Mercury has been well documented to be an endocrine system-disrupting chemical in animals and people, disrupting function of the pituitary gland, thyroid gland, enzyme production processes, and many hormonal functions at very low levels of exposure. Mercury (especially mercury vapour) rapidly crosses the blood brain barrier…
Epidemiological studies have found that human embryos are also highly susceptible to brain damage from prenatal exposure to mercury. 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.
[ Our comment – This explains problems with some vaccines! ]
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. Health Effects from Dental Staff Exposure to Mercury
VIII. Scientific Panel and Government Bodies
That Have Found Amalgam Fillings Unsafe
Toxic metals such as mercury, lead, cadmium, etc. have been documented as 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 (105,160). Exposure of humans and animals to toxic metals such as mercury, cadmium, lead, copper, aluminium, arsenic, chromium, manganese, etc. is widespread and in many areas increasing. The U.S. Centre 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. 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. The reason is that 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. The average filling has 1 gram of mercury and leaks mercury vapour continuously due to mercury’s low vapour pressure along with loss due to galvanic action of mercury with dissimilar metals in the mouth (182,192,292,348,349), resulting in significant exposure for most with amalgam fillings (see Section III). Mercury vapour 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). 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).
2. Mercury is the most toxic of the toxic metals. Mercury (vapour) 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 (14,20,25,85, 99,175,273,301/262,274); also accumulates in the motor function areas of the brain and CNS (48,291,327,329).
(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, 211,273, 291,295,327,329,301,303,395/39,262,274,303); 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 (13,56,98,102,126,145,169,170,184,213,219, 250, 257,259,286,290,291,302,324,326,329); kills or inhibits production of brain tubulin cells (66,67,161,166, 207,300); inhibits production of neurotransmitters by inhibiting: calcium-dependent neurotransmitter release (372), dihydroteridine reductase (27,122,257), nitric oxide synthase (259), and effecting phenylalanine, tyrosine and tryptophan transport to neurons) (34,122,126,257,285,288,333/255,333)
(d) is immunotoxic (damages and inhibits immune T-cells, B-cells, neutrophil function, etc.) (17,27,31,38,44,45,46,60,127,128,129,130,152,155,165,181,226,252,270,285,316,355/272) and induces ANA antibodies and autoimmune disease (38,43,45,59,60,118,131,181,226,234,269,270,313,334,342,343)
(e) is nephrotoxic (toxic to kidneys) (14,20,203,223,260,268,334)
(f) is endocrine system-disrupting chemical (accumulates in pituitary gland and damages or inhibits pituitary glands hormonal functions at very low levels (9,19,20,25,85,99,105,273,312,327,348,369/274), adrenal gland function (84,369), thyroid gland function (50,212,369), and disrupts enzyme production processes at very low levels of exposure (9,13,33,56,111,194,348,355,410-412)
(g) exposure to mercury vapour (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,etc.).
(h) reproductive and developmental toxin (2,4,9,10,22,23,24,37,38,41,61,105,149,160,275,276,281,305,338, 361,367, 20/4,39,55,149,162,255,308,339,357); damages DNA (296,327,272,392,142,38,41,42) and inhibits DNA & RNA synthesis (114/149); damages sperm, lowers sperm counts and reduces motility. (4,37,104.105,159,160/4, 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 vitamin B12 (43,96,198,263,264,338,339,347); depresses enzyme isocitric dehydrogenase (ICD) in fetus, causes reduced iodine uptake & hypothyroidism (50,91,212,222,369) & learning deficits; causes learning disabilities and impairment, and reduction in IQ (1,3,38,110,160,285c, 263,264/39), causes infertility (4,9,10,24,38,121,146,357,365,367/4,10,55,162), causes birth defects (23,35,37,38,110,142,241/241).
(i) prenatal/early postnatal exposure affects level of nerve growth factor in the brain, impairs astrocyte function, and causes imbalances in development of brain(38,119,161,175,194,305/175,255,39)
(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), and increased risk of acute myocardial infarction (35,59,202,205,212,232,306,310,351/201,308).
(k) causes immune system damage resulting in allergies, asthma, chronic fatigue syndrome CFS),and multiple sensitivities (MCS)
(8,17,45,46,52,60,75,86,87,90,97,101,128,129,131,154,168,181,212,226,228,230,265, 267,296,313,342,388/272) and neutrophil functional impairment (285/59,etc.).
(l) causes interruption of the cytochrome oxidase system/ATP energy function (84) and progressive coproporphyrinuria, resulting in low energy, digestive problems, and porphyrins in urine (34,69,70,73,210,212,226,232,260)
(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 (116,117,161,258,389,53).
(n) mercury causes significant destruction of stomach and intestine epithelial cells, resulting in damage to stomach lining (leaky gut) (222,Shelton,228) and accumulation of helicobacter pylori, a suspected major factor in stomach ulcers and stomach cancer (256).
(o) causes mitochondrial release of calcium induced by modification of the-SH groups of proteins (1,21,35,38,43,329,333), as well as damaging enzymatic process (33,111,194,252,338,410-412) (338,254), damaged sulphur oxidation processes (33,338), 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, enzyme production processes, and many hormonal functions at very low levels of exposure. Mercury (especially mercury vapour) rapidly crosses the blood brain barrier and is stored preferentially in the pituitary gland, hypothalamus, and occipital cortex in direct proportion to the number and extent of dental amalgam surfaces
(1,14,16,19,20,25,34,38,61,85,99,162,211, 273,274,287,327,348,360,366,369) Thus mercury has a greater effect on the functions of these areas. 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.
The hypothalamus regulates body temperature and many metabolic processes. Mercury damage thus commonly results in poor bodily temperature control, in addition to many problems caused by hormonal imbalances. Such hormonal secretions are affected at levels of mercury exposure much lower than the acute toxicity effects normally tested, as previously confirmed by hormonal/reproductive problems in animal populations (104). Mercury also damages the blood brain barrier and facilitates penetration of the brain by other toxic metals and substances (311).
4. Mercury’s biochemical damage at the cellular level include DNA damage, inhibition of DNA and RNA synthesis (4,38,41,42,114,142,197,272,296,392/149); alteration of protein structure (33,111,114,194,252/114); alteration of the transport of calcium (333,43,254,329); inhibitation of glucose transport (338,254), and of enzyme function and other essential nutrients (96,198,254,263,264,338,339,347,410-412); induction of free radical formation (13,54), depletion of cellular glutathione (necessary for detoxification processes) (111,126), inhibition of glutathione peroxidase enzyme (13), 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). Oxidative stress and reactive oxygen species (ROS) have been implicated as major factors in neurological disorders including stroke, PD, Alzheimer’s, ALS, etc.(13). 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).
Only a few micrograms of mercury severely disturb cellular function and inhibit nerve growth (175,147,175,226,255,305). Exposure to mercury results in metalloprotein compounds that have genetic effects, having both structural and catalytic effects on gene expression (114,241,296). Some of the processes affected by such metalloprotein control of genes include cellular respiration, metabolism, enzymatic processes, metal-specific homeostasis, and adrenal stress response systems. Significant psysiological changes occur when metal ion concentrations exceed threshold levels. Such metalloprotein formation also appears to have a relation to autoimmune reactions in significant numbers of people (114,60,313,342,368,369). Of a population of over 3000 tested by the immune lymphocyte reactivity test (MELISA,60,275), 22% tested positive for inorganic mercury and 8% for methyl mercury.
A direct mechanism involving mercury’s inhibition of cellular enzymatic processes by binding with the hydroxyl radical (SH) in amino acids appears to be a major part of the connection to allergic/immune reactive conditions such as autism, schizophrenia, eczema, psoriasis, and allergies (410-412,etc.). 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 cassein (411,412). 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), enzymatic processes involving vitamins B6 and B12, effects on the cytochrome-C energy processes, along with mercury’s adverse effects on cellular mineral levels of calcium, magnesium, zinc, and lithium. Along with these blockages of cellular enzymatic processes, mercury has been found to cause additional neurological and immune system effects in many through immune/autoimmune reactions (60,313).
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 organo-chlorine compounds (413,313,414). Much mercury in saliva and the brain is also organic, the most acutely neurotoxic form (220,272), since mouth bacteria and other organisms in the body methylate inorganic mercury to organic mercury (51, 81,225).
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 (160). Some Florida panthers that eat birds and animals that eat fish containing very low levels of mercury (about 1 part per million) have died from chronic mercury poisoning (104,160). Since mercury is an estrogenic chemical and reproductive toxin, the majority of the rest cannot reproduce. The average male Florida panther has higher estrogen levels than females, due to the estrogenic properties of mercury (105,160). Similar is true of some other animals at the top of the food chain like alligators, which are affected by mercury and other hormone disrupting chemicals…
6. In addition to having estrogenic effects, mercury has other documented hormonal effects including effects on the reproductive system resulting in lowered sperm counts, defective sperm cells, and lowered testosterone levels in males; menstrual disturbances and infertility in women; and increased neurological problems related to lowered levels of neurotransmitters dopamine, serotonin, and noreprenephrine (4,9,38,104,105,107,140,141,275,276, 288,290,365,367,372).
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 vapourized). Mercury in solid form is not stable, having low vapour pressure and being subject to galvanic action with other metals in an oral environment (182,192,292,348,349), so that within 10 years up to half has been found to have been transferred to the and body of the host (34,35,182, & section III).
8. Elemental mercury vapour 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 (38,183, 282,287,360, section III). Mercury vapour rapidly crosses the blood-brain barrier (14,85,311) and placenta of pregnant women
Developmental, learning, and behavioural effects have been found from mercury vapour 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 waters. 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.
10. Studies have found that levels of exposure to the toxic metals mercury, cadmium, and lead have major effects on classroom behaviour, learning ability, and also in mental patients and criminals behaviour (3,160).
11. Long term occupational exposure to low levels of mercury can induce slight cognitive deficits, liability, fatigue, decreased stress tolerance, etc. Higher levels have been found to cause more serious neurological problems (119,128,285,etc.). Occupational exposure studies have found mercury impairs the body’s ability to kill Candida albicans by impairment of the lytic activity of neutrophils and myeloperoxidase in workers whose mercury excretion levels are within current safety limits (285). Such levels of mercury exposure were also found to inhibit cellular respiratory burst. A population of plant workers with average mercury excretion of 20 ug/ g creatinine was found to have long lasting impairment of neutrophil function. Another study (59) found such impairment of neutraphils decreases the body’s ability to combat viruses such as those that cause heart damage, resulting in more inflamatory damage. Another group of workers with average excretion rates of 24.7 ug/gcreatinine had long lasting increases in hormonal immunological stimulation of IgG, IgA, and IgM levels. Another study (285b) found that workers exposed at high levels at least 20 years previous (urine peak levels above 600 ug/L demonstrated significantly decreased strength, decreased coordination, increased tremor, decreased sensation, polyneuropathy, etc. 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 micronuclei 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 (23,35,37,38,142,241,361/241).
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 (217). The U.S. EPA Health Standard for elemental mercury exposure (vapour) is 0.3 micrograms per cubic meter of air (2). The U.S. ATSDR health standard (MRL) for mercury vapour is 0.2 ug/ M3 of air, and the MRL for methyl mercury is 0.3 ug/kg body weight/day (217). For the average adult breathing 20 M3 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.
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 (192). Mercury in solid form is not stable due to low vapour pressure and evapourates continuously from amalgam fillings in the mouth, being transferred over a period of time to the host (15-
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 University 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. 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.
[(1).] 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, type of toothpaste used, etc.
The Tubingen study did not assess the significant exposure route of intraoral air and lungs. One study that looked at this estimated 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. Another study found similar results (83), 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 Government health guidelines for workplace exposure.
(2). The studies also determined that the number of fillings is the most important factor related to mercury level, with age of filling being much less significant (319b). Different filling composition/manufacturer can also make a difference in exposure levels (as will be further discussed). The authors of the Tubingen study calculated that based on the test results with estimates of mercury from food and oral air included, over 40 % of those tested in the study received daily mercury exposure higher than the WHO standard (PTWI). As can be seen most people with several fillings have daily exposure exceeding the Health Canada TDE and the U.S. EPA and ATSDR health guideline for mercury (2,209,199,etc.), and many tested in past studies have exceeded the older and higher WHO guideline for mercury (183), without consideration of exposure from food, etc..
