Offen 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 Aug;39 (2):141-9; & (c) 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; & A.D.Owen et al, Ann NY Acad Sci, 1996, 786:217-33; & JJ Heales et al, Neurochem Res, 1996, 21 (1):35-39; & & X.M.Shen et al, Neurobehavioral effects of NAC conjugates of dopamine: possible relevance for Parkinson’sDisease”, Chem Res Toxicol, 1996, 9 (7):1117-26; & Chem Res Toxicol, 1998, 11 (7):824-37; & (d) 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 Nov;71 (5):2049-62; & (e) Araragi S, Sato M. et al, Mercuric chloride induces apoptosis via a mitochondrial-dependent pathway in human leukemia cells. Toxicology. 2003 Feb 14;184 (1):1-9.

(57) N.Campbell & M.Godfrey, “Confirmation of Mercury Retention and Toxicity using DMPS provocation” , J of Advancement in Medicine, 7 (1) 1994; (80 cases); & (b)D.Zander et al, “Mercury mobilization by DMPS in subjects with and without amalgams”, Zentralbl Hyg Umweltmed, 1992, 192 (5): 447-54 (12 cases);

(58) Kostial K et al, Decreased Hg retention with DMSA, J Appl Toxicol, 1993, 13 (5):321-5; & Kostyniak PJ, Soiefer AL. J Appl Toxicol, 1984, 4 (4):206-10; & Butterworth RF et al, Can J Neurol Sci, 1978, 5 (4):397-400.

(59) A. Frustaci 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; & D.V. Vassalo, 1999, Effects of mercury on the isolated heart muscle are prevented by DTT and cysteine”, Toxicol Appl Pharmacol 1999 Apr 15;156 (2):113‑8; & N.G. Ilblack et al, “New aspects of murine coxsackie B3 mycocarditis: focus on heavy metals”, European Heart J, 1995, 16: supp O: 20-4; & Dahhan, Orfaly, Electrocardiogrphic Changes in Mercury Poisoning, Amer J of Cardiology, Aug, 1964; & Lorscheider F, Vimy M. Mercury and idiopathic dilated cardiomyopathy. J Am Coll Cardiol 2000 Mar 1;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 Mar;134 (3):375-83; & Review: cardiovascular effects of mercury from amalgam, www.flcv.com/cardio.html

(60) V.D.M.Stejskal, Dept. Of Clinical Chemistry, Karolinska Institute, Stockholm, Sweden LYMPHOCYTE IMMUNO‑STIMULATION ASSAY ‑MELISA” & VDM Stejskal et al, “MELISA: tool for the study of metal allergy”, Toxicology in Vitro, 8 (5):991-1000, 1994; & (c ) Metal-specific lymphocytes: biomarkers of sensitivity in man.Stejskal VD, Danersund A, Lindvall A, Hudecek R, Nordman V, Yaqob A, Mayer W, Bieger W, Lindh U.Neuroendocrinology Letters 1998

(61) E.Lutz 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; & G.Drasch et al, “Mercury Burden of Human Fetal and Infant Tissues”, Eur J Pediatr 153:607-610, 1994;

(62) Dr. J.E. Hardy, Mercury Free: the wisdom behind the growing consumer moverment to ban silver dental fillings, 1998.

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

(64) Steinberg D, Grauer F, Niv Y, Perlyte M, Kopolivic K, Dept. Of Oral Biology, Hebrew Univ. Mercury among dental personnel in Israel. Med Sci, 1995, 31 (7):428-32.

(65) Y.K.Fung et al, “In vivo mercury and methyl mercury levels in patients at different intervals after amalgam restorations”.Carlson‑MP College of Dentistry, University of Nebraska Medical Center, Lincoln. Northwest‑Dent. 1991 May‑Jun; 70 (3) 23‑6

(66) “Regional brain trace‑element studies in Alzheimer’s disease”. C.MThompson, W.R. Markesbery, et al, Univ. Of Kentucky Dept. Of Chemistry, Neurotoxicology (1988 Spring) 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.

(67) A search for longitudinal variations in trace element levels in nails of Alzheimer’s disease patients. Vance DE Ehmann WD Markesbery WR In: Biol Trace Elem Res (1990 Jul‑Dec)26‑27:461‑70; & Ehmann et al, 1986, Neurotoxicology, 7:195-206; & Thompson et al, 1988, Neurotoxicology, 9:1-7.

(68) K.A.Ritchie et al, Univ. Of Glasgow, “Psychomotor testing of dentists with chronic low level mercury exposure”, J Dent Res 74:420, IADR Abstract 160 (1995): & Occup Environ Med, 1995, 52 (12): 813-7

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

(70) D.Echeverria et al, Batelle Center for Public Health Research, Seattle, “Behavioral Effects of Low Level Exposure to Hg vapor Among Dentists”, Neurotoxicology & Teratology; 17 (2):161-168 (1995);

(71) S.C.Foo et al, “Neurobehavioral effects in Occupational Chemical Exposure”, Environmental Research, 60 (2): 267-273, 1993; & (b) D.G. Mantyla et al, “Mercury toxicity in the dental office: a neglected problem”, JADA, 92:1189-1194, 1976; & A case of mercury contamination of a dental suite, JADA, 1976, Vol 92; & (d) Symington D, Mercury poisoning in dentists, J Soc Occup Med, 1980, 30:37-39.

(72) D.L.Smith, “Mental effects of mercury poisoning”, South Med J 71:904-5, 1978.

(73) M.E.Cianciola et al, “Epidemiologic assessment of measures used to indicate exposure to mercury vapor”, Toxicol Eniviron Health, 1997, 52 (1):19-33.

(74) A.C.Bittner et al, “Behavior effects of low level mercury exposure among dental professionals”, Neurotoxicology & Teratology, 1998, 20 (4):429-39.

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

(77) I.Skare, “Mass Balance and Systemic Uptake of Mercury Released from Dental Fillings”, Water, Air, and Soil Pollution, 80 (1-4):59-67, 1995.

(78) G.Drasch et al, ” Silver Concentrations in Human Tissues: the Dependence on Dental Amalgam”, J Trace Elements in Medicine and Biology, 9 (2):82-7, 1995; & L.J. Calsakis et al, “Allergy to Silver Amalgams”, Oral Surg, 46:371-5, 1978.

(79) L.Bjorkman et al, “Mercury in Saliva and Feces after Removal of Amalgam Fillings”, Toxicology and Applied Pharmacology, 1997, 144 (1), p156-62; & Eur J Oral Sci 1998 Apr;106 (2 Pt 2):678-86 & (b) J Dent Res 75: 38-, IADR Abstract 165, 1996.

(80) M.Osterblad et al, “Antimicrobial and Mercury Resistance among Persons with and without Amalgam Fillings”, Antimicrobial Agents and Chem, 39 (11):2499, 1995

(81) L.I.Liang et al, “Mercury reactions in the human mouth with dental amalgams” Water, Air, and Soil pollution, 80:103-107;

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

(83) I.Skare et al, Swedish National Board of Occupational Safety and Health, “Human Exposure to Hg and Ag Released from Dental Amalgam Restorations”, Archives of Environmental Health 1994; 49 (5):384-394; & Review: Mercury Exposure Levels from Amalgam Fillings, DAMS, www.flcv.com/damspr1.html

(84) J.C.Veltman 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; & A.G.Riedl et al, Neurodegenerative Disease Research Center, King’s College, UK, “P450 and hemeoxygenase enzymes in the basal ganglia and their role’s in Parkinson’s disease”, Adv Neurol, 1999; 80:271-86; & Alfred V. Zamm. Dental Mercury: A Factor that Aggravates and Induces Xenobiotic Intolerance. J. Orthmol. Med. v6#2 pp67-77 (1991).

(85) J.A.Weiner et al, “The relationship between mercury concentration in human organs and predictor variables”, Sci Tot Environ, 138 (1-3):101-115, 1993; & “An estimation of the uptake of mercury from amalgam fillings in Swedish subjects”, Science of the Total Environment, v168, n3, p255-265, 1995; & 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 Nov;84 (3):211-8.& (d) Long-term effects of elemental mercury on renal function in miners of the Idrija Mercury Mine. Franko A, Budihna MV, Dodic-Fikfak M. Ann Occup Hyg. 2005 Aug;49 (6):521-7. Epub 2005 Jun 17; & Urinary mercury and biomarkers of early renal dysfunction in environmentally and occupationally exposed adults: a three-country study, Jarosińska D, Horvat M, Sällsten G, Barregård L et al, Environ Res. 2008 Oct;108 (2):224-32. Epub 2008 Aug 5

(86) (a) Guzzi, G., C., Pigatto, P. et al, (2003). Toxicol. Lett. 144 (Suppl. 1), 35-36; &A Dunsche et al, “Oral lichenoid reactions associated with amalgam: improvement after amalgam removal.” British Journal of Dermatology 2003 Jan;148:1:70-6; & (b) E.R.Smart et al, “Resolution of lichen planus following removal of amalgam restorations”, Br Dent J 178 (3):108-112, 1995 (12 cases); & H.Markow, ” Regression from orticaria following dental filling removal:, New York State J Med, 1943: 1648-1652; & G. Sasaki et al, “Three cases of oral lichenosis caused by metallic fillings”, J. Dermatol, 23 Dec, 1996; 12:890-892; & J.Bratel et al, “Effect of Replacement of Dental Amalgam on OLR”, Journal of Dentistry, 1996, 24 (1-2):41-45 (161 cases); & (c) Migration of mercury from dental amalgam through human teeth by H. H. Harris et al. (2008).J. Synchrotron Rad. 15, 123–128; & Comments on …, G.Guzzi & P.Pigatto, J. Synchrotron Rad. 16, part 3:435-36, 2009; & Mutter, J. et al (2007). Nummular dermatitis, Crit. Rev. Toxicol. 37, 537-549;

(87) L. Wong and S. Freeman, Oral lichenoid lesions (OLL) and mercury in amalgam fillings, Contact Dermatitis, Vol 48 Issue 2 Page 74 – February 2003 (33 cases); & A. Skoglund, Scand J Dent Res 102 (4): 216-222, 1994; and 99 (4):320-9, 1991 (40 cases); & P.O.Ostman et al, “Clinical & histologic changes after removal of amalgam”, Oral Surgery, Oral Medicine, and Endodontics, 1996, 81 (4):459-465; & S.H.Ibbotson et al, “The relevance of amalgam replacement on oral lichenoid reactions”, British Journal of Dermatology, 134 (3):420-3, 1996; (270 cases) www.geocities.com/ResearchTriangle/2888/relevance.html

(89) 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 Sep;13 (5):297-304 ; & M.Molin et al, “Kinetics of mercury in blood and urine after amalgam removal”, J Dent Res 74:420, IADR Abstract 159, 1995; & (b) M.Molin et al, “Mercury, selenium, And GPX before & after amalgam removal”, Acta Odontol Scand, 1990, 48:189-202.

(90) P.Koch et al, “Oral lesions and symptoms related to metals”, Dermatol, 1999, 41 (3):422-430; & “Oral lichenoid lesions, mercury hypersensitivity, …”, Contact Dermatitis, 1995, 33 (5): 323-328; & S.Freeman et al, “Oral lichenoid lesions caused by allergy to mercury in amalgam”, Contact Dermatitis, 33 (6):423-7, Dec 1995 (Denmark) & H.Mobacken et al, Contact Dermatitis, 10:11-15, 1984; & M.Jolly et al, “Amalgam related chronic ulceration of oral mucosa”, Br Dent J, 1986, 160: 434-437; & C.Camisa et al, “Contact hypersensitivity to mercury”, Cutis, 1999, 63 (3):189-

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

(92) L. Tandon et al, “Elemental imbalance studies by INAA on ALS patients”, J Radioanal Nuclear Chem 195 (1):13-19, 1995; & Y.Mano et al, “Mercury in the hair of ALS patients”, Rinsho Shinkeigaku, 1989, 29 (7): 844-848; & Mano et al, 1990, Rinsho Shinkeigaku 30: 1275-1277; & Khare et al, 1990, “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

(93) L.Barregard et al, “People with high mercury uptake from their own dental amalgam fillings”, Occup Envir Med 52: 124-128, 1995; & S.Langworth et al, “A case of high mercury exposure from dental amalgam” European J Oral Sci 1996, 104 (3):320-321; & R. Stromberg et al, “A case of unusually high mercury exposure from amalgam fillings”, Tandlakartidningen 88 (10): 570-572, 1996;

(94) F.Berglund, Case reports spanning 150 years on the adverse effects of dental amalgam, Bio-Probe, Inc., Orlando, Fl, 1995;ISBN 0-9410011-14-3 (245 cured); & Mats Hanson, A hundred and fifty years of misuse of mercury, & EFFECTS OF AMALGAM REMOVAL ON HEALTH, Mats Hanson, 5821 cases, http://iaomt.org/articles/files/files214/Hansen-%20effects%20of%20amal%20removal.pdf & Dental Materials and Health, Swedish Dept. of Health, 2003, SOU 2003:53, Appendix 10. (800 patients) http://art-bin.com/art/hanson_en.html & Tuthill JY, “Mercurial neurosis resulting from amalgam fillings”, The Brooklyn Medical Journal, December 1898, v.12, n.12, p725-742

(95) Lichtenberg, HJ “Elimination of symptoms by removal of dental amalgam from mercury poisoned patients”, J Orthomol Med 8:145-148, 1993; & Lichtenberg H, “Symptoms before and after proper amalgam removal in relation to serum-globulin reaction to metals”, Journal of Orthomolecular Medicine, 1996, 11 (4): 195-203. (119 cases) www.lichtenberg.dk/experience_after_amalgam_removal.htm

(96) Goyer RA, National Institute of Environmental Health Sciences. Toxic and essential metal interactions. Annu Rev Nutr 1997; 17:37-50; & Nutrition and metal toxicity. Am J Clin Nutr 1995; 61 (Suppl 3): 646S- 650S; & 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 Feb;39 (2):134‑142. ; & A.F.Goldberg et al, “Effect of Amalgam restorations on whole body potassium and bone mineral content in older men”, Gen Dent, 1996, 44 (3): 246-8; & K.Schirrmacher, 1998, “Effects of lead, mercury, and methyl mercury on gap junctions and [Ca2+]I in bone cells”, Calcif Tissue Int 1998 Aug;63 (2):134‑9..

(97) 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;

(98) A.Seidler et al, Possible environmental factors for Parkinson’s disease”, Neurology 46 (5): 1275- 1284, 1996; & Vroom FO, Greer M, “Mercury vapor intoxication”, 95: 305-318, 1972; & Ohlson et al, “Parkinson’s Disease and Occupational Exposure to Mercury”, Scand J. Of Work Environment Health, Vol7, No.4: 252-256, 1981; L.G. Golota, “Therapeutic properties of Unitihiol” Farm. Zh. 1980, 1: 18-22.

(100) M.Hanson et al, “The dental amalgam issue: a review”, Experientia, 47:9-22, 1991; & J.A.Weiner et al, “Does mercury from amalgam restorations constitute a health hazard”, Sci Total Environ, 1990, 99 (1-2): 1-22; & R.Marxkors, “Korrosionserscheinungen an Amalgamf llungen und Deren Auswirkungen auf den Menschlichen Organismus.” Das Deutsche Zahn rztebl. 24, 53, 117 and 170, 1970 .

(101) E.Henriksson et al, “Healing of Lichenoid Reactions following Removal of Amalgam”, J Clinical Periodontol, V22, N4, p287-94, 1995 & M.Forsbec et al, Journal of Clinical Immunology, 16 (1):31-40, Jan 1996; & A.Larsson et al, “The histopathology of oral mucosal lesions associated with amalgam”, Oral Dis 1995, 1 (3):152-8.

(102) R.L. Siblerud et al, “Evidence that mercury from silver fillings may be an etiological factor in multiple sclerosis”, Sci Total Environ, 1994, 142 (3):191-205 , & “Mental health, amalgam fillings, and MS”, Psychol Rep, 1992, 70 (3 Pt2), 1139-51;& Siblerud R.L. and Kienholz E. Evidence That Mercury From Dental Amalgam May Cause Hearomg Loss In Multiple Sclerosis Patoemts. J. Orthomol. Med, v12#4 pp 240-4 (1997); & R.L.Siblerud, “A commparison of mental health of multiple schlerosis patients with silver dental fillings and those with fillings removed”, Psychol Rep, 1992, 70 (3), Pt2, 1139-51; & (b) Amalgam dental fillings and hearing loss, International Journal of Audiology 2008; 47:770_776, Janet A. Rothwell, Paul J. Boyd

(103) A.P.Tanchyk, “Amalgam Removal for Treatment of Arthritis”, Gen Dent, v42, n4, July 1994, p354-

(104) C.F.Facemire et al, “Reproductive impairment in the Florida Panther”, Health Perspect, 1995, 103 (Supp4):79-86; & J.M.Yang 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 Nov;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 Sep;32 (4-5):239-46; & M.Maretta 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 Mar;95 (1):92-6

(105) T.Colborn (Ed.), Chemically Induced Alterations in Functional Development, Princeton Scientific Press, 1992; & ” Developmental Effects of Endocrine-Disrupting Chemicals”, Environ Heath Perspectives, V 101, No.5, Oct 1993; & B.Windham, “Health, Hormonal, and Reproductive Effects of Endocrine Disrupting Chemicals” (including mercury), Annotated Bibliography , 1996 www.flcv.com/endocrin.html ; & 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 Suppl (2): 65-71; & Trachtenberg IM, Chronic effects of mercury in organisms. U.S. Dept. Of Health, Education, and Welfare, Publ 74-473, 1974; & Review: Endocrine effects of mercury from dental amalgam, DAMS, www.flcv.com/endohg.html

(106) G.R.Bruce, “Cytotoxicity of retrofil materials”, J Endodont., v19, n6, p288-92, 1993

(107) R.L.Siblerud et al, ”Psychometric evidence that mercury from dental fillings may be a factor in depression, anger, and anxiety”, Psychol Rep, v74, n1, 1994; & Amer. J. Of Psychotherapy, 1989; 58: 575-87; Poisoning and Toxicology compendium, Leikin & Palouchek, Lexi-Comp, 1998, p705

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

(109) Y.X. Liang et al, “Psychological effects of low exposure to mercury vapor”, Environmental Med Research, 60 (2): 320-327, 1993; & T.Kampe et al, “Personality traits of adolescents with intact and repaired dentitions”, Acta Odont Scand, 44:95-, 1986; & R.Kishi et al, Residual neurobehavioral effects of chronic exposure to mercury vapor”, Occupat. Envir. Med., 1994, 51:35-41;& A.Sikora et al, “Evaluation of mental functions in workers exposed to metallic mercury”, Med Pr, 1992, 43 (2):109-21..

(110) N.Roeleveld et al, “Mental retardation and parental occupation”, Br J Ind Med 50 (10): 945-954, 1993.

(112) A.Oskarsson et al, “Mercury in breast milk in relation to fish consumption and amalgam”, Arch environ Health, 1996, 51 (3):234-41; & “Risk assessment in relation to neonatal metal exposure”, Analyst, 1998, 123 (1): 19-23; & 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 Methyl mercury Exposure in Infants. Environ Health Perspect 1994 Jan;102 (1):74‑7.

(113) T.A.Glavinskiaia et al, “Complexons in the treatment of lupus erghematousus”, Dermatol Venerol, 1980, 12: 24-28; & A.F.Hall, Arch Dermatol 47, 1943, 610-611;& S Moore, Lupus: Alternative Therapies That Work; www.shirleys‑wellness‑cafe.com/amalgam.htm

(114) M.Aschner et al, “Metallothionein induction in fetal rat brain by in utero exposure to elemental mercury vapor”, Brain Research, 1997, dec 5, 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 Spring;17 (1):107-16. & T.V. O’Halloran, “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.

(115) G.Hall, V-TOX, Mercury levels excreted after Vit C IV as chelator‑ by number of fillings Int Symposium “Status Quo and Perspectives of Amalgam and Other Dental Materials” European Academy, Ostzenhausen/Germany. April 29 ‑ May 1, 1994; & Heavy Metal Bulletin, Apr 1996, Vol.3, Issue 1, p6-8 (200 cured or significantly improved)

(116) 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 ; & J. Wireman et al, Appl Environ Microbiol, 1997, 63 (11):4494-503& (b) A.O.Summers et al, Antimicrobial Agents and Chemotherapy, 37 (4):825-834, 1993; & The Physiologist 33 (4), A-116, 1990; & (c) Mercury resistance among clinical isolates of Escherichia coli. Poiata A, Badicut I, Indres M, Biro M, Buiuc D. Roum Arch Microbiol Immunol. 2000 Jan-Jun;59 (1-2):71-9; & (d) Resistance of the normal human microflora to mercury and antimicrobials after exposure to mercury from dental amalgam fillings. Edlund C, Bjorkman L, Ekstrand J, Sandborgh-Englund G, Nord CE. Clin Infect Dis. 1996 Jun;22 (6):944-50; & (e) M.Vimy et al, ” Silver dental fillings provoke an increase in mercury and antibiotic resistant bacteria in the mouth and intestines of primates”, APUA Newsletter, Fall, 1991.

(117) (a)The effect of amalgam exposure on mercury- and antibiotic-resistant bacteria. Ready D, Pratten J, Mordan N, Watts E, Wilson M. Int J Antimicrob Agents. 2007 Apr 23; & (b) Grewal JS, Tiwari RP. Resistance to antibiotics, metals, hydrophobicity and klebocinogeny of Klebsiella pneumoniae isolated from foods. Cytobios 1999; 98 (388):113‑23; & (c) J.M.Aguiar et al, “Heavy metals and antibiotic resistance in Escherichia coli isolates from ambulatory patients”, Chemother, 1990, 2 (4):238-40.

