IAOMT Petition for Reconsideration REFERENCES

IAOMT Petition for Reconsideration


[1] Laks, D.R., Assessment of chronic mercury exposure within the U.S. population, NationalHealth and Nutrition Examination Survey, 1999-2006, Biometals, (Aug. 2009).

[2] In this section of the paper (section 9), there are several incomplete references to publishedpapers identified only by author and year. Each of these papers is discussed in Richardson,G.M., et al., Mercury vapour (Hg0): Continuing toxicological uncertainties, and establishing aCanadian reference exposure level. Regulatory Toxicology and Pharmacology, 53: 32-38 (2009).The complete citations can be obtained from this article.

[3] Castorina, R., et al., Assessment of Potential Risk Levels Associated with U.S. EnvironmentalProtection Agency Reference Values, Environmental Health Perspectives, vol. 111, no. 10(August 2003).

[4] Richardson, G.M., et al., Mercury vapour (Hg0): Continuing toxicological uncertainties, andestablishing a Canadian reference exposure level. Regulatory Toxicology and Pharmacology, 53:32-38 (2009).

[5] Schubert, et al., “Combined Effects in Toxicology—A Rapid Systematic Testing Procedure:Cadmium, Mercury & Lead.” J. of Toxicology & Environmental Health, 4:763 (1978).

[6] Ehmann, W.D. et al., Application of Neutron Activation analysis to the Study of Age RelatedNeurological Diseases, Biol Trace Elem Res. 13:19-33 (1987).

[7] Thompson, et al., Regional Brain Trace-element Studies in Alzheimer=s Disease,Neurotoxicology, 9(1):107 (Spring 1988); Vance, Trace Element Imbalances in Hair and Nailsof Alzheimer=s Disease Patients, Neurotoxicology, 9(2):197-208 (Summer 1988); Cornett, etal., Imbalances of Trace Elements Related to Oxidative Damage in Alzheimer=s Disease Brain,Neurotoxicology, 19(3):339-45 (June 1998).

[8] Wenstrup, et al., Trace Element Imbalances in Isolated Subcellular Fractions of Alzheimer=sDisease Brains, Brain Res, 12;533(1): 125-31 (Nov. 1990).

[9] Saxe SR, et al., Dental amalgam and cognitive function in older women: findings from thenun study. J Am Dent Assoc. 1995; 126:1495–1501.

[10] Haley, B.E., The relationship of the toxic effects of mercury to exacerbation of the medicalcondition classified as Alzheimer=s disease, Medical Veritas 4 (2007) 1510B1524.

[11] How Mercury Causes Brain Neuron Degeneration (video)http://www.youtube.com/watch?v=VImCpWzXJ_w

[12] Leong C.C.W., Syed N.I., Lorscheider F.L., Retrograde Degeneration of Neurite MembraneStructural Integrity of Nerve Growth Cones Following in vitro Exposure to Mercury NeuroReportVol. 12 #4, 2001.

[13] Pendergrass, J. C. et al, Mercury Vapor Inhalation Inhibits Binding of GTP to Tubulin in RatBrain: Similarity to a Molecular Lesion in Alzheimer=s Disease Brain. Neurotoxicology 18(2),315‑324 (1997).

[14] Haley, B., The Relationship of the Toxic Effects of Mercury to Exacerbation of the MedicalCondition Classified as Alzheimer=s Disease, The Nordic Journal of Biological Medicine (June-July 2003).

[15] Breitner, J.C.S., et al., Alzheimer’s disease in aging twin veterans. III. Archives of Neurology,52:763-771 (1995).

[16] Ely, J.T.A., Mercury Induced Alzheimer’s Disease: Accelerating Incidence?, Bull EnvironContam Toxicol (2001) 67(6):800-806.

[17] Mutter, Alzheimer Disease: Mercury as a Pathogenetic Factor and as a Moderator,Neuroendocrinol Lett. 2004; 25(5):275-283 (AInorganic mercury (found in dental amalgam) mayplay a major role [in the pathogenesis of Alzheimer=s Disease.@])

[18] Roses AD and Saunders AM. Apolipoprotein E genotyping as a diagnostic adjunct forAlzheimer’s disease. Int Psychogeriatr. 1997; 9 (Supp. 1):277–288 and 317–321.