(3). The main exposure paths for mercury from amalgam fillings are absorption by the lungs from intraoral air; vapour absorbed by saliva or swallowed; amalgam particles swallowed; and membrane, olfactory, venous, and neural path transfer of mercury absorbed by oral mucosa, gums, etc. (6,17,18,31,34,77,79,83,94,133,182,209,211, 216,222,319, 335,348,364) A study at Stockholm Uni. (335) made an effort to determine the respective parts in exposure made by these paths. It found that the majority of excretion is through faeces faeces, and that the majority of mercury exposure was from elemental vapour. Daily exposure from intraoral air ranged from 20 to 125ug of mercury vapour, for subjects with number of filling surfaces ranging from 18 to 82. Daily excretion through faeces amounted to from 30 to 190 ug of mercury, being more variable than other paths. Other studies had similar findings (6,15,16,18,19,25,31,36,79,80,83,115,196,386.)
The faeces mercury was essentially all-inorganic, with particles making up at most 25%, and the majority being mercury sulfuhydryl compounds- likely originating as vapour. Their study and others reviewed found that at least 80% of mercury vapour 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 faeces. A review determined that approx. 20 % of swallowed mercury sulfhydryl compounds are absorbed in the digestive tract, but approx.. 60% of swallowed mercury vapour 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 faeces (111,252), but some mercury is also excreted though the kidneys in urine and in sweat. 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), the number of fillings was highly correlated with the mercury level in urine, mean= 7 ug/L. 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 bio-accumulates in the brain/CNS(301,274,327,329,348,18,19,85), liver, kidneys, (14,85) heart (59,205,348)), and oral mucosa (174,192) with the half life in the brain being over 20 years. Elemental mercury vapour 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 vapour than for other forms (360,370). While mercury vapour and methyl Hg readily cross cell membranes and the blood-brain barrier, once in cells they form inorganic mercury 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 (274,etc.).
(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 vapour from amalgam is the single largest source of systemic mercury intake for persons with amalgam fillings, ranging from 50 to 90 % of total exposure. (14,16,17,19,36,57,61,78-83,94,129,130,138,161,167,183, 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 faeces 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 faeces usually decline between 80 to 95% (79,196,335,386)
(5). Having dissimilar metals in the teeth (e.g.-gold and mercury) causes galvanic action, electrical currents, and much higher mercury vapour levels and levels in tissues. (182,192,292,348,349,390,19,25,27,29,30,47,48,100)
Average mercury levels in gum tissue near amalgam fillings are about 200 ppm, and are the result of flow of mercury into the mucous membrane because of galvanic currents with the mucous membrane serving as cathode and amalgam as cathode (192). Average mercury levels are often 1000 ppm near a gold cap on an amalgam filling due to higher currents when gold is in contact with amalgam (30,25,35,48,58). These levels are among the highest levels ever measured in tissues of living organisms, exceeding the highest levels found in chronically exposed chloralkali workers, those who died in Minamata, or animals that died from mercury poisoning. 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). These levels are much higher than the FDA/EPA action level for prohibiting use of food with over 1 ppm mercury. Likewise the level is tremendously over the U.S. Dept. of Health/EPA drinking water limit for mercury which is 2 parts per billion (218). Studies have shown that mercury in the gums such as from root caps for root canaled teeth result in chronic inflammation, in addition to migration to other parts of the body (200,47). 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 macrophasges, multinucleated giant cells, endothelial cells, and fibroblasts. There is, in most cases chronic inflammatory response or macrophagic reaction the metals (47), usually in the form of a foreign body granuloma with multinucleated giant cells of the foreign body and Langhans types.
[(6).] The component mix in amalgams has also been found to be an important factor in mercury vapour 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 greater release of mercury vapour than conventional silver amalgams (298,299). 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 instable 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 been found to be a factor in the much higher release of mercury vapour 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). 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)
(7). Faeces is the major path of excretion of mercury from the body, having a higher correlation to systemic body burden than urine or blood, which tend to correlate with recent exposure level (35,36,79,80,183, 278). For this reason many researchers consider faeces to be the most reliable indicator of daily exposure level to mercury or other toxics. The average level of mercury in faeces of those with fillings is over 1 ppm and approx. 10 times that of a similar group without fillings (79,80,83,335,386,25,), with significant numbers of those with several filings having over 10 ppm and 170 times those without fillings (80). The saliva test is another good test for daily mercury exposure, done commonly in Europe and representing one of the largest sources of mercury exposure.
There is only a weak correlation between blood or urine mercury levels and body burden or level in a target organ (36,157,183,278,11,etc.). Mercury vapour passes through the blood rapidly (half-life in blood is 3 seconds, 370) and accumulates in other parts of the body such as the brain, kidneys, liver, thyroid gland, pituitary gland, etc. Thus blood test measures mostly recent exposure. As damage occurs to kidneys over time, mercury is less efficiently eliminated (11,36,57,183, 216,260), so urine tests are not reliable for body burden after long-term exposure. Some researchers suggest hair offers a better indicator of mercury body burden than blood or urine (279), though still not totally reliable and may be a better indicator for organic mercury than inorganic. Mercury hair levels in a population sampled in Madrid Spain ranged from 1.3 to 92.5 ppm. This study found a significant positive correlation between maternal hair mercury and mercury level in nursing infants. Hair mercury levels did not have a significant correlation with urine mercury in one study (340) and did not have a significant correlation to number of fillings (350). One researcher suggests that mercury levels in hair of greater than 5 ppm are indicative of mercury intoxication.
A new test approved by the FDA for diagnosing damage that has been caused by toxic metals like mercury is the fractionated porphyrin test (260), that measures amount of damage as well as likely source. Provocation challenge tests after use of chemical chelators such as DMPS or DMSA also are effective at measuring body burden (57), but 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. Challange 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). Several doctors use 16 ug/L as the upper bound for mercury after DMPS challange, consider anyone with higher levels to have excess body burdern (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. 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-acetylcystein (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). Also lipoic acid has been found to dramatically increase excretion of inorganic mercury (over 12 fold), but to cause decreased excretion of organic mercury (54).
(8). The number of amalgam surfaces has a statistically significant correlation to:
(a) blood plasma mercury level (17,49,79,89,133,211) (usually not as strong as other measures)
(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 (18,58,77,79,117,179,174,199,211,222,292,315,317)
(e) faeces mercury (25,79,80,83,115,117,182,335,386)
(f) pituitary gland (19,20,25,85,99,273/274)
(g) brain occipital cortex (14,16,19,25,34,85,211,273,348,366/274)
(h) renal (kidney) cortex(14,16,19,20,85,273,348,366)
(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,etc.)
(k) fetal and infant liver/brain levels (61,112,186,231) related to maternal fillings.
(9). A person with amalgam fillings has daily systemic intake from mercury vapour 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, 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).
Vapour emissions range up to 200 ug/M3 (35) and are much higher after chewing (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 over10 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)
(10). 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 vapour 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).
(11). Teeth are living tissue and have massive communication with the rest of the body via blood, lymph, and nerves. Mercury vapour (and bacteria in teeth) have paths to the rest of the body. (34,etc.) German studies of mercury loss from vapour 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).
(12). Mercury (especially mercury vapour) rapidly crosses the blood brain barrier and is stored preferentially in the pituitary gland, hypothalamus, 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).
(13). 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 fibres (5,25,34,35,327,329).
(14). 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.)
(15). Methyl mercury is more toxic to some body processes than inorganic mercury. Mercury from amalgam is methylated by bacteria and candida albicans, in the mouth and in the intestines (51,81,98,182,225). Oral bacteria streptococommus mitior, S.mutans, and S.sanguis were all found to methylate mercury (81). High levels of Vitamin 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 vapour 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).
(16). 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 and placenta was higher than that in mother’s blood (22,186). The saliva and faeces of children with amalgams have approximately 10 times the level of mercury as children without (25,315,386), 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), 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 (279). One study found a 60% increase in average cord blood mercury level between 1980 and 1990 in Japan (186).
(17). 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). The level of mercury in breast milk was found to be significantly correlated with the number of amalgam fillings (61), 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 potenital 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, immune, and reproductive systems. The fetal mercury content after maternal inhalation of mercury vapour was found to be approx. 40 times that for maternal exposure to an equivalent dose of inorganic mercury (281,287), and developmental behavioral effects from vapour 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 (22,279).
(18). There is a significant correlation between number of amalgam fillings of the mother and the level of the fetus and older infants (20,23,61,304), and also with the level in mother’s milk (19,20,38,112, 304). Fertile women should not be exposed to vapour levels above government health guidelines (38,61,182,282); the U.S. ATSDR mercury health MRL of 0.2 mcg/M3 (2,217); or have amalgams placed or removed during pregnancy (20,182,231,304,etc.).
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, headaches, chronic skin problems, metallic taste, gastrointestinal problems, asthma (8,97), stuffy nose, dry crusts in nose, rhinitis, plugged ears, ringing ears, chest pain, hyperventilation, diabetes, spacy feeling, chilly, chronic skin problems, immune and autoimmune diseases, cardiovascular problems and many types of neurological problems (26,34,35,36,38,45,59,60,69,70,71,75,91,109,148,165,204,212,199,246,255,268-270,290,291,294, 313,343). Amalgam results is 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 vapour exposure at very low levels adversely affects the immune system (17,27,31,38,45,60,84,118,129, 131,165,226,270,285,296,313,355368,369). From animal studies it has been determined that mercury damages T-cells by generating reactive oxygen species (ROS), depleting the thiol reserves of cells, damaging and decreasing the dimension of mitochondria, causing destruction of cytoplasmic organelles with loss of cell membrane integrity, inhibiting ability to secrete interleukin IL-1 and IL-2R, and in activating or inhibiting enzyme systems involving the sulphydrol protein groups (226). 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, and auto-immunity (181). One study found that insertion of amalgam fillings or nickel dental materials causes a supression of the number of T-lympocytes (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, inflamatory 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 (226). 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 immontoxic 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 functins 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 reduct in cellular glutathione when exposed to mercury, inhibiting generation of GSH by lumpocutes 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 neutraphils to kill invaders such as candida (285). Low doses also induced autoimmuntiy in some species (181,226,314,404,131,129,43). Another 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 (198,38). Several studies found adverse health effects at mercury vapour levels of 1 to 5 mcg/M3 (35). 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 surveryed (Section VI).
3. Mercury from amalgam interferes with production of cytokines, disabling early control of viruses and leading to enhanced
infection (131,251). 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.
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 follow up antibiotics) (251,131). Similar results have been found for treatment of cancer.
5. Mercury by its effect of weakening the immune system contributes to increased chronic diseases and cancer (91,180,237,239,222,234,355,38,40,etc,). Exposure to mercury vapour causes decreased zinc and methionine availability, depresses rates of methylation, and increased free radicals-all factors in increased suscepability to cancer (14,34,38,143,144,180,237,239,251,256,283). Amalgam fillings have also been found to be positively associated with mouth cancer (206,251,403).
6. Among a group of patients testing positive as allergic to mercury, low level mercury exposure was found to cause adverse immune system response, including reduction of in vitro production of tumour necrosis factor TNF alfa and interleukin-1. (152) Mercury also interrupts the cytochrome oxidase system, blocking the ATP energy function (35,232) 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).
7. 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. 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 (60,118,313,81,90,212,313,342,368,369,374,375), including to mercury preservatives such as thimersol. 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 pheny lHg, which has been commonly used in root canals and cosmetics (313). 10% of controls had significant immune reactions to HgCl and 8.3% to palladium. Removal of amalgam fillings usually results in cure of such lesions. (46,60,75,78,82, 86, 87,90,94,101,118,133,168,313). Other studies of patients suffering from chronic fatigue found similar results (374,375). Of 50 patients suffering from serious fatigue referred for MELISA test (374), 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 (374,382). 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 psycholgical symtoms (379-382,385,374,375, 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 (374,60), such as found more frequently in patients with HLA-DRA antigens (383). A significant portion of the population appear to fall in this category.
8. Patients with other systemic neurological or immune symptoms such as arthritis, myalgia, eczema, CFS, MS, diabetes, etc. also often recover after amalgam replacement (60,212,313,342,368,369, 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 (342,368). The improvement in symptoms and lymphocute 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, was able to detect subjectively when a patch test used mercury salts in a double blind study (373).