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

(119) (a) L.Ronnback et al, “Chronic encephalopaties induced by low doses of mercury or lead”, Br J Ind Med 49: 233-240, 1992; & (b) H.Langauer‑Lewowicka, ” Changes in the nervous system due to occupational metallic mercury poisoning” Neurol Neurochir Pol 1997 Sep‑Oct;31 (5):905‑13; & (c) Langauer-Lewowicka H. [Chronic toxic encephalopathies] [Polish] Med Pr. 1982;33 (1-3):113-7; & (d)[Pneuropsychological disorders after occupational exposure to mercury vapors in El Bagre (Antioquia, Colombia)] Rev Neurol. 2000 Oct 16-31;31 (8):712-6. Tirado V, Garcia MA et al; & (e) Chronic neurobehavioural effects of mercury poisoning on a group of Zulu chemical workers. Brain Inj. 2000 Sep;14 (9):797-814. Powell TJ: & (f) Neurobehavioral effects of acute exposure to inorganic mercury vapor. Appl Neuropsychol. 1999;6 (4):193-200, Haut MW, Morrow LA et al: & (g) Personality traits in miners with past occupational elemental mercury exposure. Environ Health Perspect. 2006 Feb;114 (2):290-6; Kobal Grum D, Kobal AB (120) L.Pohl, Dept. of Dental Materials Science, Umea Univ., Sweden, “The dentist’s exposure to elemental mercury during clinical work”, Acta Odontol Scand, v53, n1, p44-48, 1995; & 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.

(121) A.S.Rowland et al, “The Effect of Occupational Exposure to mercury vapor on the fertility of female dental assistants”, Occupational & Environmental Medicine, v55, n1, 1994

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

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

(124) I.Akesson et al, Dept. of Occupational Medicine, “Status of mercury and selenium in dental personnel”, Arch Environ Health, 46 (2): 102-109, 1991 & Chang SB et al, Factors affecting blood mercury concentrations in practicing dentists, Dent Res, 1992, 71 (1):66-74; & Examination of blood levels of mercurials in practicing dentists, Anal Toxicol , 1987, 11 (4):149-53.

(125) U.S. CDC, National Center for Environmental Health , National Report on Human Exposure to Environmental Chemicals, 2001, www.cdc.gov/nceh/dls/report/Highlights.htm ; & National Research Council, Toxicological Effects of Methyl mercury (2000), pp. 304‑332: Risk Characterization and Public Health Implications, Nat’l Academy Press 2000. & U.S. Centers for Disease Control, Morbidity and Mortality Weekly Report, Mar 2, 2001, www.cdc.gov/mmwr/preview/mmwrhtml/mm5008a2.html; & U.S. CDC, Second National Report on Human Exposure to Environmental Chemicals, www.cdc.gov/exposurereport/

(126) (a)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 Aug 7;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. 274: 7528-7536, 1999; &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 Jun 26;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 Aug 10;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 May 1;273 (18):11313-20; & (b) 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 Mar;19 (2):101-5; & Kim SH, Johnson VJ, Sharma RP. Mercury inhibits nitric oxide production but activates proinflammatory cytokine expression in murine macrophage: differential modulation of NF-kappaB and p38 MAPK signaling pathways. Nitric Oxide. 2002 Aug;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 Jun;103 (6):1108-14. & (c) 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 Jun;23 (2):180-92.

(127) Moszczynski et al, “The behavior of T-Cells in the blood of workers exposed to mercury”, Med Lav 85 (3):239-241, 1994; & “Lymphocytes, T and NK cells in men exposed to mercury”, Int J Occup Med Environ Health, 8 (1):1995.

(128) M.L.S.Queiroz et al, “Immunoglobulin Levels in Workers Exposed to Inorganic Mercury”, Pharmacol Toxicol 74:72-75, 1994; & “Presence of Micronuclei in lymphocytes of mercury exposed workers’, Immunopharmacol Immunotoxicol, 1999, 21 (1):141-50; & D.C.Santos, “Immunoglobulin E in mercury exposed workers”, 1997, 19 (3):383-92..

(129) P.Hultman et al, Dept. Of Pathology, Linkoping Univ., Sweden, ”Adverse immunological effects and immunity induced by dental amalgam” FASEB J 8:1183-1190, 1994; & Toxicol Appl Pharmacol, 1992, 113 (2):199-208. .

(131) 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; & S.Ellermann-Eriksen et al, “Effect of mercuric chloride on macrophage-mediated resistance mechanisms against infection”, Toxicology, 93:269-297, 1994; &M.M.Christensen et al, Institute of Medical Microbiology, “Comparison of interaction of meHgCl2 and HgCl2 with murine macrophages”, Arch Toxicol, 1993, 67 (3):205-11;

(132) K.Sato et al, “An epidemiological study of factors relating to mercury sensitization”, Arerugi 44 (2): 86-92, 1995; & T.Mori et al, “Mercury sensitization caused by environmental factors”, Nippon Eiseigaku Zasshi, 1998, 52 (4):661-6.

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

(134) A.M.Aronsson et al, “Dental amalgam and mercury”, Biol Metals, 2:25-30, 1989.

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

(136) A. Certosimo et al, “The Effect of Bleaching Agents on Mercury Release from Spherical Dental Amalgam”.

Dental Article Review and Testing, 2003, http://agd.org/library/250/251/200308_cert.pdf &;D. Gay et al, “Chewing releases mercury”, Lancet, 8123:985-98, 1979.

(137) B.Fredin, “Studies on the Mercury Release from Dental Amalgam Fillings”, Swed J Biol Med No.3, 1988, pp8-15 & Summers, Science News, 4-10-93; & G. Sallsten et al, “Long term use of nicotine chewing gum and mercury exposure from dental amalgam”, J Dent Res 75 (1):598, 1996. & (b) T.Gebel et al, “Influence of Chewing Gum on Urine Mercury Content”, Zentralbl Hyg Umweltmed, 1996, 199 (1):69-75.

(138) D. Zander et al, “Studies on Human Exposure to Mercury Amalgam Fillings”, Ubl Hyg, 1990, 190: 325-

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

(140) R.L.Siblerud, “Health Effects After Dental Amalgam Removal”, J Orthomolecular Med 5 (2): 95 -106.

(141) RL.Siblerud et al, “Evidence that mercury from dental fillings may be an etiological factor in smoking”, Toxicol Lett, v68, n3, 1993, p307- & v69 (3):305.

(142) Ariza ME; Bijur GN; Williams MV. Lead and mercury mutagenesis: role of H2O2, superoxide dismustase, and xanthine oxidase. Environ Mol Mutagen 1998;31 (4):352‑61; & M.E. Ariza et al, “Mercury mutagenesis”, Biochem Mol Toxicol, 1999, 13 (2):107-12; & M.E.Ariza et al, “Mutagenic effect of mercury”, InVivo 8 (4):559-63, 1994;

(143) P.Boffetta et al, “Carciagenocity of mercury”, Scand J Work Environ Health, 1993, 19 (1):1-7, & “Study of workers compensated for mercury intoxication”, J Occup Med, 1994, 36 (11):1260-4; & J Occup Med, 36 (11):1260-64, 1994;

(144) .Y Zaichick et al, ”Trace Elements and thyroid cancer”, Analyst, 120 (3), 1995.

(145) Carpenter DO. Effects of metals on the nervous system of humans and animals. Int J Occup Med Environ Health. 2001;14 (3):209-18; & J.M.Gorell et al, “Occupational exposure to mercury, manganese, copper, lead, and the risk of Parkinson’s disease”, Neurotoxicology, 1999, 20 (2-3):239-47; & J.M. Gorell et al, ”Occupational exposures to metals as risk factors for Parkinson’s disease”, Neurology, 1997 Mar, 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 Oct;21 (5):863-6; & Brain sites of movement disorder: genetic and environmental agents in neurodevelopmental perturbations. Neurotox Res. 2003;5 (1-2):1-26

(146) 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 Nov;42 (5):403-9; & Gerhard et al, Zentralbl Gynakol, 1992, 114, 593-602: & I.Gerhard, Therapeutikon, 1993, 7, 478-91; & E.Roller et al, J Fert Reprod, 1995, 3, 31-33; & U.Vallon et al, J Fert Reprod 1995, 3, 31

(148) H.R.Casdorph, Toxic Metal Syndrome, Avery Publishing Group, 1995.

(149) (a)B.Choi et al, “Abnormal neuronal migration of human fetal brain”, Journal of Neurophalogy, Vol 37, p719-733, 1978; & (b)L.Larkfors et al, “Methyl mercury induced alterations in the nerve growth factor level in the developing brain “, Res Dev Res, 62 (2), 1991, 287- ; & (c)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 Dec 1;70 (5):703-11;

(150) U.S. Public Health Service, “Toxicological profile of Mercury”, 1988. & J.Leiskir, ”Cytotoxity of Silver amalgam”, Scand J of Dental Res, 1974.

(151) Electric Power Research Institute, EPRI Technical Brief:”Mercury in the Environment”, 1993; & EPRI Journal, April 1990.

(152) Langworth et al, “Effects of low exposure to inorganic mercury on the human immune system”, Scand J Work Environ Health, 19 (6): 405-413.1993; & Walum E et al, Use of primary cultures to sutdy astrocytic regulatory functions. Clin Exp Pharmoacol Physiol 1995, 22:284-7; & J Biol Chem 2000 Dec 8;275 (49):38620-5; & Kerkhoff H, Troost D, Louwerse ES. Infammatory cells in the peripheral nervous system in motro 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.

(153) International Academy of oral Medicine and Toxicology, “A Scientific Response to the American Dental Association Special Report and Statement of Confidence in Dental Amalgam, IAOMT, POB 608531, Orlando, 32860-8531, http://emporium.turnpike.net/P/PDHA/mercury/asr.htm; & IAOMT, Protocol for Mercury/Silver Filling Removal, http://www.iaomt.org/documents/Safe%20Removal%20of%20Amalgam%20Fillings1.pdf

(154) K.Nordlind 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; & E.Djerasci et al, Int Dent J 19:481-8, 1969; & A.M.Robinson et al, Contact Dermatitis due to Amalgam fillings”, Arch Dermatol Syphilol, 59:p116-8, 1949; & R.R.White et al, Mercury hypersensitivity among dental students, JADA, 92:124-7, 1976;

(155) L.D.Koller, “Immunotoxicology of Heavy Metals”, Int J of Immunopharm, 2:269-279, 1980; & Amer J Vet Res, vol34, p1457-, 1973.

(156) E.G.Miller et al, “Prevalence of Mercury Hypersensitivity among Dental Students”, J Dent Res. 64:Abstract 1472, p338, 1985; & D.Kawahara et al, “Epidemiologic Study of occupational Contact Dermatitis in the Dental Clinic”, Contact Dermatitis, Vol 28, No.2, pp114-5, 1993.

(157) L.J Goldwater, “Toxicology of Inorganic Mercury”, Annals: NY Acad Sci, 65:498-503, 1957; & J.B.Nielsen et al, “Evaluation of Mercury in Hair & Blood as Biomarkers for Methyl mercury Exposure”, Arch of Toxicology, 1994, 65 (5):317-321.

(158) Wenstrup et al, “Trace element imbalances in the brains of Alzheimer’s patients”, Research, Vol 533, p125-131, 1990; & F.L.Lorscheider, B.Haley, et al, “Mercury vapor inhibits tubulin binding ”, FASEB J, 9 (4):A-3485., 1995 & Vance et al, 1988, Neurotoxicology, 9:197-208; & 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.

(159) W.Eggert-Kruse et al, “Effect of heavy metals on in vitro interaction between human sperm and cervical mucus”, Dtsch Med Wochenschr , 1992, 117 (37):1383-9 (German); E.Ernst et al, “Effect of mercury on human sperm motility”, Toxicol 1991, 68 (6):440-4; & A.Daily et al, “Declining sperm count: evidence that Young’s syndrome is associated with mercury”, BMJ, 1996, 313 (7048): 44;

(161) F.L.Lorscheider et al, “Inorganic mercury and the CNS: genetic linkage of mercury and antibiotic resistance”, Toxicology, 1995, 97 (1): 19-22; & M.C.Roberts, Dept. Of Pathobiology, Univ. Of Washington, “Antibiotic resistance in oral/respiratory bacteria”, Crit Rev Oral biol Med, 1998;9 (4):522-

(162) N.K.Mottet et al, “Health Risks from Increases in Methyl mercury Exposure”, Health Perspect; vol63 :133- 140, 1985; & (b) M.K.Mohamed et al, “Effects of methyl mercury on testicular functions in monkeys”.Toxicol, 1987, 60 (1):29-36; & M.K. Mohamed et al, Toxicol (Copenhagen), 1986, 58 (3):219-24; & N.F. Ivanitskaia, ” Evaluation of effect of mercury on reproductive function of animals”, Gig Sanit, 1991, 12: 48-51; & (c) Methylmercury alters glutamate transport in astrocytes; Neurochem Int. 2000 Aug-Sep;37 (2-3):199-206. Aschner M, Yao CP, Allen JW, Tan KH.

(163) Ahlrot-Westerlund B. Multiple Sclerosis and mercury in cerebrospinal fluid. Second Nordic Symposium on Trace Elements and Human Health, Odense, Denmark, Aug 1987; & Nutrition Research, 1985 Supplement; & Monica Kauppi and Dr Britt Ahlrot-Westerlund, Heavy Metal Bulletin 2 (3):11-12 December 1995. (Vit B12)

(164) Swedish Dental Material Commission, 2003, www.dentalmaterial.gov.se/mercury.pdf & Swedish National Dept. of Health, Mercury Amalgam Review Panel, 1987; & Heavy Metal Bulletin, Dec 2000, Vol 6, Issue 3; & Petra Ekblom, Utredare/Senior Technical Officer; Kemikalieinspektionen/National Chemicals Inspectorate Avd. Riskbegräänsning/Risk Reduction, P.O. Box 2, S-172 13 SUNDBYBERG, Sweden www.kemi.se/raw/documents/57015_kvicksilver.pdf

(165) 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.

(166) H.Basun et al, J Neural Transm Park Dis Dement Sect, “Metals in plasma and cerebrospinal fluid in normal aging and Alzheimer’s disease”, 1991, 3 (4):231-58

(167) M.L Olsted et al, “Correlation between amalgam restorations and mercury in urine”, J Dent Res, 66 (6): 1179-1182, 1987.

(168) J.Laine et al, “Immunocompetent cells in amalgam-associated oral licheinoid contact lesions”, Oral Pathol Med 1999; 28 (3): 117-21; & “Resolution of OLL after replacement of amalgam restorations”, Br J Dermatol, 1992, 126 (1):10-15 (20 cases); & (b)“Contact allergy to dental restorative materials in patients with oral lichenoid lesions”, Contact Dermatitis, 1997, 36:3, 141-6; & Adachi A, Horikawa T, “Efficacy of dental metal elimination in the management of atopic dermatitis”, J Dermatology, 1997, 24 (1), 12-19;

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

(170) Birgitta Brunes, Adima Bergli, From MS diagnosis to better health , 1996. www.melisa.org; & DAMS, Recoveries from MS after amalgam replacement, www.whale.to/d/ms1.html; & Maile Pouls, Townsend Letter, 1999, www.heall.com/healingnews/may/heavy_metals.html

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

(172) B.Nilsson et al, Dept. of Environmental Medicine, Univ. Of Umea, “Urinary mercury excretion in dental personnel”, Swed Dent J, 1986, 10 (6):221-32; & Swed Dent J, 1986, 10 (1-2):1-14; & Science of the Total Environment, 1990, 94 (3):179-85.

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

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

(175) F. Monnet-Tschudi 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;.& (c) Sorensen FW, Larsen JO, Eide R, Schionning JD; Neuron loss in cerebellar cortex of rats exposed to mercury vapor: a stereological study. Acta Neuropathol (Berl). 2000 Jul;100 (1):95-100.

(176) A.Jokstad et al, “Dental amalgam and mercury”, Pharmacol Toxicol, 70 (4), 1992, 308-13; & L.Barregard et l, “mercury exposure from dental amalgam”, Tidsskr Nor Laegeforen, 1998, 118 (1):58-62

(179) A.Lussi, “Mercury release from amalgam into saliva”, Schweiz Monatsschr Zahnmed, 1993, 103 (6):722-29; & Kindl A, Zinecker S, “Amalgam: Quecksilberdamfe bis ins Gehrin”, der Kassenarzt 4, 23, 1992; & (c ) Scalp hair and saliva as biomarkers in determination of mercury levels in Iranian women: Amalgam as a determinant of exposure; Fakour H, Esmaili-Sari A, Zayeri F. J Hazard Mater. 2009 Dec 4.

(180) Pinto OF et al, J Intl Acad Prev Med, Vol 3, No.2, 1976; & Huggins HA, Proposed role of dental amalgam toxicity in leukemia and hemotopoietic dyscrasias. International J of Biosocial and Medical Research, 1989, 11:84-93; & Schimpff SC, Young WH, Greene WH, Origin of infections in acute nonlymphocytic leukemia. Annals of International Medicine 1972, 77:707-711; & Y.Kinjo et al, “Cancer mortality in patients exposed to methyl mercury through fish diet”, J Epidemiol, 1996, 6 (3):134-8..

(181) P.W. Mathieson, “Mercury: god of TH2 cells”, 1995, Clinical Exp Immunol., 102 (2):229-30; & (b) Heo Y, Parsons PJ, Lawrence DA, Lead differentially modifies cytokine production in vitro and in vivo. Toxicol Appl Pharmacol, 196; 138:149-57; & (c) Murdoch RD, Pepys J; Enhancement of antibody and IgE production by mercury and platinum salts. Int Arch Allergy Appl Immunol 1986 80: 405-11;& (d) Parronchi P, Brugnolo F, Sampognaro S, Maggi E. Genetic and Environmental Factors Contributing to the Onset of Allergic Disorders. Int Arch Allergy Immunol 2000 Jan;121 (1):2-9.

(182) Pleva J, “Dental mercury – a public health hazard”, Rev Environ Health 10 (1):1-27 (1994) ;J Pleva, Mercury from dental amalgams: exposure and effects, Int J Risk & Safety in Med, 1992, 3: 1-22. & “Mercury- A Public Health Hazard”, Reviews on Environmental Health, 1994, 10:1-27; & Mercury poisoning from dental amalgam. J. Of Orthomol. Medicine 1989, 4 (3):141- 148; & J Orthomol Psych, Vol 12, No.3, 1983. & Emler & Cardone, Oral Roberts Univ., “An Assessment of Mercury in Mouth Air”, Journal of Dental Research, March 1985; & Vimy M. and Lorschieder, University of Calgary ” Intra oral Mercury Released from Dental Amalgam” Journal of Dental Research 1985;64:1069-1071 &” Serial Measurements of Intra Oral Mercury” Journal Dental Research 1985, 64:1072-1075.

(183) World Health Organization (WHO), 1991, Environmental Health Criteria 118, Inorganic Mercury, WHO, Geneva; & Environ metal Health. Criterion. 101, Methyl Mercury; 1990. http://www.who.int/water_sanitation_health/medicalwaste/mercurypolpaper/en/print.html

(184) T.H.Ingalls, Clustering of multiple sclerosis in Galion, Ohio, 1982-1985. Amer J Forensic Med Pathol 1989; 10: 213-5; & “Endemic clustering of multiple sclerosis in time and place”, Am J.Fors Med Path, 1986, 7:3-8; & J Forsenic Medicine and Pathology, Vol 4, No 1, 1953; & Epidemiology, etiology and prevention of MS”, Am J Fors Med & Pathology, 1983, 4:55-61; & Craelius W, Comparative epidemiology of multiple sclerosis and dental caries”, J of Epidemiological and Community Health 32:155-65.

(185) L.Jones, “Health outcomes following amalgam removal”, New Zealand Psychology Journal, Sept., 1999. http://www.melisa.org/articles/ljones.pdf

(186)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; & (b) C.N.Ong et al, “Concentrations of heavy metal in maternal and umbilical cord blood”, Biometals, 6 (1):61‑66, 1993; & (c) Y.K.Soong et al, J of Formosa Medical Assoc., 1991, 90 (1): 59-65; & (d) T. Suzuki et al, Dept. Of Human Ecology, Univ. Of Tokyo, “Mercury in human amniotic fluid” , Scand J Work Environ & Health, 3:32-35, 1977; & (e) D.A. Spencer et al, “Mercury Concentration in Cord Blood”, Arch Dis Child, 1988, 63 (2):202-3; & (f)S.Sugiyama et al, “Comparison of heavy metal concentrations in human umbilical cord blood in 1980 and 1990:, Kinki Univ. School of Medicine, Osaka, Japan; & (g)R.Sikorski et al, ”The intrapartum content of toxic metals in maternal and umbilical cord blood”, Ginekol Pol, 1989, 60 (3):151- & (h)Ask K, Akesson A, Berglund M, Vahter M.. Inorganic mercury and methylmercury in placentas of Swedish women. Environ Health Perspect 2002 May;110 (5):523-6; & (i) Ask K, Akesson A, Berglund M, Vahter M. Inorganic mercury and methylmercury in placentas of Swedish women.. Environ Health Perspect. 2002 May;110 (5):523-6.

(187) Klobusch J, Rabe T, Gerhard I, Runnebaum B, “Alopecia and environmental pollution” Klinisches Labor 1992, 38:469‑ 476; & “Schwermetallbelastungen bei Patientinnen mit Alopezie” Arch Gynecol. Obstet., 1993, 254 (1-4):278-80;& G. Kunzel et al, “Arch Gynecol. Obstet., 1993, 254:277-8.