[19] Brouwer DA., Clinical chemistry of common Apoprotein isoforms. J Chromatography BBiomed Applic. 1996; 678 (1):23–41.

[20] Godfrey ME, Wojcik DP, Krone CA., Apolipoprotein E genotyping as a potential biomarkerfor mercury neurotoxicity. J Alz Disease 2003; 5:189–195.

[21] Wojcik,et al., Mercury toxicity Presenting as chronic fatigue, memory impairment anddepression: Diagnosis, treatment, susceptibility, and outcomes in New Zealand generalpractice setting (1994-2006) Neuro Endocrinol Lett 2006;27 (4):415-423.

[22] Khatoon S, et al., Aberrant GTP β-tubulin interaction in Alzheimer’s Disease. Annals ofNeurology 1989;26:210–5. David S, Shoemaker M, Haley B. Abnormal properties of creatinekinase in Alzheimer’s Disease brain: correlation of reduced enzyme activity and active sitephotolabeling with aberrant cytosol-membrane partitioning. Molecular Brain Research1998;54:276–87. Duhr EF, Pendergrass JC, Slevin JT, Haley B. HgEDTA complex inhibits GTPinteractions with the E-Site of brain β-tubulin. Toxicology and Applied Pharmacology 1993Oct.;122(2):273–88.

[23] Ehmann, et al., Brain Trace Elements in Alzheimer’s Disease, Neurotoxicology,7(1):195-206 (Spring 1986).

[24] Thompson, et al., Regional Brain Trace-element Studies in Alzheimer’s Disease,Neurotoxicology, 9(1):107 (Spring 1988).

[25] Vance, Trace Element Imbalances in Hair and Nails of Alzheimer’s Disease Patients,Neurotoxicology, 9(2):197-208 (Summer 1988).

[26] Wenstrup, et al., Trace Element Imbalances in Isolated Subcellular Fractions of Alzheimer’sDisease Brains, Brain Res, 12;533(1): 125-31 (Nov. 1990).

[27] Mutter, Alzheimer Disease: Mercury as a Pathogenetic Factor and Apolipoprotein E asa Moderator, Neuroendocrinol Lett. 2004; 25(5):275-283 (“Inorganic mercury (found in dentalamalgam) may play a major role [in the pathogenesis of Alzheimer’s Disease.”]).

[28] Duhr, et al., Hg sup 2+ induces GTP-tubulin interactions in rat brain similar to thoseobserved in Alzheimer’s disease, 75th Annu. Meet. FASEB, Abstr. No 493, Georgia 21-25 April1991.

[29] Ely, J.T.A, et al., (1999) Urine mercury in micromercurialism: bimodal distribution anddiagnostic implications. Bull Environ. Contam. Toxicol. 63:553-9.

[30] Haley, B., Mercury toxicity: Genetic susceptibility and synergistic effects. Medical Veritas 2(2005) 535-542.

[31] Haley, B., Relationship mercury to exacerbation Alzheimer’s disease. Medical Veritas 4(2007) 1510-1524.

[32] Mutter, et al., Amalgam Disease: Article by Gottwald et al.: Poisoning, allergy, or psychicdisorder? Int. J. Hyg. Environ. Health 204, 223-229 (2001).

[33] Olivieri, et al., Mercury induces Cell Cytotoxicity and Oxidative Stress and Increase b-Amyloid Secretion and Tau Phosphorylation in SHSY5Y Neuroblastoma Cells, Journal ofNeurochemistry, Vol. 74, No. 1, 2000 231-236.

[34] Olivieri, et al., The effects of beta-estradiol on SHSY5Y neuroblastoma cells during heavymetal induced oxidative stress, neurotoxicity and beta-amyloid secretion, Neuroscience.2002;113(4):849-55.

[35] Mutter, J., et al.; Comments toxicology of Mercury and Chemical Compounds” by Clarksonand Magos (2006) Critical Reviews in Toxicology, 37:537-549 (2007).

[36] Wojcik,et al., Mercury toxicity presenting as chronic fatigue, memory impairment anddepression: Diagnosis, treatment, susceptibility, and outcomes in New Zealand general practicesetting. (1994-2006) Neuro Endocrinol Lett 2006;27 (4):415-423.

