MERCURY TOXICITY: Dependence on Dose, Diet and Genetic Susceptibility

DR. BOYD E. HALEYDR. BOYD E. HALEY

PROFESSOR AND CHAIRPROFESSOR AND CHAIR

DEPARTMENT OF CHEMISTRYDEPARTMENT OF CHEMISTRY

UNIVERSITY OF KENTUCKYUNIVERSITY OF KENTUCKY

VISUALIZATION OF MERCURY EMITTING FROM A DENTAL AMALGAM

From: www. From: www. uninformed uninformed consent.comconsent.com

David David Kennedy’s Kennedy’s IAOMT tapeIAOMT tape

Measurement of Mercury Release from a Standard Dental Filling Amalgams of known weight and surface area were Amalgams of known weight and surface area were

placed in a sealed test tube in 50 milliliters of Hplaced in a sealed test tube in 50 milliliters of H22O. O. HH22O was changed daily and Hg level measured by a O was changed daily and Hg level measured by a mercury cold vapor analyzer.mercury cold vapor analyzer.

Without brushing the amalgams released 7.54Without brushing the amalgams released 7.54g g Hg/cmHg/cm22/day./day.

With two 30 second brushings with a medium With two 30 second brushings with a medium toothbrush the amalgams released 45.5toothbrush the amalgams released 45.5g g Hg/cmHg/cm22/day, a six-fold increase./day, a six-fold increase.

This confirms the earlier observation of This confirms the earlier observation of Dr. Stock in Dr. Stock in 19261926 in Zeitschr. Angew. Chem. 39, 461-466. in Zeitschr. Angew. Chem. 39, 461-466.

Time (hr) After Treatment

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50 nM thimerosal

50 nM thimerosal+10 nM HgCl2

50 nM thimerosal+ 25 nM HgCl2

10 nM HgCl2

25 nM HgCl2

Hg & THIMEROSAL DISPLAY ADDITIVE TOXICITIES TO NEURONS IN CULTURE.

MERCURY BIRTH HAIR LEVELS VS. AMALGAM FILLINGS IN AUTISTIC AND CONTROL GROUPS

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Hair Hg level(mcg/g)

Number of amalgams:Control: autistic ratio:

4-5 6-7 8-9 >102.64 6.93 6.70 6.32 17.91

N: 15 22 29 30 43

Autistic

Control

Data from A. Holmes, M. Blaxill & B. Haley, Int. J. of Toxicology v22, in press, 2003

ACTUAL VERSUS PREDICTED BIRTH HAIR MERCURY LEVELS

-5

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Actual hair Hg level (ng/g)

Hair Hg level= (5.60)+0.04(amalgam volume)+1.15(fish consumption)+0.03(vaccine): R2= 0.79

Predicted hair Hg level(mcg/g)

AutisticsControls

Data from A. Holmes, M. Blaxill & B. Haley, Int. J. Toxicology, in press, 2003

BIRTH-HAIR MERCURY BY SEVERITY OF AUTISM

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Hair Hg level(ppm)

MildMean=0.71

n=27

Female

Male

ModerateMean=0.46

n=43

SevereMean=0.21

n=24

Data from Amy Holmes, Mark Blaxill & Boyd Haley, Int. J. Tocicology v22, in press, 2003.

CONTRAST BETWEEN BIRH HAIR Hg LEVELS AND BODY Hg LEVELS

Autistic children have much lower Hg levels Autistic children have much lower Hg levels in their birth hair, yetin their birth hair, yet

Numerous physicians have reported that Numerous physicians have reported that autistic children carry a 5 to 6-fold higher autistic children carry a 5 to 6-fold higher mercury body burden than control children.mercury body burden than control children.

The obvious explanation is micro-mercuralism The obvious explanation is micro-mercuralism & genetic susceptibility to retention toxicity.& genetic susceptibility to retention toxicity.

There is an obvious gender difference. This is There is an obvious gender difference. This is explained by testosterone effects on T-toxicity.explained by testosterone effects on T-toxicity.

ACROYDYNIA: Pink Disease

Acroydynia was prevalent from about 1880 Acroydynia was prevalent from about 1880 until 1940 affecting about 1 in 500 children. until 1940 affecting about 1 in 500 children. It was found to be caused by mercurous It was found to be caused by mercurous chloride (calomel) in baby teething powder. chloride (calomel) in baby teething powder. Removal of this teething powder from the Removal of this teething powder from the market eliminated this disease which had market eliminated this disease which had some similarity to autism.some similarity to autism.