(188) I.I. Ship et al, School of Dental Research, Univ. of Penn., Mar 1983; & P.A.Gronla et al, JADA, 1970, 81:923-25.

(189) U.S.CDC, Toxicology Division, Atlanta, Ga. and WHO, Environmental Health Criteria 101, 1990, & Mercury in Fish, Review, www.flcv.com/fishhg.html

(190) P.Urban et al, “Neurological examination on 3 groups of workers exposed to mercury vapor”, Eur J Neurology, 1999, 6 (5): 571-7; & B. Polakowska, “Neurological Assessment of Health Status in Dentists”, Med Pr, 1994, 45 (3):221-5; & L.Ekenvall et al, “Sensory perception in the hands of dentists” J Work Environ Health, 1990, 16 (5):334-9.

(191) D.Brune et al, Gastrointestinal and in vitro release of metals from conventional and copper-rich amalgams. Scand J Dent Res, 1983, 91:66-71 & (b) Dependence of kinetic variables in the short-term release of Hg (2+), Cu (2+) and Zn (2+ )ions into synthetic saliva from an high-copper dental amalgam. Campus G, Garcia-Godoy F, et al; Mater Sci Mater Med. 2007 Mar 27; & (c) “Metal release from dental materials”, Biomaterials, 1986, 7, 163-175.

(192) (a) N.Nogi, “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; & J. Bergdahl, A.J.Certosimo et al, National Naval Dental Center, “Oral Electricity”, Gen Dent, 1996, 44 (4):324-6; & B.M.Owens et al, “Localized galvanic shock after insertion of an amalgam restoration”, Compendium, 1993, 14 (10), 1302, 1304, 1306-7 & (b)M.D.Rose et al, Eastman Dental Institute, “The tarnished history of a posteria restoration”, Br Dent J 1998;185 (9):436;& & R.D.Meyer et al, “Intraoral galvanic corrosion”, Prosthet Dent, 1993, 69 (2):141-3 R.H.Ogletree et al, School of Materials Science, GIT, Atlanta, ”Effect of mercury on corrosion of eta’ Cu-Sn phase in dental amalgams”, Dent Mater, 1995, 11 (5):332-6; & (c) Johansson E, Liliefors T, “Heavy elements in root tips from teeth with amalgam fillings”, Department of Radiation Sciences, Division of Physical Biology, Box 535, 751 21 Uppsala, Sweden; & (i) Immunological findings in saliva of patients with oral discomfort and dental metal fillings in relation to presence of galvanic cell in the oral cavity. Podzimek S, Prochazkova J, Miksovsky M, Bartova J, Hana K. Neuro Endocrinol Lett. 2006 Dec;27 Suppl 1:59.

(193) E.N.Cohen et al, “Occupational disease in dentistry”, Amer. Dent Assoc, 1980, 101 (1): 21-31; & G.Bjorklund, “Risk evaluation of the occupational environment in dental care”, Tidsski Nor Laegeforen, 1991, 111 (8): 948-50; & A.Ahlbom et al, :Dentists, dental nurses, and brain tumors”, Br Med J, 1986, 202 (6521):662.

(194) Lu SC, FASEB J, 1999, 13 (10):1169‑83, “Regulation of hepatic glutathione synthesis: current concepts and controversies”; & R.B. Parsons, J Hepatol, 1998, 29 (4):595-602; & R.K.Zalups et al, “Nephrotoxicity of inorganic mercury co‑administered with L‑cysteine”, Toxicology, 1996, 109 (1): 15‑29. & T.L. Perry et al, “Hallevorden-Spatz Disease: cysteine accumulation and cysteine dioxygenase deficiency”, Ann Neural, 1985, 18 (4):482-489.

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

(196) G. Sandborgh-Englund, Pharmakinetics of mercury from dental amalgam”, Medical School Dissertation Dept. Of Basal Oral Sciences, Karolinska Institute, (Stockholm), 1998, 1-49; & G. Sandborgh-Englund et al, Mercury in biological fluids after amalgam removal. J Dental Res, 1998, 77 (4): 615-24; & Toxicological aspects on the release and systemic uptake of mercury from dental amalgam. Ekstrand J, Bjorkman L, Edlund C, Sandborgh-Englund G. Eur J Oral Sci. 1998 Apr;106 (2 Pt 2):678-86.
(197) J.Taylor, A Complete Guide to Mercury Toxicity from Dental Fillings , Scripps Publishing;

(198) Cd2+ and Hg2+ affect glucose release and cAMP-dependent transduction pathway in isolated eel hepatocytes. Aquat Toxicol. 2003 Jan 10;62 (1):55-65, Fabbri E, Caselli F, Piano A, Sartor G, Capuzzo A. & Fluctuation of trace elements during methylmercury toxication and chelation therapy. Hum Exp Toxicol. 1994 Dec;13 (12):815-23, Bapu C, Purohit RC, Sood PP; E.S. West et al, Textbook of Biochemistry, MacMillan Co, 1957, p853;& B.R.G.Danielsson et al, ”Ferotoxicity of inorganic mercury: distribution and effects of nutrient uptake by placenta and fetus”, Biol Res Preg Perinatal. 5 (3):102-109, 1984; & Danielsson et al, Neurotoxicol. Teratol., 18:129-134;?

(199) Kraub P, Deyhle M, Maier KH, Roller HD, “Field Study on the mercury content of saliva”, Heavy Metal Bull, vol.3, issue 1, April ’96; & Dr. P.Kraub & M.Deyhle, Universitat Tubingen- Institut fur Organische Chemie, “Field Study on the Mercury Content of Saliva”, 1997 (20, 000 people tested for mercury level in saliva and health status/symptoms compiled); http://www.xs4all.nl/~stgvisie/AMALGAM/EN/SCIENCE/tubingen.html www.bio.net/bionet/mm/toxicol/1999-September/002567.html

(200) V.Nadarajah et al, “Localized cellular inflammatory response to subcutaneously implanted dental mercury”, J Toxicol Environ Health, 1996, 49 (2):113-25; Kulacz & Levy , “The Roots of Disease”. Xlibris Corporation at 1-888-795-4274 www.xlibris.com; & B.E. Haley, Dental Lab, www.altcorp.com

(201) J.T. Salonen 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 Feb;148 (2):265-73; & Gualler E, et al; Mercury, fish oils, and the risk of myocardial infarction, New England J of Medicine, 2002, 347:

(203) M.J.Vimy et al, “Renal function and amalgam mercury”, Amer J Physiol, 1997, 273 (3/2):1199- ; & (b) 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.;& K.A.Nath et al, Dept. Of Medicine, Univ. Of Minnesota, “Renal oxidant injury induced by mercury”, Kidney Int, 1996, 50 (3): 1032-43; & (c)Ware RA et al, Ultrastructural changes in renal proximal tubules after chronic organic and inorganic mercury intoxication”, Environ Res, 1975, 10 (1):121-40; & (d) Bigazzi PE., “Metals and kidney autoimmunity”, Environ Health Perspect, 107 Suppl 5:753-65, (Oct 1999)& McCann et al, Intravenous gamma globulin (IVIG) treatment of autoimmune kidney disease associated with mercury ( Hg++) toxicity. J Allergy Clin Immunol 95 (1) (Pt 2):145; & (e) G.D. Nuyts et al, “New occupational risk factors for chronic renal failure”, Lancet 1995; 346 (8966):7-11: & Biometals, Vol. 10, October 1997, pp. 315‑23

(204) Tom Warren, Beating Alzheimer’s, Avery Publishing Group, 1991. www.the7thfire.com/ADApolitics.htm & www.whale.to/m/alzheimer.html

(205) M.F. Ziff et al, A Persuasive New Look at Heart Disease As It Relates to Mercury, Bio-Probe, Inc., ISBN 0-941011-08-9; & J. of American College of Cardiology V33, #6, pp1578‑1583, 1999.

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

(207) Pendergrass JC, Haley BE, Univ. Of Kentucky Dept. Of Chemistry “ The Toxic Effects of Mercury on CNS Proteins: Similarity to Observations in Alzheimer’s Disease”, IAOMT Symposium paper, March 1997 & “Mercury Vapor Inhalation Inhibits Binding of GTP …-Similarity to Lesions in Alzheimer’s Diseased Brains”, Neurotoxicology 1997, 18 (2)::315-24; & Met Ions Biol Syst, 1997, 34:461-

(208) L.T.Friberg, “Status Quo and perspectives of amalgam and other dental materials”, International symposium proceedings, G.Thieme Verlag Struttgart, 1995.

(209) Mark Richardson, Environmental Health Directorate, Health Canada, Assessment of Mercury Exposure and Risks from Dental Amalgam, 1995, Final Report; & G.M. Richardson et al, ”A Monte Carlo Assessment of Mercury Exposure and Risks from Dental Amalgam”, Human and Ecological Risk Assessment, 2 (4): 709-761; & Richardson M, in: Swedish Council for Coordinating and Planning Research, Amalgam and Health, FRN, 1999

(210) Mats Berlin, “Is amalgam in dental fillings hazardous to health?”, Lakartidningen, 1992; 89 (37):2918-23; & “Mercury in dental filling materials- environmental medicine risk analysis”, in: [Swedish Council for Coordinating and Planning Research, Amalgam and Health, FRN, 1999]; & Berlin, M; et al. Prenatal Exposure to Mercury Vapor: Effects on Brain Development. The Toxicologist, 12 (1):7 (A245), 1992; & “Expert Consulted For Amalgam Study Demands Amalgam Ban”, Swedish Dental Materials Study , “Dagens Nyheter”, April 26 2003, www.tv4.se/nyheterna/lopsedel.html www.dn.se/DNet/jsp/polopoly.jsp?d=597&a=134259&previousRenderType=6

(211) M.J.Vimy and F.L. Lorscheider, Faculty of Medicine, Univ. Of Calgary, July 1991. (Study findings) & J. Trace Elem. Exper. Med., 1990, 3, 111-123.

(212) (a) Ziff, M.F., “Documented clinical side effects to dental amalgams”, ADV. Dent. Res., 1992; 1 (6):131-134; & Ziff, S., Dentistry without Mercury, 8th Edition, 1996, Bio-Probe, Inc. , ISBN 0-941011-04-6; & Dental Mercury Detox, Bio-Probe, Inc. http://www.bioprobe.com. (Cases: FDA Patient Adverse Reaction Reports-762, Dr.M.Hanson-Swedish patients-519, Dr. H. Lichtenberg-100 Danish patients , Siblerud, RL. Health effects after dental amalgam removal. J. Orthomol. Med. 5, 1990, 95-106 (86 patients); & P. Larose. The effect of amalgam removal on 37 health symptoms in humans. Updated 1992 from study reported in Dental Health & Facts 2 (1) 1989. Foundation for Toxic-free Dentistry/Bio-Probe, Orlando (80 patients); & Zamm, AV. Removal of dental mercury: often an effective treatment for the very sensitive patient. J Orthomol. Med. 5, 1990, 138-142 (22 patients) (b) Hovmand, O. Oral galvanisme – erfaringer fra praxis. Tandlaegebladet 91, 1987, 473-476. (& (c) over 1000 additional cases of significant improvement reported directly to FDA)

(213) Dr. C. Kousmine, Multiple Sclerosis is Curable, 1995. & Review: Mercury & MS, www.flcv.com/ms.html

(214) “Amalgam declared hazardous”, Dentistry Today, February, 1989, p1.

(215) K.W. Sehnert, “Autoimmune Disorders”, Advance, Jan 1995, p47-48.

(216) T.W. Clarkson et al, in Biological Monitoring of Toxic Metals, 1988, Plenum Press, N.Y., “The prediction of intake of mercury vapor from amalgams”, p199-246 & p247-260; Environmental Health Perspective, 1993, April, 100:31-8; & F.L. Lorscheider et al, Lancet, 1991, 337, p1103.

(217) Agency for Toxic Substances and Disease Registry, U.S. Public Health Service, Toxicological Profile for Mercury , 1999; & Jan 2003 Media Advisory, New MRLs for toxic substances, MRL:elemental mercury vapor/inhalation/chronic & MRL: methyl mercury/ oral/acute; & www.atsdr.cdc.gov/mrls.html

(218) U.S. Dept. Of Health, ATSDR ToxFAQ CAS# 7349-97-6; www.atsdr.cdc.gov/tfacts46.html; & (b) U.S. EPA, K.R. Mahaffey, Methyl mercury: Epidemiology Update, presentation at EPA’s National Forum on Contaminants in Fish, in San Diego, Jan 26, 2004.

(219) D.E. Cutright et al, Dept. Of Prosthodontics, Temple Univ.“Systemic mercury levels caused by inhaling mist during high-speed amalgam grinding”, J Oral Med 28 (4):100-104, 1973 ; & (b) A.Nimmo et al, “Inhalation during removal of amalgam restorations”, J Prosthet Dent, 63 (2):1990 Feb, 228-33; & (c) Stonehouse CA, Newman AP. Mercury vapour release from a dental aspirator. Br Dent J 2001 May 26;190 (10):558-60 & (d) 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; & http://atsdr1.atsdr.cdc.gov:8080/97list.html.

(220) Sellars WA, Sellars R. Univ. Of Texas Southwestern Medical School “Methyl mercury in dental amalgams in the human mouth”, Journal of Nutritional & Environmental Medicine 1996; 6 (1): 33-37; & C Arch Environmental Health, 19, 891-905, Dec 1969.

(221) R. Golden et al, Duke Univ., “Dementia and Alzheimer’s Disease”, Minnesota Medicine, 78:p25-29, 1995; & Schofield P, Dementia associated with toxic causes and autoimmune disease. Int Psychogeriatr. 2005;17 Suppl 1:S129-47.

(222) M. Daunderer, Handbuch der Amalgamvergiftung, Ecomed Verlag, Landsberg 1998, ISBN 3‑609‑71750‑5 (in German); & “Improvement of Nerve and Immunological Damages after Amalgam Removal”, Amer. J. Of Probiotic Dentistry and Medicine, Jan 1991; & Toxicologische erfahrungen am menchen; Quecksilber in der umwelf-hearing zum amalgamproblem”, Niedersachsiscles Umweltministerium, 1991; & “Amalgam”, Ecomed-Verlag, Landsberg, 1995; & “Amalgamtest”, Forum Prakt.Allgen.Arzt, 1990, 29 (8): 213-4; & “Besserung von Nerven- und Immunschaden nach Amalgamsanierung”, Dtsch.Aschr. F. Biologische Zahnmedzin, 1990, 6 (4):152-7. ( amalgam removal & DMPS, over 5, 000 cases)

(223) Nicholson et al, “Mercury Nephrotoxicity”, Nature Vol 304: 633, 1983; & (b) Friberg et al, “Kidney injury after chronic exposure to inorganic mercury”, Archives of Environ Health, Vol 15:p64, 1967; & (c) Kazantis et al, “Nephrotic Syndrome Following Exposure to Mercury”, Quarterly J. Of Medicine, Vol 31: 403-418, 1962; & (d) L.H.Lash, Environmental Health Perspective, 1994, 102 (11); & (e) Mortada WL, Sobh MA, Mercury in dental restoration: is there a risk of nephrotoxicity? J Nephrol 2002 Mar-Apr;15 (2):171-6

(224) M.S. Hughes, Amer. J. Of Obstetrics and Gynecology, vol 143, No 4:440- 443, 1982.

(225) S. Yannai et al, “Transformations of inorganic mercury by candida albicans and Saccharomyces cerevisiae”, Applied Envir Microbiology, 1991, 7:245-247; & N.E.Zorn 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 Aug;19:43‑6 & R.E.DeSimone et al, Biochem Biophys Acta, 1973, May 28; & Yamada, Tonomura“Formation of methyl Mercury Compounds from inorganic Mercury by Clostridium cochlearium” J Ferment Technol1972 50:159‑1660

(226) (a)B.J. Shenker et al, Dept. Of Pathology, Univ. Of Penn. School of Dental Med., ”Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes: Alterations in cell viability” Immunopharmacologicol Immunotoxical, 1992, 14 (3):555-77; & M.A.Miller et al, “Mercuric chloride induces apoptosis in human T lymphocytes”, Toxicol Appl Pharmacol, 153 (2):250‑7 1998;& 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; , & (b) B.J. Shenker et al “Immune suppression of human T-cell activation”, Immunopharmacologicol Immunotoxical, 1992, 14 (3):555-77, & 14 (3):539-53; & 1993, 15 (2-3):273-90;

(227) Dr. Pierre Blaise, Health Canada, 1976 & Discovery, Feb 1997 (TV, Quebec)

(229) M.Davis, editor, Defense Against Mystery Syndromes”, Chek Printing Co., & March, 1994 (case histories documented); & Andrew Hall Cutler, PhD, PE; Amalgam Illness:Diagnosis and Treatment; 1996 , www.noamalgam.com/

(230) S. Rogers, M.D., Chemical Sensitivity, Keats Publishing; & Bauer, F; The toxicity of mercury in Dental Amalgam, CDA Journal, June 1982.

(231) Larsen, A.H. et al, “Mercury Discharge in Waste Water from Dental Clinics” Water Air and Soil Pollution, Jan 1996: 86 (1-4): 93-99 ; & Rubin, P.G. et al, Archives of Environmental Health, Jul. 1996; 51 (4):335-337; & A. Lindvall et al, “Mercury in the Dental Practice: Contamination of Ambient Air and Waste Water, FDI World Dental Congress, Aug19, 1993, Goteborg, Swe

(232) Adolph Coors Foundation, “Coors Amalgam Study: Effects of placement and removal of amalgam fillings”, 1995. (www) & International DAMS Newsletter, p17, Vol VII, Issue 2, Spring 1997. (31 cases); & (b) Antero Danersund, “Dental Materials and Psychoneuroimmunology Conference”. Danderyd Hospital, 14-16 August, 1998; www.melisa.org/archive/6th_melisa_study_group.html; & Experimental study on brain oxygenation in relation to tissue water redistribution and brain oedema. Acta Neurochir Suppl. 2000;76:279-81, Titovets E, Nechipurenko N, Griboedova T, Vlasyuk P.

(233) F.Berglund, Bjerner/Helm, Klock, Ripa, Lindforss, Mornstad, Ostlin), “Improved Health after Removal of dental amalgam fillings”, Swedish Assoc. Of Dental Mercury Patients, 1998. (www.tf.nu), (a) Lindforss, H, Marqvardsen, O, Olsson, S, Henningsson, M. Effekter på hälsan efter avlägsnandet av amalgamfyllningar (Effects on health after removal of amalgam fillings). Tandläkartidn. 86 (4), 1994, 205-211; (503 patients); & (b)Östlin, L. Amalgamutbyte – en väg mot bättre hälsa? (Amalgam removal – a road to better health?) Försäkringskassan, Stockholms län, 1991 (308 patients); & (c)Olsson, G & Lindh, U. Veränderung des allgemeinen Gesundheitszustand nach Amalgamentfernung. (Changes in general health after amalgam removal) GZM, Ganzheitl. Zahnmed. 2 (1), 1997, 22-28 (253 patients); & (d) Strömberg, R, Langworth, S. Förbättras hälsan efter borttagning av amalgam? (Does health improve after removal of amalgam?) Tandläkartidn. 90 (9), 1998, 23-29 (233 patients); & (e)LEK-studien, Landstinget Dalarna, Bjerner, B & Hjelm, H. dec. 1991, LEK-studien Dalarna. Sammanställning inför hearing med SoS:s “tungmetallgrupp”, 90-11-21 (207 patients); & (f) Klock, B, Blomgren, J, Ripa, U, Andrup B. Effekt av amalgamavlägsnande på patienter som misstänker att de lider eller har lidit av amalgamförgiftning. (Effect of amalgam removal in patients who suspect amalgam poisoning) Tandläkartidningen 81, 1989, 1297-1302 (198 patients); & (g)Sven Langworth et al, Amalgam news and Amalgamkadefonden, 1997. (www.tf.nu) http://iaomt.org/articles/files/files214/Hansen-%20effects%20of%20amal%20removal.pdf

(234) (a) Cooper GS, Dooley MA., et al, NIEHS, Occupational risk factors for the development of systemic lupus erythematosus, J Rheumatol. 2004 Oct;31 (10):1928-33; & (b) P.E. Bigazzi, “Autoimmunity and Heavy Metals”, Lupus, 1994; 3: 449-453; & (c)Pollard KM, Pearson Dl, Hultman P. Lupus-prone mice as model to study xenobiotic-induced autoimmunity. Environ Health Perspect 1999; 107 (Suppl 5): 729-735; & Nielsen JB; Hultman P. Experimental studies on genetically determined susceptibility to mercury‑induced autoimmune response. Ren Fail 1999 May‑Jul;21 (3‑4):343‑8; & Hultman P, Enestrom S, Mercury induced antinuclear antibodies in mice, Clinical and Exper Immunology, 1988, 71 (2): 269-274; & (d)Robbins SM, Quintrell NA, Bishop JM. Mercuric chloride activates the Src-family protein tyrosine kinase, Hck in myelomonocytic cells. Eur J Biochem. 2000 Dec;267 (24):7201-8; & (e) 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; & (f) Silbergeld EK, Silva IA, Nyland JF. Mercury and autoimmunity: implications for occupational and environmental health. Toxicol Appl Pharmacol. 2005 Sep 1;207 (2 Suppl):282-92. .

(235) H.J.Hamre, Mercury from Dental Amalgam and Chronic Fatigue Syndrom”, The CFIDS Chronicle, Fall 1994, p44-47.