Of the over 3,000 patients tested for lymphocyte reactivity to metals (342,368,375), the following were the percentages testing positive: nickel- 34%, inorganic mercury- 23%, phenol mercury- 13%, gold- 12%, cadmium- 11%, palladium- 11%, silver- 1%.
Other studies have also found relatively high rates of allergic reactions to inorganic mercury and nickel (81,etc.). For groups with suspected autoimmune diseases such as neurological problems, CFS, and oral lichen planus; most of the patients tested positive to inorganic mercury and most 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 Uppsula 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 (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.
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 amalgam fillings induce immune reactions in many patients (91,118)(270,286).
Mercury, nickel, palladium, and gold induce autoimmunity in genetically predisposed or highly exposed individuals (314,234,130342,).
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, 27,34,35,44,45,60,215,226,234,268,269,270, 313), including lupus (12,60,113), Chrons Disease, lichen planus (86,87,90,168), 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 (77,78,129,226,314).
11. Mercury exposure through fillings appears to be a major factor in chronic fatigue syndrome (CFS) through its effects on ATP and immune system (lymphocute reactivity, neutraphil activity, effects on T-cells and B-cells) and its promotion of growth of candida albicans in the body and the methylation of inorganic mercury by candida to the extremely toxic methyl mercury form which like mercury vapour crosses the blood-brain barrier and also damages and weakens the immune system (222,225,226,234,235,265,293,38,60,313,342,368,369,404). Mercury lymphocyte reactivity induces CFS type symptoms including profound tiredness, musculoskeletal pain, sleep distubances, gastrointestinal and neurological problems along with other CFS symptoms and fibromyalgia (342,368,369). Mercury appears to be a factor in fibromyalgia (293,369), and both inorganic and methyl mercury have been shown in animal studies to induce autoimmune reactions and disease through effects on immune system T cells (226,268,269,270/272.)
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, moodiness, depression, anger and sudden bursts of anger/rage, self-effacement, suicidal thoughts, lack of strength/force to resolve doubts or resist obsessions or compulsions, etc. Many studies of patients with major neurological diseases have found evidence amalgam fillings may play a major role in development of conditions such as depression (107,109,212,222,271,294,212,229,233, 317,320,322), schizophrenia (34,35,295), memory problems (212,222), and other more serious neurological diseases such as MS, ALS, Parkinson’s, and Alzheimer’s (see # 25).
(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 (333,329,56). Protein Kinase C (PKC) regulates intracellular and extra cellular singals across neuronal membranes, and both forms of mercury inhibit PKC at micromolar levels, as well as inhibiting phorbal ester binding (43). They also block or inhibit calcium L-channel currents in the brain in an irreversible and concentration dependent manner. Metallic mercury is much more potent than methyl mercury in such actions, with 50 % inhibitation in animal studies at 13 ppb (333,329).
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 (27,295) 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 liability, headache, fatigue, loss of sexual drive, depression, etc. are often mistakenly ascribed to psychogenic causes.. 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.)
Animal studies of developmental effects of mercury on the brain have found significant effects at extremely low exposure levels, levels commonly seen in those with amalgam fillings or in dental staff working with amalgam. One study (175) found mercury vapour decreased NGF concentration in rat’s forebrain at 4 parts per billion (ppb) tissue concentration. Another study (134) found general toxicity effects at 1 micromole (uM) levels in immature cell cultures, increased immunore activity for glial fibrillary protein at 1 nanamole (0.2 ppb) concentration, and microglial response at even lower levels. Other animal studies on rodents and monkeys have found brain cellular migration disturbances, behavioural changes, along with reduced learning and adaption capacity after low levels of mercury vapour exposure (210,264,287,149). The exposure levels in these studies are seen in the fetus and newborn babies of mother’s with amalgam fillings or who had work involving amalgam during pregnancy (61).
Epidemiological studies have found that human embryos are also highly susceptible to brain damage from prenatal exposure to mercury. 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, 305,259,210,149,305,24/39,175,255,149). Exposure of developing neuroblastoma cells to sub-cytotoxic doses of mercuric oxide resulted in lower levels of neurofilament proteins than unexposed cells (305). Mercury vapour exposure causes impaired cell proliferation in the brain and organs, resulting in reduced volume for cerebellum and organs and subtle deficiencies (38,305). 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). 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 (23,38,287,10).
(4.) Numerous studies have found long-term chronic low doses of mercury cause neurological, memory, behaviour, sleep, and mood problems (3,34,60,69,70,71,74,107, 108,109,119,140,141,199,212,222,246,255,257, 258,282,290). 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). 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 behavioural problems than the control groups.
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. Controls without CNS problems did not have such positive correlations. Mercury, nickel, palladium, and gold induce autoimmunity in genetically predisposed or highly exposed individuals (314,234,130342,). 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).
(5.) Mercury binds to hemoglobin in the red blood cells thus reducing oxygen carrying capacity (332,35), adversely affects the vascular response to norepinepherin and potassium, 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) 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. (201,202,205,212,222,306,310,35). Mercury also interrupts the cytochrome oxidase system, blocking the ATP energy function (35,232) 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). Mercury also accumulates in the heart and damages myocardial and heart valves (Turpayev, in (35)) & (59,201,205,306,351,370). 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 and root canals also can cause high porphyrins.
(6.) 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 per cent 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, and systemic effects (34,38,61,149,186,226,263,264,270,272,296,305,410-412/357).
(7.) People with amalgam fillings have an increased number of intestinal microorganisms resistant to mercury and many standard antibiotics. (35,116,117,161,389) Recent studies have found that drug resistant strains of bacteria causing ear infections, sinuitis, 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).
(8.) Mercury from amalgam binds to the -SH (sulphydryl) groups, resulting in inactivation of sulphur and blocking of enzyme function, producing sulphur metobolites with extreme toxicity that the body is unable to properly detoxify (33,114). Sulphur is essential in enzymes, hormones, nerve tissue, and red blood cells. These exist in almost every enzymatic process in the body. Blocked or inhibited sulphur oxidation at the cellular level has been found in most with many of the chronic degenerative diseases, including Parkinson’s, Alzheimer’s, ALS, lupus, rheumatoid arthritis, MCS, autism, etc. Mercury also blocks the metabolic action of manganese and the entry of calcium ions into cytoplasm (333). Mercury from amalgam thus has the potential to disturb all metabolic processes (25,21,33, 35,56,60,111,180,194,197}. Mercury is transported throughout the body in blood and can affect cells in the body and organs in different ways.
(9.) 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/alopechia after amalgam removal and detox (40,317). Another study in Japan found significantly higher levels of mercury in grey hair than in dark hair (402).
(10.) Mercury accumulates in the kidneys with increasing levels over time. One study found levels ranging from 21 to 810 ppb. Mercury exposure has been shown to adversely affect kidney function in occupational and animal studies (20,203,211,260,etc.), and also in those with more than average number of amalgam fillings (254)… 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 s lysomomes that maintain transmembrane proton gradient, and to decrease glutathione peroxidase activity in the kidneys while up-regulating 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.
(11.) Amalgam fillings produce electrical currents which increase mercury vapour release and may have other harmful effects (19,27,28,29,30,35,100,192,194). These currents are measured in 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 crown appear to cause higher mercury vapour losses (35). Some studies have also found persons with chronic exposure to electromagnetic fields (EMF) to have higher levels of mercury excretion (28).
(12.) Mercury from amalgam fillings is transferred to the fetus of pregnant women and children who breast feed at levels often 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 (10,23,38,197,210,287,361). Mercury vapour exposure causes impaired cell proliferation in the brain and organs, resulting in reduced volume for cerebellum and organs and subtle deficiencies (38,305).
(13.) 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,etc.), mercury can reduce reproductive function and cause birth defects and developmental problems in children (2,4,9,10,20,23,24,31,37,38,39,41,55,61,104,146,159, 162,224,255). 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 (9,105,146,159,395,27,35,38).
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).
Subfertile males in Hong Kong were found to have 40% more mercury in their hair than fertile controls (55). Studies in monkeys have found decreased sperm motility, abnormal sperm, increased infertility and abortions at low levels of methyl mercury (162,365).
Researchers advise pregnant women should not be exposed to mercury vapour 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 childbearing age.
(14.) Mercury causes breaks in DNA (4,38,41,42,197,272,296). 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).
(15.) Mercury has been well documented to be an endocrine system disrupting chemical in animals and people, disrupting function of the pituitary gland, hypothallamus, thyroid gland (50,369), enzyme production processes (111,194,33,56), and many hormonal functions at very low levels of exposure (9,105,146, 210, 312,369).
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(105,312). The hypothallamus regulates body temperature and many metabolic processes. Mercury damage thus commonly results in poor bodily temperature control, in addition to many problems caused by hormonal imbalances. Such hormonal secretions are affected at levels of mercury exposure much lower than the acute toxicity effects normally tested. Mercury also damages the blood brain barrier and facilitates penetration of the brain by other toxic metals and substances (311). Low levels of mercuric chloride also inhibit ATPase activity in the thyroid, with methyl mercury inhibiting ATP function at even lower levels (50). Both types of mercury were found to cause denaturing of protein, but inorganic mercury was more potent. These effects result commonly in a reduction in thyroid production (50) and an accumulation in the thyroid of radiation. Toxic metal exposure’s adverse influence on thyrocytes can play a major role in thyroid cancer etiology (144). Among those with chronic immune system problems with related immune antibodies, the types showing the highest level of antibody reductions after amalgam removal include thyreoglobulin and microsomal thyroid antigens (91)
(16.) 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).
(17.) 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(27,122,257,289,372). 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, and MS.
Such patients have abnormal inhibition of neurotransmitter production. Such symptoms improved for some patients after administration of 5-formyltetrahydrofolate or tyrosine (257).
(18.) 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).
(19.) 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 Alzheimer’s (66,67,158,166,204, 207,221,238,242,244,257,295,300),
ALS(92,97,325), MS(102,163,170,183,184,212,285,291,302,324,326), Parkinson’s(98,169,248,250,258,363,56,84),etc. Mercury
exposure causes high levels of oxidative stress/reactive oxygen species(ROS)(13), which has been found to be a major factor in neurological disease (56). 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 congugates are found to be highest in the brain substantia nigra with similar congugates formed with L-Dopa and dopamine in Parkinson’s disease(56). Mercury depletion of GSH and damage to cellular mitochrondria and the increased lipid perxodation in protein and DNA oxidation in the brain appear to be a major factor in Parkinson’s disease (33). One study found higher than average levels of mercury in the blood, urine, and hair of Parkinson’s disease patients (363). Another study (169) found blood and urine mercury levels to be very strongly related to
Parkinson’s with odds ratios of approx. 20 at high levels of Hg exposure. Another study (145) that reveiwed occupational exposure data found that occupational exposure to manganese and copper have high odds rations for relation to PD, as well as multiple exposures to these and lead, but noted that this effect was only seen for exposure of over 20 years…
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). There is considerable indication this may be a factor in ALS development (48,325,405). 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).
MS patients have been found to have much higher levels of mercury in cerebrospinal fluid compared to controls (163,35,139). 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 dyes biopsies. Studies have found mercury related mental effects to be indistinguishable from those of MS
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(122,257,289,372).
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).
Clinical tests of patients with MND, ALS, Parkinson’s, Alzheimer’s, Lupus (SLE), and rheumatoid arthritis have found that the patients generally have elevated plasma cysteine to sulphate ratios, with the average being 500% higher than controls (330,331,56), and in general being poor sulphur oxidizers. Mercury has been shown to diminish and block sulphur oxidation and thus reducing glutathione levels which is the part of this process involved in detoxifying and excretion of toxics like mercury (33). Glutathion is produced through the sulphur oxidation side of this process. Low levels of available glutathione have been shown to increase mercury retention and increase toxic effects (111), while high levels of free cysteine have been demonstrated to make toxicity due to inorganic mercury more severe (333,194,56). Mercury has also been found to play a part in neuronal problems through blockage of the P-450 enzymatic process (84).