MOST IMPORTANT CONCLUSIONS THERE APPEARS TO BE A SUBSET OF THE THERE APPEARS TO BE A SUBSET OF THE

POPULATION THAT CANNOT EFFECTIVELY POPULATION THAT CANNOT EFFECTIVELY EXCRETE MERCURY AND ARE AT GREATER RISK EXCRETE MERCURY AND ARE AT GREATER RISK TO EXPOSURES TO MERCURY THAN ARE THE TO EXPOSURES TO MERCURY THAN ARE THE GENERAL POPULATION. GENERAL POPULATION.

THIS SUSCEPTIBILITY IS LIKELY DUE TO THIS SUSCEPTIBILITY IS LIKELY DUE TO GENETIC DIFFERENCES, DIET, EXPOSURE TO GENETIC DIFFERENCES, DIET, EXPOSURE TO OTHER TOXICANTS, ANTIBIOTICS, ETC.OTHER TOXICANTS, ANTIBIOTICS, ETC.

DOES UNEXPLAINED LOW HAIR, NAIL, BLOOD OR DOES UNEXPLAINED LOW HAIR, NAIL, BLOOD OR URINE LEVELS APPEAR IN OTHER URINE LEVELS APPEAR IN OTHER NEUROLOGICAL OR SYSTEMIC DISEASES?NEUROLOGICAL OR SYSTEMIC DISEASES?

ELEVATED MERCURY IN IDIOPATHIC DILATED CARDIOMYOPATHY (IDCM).

WHERE DOES Hg COME FROM?

LEVELS ng/g LEVELS ng/g HgHg SbSb

ControlsControls 8.0 8.0 1.51.5

IDCMIDCM 178,400178,400 19.260 19.260

This is a 22,300 fold increase in Hg!This is a 22,300 fold increase in Hg!Frustaci et al., J. of American College of Cardiology, 33, (6) 1578, 1999.Frustaci et al., J. of American College of Cardiology, 33, (6) 1578, 1999. Controls were patients with valvular or ischemic heart disease. Controls were patients with valvular or ischemic heart disease. Athletic Athletic youth die of IDCM.youth die of IDCM.

M. Bauman & K. Nelson Paper

““In contrast, in the Sechylles study of >700 In contrast, in the Sechylles study of >700 children, exposure was to marine fish only, and children, exposure was to marine fish only, and boys with higher levels of hair mercury performed boys with higher levels of hair mercury performed better on some testsbetter on some tests, including the Boston Naming , including the Boston Naming Test and 2 tests of visual motor coordination.”Test and 2 tests of visual motor coordination.”

The above observation has lead some to dismiss The above observation has lead some to dismiss Hg as being causal for any neurological problems Hg as being causal for any neurological problems in youth.in youth.

However, it is likely in light of the autistic However, it is likely in light of the autistic observations that the boys with higher hair Hg observations that the boys with higher hair Hg levels were the best at excreting Hg or Methyl-Hg.levels were the best at excreting Hg or Methyl-Hg.

CARDIOVASCULAR DISEASE AND MERCURY

Two studies have found a correlation between Two studies have found a correlation between cardiovascular disease and Hg. cardiovascular disease and Hg. Guallar et al. NEJM Guallar et al. NEJM v347,1747,2003 & Salonen et al. Atherosclerosis v148, 265, v347,1747,2003 & Salonen et al. Atherosclerosis v148, 265, 2000.2000.

However, a Faeroe Island study found that blood However, a Faeroe Island study found that blood pressure was increased in 7 year old children when pressure was increased in 7 year old children when the blood Hg levels were the blood Hg levels were BELOWBELOW 10 10g/liter, but g/liter, but not when it was higher! not when it was higher! Sorensen et al. Epidemiology Sorensen et al. Epidemiology v10, 370, 1999 as reported by Clarkson et al. NEJM 2003.v10, 370, 1999 as reported by Clarkson et al. NEJM 2003.

If ingestion rates of mercury were the same then the above If ingestion rates of mercury were the same then the above results imply that low blood levels of Hg are caused by results imply that low blood levels of Hg are caused by failure to excrete the mercury.failure to excrete the mercury.