(236) G.J.Murphy, American Academy of Head, Neck, and Facial Pain, Oct 21, 1994

(237) H.D.Foster, 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 Dec;6 (4):209-21.

(239) J.M.Varga 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; & J.H.Gainer, “Activation of Rauscher leukemia virus by metals”, J Natl Cancer Inst, 1973, 51 (2).609-13.

(240) K.W. Hinkleman et al, “Mercury release during ultrasonic scaling of amalgam”, J Dent Res. 74 (SE):131, Abstract 960, 1995; & Haikel Y, Gasser P, Salek P, Voegel JC, “Exposure to mercury vapor during setting, removing, and polishing amalgam restorations”, J Biomed Mater Res 1990 Nov;24 (11):1551-8.

(241) R.Schoeny, U.S.EPA, “Use of genetic toxicology data in U.S. EPA risk assessment: the mercury study”, Environ Health Perspect, 1996, 104, Supp 3: 663-73; & C.H.Lee et al, “Genotoxicity of phenylHg acetate in humans as compared to other mercury compounds”, 392 (3):269-76.

(242) J.Constantinidis et al, Univ. Of Geneva Medical School, “Hypothesis regarding amyloid and zinc in the pathogenisis of Alzheimer’s Disease”, Alzheimer’s Dis Assoc Disord , 1991, 5 (1):31-35 & G. Bjorklund, “Can mercury cause Alzheimer’s”, Tidsskr Nor Laegeforen, 1991

(243) P.R.Walker et al, National Research Council of Canada, “Effects of aluminum and mercury on the structure of chromatin”, Biochemistry, May 2 1989, 28 (9):3911-3915.

(244) H.Basun et al, Dept. Of Geriatric Medicine, Huddinge Hospital, Sweden, “Trace metals in plasma and cerebrospinal fluid in Alzheimer’s disease”, J Neural Transm Park Dis Dement Sect 1991; 3 (4):231-

(245) P.Lokken, “Lethal mercury poisoning in a dental assistant”, Nor Tannlaegeforen Tid, Apr 1971, 81 (4):275-288 & R. Wronski et al, “A case of panarteritis nodoa associated with chronic mercury poisoning”, Dtsch Med Wohenschr, Mar 1977, 102 (9):323-325.

(246) K.Iyer et al, “Mercury Poisoning in a dentist”, Arch Neurol, 1976, 33:788-790.

(247) E.C.Lonnroth 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; & L.Kanerva et al, ”Occupational contact urticaria”, Contact Dermatitis, 1996, 35 (4): 229-33; & (c) Lee JY, Yoo JM, Cho BK, Kim HO. Contact dermatitis in Korean dental technicians. Contact Dermatitis. 2001 Jul;45 (1):13-6; & (d) High prevalence of extrapyramidal signs and symptoms in a group of Italian dental technicians. Fabrizio E, Vanacore N, Valente M, Rubino A, Meco G. BMC Neurol. 2007 Aug 8;7:24

(248) Y.Finkelstein, “The enigma of parkinsonism in chronic borderline mercury intoxication, resolved by challenge with penicillamine. Neurotoxicology, 1996, Spring, 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-

(249) C.H.Ngim et al, Dept. of Occupational Medicine, Univ. Of Singapore, “Chronic neurobehavioral effects of elemental mercury in dentists”, British Journal of Industrial Medicine, 1992; 49 (11):782-790.

(250) B.A.Rybicki 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 Sep, 141:1, 13‑22; & (c) Studies documenting mercury causes ataxia/tremor www.flcv.com/ataxiaHG.html

(251) (a) Y.Omura et al, Heart Disease Research Foundation, NY, NY, “Role of mercury in resistant infections and recovery after Hg detox with cilantro”, Acupuncture & Electro-Therapeutics Research, 20 (3):195-229, 1995; & (b) “Mercury exposure from silver fillings”, Acupuncture & Electrotherapy Res, 1996, 133- ; & (c)Omura, Yoshiaki; 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, Vol. 25 Issue 3/4, p230, 3p

(252) B.J.Shenker et al, Dept. of Pathology, Univ. of Pennsylvania, “Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes: Alterations in cellular glutathione content”, Immunopharmacol Immunotoxicol 1993, 15 (2-3):273-90;

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

(255) D.C. Rice, “Evidence of delayed neurotoxicity produced by methyl mercury developmental exposure”, Neurotoxicology, Fall 1996, 17 (3-4), p583-96; & (b) Weiss B, Clarkson TW, Simon W. Silent latency periods in methylmercury poisoning and in neurodegenerative disease. Environ Health Perspect. 2002 Oct;110 Suppl 5:851-4: &© Residual neurologic deficits 30 years after occupational exposure to elemental mercury. Neurotoxicology. 2000 Aug;21 (4):459-74., Letz R, Gerr F, Cragle D, Green RC, Watkins J, Fidler AT.

(256) D.B.Alymbaevaet al, Med Tr Prom Ekol, 6:13-15, 1995 (Russian), and Mayo Clinic, Stomach Cancer http://www.mayoclinic.com/health/stomach-cancer/DS00301

(257) I. Smith et al, “Pteridines and mono-amines: relevance to neurological damage”, Postgrad Med J, 62 (724): 113-123, 1986; & A.D.Kay et al, “Cerebrospinal fluid biopterin is decreased in Alzheimer’s disease”, Arch Neurol, 43 (10): 996-9, Oct 1986; & T.Yamiguchi et al, “Effects of tyrosine administration on serum bipterin In patients with Parkinson’s Disease and normal controls”, Science, 219 (4580):75-77, Jan 1983; & T.Nagatsu et al, “Catecholoamine-related enzymes and the biopterin cofactor in Parkinson’s”, Neurol, 1984, 40: 467-73.

(258) Ely, J.T.A., Mercury Induced Alzheimer’s Disease: Accelerating Incidence?, Bull Environ Contam Toxicol, 2001, 67: 800-6.

(259) C.K.Mittal et al, “Interaction of heavy metals with the nitric oxide synthase”, Mol Cell Biochem, 149-150:263-5, Aug 1995; & J.P.Bolanos et al, “Nitric Oxide mediated mitochondrial damage in the brain”,

(260) J.S. Woods et al, “Urinary porphyrin profiles as biomarker of mercury exposure: studies on dentists”, J Toxicol Environ Health, 40 (2-3):1993, p235-; & “Altered porphyrin metabolites as a biomarker of mercury exposure and toxicity”, Physiol Pharmocol, 1996, 74 (2):210-15, & Canadian J Physiology and Pharmacology, Feb 1996; & M.D.Martin et al, “Validity of urine samples for low-level mercury exposure assessment and relationship to porphyrin and creatinine excretion rates”, J Pharmacol Exp Ther, Apr 1996 & J.S. Woods et al, “Effects of Porphyrinogenic Metals on Coproporphrinogen Oxidase in Liver and Kidney” Toxicology and Applied Pharmacology, Vol 97, 183-190, 1989; & (b) 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 Feb 23;47 (3):267-83; & (c)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 Jan;66 (1):77-82; & (d) 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 Mar;15 (1):51-7: & (e) A cascade analysis of the interaction of mercury and coproporphyrinogen oxidase (CPOX) polymorphism on the heme biosynthetic pathway and porphyrin production. Heyer NJ, Bittner AC, Echeverria D, Woods JS. Toxicol Lett. 2006 Feb 20;161 (2):159-66. Epub 2005 Oct 7.

(261) New Scientist: This Week, Nov 22, 1997, p4 (and editorial), and Jan 10, 1998; and Neurotoxicology and Teratology, Jan 1998, Vol 19, p417.

(262) Chang LW, “The Neurotoxicology and pathology of organomercury, organolead, and organotin” J Toxicol Sci, 1990, 15 Suppl 4: 125-51; & “Latent effects of methyl mercury on the nervous system after prenatal exposure”, Environ Res 1977, 13 (2): 171-85.

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

(264) B.R. Danielsson et al, “ ”Behavioral effects of prenatal metallic mercury inhalation exposure in rats”, Neurotoxicol Teratol, 1993, 15 (6): 391-6;& A. Fredriksson 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; & “Behavioral effects of neonatal metallic mercury exposure in rats”, Toxicology, 1992, 74 (2-3):151‑160;

(265) K.Lohmann et al, “Multiple Chemical Sensitivity Disorder in patients with neurotoxic illnesses”, Gesundheitswesen, 1996, 58 (6):322-31.

(267) R. Brun, , Epidemiology of … Contact Dermatitis, 1975, 1 (4):214-217; & L.Nebenfuhrer et al, “Hg allergy …”, Contact Dermatitis, 1984, 10 (2):121-

(268) J.J.Weening et al, “mercury induced immune complex glomerulopathy”, Chap 4, p36-66, VanDendergen, 1980, & P.Duuet et al, “Glomerulonephritis induced by heavy metals”, Arch Toxicol. 50:187-194, 1982 & Transplantation Proceedings, Vol XIV (3), 1982, 482-

(269) (a)C.J.G.Robinson et al, “Mercuric chloride induced anitnuclear antibodies In mice”, Toxic Appl Pharmacology, 1986, 86:159-169. & (b) P.Andres, IgA-IgG disease in the intestines of rats ingesting HgCl”, Clin Immun Immunopath, 30:488-494, 1984; & (c) F.Hirsch et al, J Immun., 136 (9), 3272-3276, 1986 & (d)J.Immun., 136 (9):3277-3281; & (e)J Immun., 137 (8), 1986, 2548- & (f)Cossi et al, “Beneficial effect of human therapeutic IV-Ig in mercury induced autoimmune disease” Clin Exp Immunol, Apr, 1991; & (g) 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.

(270) (a)D.W.Eggleston, “Effect of dental amalgam and nickel alloys on T-lymphocytes”, J Prosthet Dent. 51 (5):617-623, 1984; & (b)Strauss FG, Eggleston DW. IgA nephropathy associated with dental nickel alloy sensitization. Am J Nephrol 1985;5 (5):395-7& J of the American Medical Assoc., Sept 96; & 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; & (d) 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.

(271) B.A.Weber, “The Marburg Amalgam Study”, Arzt und Umwelt, Apr, 1995; (266 cases) & (b) “Amalgam and Allergy”, Institute for Naturopathic Medicine, 1994; www.karlloren.com/ultrasound/p23.htm & (c) “Conjunctivitis sicca (dry eye study)”, Institute for Naturopathic Medicine, 1994; & , “Alternative treatment of Multiple Schlerosis, Tumor, or Cancer”, Institute for Naturopathic Medicine 1997 (40 MS cases), http://home, t‑online.de/home/Institut_f._Naturheilverfahren/patinf.htm”

(272) BJ Shenker, “Induction of apoptosis in human T-cells by methyl mercury”, Toxicol Appl Pharmacol, 1999, 157 (1):23-35; Immunopharmacol Immunotoxicol, 1992; 14 (3):555-77; & Immunotoxicol, 1992, 14 (3):539-53; & “Low-level MeHg exposure causes human T-cells to undergo apoptosis: evidence of mitochondrial disfunction”, Environ Res, 1998, 77 (2):149-159; & 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 Jun;4 (3):379-89 & O.Insug 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;

(273) R.Schiele et al, Institute of Occupational Medicine, Univ. Of Erlamgem- Nurnberg, “Studies of organ mercury content related to number of amalgam fillings”, Symposium paper, March 12, 1984, Cologne, Germany; (& 38); & “Quecksilber-Mobiliztion durch DMPS bei Personen mit und ohne Amalgamfullungen”, Zahnarztl. Mitt, 1989, 79 (17): 1866-1868; & J.J.Kleber, “Quecksilberverkonzen- tration im Urin nach DMPS” in [Status Quo and Perspectives of Amalgam], L.T. Friberg (ed.), Georg-Thieme Verlag, Stuttgart, New York, 1005, p 61-69.

(274) L.Friberg et al, “Mercury in the brain and CNS in relation to amalgam fillings”, Lakartidningen, 83 (7):519-521, 1986 (Swedish Medical Journal); & T.Suzuki et al, Ind Health, 4:69-75, 1966.

(275) L.M.Mikhailova et al, “Influence of occupational factors on disease of reproductive organs”, Pediatriya Akusherstvoi Ginekologiya, 33 (6):56-58, 1971; & Elghany NA, Stopford W, Bunn WB, Fleming LE. Occupational exposure to inorganic mercury vapour and reproductive outcomes. Occup Med (Lond). 1997 Aug;47 (6):333-6.

(277) Wiksztrajtis & B. Baranski, “Epidemiological survey of Lithunia dental offices”, Med. Pr., 24:248, 1973. (& 38) , ( c) Occupational exposure in dentistry and miscarriage. Lindbohm ML, Ylostalo P, et al, Occup Environ Med. 2007 Feb;64 (2):127-33. Epub 2006 Oct 19.

(278) NIDR/ADA Workshop, Biocompatibility of Metals in Dentistry, JADA, 109 (3): 469-471, Sept 1984. (& 38)

(279) Jenkins, Biological Monitoring of Toxic Trace Metals, Vol 1, Biological Monitoring and Surveillance, U.S. EPA, Sept 1980, p3; & M.J.Gonzalez et el, “Mercury in human hair; residents of Madrid, Spain”, Arch Environ Health, 1985, 40 (4):225-8; & D.Airey, Mercury in human hair: a review” Environmental Health Perspectives, 1983. 52:303-316; & “Total mercury concentrations in human hair from 13 countries”, Sci Total Environ 1983, 32 (2): 157-80; & S.A.Katz 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 Nov;88 (1‑3):221‑6; & Ziff, Validity of Hair Anlysis for Diagnosis of Mercury Status, Bioprobe Newsletter, Jan 1988, www.bioprobe.com.

(280) S.Nonaka et al, Nat. Inst. of Mental Health, Bethesda Md., “Lithium treatment protects neurons in CNS from glutamate induced excitability and calcium influx”, Neurobiology, Vol 95 (5):2642-2647, Mar 3, 1998; & 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 Oct;134 (2):321‑325 & Chuang D. Et al, National Institute of Mental Health, Science News, Nov 11, 2000, 158:309; & Science News, 3-14-98, p164; & Moore G.J. et al, Lancet Oct 7, 2000; & Science News, 10-31-98, p276.

(281) T.W. Clarkson et al, “Transport of elemental mercury into fetal tissues”, Biol. Neonate. 21:239-244, 1972; & M.R.Greenwood et al, “Transfer of metallic mercury into the fetus”, Experientia, 28:1455-1456, 1972;

(282) Press Release, Swedish Council for Planning and Coordinating Research (FRN), Stockholm, 19 February, 1998; & The Swedish Dental Material Commission _ _ Care and Consideration Kv. Spektern, SE _103 33 Stockholm, Sweden or on the web site, 2003 www.dentalmaterial.gov.se/Mercury.pdf

(283) A.Ahlbom et al, “Dentists, dental nurses, and brain tumors”, British Medical Journal, Vol292, March 8, 1986, p262.

(284) R.Glass, “Mortality of New England Dentists”, U.S. Dept. Of Health, Public Health Service, Washington D.C., 1966; & R. Simpson et al, “Suicide rates of Iowa dentists”, J. Of Amer. Dental Assoc., 1983, v107:441-; & B.B.Arnetz et al, “Suicide among Swedish Dentists”, Scand J Soc Med, 1987, 15 (4):243-6; & Vital Statistics of the U.S.-1970, National Center for Health Statistics, Table 1-26, “Deaths from 281 Selected Causes, by Age, Race and Sex, death statistics from 31 states; & U.S. Surgeon General Report, 2000

(285) R.C.Perlingeiro et al, “Polymorphonuclear phagentosis in workers exposed to mercury vapor”, Int J Immounopharmacology”, 16 (12):1011-7, 1994; & Hum Exp Toxicol 1995, 14 (3):281-6; & M.L. Queiroz et al, Pharmacol Toxicol, 1994, 74 (2):72-5; & (b) J.W.Albers et al, “Neurological abnormalities associated with remote occupational elemental mercury exposure”, Ann Neurol 1988, 24 (5):651-9 ; & © L.Soleo et al, “Effects of low exposure to inorganic mercury on psychological performance”, Br J Ind Med, 1990, 47 (2):105-9; & (d)P.J.Smith et al, “Effect of exposure to elemental mercury on short term memory”, Br J Ind Med 1983, 40 (4):413-9.; & (e)M.S.Hua et al, “Chronic elemental mercury intoxication”, Brain Inj, 1996, 10 (5):377-84; & (f) Gunther W, et al, Repeated neurobehavioral investigations in workers …, Neurotoxicology 1996; 17 (3-4):605-14; & (g) Levine SP; Cavender GD; Langolf GD; Albers JW. Elemental mercury exposure: peripheral neurotoxicity. Br J Ind Med 1982 May;39 (2):136‑9.

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

(287) M.C. Newland et al, ”Behavioral consequences of in utero exposure to mercury vapor in squirrel monkeys”, Toxicology & Applied Pharmacology, 1996, 139: 374-386; & “Prolonged behavioral effects of in utero exposure to methyl mercury or lead”, Toxicol Appl Pharmacol, 1994, 126 (1):6-15; & K.Warfvinge et al, “Mercury distribution in neonatal cortical areas …after exposure to mercury vapor”, Environmental Research, 1994, 67:196-208.

(289) 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 Feb;24 (2):109-17.

(290) D. Echeverria et al, “Neurobehavioral effects from exposure to dental amalgam: new distinctions between recent exposure and Hg body burden” FASEB J, Aug 1998, 12 (11):971-980; & (b) Echeverria, Woods JS, Heyer NJ, Rohlman DS, Farin FM, Bittner AC Jr, Li T, Garabedian C. Chronic low-level mercury exposure, BDNF polymorphism, and associations with cognitive and motor function. Neurotoxicol Teratol. 2005 Nov-Dec;27 (6):781-96; & The association between a genetic polymorphism of coproporphyrinogen oxidase, dental mercury exposure and neurobehavioral response in humans. Neurotoxicol Teratol. 2006 Jan-Feb;28 (1):39-48. Epub 2005 Dec 15; Echeverria D, Woods JS, et al. & (c)Amalgam and Health, Swedish Council for Planning and Coordination of Research, 1999; p297-307

(291) H.A.Huggins & TE Levy, “Cerebrospinal fluid protein changes in MS after Dental amalgam removal”, Alternative Med Rev, Aug 1998, 3 (4):295-300.

(292) M.Daunderer, H.Schiwara, et al, Quecksilber, Methylquecksilber, … in Korpermaterial von Amalgamtrager”, Klin Lab 38, 391-403, 1992; & M.Gradl et al, in Akute und chronische Toxizitat von Spurenelemente, Wissenschaftliche Verlagsgesellschaft nbH, Stuttgart, 1993, p65-71; & A.Gebhardt, Ermittlung der Quecksilberbelastung aus Amalgamfullurngen, Labormedizin 16, 384-386, 1992; & R.Mayer et al, “Zur Ermittlung de Quecksilberfreisetzung aus Amalgamfullungen”, Die Quintessenz 45, 1143-1152, 1994; & K.Mayer, “Risikobestimmung der Amalgambelastung”, ZWR, 105 (4):213-218 & 105 (5):280-283; & “Amalgam: zeitbombe in mund?”, ZWR, 1995, 104 (3):209-214; & JGD Birkmayer et al, “Quecksilberdepots im Organismus korrelieren mit der Anzahl der Amalgamfullungen”, Biol. Zahnmedizin, 1990, 6 (2):57-61.

(293) H.Huggins, Burton Goldberg, & Editors of Alternative Medicine Digest, Chronic Fatigue Fibromyalgia & Environmental Illness, Future Medicine Publishing, Inc, 1998, p197-; & U.Dorffer, “Anorexia Hydragyra: …”, Monatsschr. Kinderheilkd., 1989, 137 (8): 472.

(294) Siblerud, Robert L., et al. Psychometric evidence that dental amalgam mercury may be an etiological factor in manic depression. Journal of Orthomolecular Medicine, Vol. 13, No. 1, First Quarter 1998, pp. 31‑ 40 www.yourhealthbase.com/amalgams.html; & Bioplar Disorder: A possible dental connection, Dr. G. H. Smith, International Center for Nutritional Research, http://www.icnr.com/articles/bipolardentalconnection.html

(295) Cecil Textbook of Medicine, 20th Ed., Bennett & Plum, W.B. Saunders and Company, Philadelphia, 1996, p 69; & Comprehensive Psychiatry, 18 (6), 1977, pp595-598, &Poisoning & Toxicology Compendium, Leikin and Palouchek, Lexi-Comp., Cleveland, 1998; & Harrison’s Principles Of Internal Medicine, 14th Ed., McGraw-Hill, N.y., 1998; & Sunderman FW. Perils of mercury. Ann Clin Lab Sci 1988 Mar‑Apr;18 (2):89‑101.

(296) L.Bucio et al, Uptake, cellular distribution and DNA damage produced by mercuric chloride in a human fetal hepatic cell line. Mutat Res 1999 Jan 25;423 (1‑2):65‑72; & (b) Ho PI, Ortiz D, Rogers E, Shea TB. Multiple aspects of homocysteine neurotoxicity: glutamate excitotoxicity, kinase hyperactivation and DNA damage. J Neurosci Res. 2002 Dec 1;70 (5):694-702; & (c) Snyder RD; Lachmann PJ; Thiol involvement in the inhibition of DNA repair by metals in mammalian cells. Source Mol Toxicol, 1989 Apr‑Jun, 2:2, 117‑28 ; & L.Verschaeve et al, “Comparative in vitro cytogenetic studies in mercury-exposed human lymphocytes”, Muta Res, 1985, 157 (2-3):221-6; & L.Verschaeve, “Genetic damage induced by low level mercury exposure”, Envir Res, 12:306-10, 1976.