(20.) 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), and low levels of zinc (363). 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). 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. Persons with extra Apo-E4 gene copies are especially susceptible to this damage (207,221). 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). There is some evidence that some forms of leukaemia are abnormal response to antigenic stimulation by mercury or other such toxics and removal of amalgam has led to remission in some cases (35,38,180,239).
(21.) Mercury and methyl mercury impair or inhibit all cell functions and deplete calcium stores (96). This can be a major factor in bone loss of calcium (osteoporosis).
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.
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).
3. Total reduction in mercury levels in blood and urine is often over 80% within a few months (79,82,89,93,115,57).
4. 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 (40,46,57,60,75,78,82,86,87,90,
94,95,100,101,115,133,168,212,222,233,271,313,317,320,321,322,376), oral keratosis (pre cancer) (87,251), immune system/autoimmune problems (8,222,270,271,313,323,368,91,212,229,291,35,etc.), allergies (8,26,40,46,94, 95,97,165,212,222,228,229,233,271,317,322,349,376), asthma (8,75,97,222,228,271,322), chronic headaches/ migraines( 5,34,95,212
222,229,233,271,317,322,349,354,115,376), multiple chemical sensitivities (26,95,222,229,232,233, 35,115,313,320,368), epilepsy
(5,309,229), blood conditions (212,222,232,233,271, 35,95), eczema (60,212,222, 271,313,317,323,94,376,341), chron’s disease (222,229), stomach problems (95,212,222,228,229,233,271,317, 320, 322,35), lupus(12,113,222, 229,233), dizzyness/vertigo (40,95,212,222,271,322,376), arthritis(95,103,212, 222,271,313,322,358), MS (94,95,102,170,212,222,271,291,302,34,35,229), ALS (97,229,325,405,35), Parkinson’s/muscle tremor (222,248,229,271,212,94,98,35), Alzheimer’s (204), muscular/joint pain/fibromyalgia (222,293,317,322,369, 94), infertility (9,38,229,367), depression (94,107,222,271,294,212,229,233,317, 320,322, 376), schizophrenia (294,34,35), insomnia (94,212,222,271,317,322,376), anger (212,233, 320,102), anxiety & mental confusion (94,212,222,229,233,271,317,320,322,57), susceptibility to infections (40,222,251,317,349, 350), antibiotic resistant infection (251), endometriosis (229,38), Chronic Fatigue Syndrome (8,60,212,293,229,222, 232,233,271,313,317,320, 368,369,376), tachycardia and heart problems (205,59,94,115,212,222,232,233, 271,306,310,212), memory disorders (94,222), cancer/ leukaemia( 35,38,94,180), neuropathy/paraesthesia (94,212,222,322), vision disturbances (212,271,322), alopecia/hair loss (40,187,271,317,322,349), sinus problems (40,94,222,271,322), tinnitus (94,222,271,349,376), inflammation of eye (222,271,322), psoriasis (385,375,408), skin conditions (212,222), urinary/prostrate problems (212,222), etc., or in significant improvement in symptoms (35,38,40,57,78,86-91,93-
103,115,148, 165,168,170,180,182,185,199,204, 212,222,229,233, 234, 235,246, 271,282,289,312,317,320,321,322,323,376).
The above over 20,000 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 available and case histories. 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.
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.).
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, thyreeoglobulin, and microsomal thyroid antigens (91)
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, MS, etc. related to mercury and other immunotoxics (60,313).
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. Health Effects from Dental Personnel Exposure to Mercury Vapour
1) It is well documented that dentists and dental personnel who work with amalgam are chronically exposed to mercury vapour, 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 (57,64,69,99,123,124,138,171,173,222,249,290,362,397-399) and for blood (124,195,253,249,397).
Sweden, which has banned 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 to6.2 ug/L (124,172,253,64,68). The Swedish safety guideline for mercury in urine is 5.6 nmol Hg/mmol (11.6 ug/L). Study averages for other countries ranged from 3.3 to 36 microgram/litre (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), indicating daily exposure levels of over 100 ug/day. 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(57,69,290,303). 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). 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). 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. Another group of dental students had similar results (362), while another group of dental student showed comprimized immune systems compared to medical students. The total lymphocyte count, total T cell numbers (CD3), T helper/inducer (CD4), and T suppressor/cytotoxic (CD8) numbers were significantly elevated in the dental students compared to the matched control group (407).
Urinary porphyria profiles were found to be an excellent biomarker of level of body mercury level and mercury damage neurological effects, with coprorphyrin 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.
The U.S. ATSDR mercury vapour 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 vapour and respirable particles, and dental masks to only filter out about 40 % of such particles (219,247). This produces high levels of exposure to patient and dental staff. 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 facemasks and patients be supplied with outside air (120,153). Some studies note that carpeting in dental offices should be avoided as it is a major repository of mercury (188,7).
Use of such measures along with a Clean-UpTM 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 visual-motor coordination (69,70,123,249,290,395), concentration, verbal memory, visual memory (68,69,70,249,290,395), and emotional/mood tests (70,249,290,395).
Test performance was found to be proportional to exposure/body levels of mercury (68,70,249,290,395). Significant adverse neurobehavioral effects were found even for dental personnel receiving low exposure levels (less than 4 ug/l Hg in urine)(290).
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.
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(290). 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 theshhold 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.
Several dentists have been documented to suffer from mercury poisoning (72,74,193,246,247,248,374), other than the documented neurological effects. 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. (249,374.377.378). 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 (374). Tests of controls did not find such immune reactions common. 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 vapour and anaesthetics found increased health problems compared to controls, including significantly higher liver, kidney, and neurological diseases(99,193). Other studies reviewed found increased rates of brain cancer and allergies (99,193). 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 vapour 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).
4.) Both dental hygienists and patients get high doses of mercury vapour when dental hygienists polish or use ultrasonic scalars on amalgam surfaces (240,400). 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. (23,37,38,110,142,146,19,31). 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 vapour (247,). Dental staff have been found to have significantly higher prevalence of eye problems, conjunctivitis, atopic dermatitis, and contact urticarial (247,156,74).
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 (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, visio-motor, mood, and behavioural problems, which increase with years of exposure (1,34,68-73,88,123,188,246,247,248,249,290,374,395).
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), high rates of drug dependancy and disability due to psychological problems (15), and higher suicide rates than the general white population (284), 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 (10,38,277), and their children have significantly lower average IQ compared to the general population (1,279,38,110). 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). Several dental assistants have been diagnosed with mercury toxicity and some have died of related health effects (32,245,246,247,248).
Female dentists have increased rates of spontaneous abortion and perinatal mortality(193,38,10)), 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).
VIII. 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 thresh hold 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, Great Britain, France, Austria, Norway, Sweden, Japan, Australia, New Zealand, etc.
A Swedish National Mercury Amalgam Review Panel found that “from a toxicological point of view, mercury is too toxic to use as a filling material” (164). 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 coutries (387). A Swedish medical panel unanimously recommended to the government .discontinuing the use of amalgam as a dental material.(282). The U.S. EPA found that removed amalgam fillings are hazardous and must be sealed airtight and disposed 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, 36,38,57,60,61,88,94,99,125,148, 153,164,170,183,208, 209,210,212,222, 227,236, 238,282).
( 3. ) The use of mercury amalgams has been banned for children and women of childbearing 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.
(1) Denton S (MD); & Butler J; Proceedings of the First International Conference on Biocompatibility, Life Sciences Press, Oct 1990, p133-145.
(2) U.S. Environmental Protection Agency (EPA), 1999, “Integrated Risk Information System, National Centre for Environmental Assessment, Cincinnati, Ohio, http://www.epa.gov/ncea/iris.htm.
(3) Marlowe M et al, Main and interactive effects of metallic toxins on classroom behaviour., 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 Spermatogenesis., J Pharmacol Exp Thera 1975, 194(1);171- 181; & H. Ogura et al, . 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.
(6) T.M.Schulein et al,. Survey of Des Moines area dental offices for Mercury vapour., Iowa Dent. J. 70(1):35-36 1984; & D.W. Jones et al, .Survey of Mercury vapour 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 vapour in Manitoba dental offices., J Can. Dent. Assoc. 50(7):517-522, 1984; & Facts about Mercury and Dental Amalgam
(with Medical Study References) 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..
(7) L.Kantor et al,.Mercury vapour in the dental office-does carpeting make a difference?., JADA 103(9):402-407,1981; & G.F.Chop et al, .Mercury vapour related to manipulation of amalgam and to floor surfaces. .Oper. Dent. 8(1):23-27,1983; & G.C.Battistone et al, .Mercury as Occupational Hazard in Dentistry., Clinical Chemistry and Chemical Toxicity of Metals, 1977,219:205-8.
(8) Redhe,O. Sick From Amalgam R-Dental Ab, Frejavagen 33, S-79133 Falun, Sweden(100 cases).Olle Redhe; [firstname.lastname@example.org]
(9) Dr.I.Gerhard, Dr. E.Roller,et al, Tubingen Univ. Gynaecological Clinic, Heidelberg,1996; & .Heavy Metals and Fertility., J of Toxicology and Environmental Health, Part A, 54(8):593-611, 1998; & .Impact of heavy metals on hormonal and immunological factors in women with repeated miscarriages., & I. Gerhard, .Ganzheitiche Diagnostik un Therapie bie Infertilitat., Erfahrungsheilkunde,1993, 42(3): 100-106; & .Unfruchtbarkeit bei Frauen durch Umweltgifte. in Pravention, Diagnose und Therapie von Umwelterkrankungen, JD Kruse-Jarres(Ed.), 1993, p51-68.
(10) Editorial, J California Dental Assoc., 1984, 12:37.; & 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).
(11) Lamm O et al, .Subclinical effects of exposure to inorganic mercury revealed by somatosensory-evoked potentials. Eur Neurol, 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 vapour revealed by a multimodality potential study of chloralkali workers., Immunol, 1999, 117(3):482-8.
(12) Dimaval Scientific monograph, sixth Ed., Jan 1997, Dr Johann Ruprecht, Heyl Corporation
(13) 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; & S.Tan et al, .Oxidative stress induces programmed cell death in neuronal cells., J Neurochem, 1998, 71(1):95-105. & J.S. Bains et al, .Neurodegenerative disorders in humans and role of glutathione in oxidative stress mediated neuronal death., Brain Res Rev, 199, 25(3):335-58; & 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 Radical Biol Med 1995; 18(2): 321-36.
(14) Magnus Nylander, .Mercury Concentrations in the human brain and kidneys in relation to exposure from dental amalgam fillings., Proceedings, ICBM 1988; & M.Nylander et al, “Mercury concentrations in the human brain and kidneys and exposure from amalgam fillings”, Swed Dent J 1987; 11:179-187, & Prosth Dent 1987, 58:704-707; & Schupp, Riedel et al, .Amalgamfullungen auf die Quecksilberkonzentration in menschlichen., Organen.Dt.Zahnarztl.Z. 1992; 47:490-496.
(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.
(16) K. Ott et. al. Mercury burden due to amalgam fillings. Dtsch. Zahnarztl Z 39(9):199-205, 1984; &
(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.
(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.
(19) Matts Hanson. Dept. of Zoophysiology, University of Lund, Sweden. .Amalgam hazards in your teeth., J. Orthomolecular Psychiatry 1983; 2(3): 194-201; & F.L.Lorscheider et al, .Evaluation of the safety issue of mercury release from amalgam fillings., 1993, FASEB J, 7:1432-33.
(20) 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, University of Calgary, Calgary Alberta Canada, 1990 & Amer.J.Physiol.,1990, 258:R939-945; & 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.- & L.Hahn et al, Distribution of mercury released from amalgam fillings into monkey tissues., FASEB J.,1990, 4:5536
(21) R.A.Goyer,.Toxic effects of metals.in: Cassarett and Doull.s Toxicology- The Basic Science of Poisons, McGraw-Hill Inc., N.Y.,
(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
(23) W.D.Kuntz .Maternal and chord blood mercury background levels; Longitudinal surveillance.. Am J Obstet and Gynecol. 143(4): 440-443., 1982
(24) J.B. Brodsky, .Occupational exposure to Mercury in dentistry and pregnancy outcome., JADA111(11):779-780., 1985
(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 & C.Malmstrom, .Amalgam derived mercury in faeces., Journal of Trace Elements in Experimental Medicine, 5, (Abs122), 1992; Nylander et al. Fourth international symposium Epidemiology in Occupational Health. Como Italy Sept 1985
(26) A.F.Zamm, .Removal of dental mercury: often an effective treatment for very sensitive patients., J Orthomolecular Med, 1990, 5(53):138-142. (22 patients)
(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; & 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. Sounders and Company, Philadelphis, 1998; & U.S. EPA, Office of Health and Environmental Assessment, Mercury Health Effects, Update Health Issue Assessment, Final Report, 1984, EOA-600/8-84f.