[37] Pendergrass, J.C. and Haley, B.E., Inhibition of Brain Tubulin-Guanosine 5’-TriphosphateInteractions by Mercury: Similarity to Observations in Alzheimer’s Diseased Brain. In MetalIons in Biological Systems V34, Mercury and Its Effects on Environment and Biology, Chapter16. Edited by H. Sigel and A. Sigel. Marcel Dekker, Inc. 270 Madison Ave., N.Y., N.Y. 10016(1996).

[38] Pendergrass, J.C. and Haley, B.E., Mercury-EDTA Complex Specifically Blocks Brain b-Tubulin-GTP Interactions: Similarity to Observations in Alzheimer”s Disease. Status Quo andPerspective of Amalgam and Other Dental Materials (International Symposium Proceedings at98-105, (ed. by L. T. Friberg and G. N. Schrauzer.) Georg Thieme Verlag, Stuttgart-New York(1995).

[39] Pendergrass, J. C., Haley, B.E., Vimy, M. J., Winfield, S.A. and Lorscheider, F.L., MercuryVapor Inhalation Inhibits Binding of GTP to Tubulin in Rat Brain: Similarity to a MolecularLesion in Alzheimer’s Disease Brain. Neurotoxicology 18(2), 315-324 (1997).

[40] David, S., Shoemaker, M., and Haley, B., Abnormal Properties of Creatine kinase inAlzheimer’s Disease Brain: Correlation of Reduced Enzyme Activity and Active SitePhotolabeling with Aberrant Cytosol-Membrane Partitioning. Molecular Brain Researchaccepted (1997).

[41] Hock C, et al., Increased blood mercury levels in patients with Alzheimer’s disease. J NeuralTransm. Vol. 23, No. 26. (1998) 105(1):59-68.

[42] Ely, J.T.A., Mercury Induced Alzheimer’s Disease: Accelerating Incidence?, Bull Environ.Contam. Toxicol. (2001) 67:800-806.

[43] Duhr, E., et al., HgEDTA Complex Inhibits GTP Interactions with the E-Site of Brain Beta-Tubulin, Toxicology and Applied Pharmacology, 122, 273-280 (1993).

[44] Ngim, C., Epidemiologic Study on the Association between Body Burden Mercury Level andIdiopathic Parkinson’s Disease, Neuroepidemiology, 8:128-141 (1989).

[45] Smoking Teeth Interviews. DVD furnished FDA Joint Panels in 2006.

[46] DISPERSALLOY® DISPERSED PHASE ALLOY Tablets, Powder MATERIAL SAFETYDATA SHEET by Dentsply Caulk 38 West Clarke Avenue, Milford DE 19963-0359 Dateprepared 9/20/95 Dated Revised 9/24/97.

[47] Scientific American, Sept. 1996, p. 25.

[48] Encyclopedia of Occupational Health and Safety, (3rd revised edition 1983). Parmeggiani,L., Technical Editor, pp. 1334-1335.

[49] Baasch, E., Theoretische Ueberlegungen zur Aetiologie der Sclerosis multiplex. DieMultiple Sklerose eine Quecksilberallergie? Schw. Arch. Neurol. Neurochir. Psychiat. 98, 1966,1-18.

[50] Craelius, W., Comparative epidemiology of multiple sclerosis and dental caries. J.Epidemiol. Comm. Health 32:155-165 (1978).

[51] Ingalls, T.H., Epidemiology, etiology, and prevention of multiple sclerosis. Hypothesis andfact. Am. J. Forensic Med. Pathol. 4:55-61 (1983).

[52] Ingalls, T.H., Triggers for multiple sclerosis. Lancet, xx:160 (1986).

[53] Ingalls, T.H., Endemic clustering of multiple sclerosis in time and place, 1934-1984. Am. J.Forensic Med. Pathol. 71:3-8, (1986).

[54] Ahlrot-Westerlund, B., Multiple Sclerosis and Mercury in Cerebrospinal Fluid. SecondNordic Meeting on Trace Elements in Human Health and Disease. Odense, Denmark. 17-21 Aug1987.

[55] Svare, C., et al., The effect of dental amalgams on mercury levels in expired air. J DentRes 1981; 60:1668-1671.

[56] Siblerud, R.L., et al., Evidence that mercury form silver dental fillings may be an etioogicalfactor in multiple sclerosis. Sci Total Environ 1994 Mar 15;142(3):191-205.