(297) P.E.Schneider et al, “Mercury release from Dispersalloy amalgam”, IADR Abstrats, #630, 1982; & N.Sarkar, “Amalgamation reaction of Dispersalloy Reexamined”, IADR Abstracts #217, 1991; & N.K. Sarkar et al, IADR Abstracts # 895, 1976; & R.S.Mateer et al, IADR Abstracts #240, 1977; & N.K.Sarkar et al, IADR Abstracts, #358, 1978; & N.W. Rupp et al, IADR Abstracts # 356, 1979; & Kedici SP; Aksut AA; Kilicarslan MA; Bayramoglu G; Gokdemir K. Corrosion behavior of dental metals and alloys in different media. J Oral Rehabil 1998 Oct;25 (10):800‑8

(298) C. Toomvali, “Studies of mercury vapor emission from different dental amalgam alloys”, LIU-IFM-Kemi-EX 150, 1988; & A.Berglund, ”A study of the release of mercury vapor from different types of amalgam alloys”, J Dent Res, 1993, 72:939-946; & D.B.Boyer, “Mercury vaporization from corroded dental amalgam” Dental Materials, 1988, 4:89-93; &V.Psarras et al, “Effect of selenium on mercury vapor released from dental amalgams”, Swed Dent J, 1994, 18:15-23; & L.E.Moberg, “Long term corrosion studies of amalgams and Casting alloys in contact”, Acta Odontal Scand 1985, 43:163-177; & L.E. Moberg, “Corrosion products from dental alloys”, Published Dissertation, Stockholm, 1985.

(299) H. Lichtenberg, “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.

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

(301) Chang LW, Neurotoxic effects of mercury, Environ. Res., 1977, 14 (3):329-73; & Histochemical study on the localization and distribution of mercury in the nervous system after mercury intoxication, Exp Neurol, 1972, 35 (1):122-37; & Ultrastructural studies of the nervous system after mercury intoxication, Acta Neuropathol (Berlin), 1972, 20 (2):122-38 and 20 (4):316-34.

(302) D, Klinghardt, IAOMT Conference & tape, 1998; “large study by M.Daunderer (Germany) of MS patients after amalgam removal”.

(303)H.V.Aposhian, Mobilization of mercury and arsenic in humans by sodium 2, 3-dimercapto-1-propane sulfonate (DMPS).Environ Health Perspect. 1998 Aug;106 Suppl 4:1017-25. ; & Toxicology, 1995, 97 (1-3): 23-38; & “Urinary Mercury after Administrationof DMPS”, FASEB J., 6: 2472-2476, 1992.

(304) M.J.Vimy et al, “Mercury from Maternal Silver Tooth Fillings: a source of neonatal exposure”, Biological Trace Element Research, 56: 143-52, 1997.

(305) 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; & Toxicol Lett 1995; 75 (1-3):133-44.; & E.M. Abdulla 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 Mar 26;12 (4):733-7

(306) E.M.Oliveira et al, “Mercury effects on the contractile activity of the heart muscle”, Toxicol Appl Pharmacol, 1:86-91, 1994;

(307) 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.

(308) 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 Jul;10 (4):370-5;& D.O.Marsh et al, “Fetal Methyl mercury Poisoning”, Ann Neurol, 1980, 7:348-55.

(309) The Tribune, Mesa, Az., 13 Apr 1998, (Paul Mills, Apalachee Junction) ; & Kyle BP, Nordic J of Biological Med, 2000. & www.flcv.com/epilepsy.html (310R.L.Siblerud, “The relationship between mercury from dental amalgam and the cardiovascular system”, Science of the Total Envir., 1990, 99 (1-2): 23-35.

(312) Richard Hanson, The Key to Ultimate Health, 1999; & J.Lee (MD), What Your Doctor May Not Tell You About Hormones, DAMS, (800-311-6265)

(313) V.D.M.Stejskal et al, “Mercury-specific Lymphocytes: an indication of mercury allergy in man”, J. Of Clinical Immunology, 1996, Vol 16 (1);31-40.

(314) M.Kubicka-Muranyi et al, “Systemic autoimmune disease induced by mercuric chloride”, Int Arch Allergy Immunol;1996, 109 (1):11-20; & M.Goldman et al, 1991, “Chemically induced autoimmunity …”, Immunology Today, 12:223-; & K. Warfyinge et al, “Systemic autoimmunity due to mercury vapor exposure in genetically susceptible mice”, Toxicol Appl Pharmacol, 1995, 132 (2):299-309;& L.M. Bagenstose et al, “Mercury induced autoimmunity in humans”, Immunol Res, 1999, 20 (1): 67-78; &“Mercury-induced autoimmunity”, Clin Exp Immunol, 1998, 114 (1):9-12;

(315) B.Engin-Deniz et al, ”Die queckssilberkonzentration im spichel zehnjariger kinder in korrelation zur anzahl und Grobe iher amalgamfullungen”, Zeitschrift fur Stomatologie, 1992, 89:471-179;

(316) B.J.Shenker et al, Dept. Of Pathology, Univ. Of Pennsylvania School of Dental Medicine, “Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes: Alterations in B-cell function and viability” Immunopharmacol Immunotoxicol, 1993, 15 (1):87-112; & J.R.Daum, ”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, 116 (4):295-305, (Aug 1998)

(317) S.Zinecker, “Amalgam: Quecksilberdamfe bis ins Gehirn”, der Kassenarzt, 1992, 32 (4):23; “Praxiproblem Amalgam”, Der Allgermeinarzt, 1995, 17 (11):1215-1221. (1800 patients)

(318) V.Schneider, “Untersuchungen …”, Dissertation, Frankfurt, a>M., 1976.

(319) H.D.Utt, “Mercury Breath”, Journal of Calif. Dental Assoc., 1984, 12 (2):41; & (b) Motorkina, A.V., Barer GM, Volozhin AI, “Hg release from amalgam fillings into oral cavity”, Stomatologiiia (Mosk): 1997, 76 (4):9-11.

(320) U.F.Malt et al, “Physical and mental problems attributed to dental amalgam fillings”, Psychosomatic medicine, 1997, 59:32-41.

(321) R.L.Siblerud, “Relationship between dental amalgam and health”, Toxic Substances Journal, 1990b. 10:425-444; & “Effects on health following removal of dental amalgams”, J Orthomolecular Med, 5 (2): 95-106, & “Relationship between amalgam fillings and oral cavity health” Ann Dent, 1990, 49 (2): 6-10, (86 cured)

(322) P.Engel, “Beobachtungen uber die gesundheit vor und nach amalgamentfernug”, Separatdruck aus Schweiz. Monatsschr Zahnm. 1998, vol 108 (8). (75 cases amalgam removal) http://soho.globalpoint.ch/paul‑engel (89% significant improvement) www.melisa.org/articles/engel‑e.pdf

(323) Dr. Kohdera, Faculty of Dentistry, Osaka Univ., International Congress of Allergology and Clinical Immunology, EAACI, Stockholm, June 1994; & Heavy Metal Bulletin, Vol 1, Issue 2, Oct 1994. (160 cases cured-eczema); Tsunetoshi Kohdera, MD, dermatology, allergology, 31 Higashitakada‑cho Mibu Nakagyo‑ku Schimazu Clinics Kyoto 604 Japan e‑mail:smc‑inet@mbox.kyoto‑inet.or.jp www.melisa.org/archive/6th_melisa_study_group.html & P.Dallmann, ”kon nen durch Quecksilber entstehen? PeDa_Eigenverisg, 1995; & G. Ionescu, Schwermetallbelastung bei atopisher dermatitis and psoriasis- Diagnose und Therapie, Biol Med, 1996, (2): 65-68; SS Tsyganok, “Unithiol in treatment of dermatoses”, Vestn.Dermatol.Venerol., 1978, (9): 67-69. & (these clinics use MELISA test for diagnosis of immune reactivity) Neukirchen (clinic) (Germany, near Czech border). Director; Gruia Ionescu, owns 2 Clinics, cases paid by insurance companies in Germany. Email: Spezialklinik‑Neukirchen@toolpool.de fax: 0049 9947 10 51 11

(324) D. Bangsi, Ghadirian P et al, “Dental amalgam and multiple sclerosis”, International J of Epidemiology, 1998, Aug, 27 (4):667-71; & E. Mauch et al, “umweltgifte und multiple sklerose”, Der Allgremeinarzt, 1996, 20:2226-2220; & (c) McGrother CW, Dugmore C, Phillips MJ, et al: Multiple sclerosis, dental caries and fillings: a case-control study. Br Dent J, 1999 Sep 11;187 (5): 261-4.

(325) B. Arvidson (Sweden), Inorganic mercury is transported from muscular nerve terminals to spinal and brainstem motorneurons. Muscle Nerve, 1992, 15 (10);1089-94, & (b) Moller, Madsen, Danscher, Localization of mercury in CNS of the Rat, Environmental Research, 1986, 41: 29-43; & (c) M. Su et al, Selective involvement of large motor neurons in the spinal cord of rats treated with methyl mercury. J Neurol Sci, 1998, 156 (1):12-7; & Moller-Madsen B. Localization of mercury in CNS of the rat. III. Oral administration of methylmercuric chloride Fundam Appl Toxicol. 1991 Jan;16 (1):172-87

(326) E.Baasch, “Is multiple sclerosis a mercury allergy?”, Schweiz arch Neurol Neurochir Psichiatr, 1966, 98:1-19; & J. Clausen, “Mercury and MS”, Acta Neurol Scand, 1993;87:461-; & “Sur un cas de mercurialisme chronique simulant la sclerose en plaque”, Nord med Ark Stockholm 1880 xii no 17 1‑48 1 pl & P. Le Quesne, “Metal-induced diseases of the nervous system”, 1982, Br J Hosp Med, 28:534-

(327) (a)G. Danscher et al, Environ Res, “Localization of mercury in the CNS”, 1986, 41:29-43; & (b) 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; & (c) ”Ultrastructural localization of mercury after exposure to mercury vapor”, Prog Histochem Cytochem, 1991, 23:249-255; & (d) Pamphlett R, Coote P , “Entry of low doses of mercury vapor into the nervous system”, Neurotoxicology, 1998, 19 (1):39-47; & (e) Pamphlett et al, “Oxidative damage to nucleic acids in motor neurons containing Hg”, J Neurol Sci, 1998, 159 (2):121-6. (rats & primates); & (f) Pamphlett R, Waley P, “Motor Neuron Uptake of Low Dose Inorganic Mercury”, J. Neurological Sciences 135: 63‑67 (1996); & (g) Schionning JD, Danscher G, “Autometallographic inorganic mercury correlates with degenerative changes in dorsal root ganglia of rats intoxicated with organic mercury”, APMIS 1999 Mar;107 (3):303‑10

(328) P.McKeever et al, “Patterns of antigenic expression in human glioma cells”, Crit Rev Neurobiology, 1991, 6:119-147; & 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 Sep;42 (3):214-27.

(329) (a) Arvidson B; Arvidsson J; Johansson K, “Mercury Deposits in Neurons of the Trigeminal Ganglia After Insertion of Dental Amalgam in Rats”, Biometals; 7 (3) p261-263 1994; & (b)Arvidson B. Inorganic mercury is transported from muscular nerve terminasl to spinal and brainstem motorneurons. Muscle Nerve 1992, 15:1089-94; & B. Arvidson et al, Acta Neurol Scand, “Retograde axonal transport of mercury in primary sensory neurons” 1990, 82:324-237 & Neurosci Letters, 1990, 115:29-32; &Arvidson B, Arvidsson J. Retrograde axonal transport of mercury in primary sensory neurons innervating the tooth pulp in the rat. Neurosci Lett. 1990 Jul 17;115 (1):29-32. & (c) S.M. Candura 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;

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

C.M. Tanner et al, “Abnormal Liver Enzyme Metabolism in Parkinson’s”, Neurology, 1991, 41 (5): Suppl 2, 89-92; & M.T.Heafield 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; & A.Pean et al, “Pathways of cysteine metabolism in MND/ALS”, J neurol Sci, 1994, 124, Suppl:59‑61; & Steventon GB, et al; Xenobiotic metabolism in motor neuron disease, The Lancet, Sept 17 1988, p 644-47; & Neurology 1990, 40:1095-98.

(331) C.Gordon et al, “Abnormal sulphur oxidation in systemic lupus erythrmatosus (SLE)”, Lancet, 1992, 339:8784, 25-6; & P.Emory et al, “Poor sulphoxidation in patients with rheumatoid arthitis”, Ann Rheum Dis, 1992, 51:3, 318-20; & Bradley H, et al, Sulfate metabolism is abnormal in patients with rheumatoid arthritis. Confirmation by in vivo biochemical findings. J Rheumatol. 1994 Jul;21 (7):1192-6; & T.L. Perry et al, “Hallevorden-Spatz Disease: cysteine accumulation and cysteine dioxygenase defieciency”, Ann Neural, 1985, 18 (4):482-489.

(332) Trepka MJ, Heinrich J, Krause C, Schulz C, Wjst M, Popescu M, Wichmann HE, , “Factors affecting internal mercury burdens among German children”, Arch Environ Health, 1997, 52 (2):134-8; & L.Soleo et al, “Influence of amalgam fillings on urinary mercury excretion” (S.Italy), G Ital Med Lav Ergon, 1998, 20 (2): 75- 81 .

(333) A.J.Freitas et al, “Effects of Hg2+ and CH3Hg+ on Ca2+ fluxes in the rat brain”, Brain Research, 1996, 738 (2): 257-64; & P.R.Yallapragoda et al, “Inhibition of calcium transport by Hg salts” in rat cerebellum and cerebral cortex”, J Appl toxicol, 1996, 164 (4): 325-30; & E.Chavez et al, “Mitochondrial calcium release by Hg+2″, J Biol Chem, 1988, 263:8, 3582-; & A. Szucs 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; & D.Busselberg, 1995, “Calcium channels as target sites of heavy metals”, Toxicol Lett, Dec;82‑83:255‑61; & Cell Mol Neurobiol 1994 Dec;14 (6):675‑87; & Rossi AD, et al, Modifications of Ca2+ signaling by inorganic mercury in PC12 cells. FASEB J 1993, 7:1507-14.

(334) T.Nguyen et al, Mol Immunol, 1996, 3 (4):379-86; & P.Eggleton et al, “Pathophysicological roles of calreticulin in autoimmune disease”, Scand J Immunol, 1999, 49 (5): 466-73.

(335) A. Engqvist et al, “Speciation of mercury excreted in feces from individuals with amalgam fillings”, Arch Environ Health, 1998, 53 (3):205-13; & Dept. of Toxicology & Chemistry, Stockholm Univ., National Institute for Working Life, 1998 (www.niwl.se/ah/1998-02.html)

(336) G.S. Hill, “Drug Associated glomerulopathies” Toxicol Pathol, 1986, 14 (1):37-44; & M.Monestier et al, European J Immunology, 1994, 29 (3): 723-30.; & Adler SG, et al; Hypersensitivity phenomena and the kidney: role of drugs and environmental agents.; Am J Kidney Dis, 1985 Feb

(337) H.G. Abadin, et al, U.S. ATSDR, “Breast-feeding exposure of infants to mercury, lead, and cadmium: A Public Health Perspective”, Toxicol Ind Health, 1997, 13 (4): 495-517.

(338) (a)W.Y.Boadi et al, Dept. Of Food Engineering and Biotechnology, T-I Inst of Tech., Haifa, Israel, “In vitro effect of mercury on enzyme activities and its accumulation in the first-trimester human placenta”, Environ Res, 1992, 57 (1):96-106;& “In vitro exposure to mercury and cadmium alters term human placental membrane fluidity”, Pharmacol, 1992, 116 (1): 17-23; & (b)J.Urbach et al, Dept. of Obstetrics & Gynecology, Rambam Medical Center, Haifa, Israel, “Effect of inorganic mercury on in vitro placental nutrient transfer and oxygen consumption”, Reprod Toxicol, 1992, 6 (1):69-75;& © Karp W, Gale TF et al, Effect of mercuric acetate on selected enzymes of maternal and fetal hamsters” Environmental Research, 36:351-358; & W.B. Karp et al, “Correlation of human placental enzymatic activity with trace metal concentration in placenta”, Environ Res. 13:470- 477, 1977; & (d) Boot JH. Effects of SH‑blocking compounds on the energy metabolism and glucose uptake in isolated rat hepatocytes. Cell Struct Funct 1995 Jun;20 (3):233‑8; & Semczuk M, Semczuk‑Sikora A. New data on toxic metal intoxication (Cd, Pb, and Hg in particular) and Mg status during pregnancy. Med Sci Monit 2001 Mar;7 (2):332‑340; & (e) H.Iioka et al, “The effect of inorganic mercury on placental amino acid transport”, Nippon sanka Fujinka Gakkai Zasshi, 1987, 39 (2): 202-6.

(339) H.Drexler et al, “The mercury concentration in breast milk resulting from amalgam fillings and dietary habits”, Environ Res, 1998, 77 (2):124-9; & Sundberg J, Ersson B, Lonnerdal B, Oskarsson A. Protein binding of mercury in milk and plasma from mice and man‑‑a comparison between methyl mercury and inorganic mercury. Toxicology 1999 Oct 1;137 (3):169‑84; & Vimy MJ, Hooper DE, King WW, Lorscheider FL.; Mercury from maternal “silver” tooth fillings in sheep and human breast milk. A source of neonatal exposure. Biol Trace Elem Res 1997 Feb;56 (2):143-52.

(340) Herrman M. Schweinsberg F. “Mercury burden from amalgam fillings”, Zentralbl Hyg Umweltmed, 1993, 194 (3):271-91.

(341) A.Tosti et al, “Contact stomatitis”, Semin Cutan Med Surg, 1997, 16 (4):314-9; & T.Nakada et al, “Patch test materials for mercury allergic contact dermatitis”, Dermatitis, 1997, 36 (5):237-9; & Guttman-Yassky E, Weltfriend S, Bergman R. Resolution of orofacial granulomatosis with amalgam removal. J Eur Acad Dermatol Venereol. 2003 May;17 (3):344-7

(342) Stejskal VDM, Danersund A, Lindvall A, Hudecek R, Nordman V, Yaqob A et al. Metal- specific memory lymphocytes: biomarkers of sensitivity in man. Neuroendocrinology Letters, 1999; 20: 289-98; & Metal-specific lymphocyte reactivity is downregulated after dental metal replacement. Yaqob A, Danersund A, Stejskal VD, Lindvall A, Hudecek R, Lindh U., Neuro Endocrinol Lett. 2006 Feb-Apr;27 (1-2):189-97; & Stejskal V, Hudecek R, Mayer W, “Metal-specific lymphocytes: risk factors in CFS and other related diseases”, Neuroendocrinology Letters, 1998; (fatigue)

(343) P.L.Bigazzi, “Autoimmunity induced by metals”, in Chang, L., Toxicology of Metals, Lewis Publishers, CRC Press Inc. 1996., p835-52.

(344) G.A.Caron et al, “Lymphocytes transformation induced by inorganic and organic mercury”, Int Arch Allergy, 1970, 37:76-87.

(345) N.H.Nielsen et al, “The relationship between IgE-mediated and cell-mediated hypersensities”, The Glostrup Allergy Study, Denmark, British J of Dermatol, 1996, 134:669-72.

(346) 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, Issue 4, 1999, p5, 6.; & (c)Remedyfind survey of CFS/FM patients, http://remedyfind.com/rm‑192‑Mercury.asp

(347) G.Benga “Water exchange through erythrocyte membranes” Neurol Neurochir Pol 1997 Sep‑Oct;31 (5):905‑13

(348) A Kistner, “Quecksilbervergiftung durch Amalgam: Diagnose und Therapie” ZWR, 1995, 104 (5):412-417; & (c) 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 an intoxication with mercury compounds. Acta Histochem Suppl 1980; 22:367-80.

(349) M.Schaeffer et al, “Risikofaktor Amalgam-Ein Problemstoff”, Schriftenreihe mweltmedizin, Forum Medizin Verlagsgesellschaft, 1996; & (b)Nixon, DE, Mussmann GV, Moyer TP. Inorganic, organic, and total mercury in blood and urine. J Anal Toxicol, 1996; 10 (1): 17-22.

(350) F. Schweinsberg, “Risk estimation of mercury intake from different sources”, Toxicol. Lett. 1994, 72: _45- 51; & L.D. Pzheusskaia, “Disintoxication therapy of patients with nonspecific inflammatory diseases of the female genital organs”, Akush. Ginekol 1977, (4): 30-34;

(351) S.Halbach et al, “Thiol chelators and mercury effects on isolated heart muscle”, Plzen.Lek. Sborn,

1990, 62 (Supp), 39-41, 1990; & “Sulfhydryl-induced restoration of myocardial contractility after alteration by mercury”, Arch. Toxicol. 63 (Supp 13) 349-352, 1989; & N.V.Klykov, “Treatment of patients with myocardial infarction”, Vrach.Delo.1979, (12):50-3; & “Treatment of patients with chronic circulatory insufficiency” Kardiologila, 1972, 12 (1):126-31.

(352) B.Arnold, Eigenschaften und Einsatzgebiete des Chelatbildners:DMPS”, Z.Umweltmedizin 1997, 5 (1):38- ; & (b) Diagnostik un Monitorung vonSchwermetallbelastungen, I, II, ZWR, 1996, 105 (10): 586-569 & (11):665-; & (c) Therapie der Schwermetallbelastung, Mineraloscope, 1996, (1):22-23; & (d)Monaci Fet al, Concentrations of major elements and mercury in unstimulated human saliva. Biol Trace Elem Res. 2002 Dec;89 (3):193-203.