(28) F.Schmidt et al, .Mercury in urine of employees exposed to magnetic fields., Tidsskr Nor Laegeforen, 1997, 117(2): 199-202; & Sheppard AR and EisenbudM., Biological Effects of electric and magnetic fields of extremely low frequency. New York university press. 1977
(29) 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.
(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 vapour (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 Surgury, 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) S.C. Langley-Evans et al, .SO2: a potent glutathione depleting agent., Comp Biochem Physiol Pharmocol Toxicol Endocrinol, 114(2):89-98; & (b)P.E. Emory et al, .Increased Prevalence of poor sulphuoxidation in patients with Rheumatoid Arthritis., Ann Rheum Dis, 1992, 51(3): 318-20; & (c) Markovich et al, “Heavy metals (Hg,Cd) inhibit the activity of the liver and kidney sulphate transporter Sat-1”, Toxicol Appl Pharmacol, 1999,154(2):181-7; & (d)2S.A.McFadden, .Xenobiotic metabolism and adverse environmental response: sulphur-dependent detox pathways.,Toxicology, 1996, 111(1-3):43-65;
(34) Patrick Störtebecker, 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-
(35) Hal Huggins, Its All in Your Head, 1997; & Proceedings: ICBM conf. Colorado, 1988; & Centre for Progressive Medicine, 1999, http://www.hugnet.com
(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) Mohamed et al. .Lazer Light Scatering Study of the Toxic Effects of Methylmercury on sperm motility.. J Androl.,7 (1):11-15.,1986; & A. Anttila et al, Finnish Inst. Of Occupational Health, .Effects of paternal occupation exposure on spontaneous abortion., J of Occup & Environ Med, 1995, 37(8):915-21.
(38) 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, Behavioural and neuropathological effects of prenatal methyl mercury exposure in mice.. Neurobeahv. Toxicol Teratol., 1985:7;227-232; & P.Grandjean et al, .MeHg and neurotoxicity in children., Am J Epidemiol, 1999, 150(3):301-5: & Z.Annau et al, Johns Hopkins Univ., School of Public Health, .Mechanisms of neurotoxicity and their relationships to behavioural changes., Toxicology, 1988, 49(2): 219-25; & S.D.Vanay et al, .CNS aryl sulfatases inhibited by methyl mercury., Pharmacol Toxicol, 1991, 69(1):71-4.
(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.
(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.
(43) B.Rajanna et al, .Modulation of protein kinase C by heavy metals., Toxicol Lett, 1995, 81(2-3):197-203: & A.Badou et al, .HgCl2-induced IL-4 gene expression in T cells involves a protein kinase C-dependent calcium influx through L-type calcium channels., & D.B.Veprintsev, 1996, Institute for Biological Instrumentation, Russian Academy of Sciences, Pb2+ and Hg2+ binding to alpha-lactalbumin..Biochem Mol Biol Int 1996 Aug;39(6):1255-65
(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, .Auto reactive 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 Dentaries et Allergies., J Biol Buccale., 1986 : 14; 83-100 (41 cases); & D.E. Swartzendruber, Med Hyptheses, 1993, v41,n1, p31-34.
(47) 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;& 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; & J.D. Harrison et al, Amalgam tattoos: light and microscopy and electronprobe micro-analysis; & T. Kanzaki et al, Electron microscopic X-ray microanalysis of metals deposited in oral mucosa. JDermatol 1992; 19(8):487-92; & K. Nilner et al, In vitro testing of dental materials by means of macrophage cultures. JBiomed Mater Res 1986;20(8):1125-38.
(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.
(49) A.Kingman et al, National Institute of Dental Research, .Mercury concentrations in urine and blood associated with amalgam exposure in the U.S. military population., Dent Res, 1998, 77(3):461-71.
(50) J.Kawada et al, .Effects of inorganic and methyl mercury on thyroidal function., J Pharmacobiodyn, 1980, 3(3):149-59.
(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.
(52) .Bacterial Growth on Dental Restorative Materials in Mucosal Contact.. Orstavic, Arneberg, Valderhaug Acta Odontol. Scand.1981, 39:267-274
(53) C. Thornsberry, MRL Services, Franklin, Tenn, Proceedings of Infectuous Diseases Soc. Of America, San Francisco, Ca., & USA Today, April, 1997; & Science News,Vol 155, June 5, 1999, p356.
(54) M.E. Lund et al, .Treatment of acute MeHg poisoning by NAC., J Toxicol Clin Toxicol, 1984, 22(1):31-49; & 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; Z.Gregus et al, .Effect of lipoic acid on biliary excretion of glutathione and metals., Toxicol APPl Pharmacol, 1992, 114(1):88- 96; & & J.F. Balch et al, Prescription for Nutritional Healing., 2nd Ed., 1997.
(55) M.D.Dickman et al, .Hong Kong subfertility links to mercury in human hair and fish., Sci Total Environ, 1998,214:165-74.
(56) X.M.Shen et al, Neurolbehavioral 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; & A.Nicole et al, .Direct evidence for glutathione as mediator of apoptsosis in neuronal cells., Biomed Pharmacother, 1998; 52(9):349-55; & J.P.Spencer et al, .Cysteine & GSH in PD., mechinsms involving ROS., J Neurochem, 1998, 71(5):2112-22: & P.Jenner,.Oxidative mechanisms in PD., Mov Disord, 1998; 13(Supp1):24-34; & D. Offen et al, .Use of thiols in treatment of PD., Exp Neurol, 1996,141(1):32-9; & A.D.Owen et al, Ann NY Acad Sci, 1996, 786:217-33; & JJ Heales et al, Neurochem Res, 1996, 21(1):35-39.
(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) 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.
(59) A. Frustaci et al, .Marked elevation of mycardial 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.
(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.
(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) W. Kostler., President of the Austrian Oncology Society. Paper presented at the World Congress on Cancer. April 1994 Sydney Australia.
(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. 1991May-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 Reseach, Seattle, “Behavioral Effects of Low Level Exposure to Hg vapour 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; D.G. Mantyla et al, “Mercury toxicity in the dental office: a neglected problem”, JADA, 92:1189-1194, 1976.
(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 vapour., 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. Amalagam allergy associatiated 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.
(76) A. Schulte et al, “Mercury Concentrations in Children with and without Amalgam Restorations”, J.Dent Res 73(4): 980 A-334; & Schweiz Monatsschr Zahnmed, 1994,104(11):1336-40..
(77) I.Skare, “Mass Balance and Systemic Uptake of Mercury Released from Dental Fillings”, Water, Air, and Soil Pollutio, 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 Faeces after Removal of Amalgam Fillings”, Toxicology and Applied Pharmacology, 1997, 144(1), p156-62; & (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.
(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.
(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.
(86) 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).
(87) 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)
(88) M.E.Godfrey, .Chronic alilments related to amalgams., J.Adv Med,1990, 3:247
(89) 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 hypersensitity, …”, 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.
(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 Sci1996, 104:320-321; & R. Stromberg et al, “A case of unusually high mercury exposure from amalgam fillings”, Tandlakartidningen 88 (10): 570-572, 1996; & 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
(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)
(95) H.J.Lichtenberg, “Elimination of symptoms by removal of dental amalgam from mercury poisoned patients”, J Orthomol Med 8:145-148, 1993; & .Symptoms before and after removal of amalgam.,J of Orth Med,1996,11(4):195- (119cases)
(96) 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, & N.Vanacore et al, Dirparimento di Scienze Neurologiche, University La Sapienza, Roma, Med Lav (Italy), 1995, Nov, 86(6): 522-533.
(98) A.Seidler et al, Possible environmental factors for Parkinson’s disease”, Neurology 46(5): 1275- 1284, 1996; & F.O.Vroom et al, “Mercury vapour 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, .Theraputic properties of Unitihiol. Farm. Zh. 1980, 1: 18-22.
(99) M.Nylander et al, Mercury accumulation in tissues from dental staff and controls., Swedish Dental Journal, 13:235-243, 1989; & M.Nylander et al, Br J Ind Med 1991, 48(11):729-34; & .Mercury in pituitary glands of dentists., Lancet,442, Feb 26, 1986. (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 contitute 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,v142,n3, p191- , & .Mental health, amalgam fillings, and MS., Psychol Rep,1992, 70(3 Pt2), 1139-51; & T.Engalls, Am J Forensic Med Pathol, 4(1):1983, Mar, 55-61.
(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; M.Maretta et al, .Effect of mercury on the epithelium of the fowl testis., Vet Hung 1995, 43(1):153-6.
(105) T.Colborn(Ed.),Chemically Induced Atlerations in Functional Development, Princeton Scientific Press,1992; & . Developmental Effects of Endocrine-Disrupting Chemicals”, Eniron Heath Perspectives, V 101, No.5, Oct 1993; & B.Windham, “Health, Hormonal, and Reproductive Effects of Endocrine Disrupting Chemicals” (including mercury), Annotated Bibliography ,1996; & 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 Supply (2): 65-71; & Trachtenberg IM, Chronic effects of mercury in ogranisms. U.S. Dept. Of Health, Eductation, and Welfare, Publ 74-473, 1974,
(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 vapour”, 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 vapour., Occupat. Envir. Med., 1994, 51:35-41;& A.Sikora et al, .Evaluation of mental functions in workers exposed to metalic 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.
(111) T.W.Clarkson et al, “Billiary secretion of glutathione-metal complexes”, Fundam Appl Toxicol,1985,5(5):816-31; & D.Quig, Doctors Data Lab,”Cysteine metabolism and metal toxicity”, Altern Med Rev, 1998;3:4, p262-270, & J.de Ceaurriz et al, Role of gamma- glutamyltraspeptidase (GGC) and extracellular glutathione in disopition of inorganic mercury”,J Appl Toxicol,1994, 14(3): 201-; & W.O. Berndt et al, “Renal glutathione and mercury uptake”, Fundam Appl Toxicol, 1985, 5(5):832-9; & R.K. Zulups et al, J Toxicol Environ Health, 1995, 44(4): 385-99; D.Jay, .Glutathione inhibits SOD activity of Hg., Arch Inst cardiol Mex, 1998,68(6):457-61.
(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.
(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.
(114) M.Aschner et al, .Metallothioein induction in fetal rat brain by in utero exposure to elemental mercury vapour., Brain Research, 1997, dec 5, 778(1):222-32; & T.V. O.Halloran, .Transition metals in control Of gene expression., Science, 1993, 261(5122):715-25; & R.L.Matts et al, J Biol Chem, 1991, 266(19): 12695-702; & Matts RL, Schatz JR, Hurst R, Kagen R. Toxic heavy metal ions inhibit reduction of disulfid bonds. J Biol Chem 1991; 266(19): 12695-702; Boot JH. Effects of SH-blocking compounds on the energy metablolism in isolated rat hepatocytes. Cell Struct Funct 1995; 20(3): 233-8.
(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) A.O.Summers et al, Antimicrobial Agents and Chemotherapy, 37(4):825-834,1993; & The Physiologist 33(4), A-116,1990; & J. Wireman et al, Appl Environ Microbiol, 1997, 63(11):4494-503. & 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) C.Edlund et al, “Resistance of the Normal Human Microflora to mercury and antimicrobials”, Clin Infect Dis 22(6):944-950, 1996.
(118) Tibbling L, Stejskal VDM, et al, Immunolocial and brain MRI changes in patients with suspected metal intoxication”, Int J Occup Med Toxicol 4(2):285-294,1995.
(119) L.Ronnback et al, “Chronic encephalopaties induced by low doses of mercury or lead”, Br J Ind Med 49:233-240, 1992; & H.Langauer-Lewowicka,. Changes in the nervous system due to occupational metallic mercury poisoning. Neurol Neurochir Pol 1997 Sep-Oct;31(5):905-13; & Kim P, Choi BH. .Selective inhibition of glutamate uptake by mercury in cultured mouse astrocytes., Yonsei Med J 1995; 36(3): 299-305*. Facts about Mercury and Dental Amalgam (with Medical Study References)
(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.