Hg Levels in Human Brain Saxe et al, determined Hg levels in the brains of 101 human Saxe et al, determined Hg levels in the brains of 101 human

subjects, both AD and normals, mostly Catholic Nuns subjects, both AD and normals, mostly Catholic Nuns (Alzheimer’s Disease, Dental Amalgam and Mercury, JADA v130, p191-199, 1999)(Alzheimer’s Disease, Dental Amalgam and Mercury, JADA v130, p191-199, 1999)..

The histogram in this paper showed 6 of 101 subjects with The histogram in this paper showed 6 of 101 subjects with brain Hg levels above 200 ng/g wet weight (C=236, 248, brain Hg levels above 200 ng/g wet weight (C=236, 248, 319: AD=394, 622, 698). 319: AD=394, 622, 698). This represents between 1.2 & 3.5 This represents between 1.2 & 3.5 micromolar, or highly toxic levels of Hg in 6% of these micromolar, or highly toxic levels of Hg in 6% of these subjects. At 100 ng/g Hg this increases to about 15% of subjects. At 100 ng/g Hg this increases to about 15% of subjects with highly toxic levels of brain mercury.subjects with highly toxic levels of brain mercury.

Hg levels were double in the control olfactory tissue!Hg levels were double in the control olfactory tissue! Where does this Hg come from? Why is it elevated in Where does this Hg come from? Why is it elevated in

certain individuals? certain individuals? This also appears to be an inability to This also appears to be an inability to excrete the mercuryexcrete the mercury as the authors state Hg levels were not as the authors state Hg levels were not correlated with number of amalgam fillings.correlated with number of amalgam fillings.

Hg levels in AD brain Ehmann, Markesbery, et al. Transactions of the Ehmann, Markesbery, et al. Transactions of the

American Nuclear Society, 41, 206-207, 1982 entitled American Nuclear Society, 41, 206-207, 1982 entitled “Brain Trace Element Studies of Aging and Disease “Brain Trace Element Studies of Aging and Disease by INAA” INAA= instrumental neutron activation by INAA” INAA= instrumental neutron activation analysis. analysis.

Tested for Ag, Br, Co, Cr, Cs, Fe, Hg, Rb, Sb, Sc, Se Tested for Ag, Br, Co, Cr, Cs, Fe, Hg, Rb, Sb, Sc, Se and Zn. and Zn.

QuoteQuote: : “ In the comparison of Alzheimer’s disease “ In the comparison of Alzheimer’s disease and control brains, the largest differences were and control brains, the largest differences were observed for bromine and mercury, both being observed for bromine and mercury, both being enriched in Alzheimer’s brains (p < 0.05).”enriched in Alzheimer’s brains (p < 0.05).”

Hg levels in hair & nails of AD Ehmann, Markesbery et al. Neurotoxicology 9(2)197-208. Trace Ehmann, Markesbery et al. Neurotoxicology 9(2)197-208. Trace

Element Imbalances in Hair and Nails of Alzheimer’s Diseased Element Imbalances in Hair and Nails of Alzheimer’s Diseased Patients. Patients.

QuoteQuote “The concentrations of 17 elements in the hair and nails of 180 “The concentrations of 17 elements in the hair and nails of 180 Alzheimer’s disease (AD) and control subjects have been determined Alzheimer’s disease (AD) and control subjects have been determined by instrumental neutron activation analysis (INAA). by instrumental neutron activation analysis (INAA).

““Mercury is decreased in the nail of AD subjects compared to Mercury is decreased in the nail of AD subjects compared to controls”controls”

““Perhaps one reason for the lowering of nail Hg in AD subjects could Perhaps one reason for the lowering of nail Hg in AD subjects could be the presumably lower exposure rate of the AD patients to be the presumably lower exposure rate of the AD patients to environmental Hg. This would not explain the elevated brain Hg, environmental Hg. This would not explain the elevated brain Hg, however.” however.”

Hg in nails of AD subjects

Ehman, Markesbery et al. Biological Trace Element Ehman, Markesbery et al. Biological Trace Element Research, pp461-470. Editor:G.N. Schrauzer, 1990 by the Research, pp461-470. Editor:G.N. Schrauzer, 1990 by the Humana Press, Inc. Humana Press, Inc.

A Search for Longitudinal Variations in Trace Element A Search for Longitudinal Variations in Trace Element Levels in Nails of Alzheimer’s disease patients. Levels in Nails of Alzheimer’s disease patients.