(353) P.P Guida, “Therputic efficacy of unithiol in Buschke’s Scleroderma”, Vrach. Delo.1983, (8): 36-38; & A.A.Dubinskii et al, “Morpholcial changes in the skin in Scleroderma after treatment with unithiol”, Vrach.Delo.1978, (10): 112-114.

(354) W.Behnke, “Kopfschmerz un Migrane: Schon mal an Amalgam gegcht?”, Der Allgemeinarzt, 1995, 17 (11): 1222-1223; & J.Lechner, “Quecksilberbelastung, …”, Dtsch. Z. Biol. Zahnmed. 1992, 8 (1): 8-14.

(355) W.Kostler, “Beeinflubung der zellularen Immunabwehr drch Quecksilberfreisetzung”, Forum Prakt. Allgem. Arzt, 1991, 30 (2):62-3; & P.Schleicher, “Schwermetalle schadigen das Immunsystem”, Mineraloscope, 1996, (1): 37; & “Immunschaden durch Toxine” Argumente+Fakten der Medizin, 1992, 05; & W. Scheicher, Dissertation, Universitat Karlsruhe, 1977.

(356) M.Daunderer, Die Amalgamvergiftung und ihre medizinische Folgen”, Forum Prakt.Allgem.Arzt, 1991, 30 (2): 44-66; & M.Daunderer, “Jugendicher starb an Amalgam”, Forum Prakt.Allgen. Arzt, 29 (11): 294

(357) S.B.Elhassani, “The many faces of methyl mercury poisoning”, J Toxicol Clin Toxicol, 1982 (8): 875-9; & N.Neuburger et al, “Kompendium Umweltmedizin”, MediVerlagsgesellschaft, Hamburg, 1996; & O.Oster et al, “Die Pathobiochemie, Diagnose und Therapie der Metall- und Metalloidintoxikation-2. Die Quecksilberintoxikation, Intensivmed, 1985, 22 (3):130-9

(358) N.I. Shtelmakh et al, “Comparative treatments of rheumatoid arthritis”, Vrasch. Delo., 1982, (1):49-52 (359) G. Tapparo, :Toxische Untersunchungen zu Amalgam”, Die Zahn Arztwoche, 1992

(360) 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 .

(361) K.H.Friese, “Konnen Amalgamplomben angebornene Innenohrschaden verusachen?”, Therapeutikon, 1993, 7 (11): 492-496; & “Amalgamvergiftung- moglicher Zusammenhang mit angeborener Schwerhorlgkeit, Der Naturarzt, 1995, 135 (8): 13-15; & E.Bonnet, “Okopadiatrie-Verbindung zur Naturheilkunde”, Arztezeitschr Naturheikunde, 1995, 36 (4): 272-78.

(362) G.Bohmer et al, “Quecksilber-Mobilisation mit dern DMPS bei arztlichem und zahnarztlichem Personal im Vergleich”, Der Artikulator (30): 11-12, 1989; & W.Legrum, “Wie problematisch ist der Dentalwerkstoff Amalgam?”, Dtsch. Med. Wochenschr., 1990, 115 (39): 1490-1494; & M.Cikrt et al, “Mobiliztion of mercury using DMPS”, 1993, Plzen Lek. Sborn. 68 (Supp) 119; & R.Hickel et al, “Die Quecksilberbelastung von Zahnmedizinstudenten anch beruflicher Amalgaexposition, Dtsch. Zahnarztl.Z 1995, 50 (7): 506-10.

(364) W. Bayer, Erfahrungsheikunde 1992, 41 (10): 628-633; & B.Gabard, Arch Toxicol, 1978, 39 (4): 289- 298; & H. Pscheidl, “Amalgamvergiftung- eine chronische Krankheit und ihre Therapie”, ACD, 1994, 3 (4):153-166.

(365) C. Schulte-Uebbing, “Umweltbedingte Frauenkranheiten”, Sonntag-Verlag, Stuttgart, 1996; & Umweltmedizin in der Frauenheilkunde, Arztezeitschr. Naturheilkunde, 35 (2):9-17.

(366) (a)“Tooth amalgam and pregnancy”, Geburtshilfe Frauenheikd. 1995, 55 (6): M63-M65; & (b) T. Zinke, “There are new realizations to the Amalgam problem”, in Status Quo and perspectiveves of Amalgam and Other Dental Materials, L.F. Friberg (Ed.), Georg=Thieme-Verlag, Stuttgart, New York, 1995, p1-7.

(367) (a) Gerhard I, “Amalgam from gynacological view”, Der Frauenarzt, 1995, 36 (6): 627-28; & (b)“Schdstoffe und Fertillitatsstorungen”, Schwermetalle und Mineralstoffe, Geburtshilfe Frauenheikd, 1992, 52 (7):383-396; & (c) Gerhard I, “Reproductive risks of heavy metals and pesticides in women”, in: Reproductive Toxicology, M.Richardson (ed.), VCH Weinhelm, 1993, 167-83; & (d)Gerhard I, “Infertility with women by environmental illnesses, JD. Kruse-Jarres (Ed.), 1993, 51-68.

(368) Olin R, Paulander J, Axelsson P; FMS, CFS, and TMS- Prevalences in a Swedish County, An oral examination based study, Preventive Dental Health Care Center, Karlstad, Sweden, 1998.

(369) 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. Neuro Endocrinol Lett. 2004 Jun;25 (3):211-8. http://www.melisa.org/pdf/Mercury-and-autoimmunity.pdf & 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.

(370) 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; 991 (1):85-9.

(371) 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.

(372) 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.

(373) 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; & ‘The frequency of mercury intolerance in patients with CFS and healthy controls”, Contact Dermatitis. 1999 Jul;41 (1):60‑1

(374) 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.

(375) Contact allergy to gold in dental patients; Räsänen L; Kalimo K; Laine J; et al, Br J Dermatol, 1996 Apr, 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 Aug;31 (2):89‑91; & High frequency of contact allergy to gold sodium thiosulfate. An indication of gold allergy? , Björkner B; Bruze M; Möller H , Contact Dermatitis, 1994 Mar, 30:3, 144-51

(376) 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 (6, 744 patients in 34 clinics); & Treatment of Health Complaints Attributed to Amalgam, J Dent Res 87 (4):349-353, 2008, D. Melchart, S. Vogt, W. Köhler, A. Streng, W. Weidenhammer, L. Kremers, R. Hickel, N. Felgenhauer, T. Zilker, E. Wühr, and S. Halbach , (90 patients)

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

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

(380) Komaroff AL, Buchwald DS. Chronic fatigue syndrom: an update. Ann Rev Med 1998; 49: 1-13; & Buchwald DS, Wener MH, Kith P. Markers of inflamation and immune activation in CFS. J Rheumatol 1997; 24:372-76.

(381) 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. In Vitro Cell Dev Biol 1990 Jan;26 (1):24‑8. Toxic effect of heavy metals on cells isolated from the rat adrenal and testis.

(382) Sterzl I, Fucikova T, Zamrazil V. The fatigue syndrome in autoimmune thyroiditis with polyglandular activation of autoimmunity. Vnitrni Lekarstvi 1998; 44: 456-60; & (b) Sterzl I, Hrda P, Prochazkova J, Bartova J, Reactions to metals in patients with chronic fatigue and autoimmune endocrinopathy. Vnitr Lek 1999 Sep;45 (9):527‑31 ; & & (c)Kolenic J, Palcakova D, Benicky L, Kolenicova M – “The frequency of auto-antibody occurrence in occupational risk (mercury)” Prac Lek 45 (2):75-77 (1993)

(383) 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.

(384) Kuklinski B. Glutathione Transferasen und Krankheit. Seitschrift fur Umweltmedizin 1999; 7:39-45.

(385) (a) Kohdera T, Koh N, Koh R. Antigen-specific lymphocyte stimulation test on patients with psoriasis vulgaris. XVI International Congress of Allergology and Clinical Immunology, Oct 1997, Cancoon, Mexico; & (b)Ionescu G, . Heavy metal load with atopic Dermatitis and Psoriasis, Biol Med 1996; 2:65-68; & (c) A subset of patients with common variable immunodeficiency. Blood 1993, 82 (1): 192-20.

(386) Great Smokies Diagnostic Lab, research web pages (by condition) http://www.gsdl.com; & Doctors Data Lab , http://www.doctorsdata.com , inquiries @doctors data.com, www.doctorsdata.com, & MetaMetrix Lab, www.metametrix.com; & (d) Biospectron Lab, LMI, Lennart Månsson International AB, lmi.analyslab@swipnet.se http://home.swipnet.se/misac/research11.html#biospectrons & (e) Great Plains Laboratory www.greatplainslaboratory.com/test19.html

(387) Caulk, Inc. (amalgam manufacturer), http://www.caulk.com/mSDSDFU/DISPERSDFU.html.

(388) Sata K, Kusada Y, Zhang Z, Ueda K, Ishi Y, Mori T, et al. An epidemiological study of mercury sensitization. Allergology International 1997; 46:201-6.

(389) Brunker P, Rother D, Sedlmeier R. J Mol Gen Genet 1996; 251 (3); & Williams MV. Environ Mol Mutagen 1996; 27 (1): 30-3; & F Fekete and K Johnson, Antibiotic Resistance and Mercury, Science News – June 24, 2002

(390) (a)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; & (b) 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 20 (6):483-9 (2000) www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11180271&form=6&db=m&Dopt=r; & (c) Barregard L, Lindstedt G, Schutz A, Sallsten G – “Endocrine function in mercury exposed chloralkali workers” Occup Environ Med 51 (8):536-40 (1994) www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid= 7951778&form=6&db=m&Dopt=r & (d) Watanabe C – “Selenium deficiency and brain functions: the significance for methylmercury toxicity” Nippon Eiseigaku Zasshi 55 (4):581-9 (2001); & (e) 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 Apr;80 (3):208-14.

(391) 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. (article in German with English abstract)

(392) Gebbart E. Chromosone Damage in Individuals exposed to heavy metals. Curr Top Environ Toxicol Chem 1985; 8: 213-25.

(394) Blatter B, van der Star M, Roeleveld N. Int Archieves of Occup and Environ Health 1987; 59: 551-7.

(395) Baranski B. Environmental Health Perspectives 1993; 101 (suppl 2): 85-90; & (b)Baranski B. Effect of mercury on the sexual cycle and prenatal and postnatal development of progeny. Med Pr 1981; 32 (4): 271-6; & (c) Hooper A, Mercury poisoning in Dentistry, Wisconsin Medical J, Aug 1980, vol 79; & (d) Shapiro IM, Cornblath DR, Sumner AJ. Neurophysiological and neuropsychological function in mercury-exposed dentists. The Lancet 1982; 1:1147-1150; & (e) Uzzell BP and Oler J. Chronic low-level mercury exposure and neuropsychological functioning. J of Clin and Exper Neuropsych 1986; 8:581-93;

(396) Epidemiologisk undersokning av fosterkador hos 1.2 milj. barn, fodda sedan 1967; Norgeyrkesmed. Avd. Haukelands sykehus. Aftenposton 6 mpv 1997.

(397) Hudecek R, Danersund A. In: Amalgam and Health: The Swedish Council for Planning and Research Coordination, 1999, p78-84.

(398) 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 Winter;30 (2):65-83.

(399) 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;

(400) Kim DE, Song KB, Kim YJ. Mercury contents in hair of dental personnel and evaluation of various

agents suppressing mercury vaporization. Taehan Chikkwa Uisa Hyophoe Chi 27 (7): 649-59.

(401) 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] [Article in Polish] Med Pr. 2002;53 (2):161-5.

(402) Ando T, Wakisaka I, Hatano H. Mercury concentration in gray hair. Nippon Eiseigaku Zasshi 1989; 43 (6):1063-8.

(403) 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 Sep, 106:9, 834-5; & Pierson HF. “Pharmacological perturbation of murine melanoma growth by copper chelates.Cancer Lett, 1985 Mar, 26:2, 221-33.

(404) M. E. Godfrey, Candida, Dysbiosis and Amalgam. J. Adv. Med. vol 9 no 2 (1996); & Romani L, Immunity to Candida Albicans: Th1, Th2 cells and beyond. Curr Opin Microbiol 1999, 2 (4):363-7; & Alfred V. Zamm. CANDIDA ALBICANS THERAPY: Dental mercury removal, an effective adjunct. J. Orthmol. Med. v1#4 pp261-5 (1986)

(405) Stejskal J, Stejskal V. The role of metals in autoimmune diseases and the link to neuroendocrinology Neuroendocrinology Letters, 20:345‑358, 1999. www.melisa.org

(406) Goering Pl, Rowland AS. Toxicity assessment of mercury vapor from dental amalgams. Fundam. Appl Toxicol 1992; 19:319-329.

(407) Wehner‑Caroli J; Scherwitz C; Schweinsberg F; Fierlbeck G. Exacerbation of pustular psoriasis in mercury poisoning. Hautarzt 1994 Oct;45 (10):708‑10.

(408) 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.

(409) Bernard S, Enayati A, Redwood L, Roger H, Binstock T. Autism: a novel form of mercury poisoning. Med Hypotheses 2001 Apr;56 (4):462-71. http://www.autism.com/ari/mercurylong.html : & Yazbak FE (MD, FAAP) Autism 99 : A National Emergency, www.garynull.com/documents/autism_99.htm & Amy Holmes, MD, Autism Treatment Clinic, Baton Rouge, La, http://www.healing-arts.org/children/holmes.htm#wethink

(410) J.R. Cade et al, Autism and schizophrenia linked to malfunctioning enzyme for milk protein digestion. Autism, Mar 1999.

(411) Puschel G, Mentlein R, Heymann E, ‘Isolation and characterization of dipeptyl peptidase IV from human placenta’, Eur J Biochem 1982 Aug;126 (2):359-65; & Kar NC, Pearson CM. Dipeptyl Peptidases in human muscle disease. Clin Chim Acta 1978; 82 (1-2): 185-92; & Seroussi K, Autism and Pervasive Developmental Disorders , 1998, p174, etc.; & 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 Jul;44 (1):13-8

(412) (a) 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 autsim a hypoglutamatergic disorer? J Neural Transm 1998, 105 (4-5): 525-35. & (b)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; & (c)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;

(413) Autism-Mercury@egroups.com, web group of parents with autistic kids and autism doctors and researchers; www.flcv.com/autismc.html & Autism, PDD, and Immune Reactive Conditions; the mercury connection, www.flcv.com/kidshg.html & Edelson SB, Cantor DS. Autism: xenobiotic influences. Toxicol Ind Health 1998; 14 (4): 553-63; www.edelsoncenter.com/Autism/autism.htm & Liska, DJ. The detoxification enzyme systems. Altern Med Rev 1998. 3 (3):187-98.

(414)Wecker L, Miller SB, Cochran SR, Dugger DL, Johnson WD. Trace element concentrations in hair from autistic children. Defic Res 1985; 29 (Pt 1): 15-22.

(415) 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 Inflamation 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.

(416) (a) 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 & (b)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:& (c) Leigh Pn. Pathologic mechanisms in ALS and other motor neuron diseases. In: Calne DB (Ed.), Neurodegenerative Diseases, WB Saunder Co., 1997, p473-88; & P.Froissard et al, Universite de Caen, “Role of glutathione metabolism in the glutamate-induced programmed cell death of neuronal cells” Eur J Pharmacol, 1997, 236 (1): 93-99; & (d) 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; & (e) 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;

(417) 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 .

(419) Lipozencic J; Milavec‑Puretic V; Pasic A. Contact allergy and psoriasis. Arh Hig Rada Toksikol 1992 Sep;43 (3):249‑54; & Roujeau JC et al, Acute generalized exanthematous pustulosis. Analysis of 63 cases; Arch Dermatol 1991 Sep;127 (9):1333‑8; & Yiannias JA; Winkelmann RK; Connolly SM. Contact sensitivities in palmar plantar pustulosis (acropustulosis). Contact Dermatitis 1998 Sep;39 (3):108‑11

(420) 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

(421) Yoshida M; Kishimoto T; Yamamura Y; Tabuse M; Akama Y; Satoh H. Amount of mercury from dental amalgam filling released into the atmosphere by cremation. Nippon Koshu Eisei Zasshi 1994 Jul;41 (7):618‑24.

(422) Reese Km. Mercury emissions from crematoria. Chem & Engin News, 12-7-98, p80-81; & Lancet 1998; 352, 1602.

(423) T.Barber, “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 Feb;26 (2):167‑72; & Patten BM, Mallette LE. Motor neuron disease: retrospective study of associated abnormalities. Dis Nerv Syst 1976 Jun;37 (6):318‑21; & Kantarjian A, “A syndrome clinically resembling amyotrophic lateral sclerosis following chronic mercurialism”, Neurology 11:639‑644 (1961)

(424) 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 Sep;44 (3 Suppl 1):S85‑8.

(425) (a) 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 Feb;90 (2):198‑204; & (b) Hu H; 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 Oct;10 (5):441‑6; & (c) 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 Mar;96 (3):348‑57; & (d) HultmanP, Johansson U, Turley SJ; Adverse immunological effects and autoimmunit induced by dental amalgam in mice. FASEB J 1994; 8: 1183-90; & (e) 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; & (f) Abedi-Valugerdi M, Hansson M, Moller G., “Genetic control of resistance to mercury-induced immune/autoimmune activation”, Scand J Immunol, 54 (1-2):190-7 (Jul-Aug 2001)

(426) 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, 77 (6):1415-25, (Jun 1998)

(427) 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. V. Study on the human amnion of the antagonism between magnesium, taurine and polluting metals. [ French] Magnesium. 1985;4 (5-6):325-32.

(428) O’Carroll RE, Masterton G, Goodwin GM. The neuropsychiatric sequelae of mercury poisoning. The Mad Hatter’s disease revisited. Br J Psychiatry 1995, 167 (1): 95-8; & PUBLIC HEALTH REPORTS, PUBLIC HEALTH BULLETIN #263. March 28, 1941. Mercurialism and its control in the felt hat industry.

(429) Rodier P.M. Developing brain as a target of toxicity. Environ Health Perspect 1995; 103 (Supp 6): 73-76; & Rice, DC, Issues in developmental neurotoxicology: interpretation and implications of the data. Can J Public Health 1998; 89 (Supp1): 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 (supp 3):511-533; & (c)Crinnion WJ. Environmental toxins and their common health effects. Altern Med Rev 2000, 5 (1):52-63; & 5 (3):209-23.

(430) Fukino H, Hirai M, Hsueh YM, Yamane Y. Effect of zinc pretreatment on mercuric chloride-induced lipid peroxidation in the rat kidney. Toxicol Appl Pharmacol 1984, 73 (3): 395-401.

(431) Smith T, Pitts K, Mc Garvey JA, Summers AO. Bacterial oxidation of mercury metal vapor. Appl Environ Microbiol 1998, 64 (4): 1328-32.

(432) 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;

(433) Sheiner EK, Sheiner E, Hammel RD, Potashnik G, Carel R. Effect of occupational exposures on male fertility: literature review. Ind Health. 2003 Apr;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 Feb;41 (1):75-7; & Epidemiologisk undersokning av fosterkador hos 1.2 milj. barn, fodda sedan 1967; Norge yrkesmed. Avd. Haukelands sykehus. Aftenposton 6 mpv 1997; & John Aitken, Head- Dept. Of Biological Sciences, University of Newcastle in Australia. “Sperm on the wane”, paper for Conference on Male-Mediated Developmental Toxicity. Montreal, June 22, 2001, The Gazette, June 22, 2001;

(434) Gazzetta Ufficiale Repubblica Italiana, November 9th 2001, General Series n.261 MINISTRY OF HEALTH’s DECREE, October 10th 2001, Prohibition of utilization and commercialization within the Italian territory of not predosed dental amalgam; Precautionary measures and warnings to be included with dental amalgams sold in Italy

(435) Norwegian Board of Health, Report 2652, http://www.helsetilsynet.no; & Norwegian Directorate for Health and Social Welfare, Press Rlease: July 1, 2003, “National Clinical Guideline for the Use of Dental Filling Materials” www.shdir.no/index.db2?id=11566 “Exit amalgam? Use of amalgam in dental practice in Norway 2002″ Journal of the Norwegian Dental Association (Den norske Tannlegeforenings Tidende 2004; 114 no. 6, p 284-286) www.tannlegetidende.no/pls/dntt/pa_dtdm.xpnd?vp_seks_id=96963&b_start=1 & Norway and Sweden ban amalgam dental fillings. www.naturalnews.com/022943.html

(436) Schiwara, H.-W. (Medical Laboratory) Arzte fur Laboratoriumsmedizen, D-28357 Bremen; & Heavy Metal Bul, 1999, 1:28

(437) Affinity Labeling Technology, Inc. (Dental Lab), oral toxicity testing technology and tests, see research web pages on amalgam toxicity, root canals, cavitations. http://www.altcorp.com; & (b) Thomas E. Levy , MD, FACC, and Hal A. Huggins, DDS, MS; Routine Dental Extractions Routinely Produce Cavitations, Journal of Advancement in Medicine Volume 9, Number 4, Winter 1996 & www.flcv.com/damspr11.html & (c) American College of Medical Genetics Working Group findings on ApoE4 strong connection to Alzheimer’s, JAMA, 1995, 274:1627-29. ; & Duke Univ. Medical Center, www.genomics.duke.edu/pdf/Alzheimer.pdf & (d) Godfrey ME, Wojcik DP, Krone CA. Apolipoprotein E genotyping as a potential biomarker for mercury neurotoxicity. J Alzheimers Dis. 2003 Jun;5 (3):189-95.