[57] Stejskal, Role of Metals in Autoimmunity and Link to Neuroendocrinology,Neuroendocrinology Letters 1999.

[58] Ely, et al., Urine Mercury in Micromercurialism: Bimodal Distribution and DiagnosticImplications, Bull. Environ. Contam. Toxicol. (1999) 63:553-559.

[59] Brown, I.A., Chronic Mercurialism, a cause of the clinical syndrome of amyotrophic lateralsclerosis. AMA Arch. Neural Psych 72:674-681 (1954).

[60] Kantarjian, A.D., A syndrome clinically resembling amyotrophic lateral sclerosis followingchronic mercurialism. Neurology 11:639-44 (1961).

[61] Barber, T.E., Inorganic mercury intoxication reminiscent of amyotrophic sclerosis. J.Occupat. Med. 20:667-9 (1978).

[62] Adams, C.R., et al., Mercury intoxication simulating amyotrophic lateral sclerosis. J.Amer. Med. Assoc. 250:642-3 (1983).

[63] Mano, Y., Amyotrophic lateral sclerosis and mercury-preliminary report. Department ofNeurology, Nara Medical University. Rinsho Shinkeigaku Nov 1990, 30 (11) pl275-7, ISSN0009-918X; Mano, et al., Mercury in hair of patients with ALS. Rinsho Shinkeigaku July 1989,29 (7) p844-8, ISSN 0009-918X.

[64] Haley, B., et al., GTP-binding proteins in amyotrophic lateral sclerosis cerebrospinal fluid.Ann Neurol (1995).

[65] Redhe, P., et al., Recovery From Amyotrophic Lateral Sclerosis and From Allergy AfterRemoval of Dental Amalgam Fillings. Int J Risk Saf Medicine, 4:229-36 (1994).

[66] Schwarz, S., et al., Amyotrophic lateral sclerosis after accidental injection of mercury. JNeurol Neurosurg Psychiatry 1996 Jun;60(6):698.

[67] Khare, S.S., et al., Trace element imbalances in amyotrophic lateral sclerosis,Neurotoxicology, Vol. 11, No. 3, pages 521-532, 47 references (1990).

[68] Geier, D.A., et al., A Prospective Study of Prenatal Mercury Exposure from MaternalDental Amalgams and Autism Severity, Acta Neurogiol Exp (2009) 69:1-9.

[69] Holmes A.S. et al, Reduced Levels of Mercury in First Baby Haircuts, of Autistic Children,Int J Tox, 22:277–285, (2003).

[70] Boyd, N.D., et al., Mercury from dental “silver” tooth fillings impairs sheep kidneyfunction. American J. Physiol, 261 (RICP 30): R1010-4 (1991).

[71] Hahn, L.J., et al., Dental “silver” tooth fillings: a source of mercury exposure revealed bywhole body scan and tissue analysis. FASEB J, 3:2641-6 (1989).

[72] Mortada, W.L., et al.. Urology and Nephrology Center, Mansoura University, Faculty ofScience, Egypt. J Nephrol 2002 Mar-Apr;15(2):171-6.

[73] Vimy, M.J., et al., “Glomerular filtration impairment by mercury released from dental”silver” fillings in sheep.” Department of Medicine, Pathology, and Physiology, University ofCalgary, Alberta, Canada. The Physiologist August 15 (1990).

[74] Hahn, L.J., et al., Whole-body imaging of the distribution of mercury released from dentalfillings into monkey tissues. FASEB, Vol. 4, Nov. 1990, pp. 3256-3260.

[75] Warfvinge, et al., Systemic Autoimmunity Due to Mercury Vapor Exposure in GeneticallySusceptible Mice: Dose-Response Studies. Toxicol Appl Pharmacol, 132:299-309 (1995).

[76] Hultman, P., et al., Adverse Immunological Effects and Autoimmunity Induced by DentalAmalgam and Alloy in Mice. FASEB J, 8:1183-90 (1994).

[77] Rothwell, J.,, et al.,, Amalgam dental fillings and hearing loss. Int J Audiol. 2008 Dec;47(12):770-6.