QuoteQuote “Mercury tended to decrease in nail with “Mercury tended to decrease in nail with increasing age of patient, and with the duration and increasing age of patient, and with the duration and severity of the dementia.” severity of the dementia.”

Hg in nails of AD subjects Ehman, Markesbery et al. Biological Trace Element Ehman, Markesbery et al. Biological Trace Element

Research, pp461-470. Editor:G.N. Schrauzer, 1990 Research, pp461-470. Editor:G.N. Schrauzer, 1990 by the Humana Press, Inc. by the Humana Press, Inc.

A Search for Longitudinal Variations in Trace A Search for Longitudinal Variations in Trace Element Levels in Nails of Alzheimer’s disease Element Levels in Nails of Alzheimer’s disease patients. patients.

Quote: Quote: “This decrease is counter to the elevated “This decrease is counter to the elevated levels of Hg observed in AD brain, as compared levels of Hg observed in AD brain, as compared to age-matched controls.”to age-matched controls.”

Hg Brain/Nail or Hair Ratios in AD versus Normal Subjects

In a manner similar to that observed for autistic In a manner similar to that observed for autistic children the body burden of mercury in AD subjects children the body burden of mercury in AD subjects appears to be elevated compared to controls appears to be elevated compared to controls whereas whereas the mercury levels in the hair and nails was found to the mercury levels in the hair and nails was found to be significantly lower.be significantly lower.

Perhaps these AD subjects could not excrete Hg as Perhaps these AD subjects could not excrete Hg as effectively as the normal subjects.effectively as the normal subjects.

Do other experiments show any correlation between Do other experiments show any correlation between amalgam and brain Hg levels? Yes.amalgam and brain Hg levels? Yes.

Brain Hg levels versus Number Amalgam SurfacesFrom Dr. Magnus Nylander’s Research. The scatter in this graph, where high levels of Hg are observed with low amalgam surface count and low levels are observed with high amalgam count, and vice versa, is what would be expected if the individual subjects were differentially capable of excreting mercury. Similar results are seen doing similar analysis on fetal tissue and comparing Hg levels to birth mother’s amalgam count.

The low Hg levels found in alcohol abusers also implies that diet may play a role in mercury retention.

Time (hr) After Treatment

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500 nM Al(OH)3

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50 nM Thimerosal1.75 µg Neomycin/ml

50 nM Thimerosal500 nM Al(OH)3

1.75 µg Neomycin/ml

Al:NEOMYCIN:TESTERONE EFFECTS

+ TESTOSTERONE

SYNERGISTIC TOXICITIES on NEURONS IN CULTURE

50 NANOMOLAR

DR. MARK LOVELL

COLLABORATOR

Antibiotics, Milk and Hg Half-Life In a study where rats were given high doses of In a study where rats were given high doses of

oral antibiotics the oral antibiotics the half-life for excretion of half-life for excretion of mercury increased from 10 days to >100 daysmercury increased from 10 days to >100 days..

If the rats were also on a milk diet the If the rats were also on a milk diet the excretion excretion half-life increased to over 300 dayshalf-life increased to over 300 days..(Rowland, (Rowland, Archives of Environmental HealthArchives of Environmental Health 1984: 39(6); 401-408) 1984: 39(6); 401-408)

It appears obvious that the cellular retention of It appears obvious that the cellular retention of Hg is dependent on genetics, diet and medical Hg is dependent on genetics, diet and medical treatment. Increased cellular retention is an treatment. Increased cellular retention is an excretion problem.excretion problem.

Axonal Transport - A Process Essential for the Survival of Neurons

Dendrite

Microtubule, made of polymerized tubulin dimers.

MembraneBound Organelle

DynienAxon

Kinesin

Autoradiogram of [32P]8N3GTP Photolabeled Control & AD Brain Hippocampus Homogenates

EDTA Prevents Cd, Cu & Zn, But Not Hg, Inhibition of [32P]8N3GTP Photolabeling of Brain ß-Tubulin

Partitioning of ß-Tubulin is Aberrant in Alzheimer’s Diseased Brain Homogenates

NORMALSNORMALSNORMALS ALZHEIMERS

ANTIBODY DETECTION OF BETA-TUBULIN

MERCURY AND ALZHEIMER’S DISEASE Exposure of neuroblastoma cells to 10Exposure of neuroblastoma cells to 10-9-9 molar mercury molar mercury

increases increases Tau phosphorylation and secretion of beta-Tau phosphorylation and secretion of beta-amyloidamyloid. Both of these events occur in Alzheimer’s . Both of these events occur in Alzheimer’s diseased brain. Amyloid plaque formation is the diseased brain. Amyloid plaque formation is the “diagnostic hallmark” of Alzheimer’s disease. “diagnostic hallmark” of Alzheimer’s disease. Olivieri et al. J. Olivieri et al. J. Neurochemistry, 74, 231, 2000.Neurochemistry, 74, 231, 2000.