(438) Stefanovic V. et al, Kidney ectopeptidases in mercuric chloride-induced renal failure. Cell Physiol Biochem 1998; 8 (5): 278-84.

(439) Part 1, mercuric chloride intoxication. Bull Environ Contam Toxicol 1978; 20 (6): 729-35 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 Dec;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 Dec;5 (4):389-400.

(440) Kidd RF. Results of dental amalgam removal and mercury detoxification. Altern Ther Health Med 2000 Jul;6 (4):49‑55; & Gary Null, www.garynull.com/Documents/Dental/Amalgam/Amalgam6.htm

(441) (a) National Academy of Sciences, National Research Council, Committee on Developmental Toxicology, Scientific Frontiers in Developmental Toxicology and Risk Assessment, June 1, 2000, 313 pages; & Evaluating Chemical and Other Agent Exposures for Reproductive and Developmental Toxicity Subcommittee on Reproductive and Developmental Toxicity, Committee on Toxicology, Board on Environmental Studies and Toxicology, National Research Council, National Academy Press, 262 pages, 6 x 9, 2001; & (b) National Environmental Trust (NET), Physicians for Social Responsibility and the Learning Disabilities Association of America, “Polluting Our Future: Chemical Pollution in the U.S. that Affects Child Development and Learning” Sept 2000; www.safekidsinfo.org

(442) Olanow CW, Arendash GW. Metals and free radicals in neurodegeneration. Curr Opin Neurol 1994, 7 (6):548-58; & Kasarskis EJ (MD), Metallothionein in ALS Motor Neurons (IRB #91-22026), FEDRIP DATABASE, National Technical Information Service (NTIS), ID: FEDRIP/1999/07802766.

(443) Troy CM, Shelanski ML. Down-regulation of copper/zinc superoxide dismustase 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.

(444) (a) 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, April 2001;& C.Schultz et al, CoQ10 slows progression of Parkinson’s Disease; Archives of Neurology, October 15, 2002 & Matthews RT, Yang L, Browne S, Baik M, Beal MF. Coenzyme Q10 administration increases brain mitochondrial concentrations and exerts neuroprotective effects. Proc Natl Acad Sci U S A 1998 Jul 21;95 (15):8892-7; & Schulz JB, Matthews RT, Henshaw DR, Beal MF. Neuroprotective strategies for treatment of lesions produced by mitochondrial toxins: implications for neurodegenerative diseases. Neuroscience 1996 Apr;71 (4):1043-8; & Idebenone – Monograph. A potent antioxidant and stimulator of nerve growth factor. Altern Med Rev 2001 Feb;6 (1):83-86; & (b)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; & (c) C. Gooch et al, Eleanor & Lou Gehrig MDA/ALS Center at Columbia-Presbyterian Medical Center in New York; ALS Newsletter Vol. 6, No. 3 June 2001; & (d) Kidd PM., Neurodegeneration from mitochondrial insufficiency: nutrients, stem cells, growth factors, and prospects for brain rebuilding using integrative management. Altern Med Rev. 2005 Dec;10 (4):268-293.

(445) Clifford Consulting & Research, Inc, Dental Materials Reactivity Testing, Colorado Springs, Colo, www.ccrlab.com & Peak Energy Performance, inc., Dental Materials Biocompatibility Testing, www.peakenergy.com

(446) P.W.Phillips, Skinner’s Science of Dental Materials, 1980; & ImmunoSciences Lab; www.immuno‑sci‑lab.com/

(447) Amalgam/mercury poisoned patients organizations, DAMS: Assoc. Of Dental Mercury Patients-U.S., www.amalgam.org; & Swedish Association of Dental Mercury Patients, www.tf.nu/eng/infoeng1.html

(448) Dr. J. Mercola, Optimal Center Newsletter, Aug 2000, http://www.mercola.com; & J Steroid Biochem Mol Biol 1999, 69:97-107; & Mult Scler 1997, 3:105-12). & (c) (Human Reproduction Jun 2000, Supp1:1-13,

(449) Schaumburg H, Spencer P: Toxic Neuropathies. Neurology 29:431, 1979; & Levine SP; Cavender GD; Langolf GD; Albers JW. Elemental mercury exposure: peripheral neurotoxicity. Br J Ind Med 1982 May;39 (2):136‑9

(450) Dr. S J Walsh and L M Rau, University of Connecticut Health Center, “Autoimmune Disease Overlooked as a Leading Cause of Death in Women. Am J Public Health 2000;90:1463‑1466.

(451) 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, David; Rosenbaum, Jerrold; Norman, Robert. Aggression in cat and human precipitated by a cholinesterase inhibitor. The journal Psychosomatics, July 1986, vol. 27, #7, pgs. 535‑536; & Devinsky, Orrin; Kernan, Jennifer: Bear, David. Aggressive Behavior Following Exposure to Cholinesterase Inhibitors. Journal of Neuropsychiatry, vol. 4, #2, Spring 1992, pgs. 189‑199.

(452) Uppsala Amalgam Clinic, Sweden, (www.melisa.org), (over 800 patients, CFS, MCS, neurological)

(453) Blumer W, “Mercury toxicity and dental amalgam fillings”, Journal of Advancement in Medicine, v.11, n.3, Fall 1998, p.219

(455) Lindvall A, Lindh U, Danersund A, Metal Profiles in 25 Patients with Long-Term Illness. Presented at Eurotox 93 Congress & Lindh, U. Nucl Instr and Meth B30:404. 1988 & Hallgren, R; Feltelius, N; Lindh, U.J. Rheumatol. 15:308. 1988

(456) Panasiuk J , Peripheral blood lymphocyte transformation test in various skin diseases of allergic origin. (nickel & lupus) Przegl Dermatol 1980;67 (6):823‑9 [Article in Polish] ; & Barnett JH, Discoid lupus erythematosus exacerbated by contact dermatitis. Cutis 1990 Nov;46 (5):430‑2 (nickel & lupus) & Nickel Allergy Is Found in a Majority of Women with Chronic Fatigue Syndrome and Muscle Pain– And May Be Triggered by Cigarette Smoke and Dietary Nickel Intake; Journal of Chronic Fatigue Syndrome, Vol. 8 (1) 2001

(457) International Labor Organization, Mental health in the workplace in Finland, Germany, United Kingdom and United States. Oct 2000, www.ilo.org/public/english/bureau/inf/pr/2000/37.htm (not used)

(458) 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 Jan 1;142 (1):390‑399

(459) Isny Clinic (South Germany) Kurt Muller , MD, member of Editorial board for Ganzheitliches Medicine Journal. Wassertornstrasse 6 , Isny, BRD fax: 0049 7562 550 52

(460) Edwards AE, Depression and Candida, JAMA, 1985, 253 (23): 3400; & Crook WG, Depression associated with Candida albicans infections, JAMA, 1984, 251:22.

(461) 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 fatty acids and zinc with ADHD. J Child Psychol Psychiatry 1996; 37 (2):225-7; & Maes M, Vandoolaeghe E, Neels H, Demedts P, Wauters, A, Meltzer HY, Altamura C, Desnyder R. 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.

(462) Olivieri G; Brack C; Muller‑Spahn F; Stahelin HB; Herrmann M; Renard P; Brockhaus M; Hock C. Mercury induces cell cytotoxicity and oxidative stress and increases beta‑amyloid secretion and tau phosphorylation in SHSY5Y neuroblastoma cells. J Neurochem 2000 Jan;74 (1):231‑6; & (b) 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 Jun 1;32 (11):1076-83; & (c) Ho PI, Collins SC, et al; Homocysteine potentiates beta-amyloid neurotoxicity: role of oxidative stress. J Neurochem. 2001 Jul;78 (2):249-53.

(463) Johnson S. The possible role of gradual accumulation of copper, cadmium, lead and iron depletion of zinc, magnesium, selenium, vitamins B2, B6, D, and E and essential fatty acids in multiple sclerosis. Med Hypotheses 2000 Sep;55 (3):239‑41.

(464) Walsh, WJ, Health Research Institute, Autism and Metal Metabolism, www.hriptc.org/autism.htm, Oct 20, 2000; & Walsh WJ, Pfeiffer Treatment Center, Metal‑Metabolism and Human Functioning, 2000, ; http://www.hriptc.org/metal_metabolism.html & © HRI-Pfeiffer Center Autism Study; paper presented to Dan Conference, Jan 2001;

(465) Walsh WJ, Health Research Institute, Biochemical Treatment of Mental Illness and Behavior Disorders, Minnesota Brain Bio Assoc, Nov 17, 1997; http://www.hriptc.org/Minnesota.htm; & William J. Walsh, Laura B. Glab, and Mary L. Haakenson; Pfieffer Treatment Center, Biochemical Therapy and Behavior Outcomes; 2000, http://www.hriptc.org/btbres.htm

(466) Chen KM, Department of Neurology, Guam Memorial Hospital; Disappearance of ALS from Guam: implications for exogenous causes, 2000.

(467) Interpretation of Diagnostic Tests, A Synopsis of Laboratory Medicine, J.B. Wallach, Fifth Edition.

(468) Overzet K, Gensler TJ, Kim SJ, Geiger ME, van Venrooij WJ, Pollard KM, Anderson P, Utz PJ. Small nucleolar RNP Scleroderma autoantigens associate with phosphorylated serine/arginine splicing factors during apoptosis. Arthritis Rheum 2000 Jun;43 (6):1327‑36

(470) Dr. Garth Nicholson, Institute for Molecular Medicine, Huntington Beach, Calif., www.immed.org & Michael Guthrie, R.Ph. ImmuneSupport.com 07‑18‑2001 Mycoplasmas – The Missing Link in Fatiguing Illnesses, www.immunesupport.com/library/showarticle.cfm?ID=3066; & New Treatments for Chronic Infections Found in Fibromyalgia Syndrome, Chronic Fatigue Syndrome, Rheumatoid Arthritis, and Gulf War Illnesses, www.immed.org/reports/autoimmune_illness/rep1.html ; & Prof. Garth L. Nicolson, Chronic Fatigue Syndrome, Fibromyalgia Syndrome and Other Fatigue Conditions, www.immed.org/illness/fatigue_illness_research.html; & Dr. G. Nicholson, Institute for Molecular Medicine, New Treatments for Chronic Infections Found in Fibromyalgia Syndrome, Chronic Fatigue Syndrome, Rheumatoid Arthritis, Multiple Sclerosis, Amyotrophic Lateral Sclerosis, and Gulf War Illnesses, www.immed.org/reports/autoimmune_illness/rep1.html & (b) Immunosciences Lab, www.immuno‑sci‑lab.com/index2.html

(471) 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; & Spect Imaging: comparison of findings in patients with CFS, AIDA dementia complex, and major unipolar depression, Am J Roentgenol 1994, 162 (4): 943‑51; & Ichiso M, Salit IE, Abbey SE. Assessment of regional cerebral perfusion by SPECT in CFS. Nucl Med Commun 1992; 13:767-72.

(472) Patarca-Monero R, Klimas NG, Fletcher MA. Immunotherapy of chronic fatigue syndrome. Journal of Chronic Fatigue Syndrome. 2001, 8 (1): 3-37; & DeBecker P, De Meirleir K, Joos E, Velkeniers B. DHEA response to I.V. ACTH in patients with CFS. Horm Metab Res 1999, 31 (1): 18-21.

(473) 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.

(474) Richards SCM, Bell J, Cheung, YL, Cleare A, Scott DL. Muscle metabolites detected in urine in FM and CFS suggest ongoing muscle damage. Conference Proceedings of the British Society of Rheumatologists, April 2001, Scotland, Abstract 382; http://freespace, virgin.net/david.axford/me_nb_o4.htm.

(475) Hugh Fudenberg, MD, paper: NVIC International Vaccine Conference, Arlington, VA September, 1997. (http://members.aol.com/nitrf

(476) Dr Thomas Verstraeten, US Centres for Disease Control and Prevention, Summary Results: Vaccine Safety Datalink Project ‑ a database of 400, 000 children , May 2000; & Geier M.R., Geier DA; Timerosal in Childhood Vaccines, Neurodevelopmental Disorders, and Heart Disease in the U.S. ; J of Amer Physicians and Surgeons, Vol 8 (1), Spring 2003

(477) Lars Landner and Lennart Lindestrom. Swedish Environmental Research Group (MFG), Copper in society and the Environment, 2nd revised edition. 1999.

(478) Ganser, AL; Kirschner, DA. The interaction of mercurials with myelin: Comparison of in vitro and in vivo effects. Neurotoxicol, 6 (1):63‑77, 1985; & Windebank, AJ. Specific Inhibition of Myelination by Lead in vitro; Comparison with Arsenic, Thallium, and Mercury. Exp Neurol, 94 (1):203‑12, 1986; & International Labor Organization (ILO). Encyclopaedia of Occupational Health and Safety, 3rd Ed., Vol. 2. ED: Parmeggiani, L., pp. 1332‑59 1983.

(479) Amphotericin B, HgCl2 and Peritoneal Transport in Rabbits, Zweers MM, Douma CE, van der Wardt AB, Krediet RT, Struijk DG. Department of Nephrology, Academic Medical Center, Amsterdam, The Netherlands. Accepted Abstracts : The 3rd European Peritoneal Dialysis Meeting ‑‑ 5‑7 April 1998, Edinburgh, U.K; & Structural basis of aquaporin inhibition by mercury. J Mol Biol. 2007 May 4;368 (3):607-17; Savage DF, Stroud RM; & Mercury chloride decreases the water permeability of aquaporin-4-reconstituted proteoliposomes. Biol Cell. 2008 Jan 2; Yukutake Y, Tsuji S, Hirano Y, Adachi T, Takahashi T, et al

(480) 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.

(483) Thomas DE et al, Tryptophan and nutritional status in patients with senile dementia, Psychological Med 1986, 16:297-305; & Yaryura-Tobias JA et al, Changes in serum tryptophan and glucose in psychotics and neurotics, Nutrition, No.4557, p1132; Carney MWP, Brit Med J, 1967, 4:512-516.

(484) 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; & J Family Practice, 1988, 27 (6): 603-606; & Anderson RA et al, Effects of supplemental chromium on patients with reactive hypoglycemia, Metabolism, 1987, 36 (4): 351-355; & Metabolism, 1983, 32 (9): 894-99.

(485) Dr. Hulda Clark, The Cure for all Diseases, New Century Press, 2000, www.drclark.net (amalgam replacement and treatment for parasites/bacteria) (U.S. CDC confirms parasites common in those with chronic immune conditions) & U.S. Center for Disease Control, Parasites (widespread exposures), www.dpd.cdc.gov/dpdx/HTML/Para_Health.htm ;www.cdc.gov/ncidod/diseases/list_parasites.htm http://www.cdc.gov/ncidod/dpd/parasites/ascaris/prevention.htm www.cdc.gov/healthypets/browse_by_diseases.htm ;www.cdc.gov/ncidod/diseases/index.htm

(486) Dr. Hulda Clark, The Cure for All Cancers, 1998, www.drclark.net; & A Cancer Therapy, The Results of Fifty Cases (1975)–Dr Max Gerson, Gerson Clinics, www.gerson.org. & Charlotte Du Bois and John Lubecki, The End of Cancer, Nelson’s Books, 2003; & The Cancer Homepage www.curezone.com/diseases/cancer/cancer_dental_risk.asp & Dr. Hulda Clark, The Cure of HIV/AIDS, New Century Press, 1993.

(487) 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.

(488) 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 Dec 24;274 (52):37111‑6

(489) Waggoner DJ, Bartnikas TB, Gitlin JD. The role of copper in neurodegenerative disease. Neurobiol Dis 1999 Aug;6 (4):221‑30; & (b) Torsdottir G, Kristinsson J, Gudmundsson G, Snaedal J, Johannesson T. Copper, ceruloplasmin and superoxide dismustase (SOD) in amyotrophic lateral sclerosis. Pharmacol oxicol 2000 Sep;87 (3):126‑30; & © Estevez AG, Beckman JS et al, Induction of nitric oxide‑dependent apoptosis in motor neurons by zinc‑deficient superoxide dismustase. Science 1999 Dec 24;286 (5449): 2498‑500; & (d) Cookson MR, Shaw PJ. Oxidative stress and motor neurons disease. Brain Pathol 1999 Jan;9 (1):165‑86.

(490) Rojas M, Olivet C . Occupational exposure and health effects of metallic mercury among dentists and dental assistants: a preliminary study. Valencia, Venezuela; 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 Jul;15 (3):673‑82.

(491) 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 .

(492) 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 Apr;13 (2):257‑267; & (b) 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 Apr;53 (2):85-91; & © Examination of urinary mercury levels in dentists in Turkey. Karahalil B, Rahravi H, Ertas N. Hum Exp Toxicol. 2005 Aug;24 (8):383-8.

(493) Moller AT, Spangenberg JJ. Stress and coping amongst South African dentists in private practice. J Dent Assoc S Afr 1996 Jun;51 (6):347‑57; & Stefansson CG, Wicks S. Health care occupations and suicide in Sweden 1961‑1985. Soc Psychiatry Psychiatr Epidemiol 1991 Dec;26 (6):259‑64

(494) (a)Kobayashi MS, Han D, Packer L. Antioxidants and herbal extracts protect HT-4 neuronal cells against glutamate-induced cytotoxicity. Free Radic Res 2000 Feb;32 (2):115-24 (PMID: 10653482; & (b)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 Aug;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 Aug;15 (5):449-51 ;& (c)Li Y, Liu L, Barger SW, Mrak RE, Griffin WS. Vitamin E suppression of microglial activation is neuroprotective. J Neurosci Res 2001 Oct 15;66 (2):163-70.

(496) Doble A. The role of excitotoxicity in neurodegenerative disease: implications for therapy. Pharmacol Ther 1999 Mar;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 Mar 1;63 (5):377‑87; & Cookson MR, Shaw PJ. Oxidative stress and motor neurons disease. Brain Pathol 1999 Jan;9 (1):165‑86

(497) Torres‑Aleman I, Barrios V, Berciano J. The peripheral insulin‑like growth factor system in amyotrophic lateral sclerosis and in multiple sclerosis. Neurology 1998 Mar;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 Nov;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 Dec 8;275 (49):38620-5;

(498) Lai EC, Rudnicki SA. Effect of recombinant human insulin‑like growth factor‑I on progression of ALS. A placebo‑controlled study. Neurology 1997 Dec;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 Sep;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 Aug;20 (8):326‑31; & Couratier P, Vallat JM. Therapeutic effects of neurotrophic factors in ALS; Rev Neurol (Paris). 2000 Dec;156 (12):1075‑7. French.

(499) 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 Feb;83 (2):309‑19.

(501) Anthony Iacopino.Conference Paper, American Academy of Periodontology (AAP) at the US National Institutes of Health in Bethesda, Maryland, April, 2001; Diabetes: A Silent Epidemic, Newsweek, Sep 4, 2000& (b)Harris Coulter, Childhood Vaccinations and Juvenile‑Onset (Type‑1) Diabetes, Testimony before the Congress of the United States, House of Representatives, Committee on Appropriations, subcommittee on Labor, Health and Human Services, Education, and Related Agencies, April 16, 1997, www.909shot.com/hcdiabetes.htm; & (c) Dr. Bart Classen, Vaccines are the largest cause of insulin-dependent diabetes in young children, paper given at American College for Advancement in Medicine., Nashville, Tenn., May 14, 2001; & (d) Narayan KMV, Boyle JP, Lifetime risk for diabetes mellitus in the U.S. JAMA, 2003, 290 (14):1884-90; (e) W. Block, Lipoic Acid Helps Fight Diabetes, Life Enhancement, Dec 2003; www.life-enhancement.com & Review of mercury/diabetes connection, www.flcv.com/diabetes.html

(502) Dr. R.C. Atkins, The Vitamin and Nutrient Solution to Chronic Health Problems, , 1998, ISBN 0-684-81849-3; & Dr. Rona, Return to the Joy of Health, www.srvitamins.com

(503) Rupp, Paffenberger, Significance to health of mercury used in dental practice, Reports of Councils and Bureaus, JADA, Vol 182, June 1971; & Rao, Hefferen, Biocompatibility of Dental Materials, Vol III, D.C. Smith and D.F. Williams, Eds., CRC Press, Boca Raton, Fl 1982, Toxicity of Mercury; & Center for Chemical Hazard Assessment, Potential Occupational Hazards: Dentistry, Syracuse Research, Contract No.210-78-0019, 1980; & Merck Manuel, 14th Edition, p1552; & Faria Md Mde A; Chronic occupational metallic mercurialism; Rev Saude Publica 2003 Feb;37 (1):116-27.

(504) Gosselin, Smith, Hodge, Clincial Toxicology of Commercial Products, Williams and Wilkins Publisher, Baltimore, 5th Ed, 1984; & Katzung, MD, Basic Clinical Pharmacology, 2nd Ed.; & Thienes, Haley, Clinical Toxicology, Lea & Febeger, Philadelphia, 5th Ed, 1972.