[78] See, Djerassi, E., et al., (1969) The possibilities of allergic reactions from silver amalgamrestorations. Int Dent J 19:481-488, attached hereto as Exhibit 117. (None of controls had allergyto dental amalgam. Of 180 subjects, 16.1 % exhibited an allergic response to amalgam and 11% were allergic to mercury. Of the subjects who had amalgam fillings for up to five years, 5.8percent showed positive reactions. For subjects who had amalgam fillings for more than fiveyears, 22.52 % had positive reactions.)

[79] North American Contact Dermatitis Group, Epidemiology of Contact Dermatitis in NorthAmerica, Arch Dermatol, vol. 108, (Oct.1973), attached hereto as Exhibit 118. (5.0% reacted toammoniated Hg; 8.0% reacted to thimerosal a mercury containing preservative.)

[80] White, R.R., et al., (1976) Development of mercury hypersensitivity among dental students,J. Am Dent. Assoc. 92:1204-1207, attached hereto as Exhibit 119. (Authors patch-tested 396dental students. Of those subjects having amalgam fillings for two years or less, 3.8 % hadpositive mercury patch tests, while 6.0% of those with amalgam fillings for more than five yearswere positive.)

[81] Miller, E.G., et al., (1987) Prevalence of mercury hypersensitivity in dental students. J.Prosthet. Dent. 58:235-237 (Exhibit 120) (Authors tested 171 dental students and found a greatercorrelation to the number of amalgam fillings subjects had than to the length of time the fillingswere in place. The percentage of the subjects testing positive to mercury ranged from 26.9% to38.7% by class.)

[82] Frustaci, A., et al., Marked elevation of myocardial trace elements in idiopathic dilatedcardiomyopathy compared with secondary cardiac dysfunction. J American College ofCardiology 33(6) 1578 (1999).

[83] Snapp, K.R., et al., Contribution of Dental Amalgams to Blood Mercury Levels. J Dent Res65:311, 1981 Abstract #1276, Special issue.

[84] Molin, M., Mercury Released from Dental Amalgam in Man, Swedish Dental J. Supp. 711990.

[85] Molin, M., Mercury, selenium, and glutathione peroxidase before and after amalgamremoval in man. Acta Odontol Scand 48:189-202 (1990).

[86] Molin, M., Kinetics of mercury in blood and urine after amalgam removal. J Dent Res74:420 IADR Abstract 159 (1995).

[87] Zander H.A., Effects of silicate cement and amalgam on the gingiva JADA, Vol. 55:11-15(1957), reported “materials used in restorative dentistry may be a contributing factor in gingivaldisease.”

[88] App G. R., Effect of Silicate, Amalgam, and Cast Gold on the Gingiva. J. Prost Dent Vol.11 #3 pp.522-532 (1961), suggested that there was greater chronic inflammation around amalgamsites than non-amalgam areas.

[89] Trott and Sherkat, J CDA, 30:766-770 (1964), demonstrated that the presence of amalgamcorrelates with gingival disease. Such disease was not present at contralateral amalgam-free sites.

[90] Sotres, L. S., et al., A Histologic Study of Gingival Tissue Response to Amalgam, Silicateand Resin Restorations J. Periodo. l40: 543-546 (1969), confirmed the Trott and Sherkatfindings.

[91] Turgeon, et al., (J CDA 37:255-256 (1972)) reported the presence of very significanterythema around amalgam restorations that was not present at control non-amalgam sites.

[92] Trivedi, S.C. and Talim, S.T. The response of human gingiva to restorative materials, J.Prosth. Dentistry, 29:73-81 (1973), demonstrated that 62.5% of amalgam sites have inflammatoryperiodontal tissue reaction.

[93] Goldschmidt, P.R. et al., Effects of amalgam corrosion products on human cells. J. Perio.Res., 11:108-115 (1976), demonstrated that amalgam corrosion products were cytotoxic togingival cells at concentrations of 10-6; that is, micrograms/gram of tissue.

[94] Fisher, D., et al., A 4-year follow-up study of alveolar bone height influenced by twodissimilar Class II amalgam restorations Journal of Oral Rehabilitation Vol. 11, pp 399-405(1984).

[95] Lorscheider, F.L., et al., Mercury Exposure from Silver Tooth Fillings: Emerging EvidenceQuestions a Traditional Dental Paradigm. FASEB J., 9:504-8 (1995).





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