(121) A.S.Rowland et al,.The Effect of Occupational Exposure to mercury vapour 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 personel”, 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) G. Hall, “Perspectives of Amalgam and Other Dental Materials”, European Acadamy Symposium Article, Ostzenhausen,Germany, April 29, 1994.
(126) K.R.Hoyt et al, .Mechanisms of dopamine-induced cell death and differences from glutamate Induced cell death., Exp Neurol 1997, 143(2):269-81; & P.Froissard et al, Universite de Caen, .Role of glutathione metabolism in the glutamate induced programmed cell death of neuronal cells. Eur J Pharacol, 1997, 236(1): 93-99.
(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, .Immunoglubuline 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. .
(130) S. Enestrom et al, “Does amalgam affect the Immune System?” Int Arch Allergy Immunol 106:180-203,1995.
(131) S.Ellermann-Eriksen et al, “Effect of mercuric chloride on macrophage-mediated resistance mechinisms against infection”, Toxicology, 93:269-297,1994; & M.Kubicka-Muranyi et al, .Systemic autoimmune disease induced by mercuric chloride., Int Arch Allergy Immunol;1996, 109(1):11-20 & M.M.Christensen et al, Institute o Medical Microbiology, .Comparision 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 evapouration rate from dental amalgam fillings”, Scand J Dent Res, 100(6): 354-360, 1992.
(136) 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 Mercuy Amalgam Fillings”, Ubl Hyg, 1990, 190: 325-
(139) G.Sallsten et al, .Mercury in cerebrospinal fluid in subjects exposed to mercury vapour., Environmental Research, 1994; 65:195-206.
(140) R.L.Siblerud, “Health Effects After Dental Amalgam Removal”, J Orthomolecular Med 5(2): 95 -106.
(141) L.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) M.E. Ariza et al, .Mercury mutagenisis., 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, “Carciagenicity 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) J.M.Gorell et al, .Occupational exposure to mercury, manganese, copper, lead, and therisk 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.
(146) 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.
(147) .M.Wood,”Mechinisms for the Neurotoxicity of Mercury”, in Organotransitional Metal Chemistry, Plenum Publishing Corp, N.Y, N.Y, 1987. & R.P. Sharma et al, .Metals and Neurotoxic Effects., J of Comp Pathology, Vol 91, 1981.
(148) H.R.Casdorph, Toxic Metal Syndrome, Avery Publishing Group, 1995.
(149) B.Choi et al, “Abnormal neuronal migration of human fetal brain”, Journal of Neurophalogy, Vol 37, p719-733, 1978; & 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.
(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.
(153) International Acadamy 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.
(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, J Amer Dent assoc, 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, .Prevelence 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 Methylmercury Exposure., Arch of Toxicology, 1994,65(5):317-321.
(158) Wenstrup et al, .Trace element imbalances in the brains of Alzheimers patients., Research, Vol 533,p125-131,1990; & F.L.Lorscheider,B.Haley,et al, .Mercury vapour inhibits tubulin binding…., FASEB J,9(4):A-3485.,1995 & & Vance et al, 1988, Neurotoxicology, 9:197-208; & l> de Saint-Georges et al, .Inhibition by mercuric chloride fo the in vitro polymeriztion 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 interacton 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..
(160) B.Windham, “Health Effects of Toxic Metals: An Anotated Bibliography”,1995.
(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 Methylmercury Exposure.,Health Perspect; vol63 :133-140,1985; & 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.
(163) Ahlrot-Westerlund B. Multiple Schlerosis and mercury in cerebrospinal fluid. Second Nordic Symposium on Trace Elements and Human Health, Odense, Denmark, Aug 1987; & Nutrition Research, 1985 Supplement .
(164) Swedish National Dept. of Health, Mercury Amalgam Review Panel, 1987.
(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; & .Contact allergy to dental restorative materials in patients with oral lichenoid lesions., Contact Dermatitis, 1997,36:3,141-6; & .Resolution of OLL after replacement of amalgam restorations., Br J Dermatol, 1992,126(1):10-15(20 casess); & A. Adachi et al, .Efficacy of dental metal elimination in the management of atopic dermatitis., J Dermatology,1997, 24:1,141-6;
(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) 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.
(171) A.Jokstad, .Mercury excretion and ocuupational exposure of dental personnel.,Community Dent Oral Epidemiology, Facts about Mercury and Dental Amalgam (with Medical Study References) 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) L.Larkfors et al,”Methylmercury induced alterations in the nerve growth factor level in the developing brain “, Res Dev Res,62(2),1991,287- ; & Soderstrom et al, .The effect of mercury vapour on cholinergic neurons in the fetal brain, Brain Research & Developmental Brain Res, 1995, 85:96-108; & Toxicol Lett 1995; 75(1-3):133-44.
(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
(177) S.Olsson et al, “Daily dose calculations from measurements of intra-oral mercury vapour”, J Dent Res, 71(2):414-23,1992.
(178) J.Lenihan et al, .Mercury hazards in dental practice., Br Dent J, 1973, 135: 363-376; & G.S.Nixon et al, J Oral Ther Pharm, 1965, 1: 512.
(179) A.Lussi,”Mercury release from amalgam into saliva”, Schweiz Monatsschr Zahnmed,1993, 103(6):722-
(180) Pinto OF et al, J Intl Acad Prev Med, Vol 3, No.2, 1976; & Y.Kinjo et al, .Cancer mortality in patients exposed to methylmercury 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; Parronchi P, Brugnolo F, Sampognaro S, Maggi E. Int Arch Allergy Immunol 2000 Jan;121(1):2-9. Genetic and Environmental Factors Contributing to the Onset of Allergic Disorders.
(182) 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.
(183) World Health Organization(WHO),1991, Environmental Health criteria 118, Inorgtanic Mercury, WHO, Geneva; & Envir. H. Crit. 101, Methyl Mercury;
(184) T.H.Ingalls, 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; & .Endemic clustering of MS., Am J.Fors Med Path, 1986,7:3-8
(185) L.Jones, .Health outcomes following amalgam removal., New Zealand Psychology Journal, Sept.,1999.
(186) J.Yang et al, .Maternal-fetal transfer of metallic mercury via the placenta and milk., Lab Sci, 1997,27(2):135-41; & C.N.Ong et al, “Concentrations of heavy metal in maternal and umbilical cord blood”, Biometals, 6(1):61-66, 1993; & J.Yang et al, .Maternal-fetal transfer of metallic mercury via placenta and milk”, Ann Clin Lab Sci, 27(2):135-141, Mar 1997); & Y.K.Soong et al, J of Formosa Medical Assoc., 1991, 90(1): 59-65; & T. Suzuki et al, Dept. Of Human Ecology, Univ. Of Tokyo, .Mercury in human amnotic fluid.,Scand J Work Environ & Health, 3:32-35,1977; & D.A. Spencer et al,.Mercury Concentration in Cord Blood., Arch Dis Child, 1988, 63(2):202-3; & 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; & R.Sikorski et al,.The intrapartum content of toxic metals in maternal and umbilical cord blood., Ginekol Pol, 1989,60(3):151-5.
(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.
(190) P.Urban et al, .Neurological examination on 3 groups of workers exposed to mercury vapour., 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, Scand J Dent Res, 1983,19:66-71 & Sci Tot Envir,1985,44:…; & .Metal release from dental materials., Biomaterials, 1986, 7, 163-175.
(192) 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; & M.D.Rose et al, Eastman Dental Institute, .The tarnished history of a posteria restoration., Br Dent J 1998;185(9):436; & J. Bergdahl, A.J.Certosimo et al, National Naval Dental Center, .Oral Electricity., Gen Dent, 1996, 44(4):324-6; & 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; & R.D.Meyer et al, .Intraoral galvanic corrosion.,Prosthet Dent, 1993,69(2):141-3; & B.M.Owens et al, .Localized galvanic shock after insertion of an amalgam restoration., Compenium, 1993, 14(10),1302,1304,1306-7. Facts about Mercury and Dental Amalgam (with Medical Study References)
(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 defieciency., 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 Disertation Dept. Of Basal Oral Sciences, Karolinska Institutet,(Stolckholm),1998,1-49; & G. Sandborgh-Englund et al, J Dental Res, 1998, 77(4): 615-24; (197) J.Taylor, A Complete Guide to Mercury Toxicity from Dental Fillings, Scripps Pulbishing;
(198) 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, Nurotoxicol. Teratol., 18:129-134;? M.Burk et al, Magnesium, 4(5-6): 325-332, 1985 ?
(199) Dr. P.Kraub & M.Deyhle, Universitat Tubingen- Institut fur Organische Chemie, .Field Study on the Mercury Content of Saliva., 1997 http://www.uni-tuebingen.de/KRAUSS/amalgam.html; (20,000 people tested for mercury level in saliva and health status/symptoms compiled) (200) V.Nadarajah et al, .Localized cellular inflamatory response to subcutaneously implanted dental mercury., J Toxicol Environ Health, Oct 11: 49(2):113-25.
(201) J.T. Salonen et al, .Intake of mercury from fish and the risk of myocardial infarction and cardiovasculr disease in eastern Finnish men., Circulation, 1995; 91(3):645-55.
(202) T.Kishimoto et al, .Methylmercury injury of Cultured Human Vascular EndothelialCells., Journal of Trace Elements in Experimental Medicine, 6(4): 155-163, 1993.
(203) M.J.Vimy et al, .Renal function and amalgam mercury., Amer J Physiol, 1997,273(3/2):1199- ; &(b) 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) 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.
(204) Tom Warren, Beating Alzheimer.s, Avery Publishing Group, 1991.
(205) M.F. Ziff et al, A Persuasive New Look at Heart Disease As It Relates toMercury, 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) Boyd Haley, Univ. Of Kentucky . The Toxic Effects fo Mercury on CNS Proteins: Similarity to Observations in Alzheimer.s Disease., IAOMT Symposium paper, March 1997 & .Mercury Vapour Inhaltion Inhibits Binding of GTP …- Similarity to Lesions in Alzheimers Diseased Brains., Neurotoxicology, 18:315- June 1997 & 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 ofMercury 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.
(210) Mats Berlin, .Is amalgam in dental fillings hazardous to health?., Lakartidningen, 1992; 89(37):2918-23; & .Prenatal exposure to mercury vapour: Effects on brain development., Fundamental and Applied Toxicology, 1,112, 1: 7(?) & M.Berlin, .Mercury in dental filling materials- environmental medicine risk analysis., paper for the Swedish Council for Coordinating and Planning Research, 1998.
(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) Ziff, M.F., .Documented Clinical Side Effects to Dental Amalgams., ADV. Dent. Res.,1992; 1(6):131-134; & S.Ziff,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,Dr. P.Larose- 80 Canadian patients, Dr. R.Siblerud, 86 Colorado patients, Dr.A.V.Zamm, 22 patients)
(213) Dr. C. Kousmine, Multiple Scherosis is Curable, 1995.
(214) .Amalgam declared hazardous., Dentistry Today, February, 1989, p1. Facts about Mercury and Dental Amalgam (with Medical Study References)
(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 vapour 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; & Apr 19,1999 Media Advisory, New MRLs for toxic substances, MRL:elemental mercury vapour/inhalation/chronic & MRL: methy mercury/ oral/acute; & http://www.atsdr.cdc.gov/mrls.html.
(218) U.S. Dept. Of Health, ASTDR ToxFAQ CAS# 7349-97-6.
(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 ; & A.Nimmo et al, .Inhalation during removal of amalgam restorations., J Prosthet Dent, 63(2):1990 Feb, 228-33.
(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.
(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 amalgam problem.,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 3,000 cases)
(223) Nicholson et al, .Mercury Nephrotoxicity., Nature Vol 304: 633, 1983; & Friberg et al, .Kidney injury after chronic exposure to inorganic mercury., Archives of Environ Health, Vol 15:p64, 1967; & Kazantis et al, .Nephrotic Syndrome Following Exposure to Mercury., Quarterly J. Of Medicine, Vol 31: 403-418, 1962; & L.H.Lash, Environmental Health Perspective,1994,102(11).