(506) Leistevuo J, Pyy L, Osterblad M, Dental amalgam fillings and the amount of organic mercury in human saliva. Caries Res 2001 May‑Jun;35 (3):163‑6; & Leistevuo J et al., Dental amalgam fillings and the amount of organic mercury in human saliva, Corks Res, 35 (3):163-6 (2001 May-Jun)

(507) Appel SH, Beers D, Siklos L, Engelhardt JI, Mosier DR. Calcium: the Darth Vader of ALS. Amyotroph Lateral Scler Other Motor Neuron Disord 2001 Mar;2 Suppl 1:S47-54; & Niebroj-Dobosz I, Jamrozik Z, Janik P, Hausmanowa-Petrusewicz I, Kwiecinski H. Anti-neural antibodies in serum and cerebrospinal fluid of amyotrophic lateral sclerosis (ALS) patients. Acta Neurol Scand 1999 Oct;100 (4):238-43; & Appel SH, Stockton-Appel V, Stewart SS, Kerman RH. Amyotrophic lateral sclerosis. Associated clinical disorders and immunological evaluations. Arch Neurol 1986 Mar;43 (3):234-8: Pestronk A, Choksi R. Multifocal motor neuropathy. Serum IgM anti-GM1 ganglioside antibodies in most patients detected using covalent linkage of GM1 to ELISA plates. Neurology 1997 Nov;49 (5):1289-92; & Pestronk A, Adams RN, Cornblath D, Kuncl RW, Drachman DB, Clawson L. Patterns of serum IgM antibodies to GM1 and GD1a gangliosides in amyotrophic lateral sclerosis. Ann Neurol 1989 Jan;25 (1):98-102

(508) Bonar DB, McColgan B, Smith DR, Darke C, Guttridge MG, Williams HSmyth PPA, Hypothyroidism and aging: The Rosses’ Survey. Thyroid 2000, 10 (9):821-827; & Canaris GJ, Manowitz NR, Mayor G, Ridgway EC. The Colorado thyroid disease prevalence study. Arch Tntern Med 2000, 160 (4):526-34; & GS Connection 11 (12): Prevelence of Thyroid Imbalance, Thyroid in Pregnancy, GSDL, www.gsdl.com

(509) Klein RZ, Sargent JD, Larsen PR, Waisbren Se, Haddow JE, Mitchell ML, Relation of severity of maternal hypothyroidism to cognitive development of offspring. J Med Screen 2001: 8:18-20; & (b) de Escobar DM, Orbregon MF, del Rey FE, Is neuropsychological development related to maternal hypothyroidism or to maternal hypothyroxinemia? C Clin Endocrin Metab 2000; 3975-3987; & © Abstract # 274: Wolfberg, Adam J. and David A. Nagey, “Thyroid Disease During Pregnancy and Subsequent Congenital Anomalies.”St Johns Univ., kblum@jhmi.edu ; & Birth Defect News, Jan 2002, p2; & (d) Allan W. (MD), Maternal thyroid deficiency and pregnancy complications, Journal of Medical Screening, 2000; & (e) Thyroid Imbalances in Pregnancy Linked to Poor Child Neurodelopment, Great Smokies Diagnostic Lab, www.gsdl.com/news/connections/vol11/conn20010228.html

(510) (a)Morris MS, Bostom AG, Jacques PJ, Selhub J, Rosenberg IH, Hyperhomocysteinemia and hypercholesterolemia associated with hypothyroidism in the third U.S. National Health and Nutrition Examination Survey, Artherosclerosis 2001, 155:195-200; & (b) Shanoudy H. Soliman A, Moe S, Hadian D, Veldhuis F, Iranmanesh A, Russell D, Early manifestations of “sick eythyroid syndrome” in patients with compensated chronic heart failure, J Card Fail 2001, 7 (2):146-52; & (c)AE. Hak, HAP. Pols, TJ. Visser, et al., The Rotterdam Study., Subclinical hypothyroidism is an independent risk factor for atherosclerosis and myocardial infarction in elderly women, Ann Int Med, 2000, vol. 132, pp. 270–278 & (d)Thyroid Dysfunction Linked to Elevated Cardiac Risk, GSDL, www.gsdl.com/news/connections/vol12/conn20010411.html.; & (e) Biondi B, Palmieri EA, Lombardi G, Fazio S. Effects of subclinical thyroid dysfunction on the heart. Ann Intern Med 2002 Dec 3;137 (11):904-14; & (f) B.G. Nedreboe, O. Nygard, et al, Plasma Total Homocysteine of hypothyroid patients during 12 months of treatment, Haukeland Univ. Hospital, Bergen, Norway, bjoern.gunnar.nedreboe@haukeland.no (references 7 other studies with similar findings); & (g) Hussein, WI, Green, R, Jacobsen, DW, Faiman, C. Normalization of hyperhomocysteinemia with L-thyroxine in hypothyroidism. Ann Intern Med 1999; 131:348;

(511) Abramson J, Stagnaro-Green A, Thyroid antibodies and fetal loss, Thyroid 2001, 11 (1): 57-63; & Thyroid Antibodies May Spur Pregnancy Loss, GSDL, www.gsdl.con/news/connections/vol12/conn20010411.html (512) Zeeman Mercury Spectrometer RA-915 Demonstration, Fifth International Conference on Mercury, Rio de Janeiro, Brazil, May 23-28, 1999. (methyl mercury sniffer)

(513) (a) In vitro and in vivo effects of mercuric chloride on thymic endocrine activity, NK and NKT cell cytotoxicity, cytokine profiles (IL-2, IFN-gamma, IL-6): role of the nitric oxide-L-arginine pathway. Int Immunopharmacol. 2006 Mar;6 (3):376-89. Epub 2005 Nov 9. Santarelli L, Bracci M, Mocchegiani E. & Valentino M, Santarelli L, Pieragostini E, Soleo L, Mocchegiani E. In vitro inhibition of thymulin production in mercury-exposed thymus of young mice. Sci Total Environ 2001 Apr 10;270 (1-3):109-112 ; & (b) Nordlind K. Stimulating effect of mercuric chloride and nickel sulfate on DNA synthesis of thymocytes and peripheral lymphoid cells. Int Arch Allergy Appl Immunol 1983;72 (2):177-179; & Chen M, von Mikecz A. Specific inhibition of rRNA transcription and dynamic relocation of fibrillarin induced by mercury. Exp Cell Res 2000 Aug 25;259 (1):225‑238; & © Dieter MP, Luster MI, Boorman GA, Jameson CW, Dean JH, Cox JW. Immunological and biochemical responses in mice treated with mercuric chloride.. Toxicol Appl Pharmacol 1983 Apr;68 (2):218‑228; & (d) Hansson M, Djerbi M, et al; Exposure to mercuric chloride during the induction phase and after the onset of collagen-induced arthritis enhances immune/autoimmune responses and exacerbates the disease in DBA/1 mice.
Immunology. 2005 Mar;114 (3):428-37; & (e)Arnett FC, Fritzler MJ, Ahn C, Holian A. Urinary mercury levels in patients with autoantibodies to U3-RNP (fibrillarin). J Rheumatol. 2000 Feb;27 (2):405-10

(514) Kusaka Y. Occupational diseases caused by exposure to sensitizing metals. Sangyo Igaku 1993, 35:75-87; & (b) Firestein GS. Rheumatoid arthitis, in:Kelley G, HarrisL, Sledge J, (Eds ( Textbook of Rheumatology, USA: WB Saunders Company 1997; p851-88; & (c) Parnham M, Blake D. Antioxidants as antirheumatics. Agents Actions Suppl 1993, 44:189-95; & (d Karatas GK, Tosun AK, Karacehennem E, Sepici V. Mercury poisoning: an unusual cause of polyarthritis. Clin Rheumatol. 2002 Feb;21 (1):73-5.

(516) Fassbender K, Mossner R. Mood disorders and dysfunction of the hypothalamic-pituitary-adrenal axis in conditions such as MS: association with cerebral inflammation. Arch Neurol 1998: 55: 66-72; & (b) Wilder RL. Neuroendocrine-immune system interactions and autoimmunity. Annu Rev Immunol 1995; 13:307-38.

(517) Earl C, Chantry A, Mohammad N. Zinc ions stabilize the association of basic protein with brain myelin membranes. J Neurochem 1988; 51:718-24; & Riccio P, Giovanneli S, Bobba A. Specificity of zinc binding to myelin basic protein. Neurochem Res 1995; 20: 1107-13; & Sanders B. The role of general and metal-specific cellular responses in protection and repair of metal-induced damage: stress proteins and metallothioneins. In: Chang L (Ed.), Toxicology of Metals. Lewis Publishers, CRC Press Inc, 1996, p835-52; & Mendez-Alvarez E, Soto-Otero R, et al, Effects of aluminum and zinc on the oxidative stress caused by 6-hydroxydopamine autoxidation: relevance for the pathogenesis of Parkinson’s disease. Biochim Biophys Acta. 2002 Mar 16;1586 (2):155-68.

(518) Landay AL, Jessop C, Lenette ET, chronic fatigue syndrome: clinical condition associated with immune activation. Lancet 1991; 338:707-12; & (b)Caliguri M, Murray C, Buchwald D. Phenotypic and functional deficiency of natural killer cells in patients with CFS. J Immunol 1987; 139:3306-13; & (c)Barker E, Fujirmura SF, Fadern MB. Immunologic abnormalities associated with CFS. Clin Infect Dis 1994; 18: 136-41.

(519) 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; & (b)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.

(520) Mitchell JD. Heavy metals and trace elements in amyotrophic lateral sclerosis. Neurol Clin 1987 Feb;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 clincal onset and prgression? Neuroepidemiology 1990, 9:255-62; Roelofs-Iverson RA, Elveback LR. ALS and heavy metals, Neurology 1984, 34:393-5; & ArmonC, 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 Nov-Dec; 86 (6):522-33.

(521) 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; & 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 Sep;36 (5):687-97.

(522) 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 Nov;102 (5):467-72

(523) CBS Television Network, ” 60 Minutes”, television program narrated by Morley Safer, December 12, 1990, www.vimy‑dentistry.com/tttoc.htm#_Toc499123411

(524) (a) Urushitani M, Shimohama S. The role of nitric oxide in amyotrophic lateral sclerosis. Amyotroph Lateral Scler Other Motor Neuron Disord 2001 Jun;2 (2):71-81; & (b) Torreilles F, Salman-Tabcheh S, Guerin M, Torreilles J. Neurodegenerative disorders: the role of peroxynitrite.Brain Res Brain Res Rev 1999 Aug;30 (2):153-63; & (c)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 Apr;47 (4):524-7; & (d) 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

(526) Ahlbom II, Cardis E, Green A, Linet M, Savitz D, Swerdlow A. Review of the Epidemiologic Literature on EMF and Health. Environ Health Perspect 2001 Dec;109 Suppl 6:911-933.

(527) Cline Medical Center, Vancouver Island, http://www.oceansidemedicine.com/Default.htm

(528) Doctors Data Inc.; Fecal Elements Test; P.O.Box 111, West Chicago, Illinois, 60186-0111; www.doctorsdata.com

(529) (a)Dr. D.A. Carroll, O.D.& Dr. B.C. Lane, Preventing mercury related cataracts, www.medicalvisioncenter.com/prevention.html; & Alan Thal, MD, Cataract reversal through mercury detox, www.digitalnaturopath.com/treat/T33633.html; & Dr, Ben Lane, O.D., Methylmercury in seafood contributes to cataract development, Medical World News, December 20, 1982; & Dr. Victoria Buntine, Mercury Effects, Healthinasia Incorporated, 2001, www.healthinasia.com/mercury.html, & Dr. G. E. Poesnecker, Its Only Natural, 2001, www.oneflesh.org/only‑22.html; & (b) Rudolph CJ, Samuels RT, McDanagh EW. Cheraskin E. Visual Field Evidence of Macular Degeneration Reversal Using a Combination of EDTA Chelation and Multiple Vitamin and Trace Mineral Therapy.In: Cranton EM, ed. A Textbook on EDTA Chelation Therapy, Second Edition. Charlottesville, Virginia: Hampton Roads Publishing Company; 2001, & (c) Olynyk F, Sharpe DH: Mercury poisoning in paper pica. (retinitis pigmentosa) N Engl J Med 1982 Apr 29;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 mercury poisoning) and incidence of complications with aging. J Environ Sci Health B 1995 Sep;30 (5):699‑715; & (d) Cavalleri A, Belotti L, Gobba FM, Luzzana G, Rosa P & Seghizzi P. Colour vision loss in workers exposed to elemental mercury vapour. Toxicology Letters 77 (1‑3):351‑356 (1995); & Urban P, Gobba F, Nerudova J, Lukas E, Cabelkova Z, Cikrt M, .Color Discrimination Impairment in Workers Exposed to Mercury Vapor. Neurotoxicology. 2003 Aug;24 (4-5):711-716;

(530) Cancer case histories followed by doctors, www.whale.to/d/cancer.html ; & Increased levels of transition metals in breast cancer tissue; Ionescu JG, Novotny J, Stejskal VD, Latsch A, Neuro Endocrinol Lett. 2006 Aug 5;27 (Suppl1)

(531) Dr. Ewan Macdonald, KA Ritchie et al , Health and neuropsychological functioning of dentists exposed to mercury. Occup Environ Med. 2002 May;59 (5):285-6; & Wesnes K., A pilot study of the effect of low level exposure to mercury on the health of dental surgeons. Occupational & Environmental Medicine. 52 (12):813-7, 1995

(532) El-essawy Dental Clinic www.el-essawy.com (large number of cases-most chronic conditions improve after amalgam replacement) www.wholisticresearch.com/info/artshow.php3?artid=7

(533) Tetsuya Endo, Koichi Haraguchi and Masakatsu Sakata , Hokkaido Univeristy, High levels of mercury found in whalemeat, The Science of the Total Environment. 2002

(534) Tirado V, Garcia MA, Franco A., Pneuropsychological disorders after occupational exposure to mercury vapors, Rev Neurol 2000 Oct 16-31;31 (8):712-6; & Powell TJ. Chronic neurobehavioural effects of mercury poisoning on a group of chemical workers. Brain Inj 2000 Sep;14 (9):797-814

(535) K. Sullivan, Evidence Implicating Amalgam in Alzheimer’s Disease, www.bhoffcomp.com/coping/amalgam.html

(536) Dr. J. Mercola; Fixing teeth, Threatening Lives with Mercury; www.mercola.com/2002/aug/14/mercury.htm

(537) Amalgam replacement with detox using NDF, case histories, www.healthydetox.org/cases.html

(538) C. Malmstrom, DDS, Medical Research and Development, http://home.swipnet.se/misac/maineng.html & http://home.swipnet.se/misac/infpatient.html (Over 2000 cases, about 90% signif. improvement) & Malmstrom detox high fiber diet ( http://home.swipnet.se/misac/vararticles8.html) & Health, Teeth, and Mercury Toxicity, www.earthtym.net/merc‑tox.htm; & Eric Davis Dental Center, www.ericdavisdental.com/the_program.htm

(540) Wisconsin Bureau of Public Health, Imported seabass as a source of mercury exposure: a Wisconsin Case Study, Environ Health Perspect 1995, 103 (6): 604-6; & J. Hightower, “Methylmercury Contaminmation in Fish: Human Exposures and Case Reports, ” Environmental Health Perspectives; Nov 1, 2002.

(541) 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 Jul;81 (1):1-19; & (b)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 Winter;16 (4):729005‑10

(542) DAMS, Inc.; www.flcv.com/damspr5.html

(543) U.S. Centers for Disease Control, National Center for Health Statistics, NHANES III study (thousands of people’s health monitored), www.flcv.com/NHanes3.html ; & www.mercola.com/article/mercury/no_mercury.htm & Review: cancer related to mercury exposure, B. Windham (Ed) www.flcv.com/cancerhg.html ; & (b) Laks, Dan R. Assessment of chronic mercury exposure within the U.S. population, National Health and Nutrition Examination Survey, 1999–2006. Biometals. August 2009; & Laks, D.R. et al, Mercury has an affinity for pituitary hormones, Medical Hypotheses, Dec 2009; & (c) An Investigation of Factors Related to Levels of Mercury in Human Hair, Environmental Quality Institute, October 01, 2005, www.greenpeace.org/raw/content/usa/press/reports/mercury-report.pdf www.greenpeace.org/usa/assets/binaries/addendum-to-mercury-report

(544) Behan P and Chaudhuri A, Astrocyte malfunction as cause of MS, Journal of the Royal College of Physicians of Edinburgh; Nov 2002, http://news.bbc.co.uk/1/hi/health/2462005.stm

(545) Ritchie KA, Gilmour WH, Macdonald EB, et al, Health and neuropsychological functioning of dentists exposed to mercury. Occup Environ Med 2002 May;59 (5):287-93; & (b) Mercury vapour levels in dental practices and body mercury levels of dentists and controls. Br Dent J. 2004 Nov 27;197 (10):625-32; discussion 621. Ritchie KA, Burke FJ, et al

(546) Rob Edwards and Duncan Graham-Rowe. “Electrical connection” New Scientist 6 March 2002; & Dr. Mae-Wan Ho, National Radiological Protection Board (NRPB), “Electromagnetic Fields Double Leukemia Risks” 2002; & Richard Doll et al, Cancer Studies Unit, Oxford Univ., March 2002; & London SJ; Bowman JD; Sobel E; Thomas DC; Garabrant DH; Pearce N; Bernstein L; Peters JM. Exposure to magnetic fields among electrical workers in relation to leukemia risk in Los Angeles County. Am J Ind Med 1994 Jul;26 (1):47-60; & Caplan LS; Schoenfeld ER; O’Leary ES; Leske MC. Breast cancer and electromagnetic fields–a review. Ann Epidemiol 2000 Jan;10 (1):31-44;

(547) Canada-wide Standards: A Pollution Prevention Program for Dental Amalgam Waste, J Can Dent Assoc 2001; 67:270-3 www.cda-adc.ca/jcda/vol-67/issue-5/270.html & A.O. Adegbembo, P.A. Watson, S.J. Lugowski, 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.

(548) Association of Metropolitan Sewerage Agencies (AMSA), Evaluation of Domestic Sources of Mercury , Aug 2000, www.amsa‑cleanwater.org/pubs/mercury/mercury.cfm; & Association of Metropolitan Sewerage Agencies (AMSA)/U.S. EPA, Mercury Source Control Program Evaluation ( www.amsa-cleanwater.org/advocacy/mercgrant/finalreport.pdf ), Larry Walker Associates, Final Report, March 2002,

(549) Dentist the Menace: The Uncontrolled Release of Dental Mercury in the Environment, Mercury Policy Project and Healthcare Without Harm, June 2002, www.mercurypolicy.org/new/documents/DentistTheMenace.pdf

(550) J. S. Malpas, M.D., Treatment Options for Multiple Myeloma, New England Journal of Medicine, December 12th, 2002; & Riccardi et al, British Journal of Cancer 2000;82:1254-60.

(551) Dr. Harald Hamre (Norwegian physician treating mercury toxicity) , Amalgam and Illness, 1998.

(552) 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 Oct-Dec;23 (5-6):459-82. (750 cases)

(553) 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 Jul-Aug;57 (4):366-70; & Council of European Communities Directive 84/156/EEC.

(554) Swedish newspaper “Dagens Nyheter” April 26, 2003, “Healthy Enough to Work Again without Amalgam” “

(555) 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; Bellabarba D, and Tremblay R; Effect of thimerosal on serum binding of thyroid hormones, Can J Physsiol Pharmacol, 173, 51:156-159: & Hokkfen B, Kodding R, Hesch RD; Regulation of thyroid hormone metabolism in rat liver fractions, Biochim Biophys Acta 1978, 539: (1): 114-24.

(556) Aspen Clinic for Preventive and Environ-mental Medicine in Colorado, http://curezone.org/testimonials/003.htm; & Alpine Holistic Health Clinic, Dr. Lewis Cone, Plano, Texas, www.drlewiscone.com/toxic_metals.htm; & ICNR Case Study #11 www.icnr.com/cs/cs_11.html

(557) Psychiatric Disturbances and Toxic Metals, Townsend Letter for Doctor’s & Patients April 2002; & Alternative & Complementary Therapies (a magazine for doctors), Aug 2002.

(558) American Assoc. of Clinical Endocrinologists and American College of Endocrinolog. AACE clinical practice guidelines for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocr Pract., 1995, 1: 54-62.

(559) Choy CM, Lam CW, et al, 2002, Infertility, blood mercury concentrations, and dietary seafood consumption: a case control study, BJOG: An International Journal of Obstetrics and Gynaecology, 109: 1121-1125.

(560) Nath J, Safar R. Late-onset bipolar disorder due to hyperthyroidism. Acta Psychiatr Scand 2001;104:72-75.

(561) 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.

(562) 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.

(563) Aydin, N ;Karaoglanoglu, S; 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.

(564) 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 Nov 23;276 (47):44284-96. Epub 2001 Sep 11

(565) 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 Jan;80 (1):50-63.

(566) 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 273: 20354-20362, 1998

(567) Kim CY, Satoh H, et al, Protective effect of melatonin on methylmercury-Induced mortality in mice. Tohoku J Exp Med. 2000 Aug;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 Jan;74 (1):231-6.

(568) Bemis JC, Seegal RF; 2000, PCBs and methylmercury alter intracellular calcium concentrations in rat cerebellar granule cells. Neurotoxicology, 21 (6): 1123-1134.

(578) Urinary mercury concentrations associated with dental restorations in adult women aged 16-49 years: United States, 1999-2000. Occup Environ Med. 2005 Jun;62 (6):368-75. Dye BA, Schober SE, Dillon CF, Jones RL, Fryar C, McDowell M, Sinks TH.
(579) Evaluation of the mercury exposure of dental amalgam patients by the Mercury Triple Test.
Hansen G, Victor R, Engeldinger E, Schweitzer C. Occup Environ Med. 2004 Jun;61 (6):535-40

(580) Determination of mercury in blood, urine and saliva for the biological monitoring of an exposure from amalgam fillings in a group with self-reported adverse health effects. Zimmer H, Ludwig H, et al, Int J Hyg Environ Health. 2002 Apr;205 (3):205-11.