Exposure of cultured neurons to 10Exposure of cultured neurons to 10-7-7 to 10 to 10-10-10 molar mercury molar mercury rapidly causes rapidly causes the stripping of tubulinthe stripping of tubulin from the neurofibrils from the neurofibrils forming the neurite processes forming the neurite processes leading to the formation of leading to the formation of neurofibillary tanglesneurofibillary tangles, a “diagnostic hallmark”, a “diagnostic hallmark” of of Alzheimer’s disease. Alzheimer’s disease. Leong et al. NeuroReports 12(4), 733, 2001Leong et al. NeuroReports 12(4), 733, 2001

Therefore, Hg exposure can create these diagnostic Therefore, Hg exposure can create these diagnostic hallmarks of Alzheimer’s Disease!hallmarks of Alzheimer’s Disease!

HgEDTA Induces Aberrant [32P]8N3GTP-ß-Tubulin Interactions Indicative of AD

EFFECT OF SEQUENTIAL AMALGAM EXTRACTION SOLUTIONS ON THE VIABILITY OF BRAIN TUBULIN

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% Active

PROTEINS INVOLVED IN Hg EXCRETION

GLUTATHIONEGLUTATHIONE (carries Hg through bilary transport, (carries Hg through bilary transport, rapidly oxidized by excess Hgrapidly oxidized by excess Hg2+2+. . Note: HgNote: Hg2+2+ must go must go intracellular to interact with GSH, then be excreted for intracellular to interact with GSH, then be excreted for clearance in the bilary transport system of the liver.clearance in the bilary transport system of the liver.

GLUTATHIONE TRANSFERASEGLUTATHIONE TRANSFERASE, a recent gene product , a recent gene product identified with AD risk.identified with AD risk.

METALLOTHIONINEMETALLOTHIONINE (Dr. W.Walsh’s work, regulated by (Dr. W.Walsh’s work, regulated by estrogen and testosterone). This may explain gender estrogen and testosterone). This may explain gender susceptibility.susceptibility.

APO-EAPO-E (apo-lipoprotein-E, a brain “housekeeping protein” (apo-lipoprotein-E, a brain “housekeeping protein” that carries cholesterol from the brain through the CSF, that carries cholesterol from the brain through the CSF, through the blood-brain barrier for excretion by the liver through the blood-brain barrier for excretion by the liver bilary transport system.) This may explain additional bilary transport system.) This may explain additional excretion deficit.excretion deficit.

Biochemical Differences Between the Three Most Common Apolipoprotein E Isoforms is Reflected in Hg Binding Capacity

HIGH RISK FOR EARLY AD

LOW RISK FOR EARLY AD2 Mercury binding sites

1 Mercury binding site

No Mercury binding sites

RELATIONSHIP TO NUMBER OF APO-E –SH GROUPS AND AGE OF AD ONSET

APO-EAPO-E 22 33 44

22 44 (>90) (>90) 33 (>90) (>90) 22 (80-90) (80-90)

33 33 (>90) (>90) 22 (80-90) (80-90) 11 (70-80) (70-80)

44 22 (80-90) (80-90) 11 (70-80) (70-80) 00 (<70) (<70)

RED = APO-E GENOTYPE COMBINATION

YELLOW = NUMBER OF –SH GROUPS IN COMBINATION

WHITE = APPROXIMATE AGE OF ONSET OF AD

M. Godfrey, et al. APO-E Geneotyping as a Potential Biomarker for Mercury Neurotoxicity. J. of Alzheimer’s Disease (June 2003)

400 subjects with a mean of 13.7 amalgams, with previously 400 subjects with a mean of 13.7 amalgams, with previously diagnosed neurological problems, were compared to 426 diagnosed neurological problems, were compared to 426 blood donors with regards to APO-E geneotype. blood donors with regards to APO-E geneotype.