(224) M.S. Hughes, Amer. J. Of Obstetrics and Gynecology, vol 143, No 4:440- 443, 1982.
(225) S. Yannai et al, .Transformationss 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; & W.P.Ridley et al, Environ Health Perspectives, 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 Chlostridium cochlearium. J Ferment Technol1972 50:159-1660
(226) 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. and .Immune suppression of human T-cell activation., Immuno-pharmacological Immuno-toxical, 1992, 14(3):555-77, & 14(3):539-53; & 1993, 15(2-3):273-90; & M.A.Miller et al, .Mercuric chloride induces apoptosis in human T lymphocytes., Toxicol Appl Pharmacol, 153(2):250-7 1998 ; & L.M.Bagentose 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; & Goering PL, Thomas D, Rojko JL, Lucas AD. Mercuric chloride induced apoptosis is dependent on protein synthesis. Toxicol Lett 1999; 105(3): 183-95.(227) Dr. Pierre blais, Health Canada, 1976 & Discovery, Feb 1997 (TV,Quebec)(228) Dr. T. Rau, Paracelsus Alergy Clinic, Lustmuhle, Switzerland,1996(www); & Dr. B. Shelton, Director, The Allergy Center, Phoenix, Arizona, in (293); & E. Cutler,Winning the War against Asthma & Allergies, DAMS(800-311-6265)
(229) M.Davis,editor, Defense Against Mystery Syndromes., Chek Printing Co., & March, 1994(case histories documented)
(230) S. Rogers, M.D., Chemical Sensitivity, Keats Publishing,
(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, Juul 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) & Internations DAMS Newsletter, p17, Vol VII, Issue 2, Spring 1997. (31 cases)
(233) Sven Langworth et al,.Amalgamnews and Amalgamkadefonden, 1997 and Svenska Dogbladet,1997 (286 cases); & 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) (over 1000 cases) (Sweden has banned amalgam fillings & Gov.t maintains health records on all citizens)
(234) P.E. Bigazzi, .Autoimmunity and Heavy Metals., Lupus, 1994; 3: 449-453.
(235) H.J.Hamre, Mercury from Dental Amalga and Chronic Fatigue Syndrom., The CFIDS Chronicle, Fall 1994, p44-47. Facts about Mercury and Dental Amalgam (with Medical Study References)
(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.
(238) World Health Organizaition Scientific Panel Members( Dr. Lars Friburg- chairman, Dr. Fritz Lorscheider, Professor of Medical Physiology, Univ. Of Calgary; Dr. Murray Vimy, Professor of Oral Biology and Dental Medicine, Univ. Of Calgary Medical School. *** Dr. Vasken Aposhian, Dept. Head, Molecular and Cellular Biology, Univ. Of Arizona; Dr. David Eggleston, Uni. Of California, researcher on mercury in the brain; Dr. Boyd Haley, Univ. Of Kentucky researcher on mercury in the brain and Alzheimer.s Disease ( http://www.altcorp.com/); Dr. Gustav Drasch, Univ. Of Munich, researcher on mercury in brains of dead infants and fetuses; Dr. D. Echeverria, Neuro-Toxicologist, researcher on reproductive problems and birth defects in dental workers; BBC Panorama Program on Dental Amalgam:.The Poison in Your Mouth., June 1994.
(239) J.M.Varga et al, .High incidence of cross stimulation by natural allergens of rat basophilic lekemia 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;
(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 Alzheiemer Disease., Alzheimer 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 assciated 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.
(248) Y.Finkelstein,.The enigma of parkinsonism in chronic borderline mercury intoxication, resolved by challenge with penicillamine. Neurotoxicology, 1996, Spring, 17(1): 291-5.
(249) C.H.Ngim et al, Dept. of Occupational Medicine, Univ. Of Singapore,.Chronic neurobehavioral effects of elemental mercury in dentists., Brithish 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
(251) 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-Theraputics Research, 20(3):195-229, 1995; & .Mercury exposure from silver fillings., Aculpunture & Electrotherapy Res, 1996, 133-
(252) B.J.Shenker et al, Dept. of Pathology, Univ. of Pennsylvania, .Immunotoxic effects of mercuric compounds on human lymphoctes and monocytes: Alterations in cellular glutathione content., Immunopharmacol Immunotoxicol 1993, 15(2-3):273-90.
(253) S.Langworth et al, .Exposure to mercury vapour and impact on health in the dental profession in Sweden., J Dent Res, 1997, 76(7):1397-404.
(254) al-Saleh I, Shinwari N. Urinary mercury levels in females: influence of dental amalgam fillings. Biometals 1997; 10($): 315-23.
(255) D.C. Rice, .Evidence of delayed neurotoxicity produced by methylmercury developmental exposure., Neurotoxicology, Fall 1996, 17(3-4), p583-96.
(256) D.B.Alymbaevaet al, Med Tr Prom Ekol, 6:13-15, 1995 (Russian)
(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) J.M.Aguiar et al, .Heavy metals and antibiotic resistance in Escherichia coli isolates from ambulatory patients., Chemother, 1990, 2(4):238-40. Facts about Mercury and Dental Amalgam (with Medical Study References)
(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 Pharocol, 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 Porphyinogenic Metals on Coproporphrinogen Oxidase in Liver and Kidney. Toxicology and Applied Pharmacology, Vol 97, 183-190, 1989.
(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 neurotxicology 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) H.Iioka et al, .The effect of inorganic mercury on placental amino acid transport., Nippon sanka Fujinka Gakkai Zasshi, 1987, 39(2): 202-6.
(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 vapour and methylmercury produce interactive behavioral changes in adult rats., Neurotoxicol Teratol, 1996, 18(2): 129-34; & .Behavioural 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 neuroltoxic illnesses., Gesundheitswesen, 1996,58(6):322-31.
(266) N.Matsuo et al, .Mercury concentration in organs of contemporary Japanese., Environ Health, 1989, 44(5): 298-303; & R.Schiele et al, .Study on the normal mercury concentrations of human organs., Zentralbl Bakteriol Mikrobiol Hyg (B), 1981, 173(1-2_:45-62; & T. Suzuki et al, .The hair-organ relationship in mercury concentration in contemporary Japan., Arch Environ Health, 1993, 48(4):221-9; & K.Schmid et al, Zentralbl Hyg Umweltmed, 1996,199(1):24-37,.Hazardous burden by country.
(267) R. Brun, ,Epideology 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, .Benefiecial effect of human therapeutic IV-Ig in mercury indueced autoimune disease. Clin Exp Immunol, Apr, 1991; & (g)El-Fawai HA, Waterman SJ, De Feo A, Shamy MY. Neuroimmunotoxicology: Humoral Assesment of Neurotoxicity and Autoimmune Mechinisms. Contact Dermatitis 1999; 41(1): 60-1.
(270) D.W.Eggleston, .Effect of dental amalgam and nickel alloys on T-lympocytes.,J Prosthet Dent. 51(5):617-623,1984; & D.W.Eggleston et al, J Prosthet Dent, 1987,58(6),704-7; & J of the American Medical Assoc., Sept 96.
(271) B.A.Weber, .The Marburg Amalgam Study., Arzt und Umwelt, Apr, 1995; (266 cases) & (b) B.A. Weber, .Amalgam and Allergy., Institute for Naturopathic Medicine, 1994; & © B.A. Weber, .Conuctivitis sicca(dry eye study).,Institute for Naturopathic Medicine, 1994; B.A.Weber, .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; Immuno-pharmacol Immuno-toxicol, 1992; 14(3):555-77; & Immuno-toxicol, 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; & O.Insug et al, .Mercuric compounds inhibit hunan moncyte 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 etal, Ind Health,4:69-75,1966.
(275) L.M.Mikhailova et al, .Influence of occupational factors on disease of reproductive organs., Pediatriya Akusherstvoi Facts about Mercury and Dental Amalgam (with Medical Study References) Ginekologiya,33(6):56-58,1971
(276) ATSDR/EPA Priority List for 1999: Top 20 Hazardous Substances, Agency for Toxic Substances and Disease Registry,U.S. Department of Health and Human Services, http://www.atsdr.cdc.gov/99list.html; & U.S. Environmental Protection Agency, Hazardous Air Pollutant Hazard Summary Fact Sheets, EPA: In Risk Information System, 1995.
(278) NIDR/ADA Workshop, Biocompatibility of Metals in Dentistry, JADA, 109(3): 469-471, Sept 1984. (& 38)
(279) 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 form 13 coutnries., 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..
(280) S.Nonaka et al, Nat. Inst. of Mental Health, Bethesda Md., .Lithium treatment protects neurons in CNS from glutamate induced excitibility and calcium influx., Neurobiology, Vol 95(5):2642-2647, Mar 3, 1998.
(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.
(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.
(285) R.C.Perlingeiro et al, .Polymorphonuclear phagentosis in workers exposed to mercuryvapour., Int J Immouno- pharmacology., 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 pyschological 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.
(286) M. Lai et al, .Sensitivity of MS detections by MRI., Journal of Neurology, Neruosurgury, and Psychiatry, 1996, 60(3):339-
(287) M.C. Newland et al,.Behavioral consequences of in utero exposure to mercury vapour 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 vapour., Environmental Research, 1994, 67:196-208.
(288) M.Hobson & B.Ajanna, .Influence of mercury on uptake of dopamine and norepinephrine., Toxicol Letters, Dep 1985, 27:2-3:7-14.
(289) J.Mai et al, Biological Trace Element Research,1990;24:109-117.
(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; & 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) .Do amalgam fillings influence manic depression?.,Journal of Orthomol. Medicine , 1998, http://www.depression.com/news/news_981116.htm.
(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.
(296) L.Bucio et al, Uptake, cellular distribution and DNA damage produced by mercuric chloride in a human Facts about Mercury and Dental Amalgam (with Medical Study References) fetal hepatic cell line. Mutat Res 1999 Jan 25;423(1-2):65-72; & 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, .Amalgamtion 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.
(298) C. Toomvali, .Studies of mercury vapour emission from different dental amalgam alloys., LIU-IFM-Kemi-EX 150, 1988; & A.Berglund,.A study of the release of mercury vapour from different types of amalgam alloys., J Dent Res, 1993, 72:939-946; & D.B.Boyer, .Mercury vapourization from corroded dental amalgam. Dental Materials, 1988, 4:89-93; &V.Psarras et al, .Effect of selenium on mercury vapour 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 vapour 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 localisation 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 et al, .Mobilization of Mercury in Humans by DMPS., Envir. Health Perspectives, Vol 106, Supp. 4, Aug.1998; & Toxicology, 1995, 97(1-3): 23-38; & .Urinary Mercury after Administration DMPS., FASEB J., 6: 2472-2476,
(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) S. Soederstroem et al, .The effect of mercury vapour on chloinergic neurons in the fetal brain.,Developmental Brain Research,85(1):96-108.1995; & 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.
(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) N.Sorenson et al, .Prenatal methyl mercury expsoure as a cardiovascular risk factor at 7 years of age. Epidemiology, 1999, 10(4):370-4: & D.O.Marsh et al, .Fetal Mehylmercury Poisoning., Ann Neurol, 1980, 7:348-55.
(309) The Tribune, Mesa, Az., 13 Apr 1998, (Paul Mills, Apalachee Junction)
(310) R.L.Siblerud, .The relationship between mercury from dental amalgam and the cardiovascular system., Science of the Total Envir., 1990, 99(1-2): 23-35.
(311) Chang LW, Hartmann HA,.Blood-brain barrier dysfunction in experimental mercury intoxication.. Acta Neuropathol (Berl) 1972;21(3):179-84; & Ware RA, Chang LW, Burkholder PM, .An ultrastructual study on the bloodbrain barrier disfunction following mercury intoxication.,Acta Neurolpathol(Berlin), 1974,30(3): 211-214; & Prenatal and neonatal toxicology and pathology of heavy metals. Adv Pharmacol Chemother., 1980, 17:195-231.
(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.Goldman et al,1991,.Chemically induced autoimmunity ….,Immunology Today,12:223-; & K. Warfyinge et al, .Systemic autoimmunity due to mercury vapour exposure in genetically susceptible mice., Toxicol Appl Pharmacol, 1995, 132(2):299-309; Pollard KM, Pearson Dl, Hultman P. Lupus-prone mie as model to study xenobiotic-induced autoimmunity. Envriron Health Perspect 1999; 107(Suppl 5): 729-735.
(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. Immuno-pharmacolImmunotoxicol, 1993, 15(1):87-112; & J.R.Daum,.Immuno-toxicology of mercury and cadmium on B-lumphocutes., Int JImmuno-pharmacol, 1993, 15(3):383-94..
(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) Facts about Mercury and Dental Amalgam (with Medical Study References)
(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) A.V. Motorkina et al, .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. (99 cured)
(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
(323) Dr. Kohdera, Faculty of Dentistry, Osaka Univ, Internationsl Congress of Allergology and Clinical Immunology, EAACI, Stockholm, June 1994; & Heavy Metal Bulletin, Vol 1, Issue 2, Oct 1994. (160 cases cured-eczema); & P.Dallmann,.konnen durch Quecksilber entstehen? PeDa_Eigenverisg, 1995; & G. Ionescu, Biol Med, 1996, (2): 65-68; SS Tsyganok, .Unithiol in treatment of dermatoses., Vestn.Dermatol.Venerol., 1978, (9): 67-69.
(324) D. Bangsi 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.
(325) C.R. Adams et al, .Mercury intoxication simulating ALS., JAMA, 1983, 250(5):642-5; & T.Barber, .Inorganic mercury intoxification similar to ALS., J of Occup Med, 1978, 20:667-9; & M. Su et al, J Neurol Sci,1998, 156(1):12-7; & B. Arvidson(Sweden), Inorganic mercury is transported from muscular nerve terminals to spinal and brainstem motorneurons. Muscle Nerve, 1992, 15(10);1089-94,
(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 enplaque”,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) G. Danscher et al, Environ Res, .Localization of mercury in the CNS., 1986, 41:29-43; & 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; &.Ultrastructural localization of mercury after expsoure to mercury vapour., Prog Histochem Cytochem, 1991, 23:249-255; & R.Pamphlett et al, .Entry of low doses of mercury vapour into the nervous system., Neurotoxicology, 1998, 19(1):39-47; & Pamphlett et al, .Oxidative damage to nucleic acids in motor neurons containing Hg., J Neurol Sci,1998,159(2):121-6. (rats & primates)
(328) P.McKeever et al, .Patterns of antigenic exproession in human glioma cells., Crit Rev Neurobiology, 1991, 6:119-147.
(329) 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; & 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) C.M. Tanner et al,.Abnormal Liver Enzyme Metablolism in Parkinson.s.,Neurology, 1991, 41(5): Suppl 2, 89-92; & M.Watanabe et al, Amino Acids, 1998, 15(2): 143-50 & 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.
(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; & P.Emory et al, Br J Rheumotol, 1992, 31:7,449-51.
(332) M.J.Trepka et al, .Factors afftecting 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, 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
(334) T.Nguyen et al, Mol Immunol,1996,3(4):379-86; & P.Eggleton etal, .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 faeces 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.
(337) H.G. Abadin, et al, U.S. ATSDR, .Breast-feeding exposure of infants to mercury, lead, and cadmium: A Public, 1997, 13(4): 495-517.
(338) 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 acticities and its accumulation in the first-trimester human placento., Environ Res, 1992, 57(1):96-106;& .In vitro exposure to mercury and cadmium alters term human placental membrane fluidlty., Pharmacol, 1992, 116(1): 17-23; & 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;& W.B. Karp etal, .Correlation of human placental enzymatic activity with trace metal concentration in pl acenta., Environ Res. 13:470-477,1977.
(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.
(340) Herrman M. Schweinsberg F. .Mercury burden from amalgam fillings., Zentralbl Hyg Umweltmed, 1993,194(3):271-
(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 dematitis., Dermatitis, 1997, 36(5):237-9.
(342) V.Stejskal, .MELISA: A New Technology for Diagnosing and Monitoring of Metal Sensitivity., Proceedings: 33rd Annual Meeting of American Acadamy of Environmental Medicine, Nov. 1998, Baltimore, Maryland.
(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) D.J.Clauw, .The pathogenesis of chronic pain and fatigue syndroms: fibromyalgia. Med Hypothesis, 1995, 44:369-78.
(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; & Mass C, Bruck W. .Study on the significance of mercury accumulation in the brain from dental amalgam fillings through direct mouth-nose-brain transport., Zentralbl Hyg Umweltmed 1996; 198(3): 275-91.
(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, 72:345-51; & L.D. Pzheusskaia, .Disintoxication therapy of patients with nonspecific inflammatory diseases of the 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; & .Sulhydryl-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 insufficiencey. Kardiologila, 1972,12(1):126-31.
(352) B.Arnold, Eigenschaften und Einsatzgebiete des Chelatbildners:DMPS., Z.Umweltmedizin 1997,5(1):38- ; & Diagnostik un Monitorung vonSchwermetallbelastungen,I,II, ZWR,1996, 105(10):586-569 & (11):665-; & Therapie der Schwermetallbelastung, Mineraloscope, 1996,(1):22-23.(353) P.P Guida, .Theraputic efficacy of unithiol in Buschke.s scherodrma., 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, University 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 methylmercury 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 arthities., 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 Facts about Mercury and Dental Amalgam (with Medical Study References) chloride, phenylmercury acetate, or mercury vapour, 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.
(363) J.W.Reinhardt, Univ. Of Iowa College of Dentistry, .Side effects: mercury contribution to body burden from dental amalgam., Adv Dent Res, 1992, 6: 110-3.
(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) .Zahnamalgam und Schwangerschaft., Geburtshilfe Frauenheikd. 1995, 55(6): M63-M65; & T. Zinke, .Gibt es neue Erkenntnisse zur Amalgamproblematic?., 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) I. Gerhard, .Amalgam aus gynakologischer Sicht., Der Frauenarzt, 1995,36(6): 627-28; & .Schdstoffe und Fertillitatsstorungen., Schwermetalle und Mineralstoffe, Geburtshilfe Frauenheikd, 1992, 52(7):383-396; & .Reproductive risks of heavy metal and pesticides in women., in: Reproductive Toxicology, M.Richardson(ed.), VCH Weinhelm, 1993, 167-83; &.Unfruchtbarkeit bei Frauen durch Umwelterkrankungen, JD. Kruse-Jarres(Ed.), 1993, 51-68.
(368) Stejskal VDM, Danersund A, Lindvall A, Hudecek R, Nordman V, Yaqob A et al. Metal- specific memory lymphoctes: biomarkers of sensitivity in man. Neuroendocrinology Letters, 1999.
(369) Sterzl I, Prochazkova J, Stejaskal VDM et al, Mercury and nickel allergy: risk facotrs in fatigue and autoimmunity. Neuroendocrinology Letters 1999; 20:221-228.
(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. Biochim Biophys Acta 1989; 991(1):85-9.
(371) Halbach S. Estimation of mercury dose by a novel quantitation 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. Neuroltoxicol Teratol 1998; 10(5):393-416.
(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) Sterzl I, Prochazkova J, Stejskal VDM. Mercury and nickel allergy: risk factors in fatigue and autoimmunity. Neuroendocrinology Letters 1999, 20:221-228.
(375) Stejskal VDM, Danersund A, Lindvall A. Metal-specific memory lympocytes: biomarkers of sensitivity in man. Neuroendocrinology Letters 1999.
(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)
(377) Murtomaa H, Haavio-Manila e, Kandolin I. Burnout and its causes in Finnish dentists. Comunity Dental Oral Epidemiol 1990;18:208-12.
(378) Cheraskin E, Ringsdorf Wm, Medford FH. Daily vitamin C consumption and fatigabilit. J Am Gerialr Soc 1976; 24:136-37.
(379) MacDonald EM, Mann AH, Thomas HC. Interferons as mediatorors of psychiatric morbidity. The Lancet 1978; Nov 21, 1175-78; & Hickie I, Lloyd A. Are cytokines associated with neuropsychiatric syndrome in humans? Int J Immunopharm 1995; 4:285-
(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 sydrome. 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.
(382) Sterzl I, Fucikova T, Zamrazil V. The fatigue syndrome in autoimmune thyroiditis with polyglanular activation of autoimmunity. Vnitrni Lekarstvi 1998; 44: 456-60.
(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. Facts about Mercury and Dental Amalgam (with Medical Study References)
(385) Kohdera T, Koh N, Koh R. Antigen-specific lympocyte stimulation test on patients with psoriasis vulgaris. XVI International Congress of Allergology and Clinical Immunology, Oct 1997, Cancoon, Mexico; & Ionescu G. Schwermetallbelastung beiatopischer Dermatitis und Psoriasis. Biol Med 1996; 2:65-68.
(386) Biospectron Lab ……. & Doctors Data Lab ………..
(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.
(390) Ellingsen DG, Nordhagen HP, Thomassen Y. Uninary selenium excretion in workers with low exposure to mercury vapour. J Appl toxicol 1995; 15(1): 33-6.
(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.
(393) Furuhjelm M, Jonson B. Int J of Fertility 1962, 7(1); 17-21; & Dr. J.K Sherman, Univ. Of Arkansas, study reported in Washington Star Newspaper, Jan 7, 1979.
(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; & & Baranski B. Effect of mercury on the sexual cycle and prenatal and postnatal development of progeny. Med Pr 1981; 32(4): 271-6.
(395) Shapiro IM, Cornblath DR, Sumner AJ. Neurophysiological and neuropshchological function in mercury- exposed dentists. The Lancet 1982; 1:1147-1150; & Szzell BP and Oler J. Chronic low-level mercury exposure and neuropshycological functioning. J of Clin and Exper Neuropsych 1986; 8:581-93.
(396) Epidemiologisk undersokning av fosterkador hos 1.2 milj. barn, fodda sedan 1967; Norge yrkesmed. Avd. Haukelands sykehus. Aftenposton 6 mpv 1997.
(397) Hudecek R, Danersund A. Removal of Incompatible Dental Material in Patients with Intolerance of Dental Materials. 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.
(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 vapourization. Taehan Chikkwa Uisa Hyophoe Chi 27(7): 649-59.
(401) Sikorski R, Juszkiewicz T. Women in dental surguries: reproductive hazards in occupational exposure to mercury. Int Arch Occup Environ Health 1987; 59(6):551-7.
(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 Xray 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)
(405) Jenny Stejskal, Vera Stejskal. The role of metals in autoimmune diseases and the link to neuroendocrinology Neuroendocrinology Letters, 20:345-358, 1999. see #218
(406) Goering Pl, Rowland AS. Toxicity assessment of mercury vapour drom dental amalgams. Fundam. Appl Toxicol 1992; 19:319-329.
(407) Eedy DJ, Burrows D, Dlifford T, Fay A. Elevated T cell subpopulations in dental students. J prosthet Dent 1990; 63(5):593-6.
(408) Wehner-Caroli J; Scherwitz C; Schweinsberg F; Fierlbeck G. Exacerbation of pustular psoriasis in mercury poisoning. Hautarzt 1994 Oct;45(10):708-10.
(409) Autism: a unique form of mercury poisoning. http://www.canfoundation.org/newcansite/sciwatch/invest.html
(410) J.R. Cade et al, Autism and schizophrenia linked to malfunctioning enzyme for milk protein digestion. Autism, Mar1999.
(411) Puschel et al, Mercury inhibits activity of dipetyl-peptidase IV. European J Biochem 1982; 126:359-365.
(412) Stefanovic V. et al, Kidney ectopeptidases in mercuric chloride-induced renal failure. Cell Physiol Biochem 1998;8(5): 278-84.
(413) Autism-Mercury@egroups.com, web group of parents with autistic kids and autism doctors and researchers; & http://www.edelsoncenter.com.
(414) Reichrtova E et al, .Cord Serum Immunoglobulin E Related to Enviornmental Contamination of Human Placentas with Oganochlorine Compounds., Envir Health Perspec, 1999, 107(11):895-99.
(415) Wecker L, Miller SB, Cochran SR, Dugger DL, Johnson WD. Trace element concentrations in hair from autistic children. Facts about Mercury and Dental Amalgam (with Medical Study References) Defic Res 1985; 29(Pt 1): 15-22
Thank you Mr. Windham – great work!
We are keeping a copy of this work off-line,
in case your original is ever lost.