It was found that the symptomatic cohort was significantly It was found that the symptomatic cohort was significantly elevated in percentages of 4/4 (3.5 vs 1.0 ) elevated in percentages of 4/4 (3.5 vs 1.0 ) and and low in the low in the 2/2 (0.25 vs 1.4)2/2 (0.25 vs 1.4) in comparison to the blood donors. in comparison to the blood donors.

In mixed geneotypes 2/3 (9.5 vs 20) and 3/4 (30.8 vs 25) In mixed geneotypes 2/3 (9.5 vs 20) and 3/4 (30.8 vs 25) similar skewed ratios were found.similar skewed ratios were found.

The 3/3 homozygote was found at 54.8 and 51.4 in the The 3/3 homozygote was found at 54.8 and 51.4 in the symptomatic and blood donor groups, respectively.symptomatic and blood donor groups, respectively.

Effect of Removal of Amalgams & Antioxidant Therapy on Patient Symptoms and Blood Hg Levels.

U. Lindh et al., Neuroendocrinology Letters, v23, 459, 2002.

Controls matched with test groups in age, gender & socio-economic conditions. They were subjectively healthy persons not suffering from any disease.

CONCLUSIONS WITH REGARD TO AD MOST, IF NOT ALL, ABERRANT BIOCHEMISTRY IN MOST, IF NOT ALL, ABERRANT BIOCHEMISTRY IN

AD BRAIN CAN BE MIMICKED BY Hg.AD BRAIN CAN BE MIMICKED BY Hg. THE DIAGNOSTIC HALLMARKS OF AD BRAIN CAN THE DIAGNOSTIC HALLMARKS OF AD BRAIN CAN

BE PRODUCED BY Hg CONCENTRATIONS LOWER BE PRODUCED BY Hg CONCENTRATIONS LOWER THAN REPORTED IN HUMAN BRAIN.THAN REPORTED IN HUMAN BRAIN.

THE BIOLOGICAL PLAUSIBILITY OF Hg BEING THE BIOLOGICAL PLAUSIBILITY OF Hg BEING CAUSAL IN AD IS MORE COMPLETE THAN CAUSAL IN AD IS MORE COMPLETE THAN THIMEROSAL CAUSATION OF AUTISM. THIMEROSAL CAUSATION OF AUTISM.

WHILE THERE HAS BEEN NO SIGNIFICANT WHILE THERE HAS BEEN NO SIGNIFICANT EPIDEMIOLOGICAL STUDY ON Hg EXPOSURE AND EPIDEMIOLOGICAL STUDY ON Hg EXPOSURE AND AD, AND REASONABLE PEOPLE COULD DISAGREE AD, AND REASONABLE PEOPLE COULD DISAGREE ABOUT THE CAUSALITY, THERE IS NO DOUBT ABOUT THE CAUSALITY, THERE IS NO DOUBT THAT EXPOSURE TO Hg WOULD EXACERBATE AD!THAT EXPOSURE TO Hg WOULD EXACERBATE AD!

CONCLUSION REGARDING AMALGAM FILLINGS

DUE TO THE ENHANCEMENT OF Hg TOXICITY DUE TO THE ENHANCEMENT OF Hg TOXICITY AND RETENTION BY FACTORS FOUND IN THE AND RETENTION BY FACTORS FOUND IN THE DIET, ANTIBIOTICS, OTHER TOXICANTS SUCH AS DIET, ANTIBIOTICS, OTHER TOXICANTS SUCH AS PbPb2+2+ & Cd & Cd2+2+, AND GENETIC SUSCEPTIBILITY , AND GENETIC SUSCEPTIBILITY THERE CANNOT BE ANY REASONABLE THERE CANNOT BE ANY REASONABLE PREDICITION OF A SAFE LEVEL OF MERCURY PREDICITION OF A SAFE LEVEL OF MERCURY EXPOSUREEXPOSURE WITHIN THE LEVELS PRODUCED BY WITHIN THE LEVELS PRODUCED BY HAVING AMALGAM FILLINGS.HAVING AMALGAM FILLINGS.

MERCURY FROM THE BIRTH MOTHER’S MERCURY FROM THE BIRTH MOTHER’S AMALGAMS IS FOUND IN THE CHILD ON BIRTH.AMALGAMS IS FOUND IN THE CHILD ON BIRTH.