VOLUME I Not found

VOLUME 2

Vol. 2 #1. Specification Program, ADA Guide to Dental Materials and Devices, 7th ed., chapt I:1-12 (1974-1975).

Vol. 2 #1A. Evaluation Programs, ADA Guide to Dental Materials and Devices, 7th ed., chapt II:13-15,18 (1974-1975).

Vol. 2 #1B. Amalgam and Mercury, ADA Guide to Dental Materials and Devices, 7th ed., chapt III: 19-35 (1974-1975).

Vol. 2 #1C. Recommended Standard practices for Biological and Clinical Evaluations, ADA Guide to Dental Materials and Devices, 7th ed. Chapt XVI:160-169 (1974-1975).

Vol. 2 #1D. Specifications for Dental Materials, ADA Guide to Dental Materials and Devices, 7th ed., 170-173;186-187 (1974-1975).

Vol. 2 #1E. List of Certified Dental Materials and Devices, ADA Guide to Dental Materials and Devices , 7th ed., 261-274 (1974-1975).

Vol. 2 #1F. Index to Manufacturers and Distributors of Certified and/or Classified Products, ADA Guide to Dental Materials and Devices, 7th ed., 275-282 (1974-1975).

Vol. 2 #1G. Publications and Educational Material, ADA Guide to Dental Materials and Devices , 7th ed., 283-288 (1974-1975).

Vol. 2 #1H. The International System of Units, ADA Guide to Dental Materials and Devices , 7th.ed., 289 (1974-1975).

Vol. 2 #2. Dental Mercury Hygiene, JADA vol. 122 (August 1991).

Vol. 2 #3. Pleva, J. PhD., Corrosion and Mercury Release from Dental Amalgam, Journal of Orthomolecular Medicine v.4, no 3:141-145;152-157 (1989).

Vol. 2 #4. Craig, R.G.,PhD., Amalgam, Restorative Dental Materials, 8th ed.:248-249 (1989).

Vol. 2 #5. Lussi, A., et.al., Mercury and copper release from amalgams in different soft drinks, Dental Materials, 279-281 (1990).

Vol. 2 #6. Craig, R.G., Biocompatibility of mercury derivatives, Dental Materials, v.2, no.3:91-96 (1986).

Vol. 2 #7. Okabe, T., Mercury in the structure of dental amalgam, Dental Materials, v.3,no.1:1-7 (1987).8. Gjerdet, N.R., et.al., Porosity, strength, and mercury content of amalgam made by different dentists in their own practice, Dental Materials, v.1:150-153 (1985).

Vol. 2 #9. Boyer, D.B., Mercury vaporization from corroded dental amalgam., Dental materials, v.4, no.2:89-93 (1988).

Vol. 2 #10. Phillips, R.W., Skinner’s Dental Amalgam: Technical Considerations, Science of Dental Materials, 8th ed.:335-336 (1982).

Vol. 2 #11. Mann, J., et.al., Mercury: Health Hazards in Dentistry, NY State Dental Journal, 21-25 (June/July 1986).

Vol. 2 #12. Device for Storing, Transporting and Mixing Reactive Ingredients, Johnson & Johnson.

Vol. 2 #13. Directions for Use Tytin Whitecap Capsules.

Vol. 2 #14. Recommendations in Dental Mercury Hygiene, Australian Dental Journal, vol. 32, no.2:136-137 (1987).

Vol. 2 #14A. Guidelines for the Safe Handling of Mercury, J. Canad. Dent. Assoc., v.51, no.7 (July 1985).

Vol. 2 #15. Missing Brown, E.M., DDS, Form letter to Doctor regarding 60 Minutes report on safety of silver amalgam fillings (December 1990).

Vol. 2 #16. Recommendations in dental mercury hygiene, JADA, v.109:617-619 (October 1984).

Vol. 2 #17. Safety & Infection control in the dental office, ADA:12-13 (1990).

Vol. 2 #18. Craig, R.G., PhD., et.al., Amalgam, Restorative dental materials, 5th ed.:203 (1975).

Vol. 2 #19. Missing Dental Mercury Hygiene, JADA vol. 122 (August 1991).

Vol. 2 #20. Smith, R.G., Dose-Response Relationship Associated with Known Mercury Absorption at Low Dose Levels of Inorganic Mercury, Environmental Mercury Contamination: 207-222 (1972).

Vol. 2 #21. Ericson, A., et.al., Pregnancy outcome in women working as dentists, dental assistants or dental technicians, Occupational Environmental Health, 329-333 (1989)

Vol. 2 #22. Inorganic Mercury, Environmental Health Criteria 118-World Health Organization, 29-33;86-113 (1991).

Vol. 2 #23. Missing Ngim, C.H., et.al., Epidemiologic Study on the Association between Body Burden Mercury Level and Idiopathic Parkinson’s Disease, Neuroepidemiology, v8:128-141 (1989).

Vol. 2 #24. Mercury, Material Safety Data Sheet-Fisher Scientific Chemical Div. , 1-7 (1988).

Vol. 2 #25. Department of Health Services Title 26 Register 91, no. 14: 755;805-806 (1991).

Vol. 2 #26. Hahn, L.J., et.al., Whole-body imaging of the distribution of mercury released from dental fillings into monkey tissues, FASEB , v.4:3256-3260 (November 1990).

Vol. 2 #27. Missing Eggleston, D.W., DDS., et.al., Correlation of dental amalgam with mercury in brain tissue, Journal of Prosthetic Dentistry v.58 no.6,:704-707 (December 1987). Found in Vol. 25 #6

Vol. 2 #28. Vimy, M.J., et.al., Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings, The American Physiological Society:R939-R945 (1990).

Vol. 2 #29. Siblerud, R.L., A Comparison of Mental Health of Multiple Sclerosis Patients with Silver/Mercury Dental Fillings and Those with Fillings Removed, Psychological Reports , v.70: 1139-1151 (1992).

Vol. 2 #30. Malmstrom, C. DDS., et.al., Amalgam-derived mercury in feces, Conference on Trace Elements in Health and Disease, Stockholm, (May 1992).

Vol. 2 #31. Enwonwu, C.O., Mercury Vapor in Dentistry: Critical Review of the Literature, Environmental Research, v.42:257-274 (1987).

Vol. 2 #32. Summers, A.O., et.al., “Silver” Dental Fillings Provoke an Increase in mercury and Antibiotic Resistant Bacteria in the Mouth and Intestines of Primates, APUA Newsletter, (1991).

Vol. 2 #33. Missing Gallowy, W.D., et.al., Toxicity Assessment of Mercury Vapor from Dental Amalgams, Symposium Abstracts:242-246.

Vol. 2 #34. Clarkson, T.W., Mercury, Journal of the American College of Toxicology, v.8, no.7:1291 (1989).

Vol. 2 #35. Missing Thompson, C.M., et.al., Regional Brain Trace-Element Studies in Alzheimer’s Disease, NeuroToxicology, v.9, no.1:1-6 (1988).

Vol. 2 #36. Warren, J., Alzheimer’s may be linked to mercury, UK scientists say, Lexington Herald-Leader (1990).

37. Clarkson, T.W., PhD, Mercury-An Element of Mystery, The New England Journal of Medicine, v.323, no.16: 1137-1139 (October 1990).

Vol. 2 #38. Ellenhorn, M.J., MD, et.al., Mercury, Medical Toxicology, 1048-1052.

Vol. 2 #39. Occupational Exposure to Inorganic Mercury, U.S. Dept. of Health, Education and Welfare 1-51;69-83 (1973).

Vol. 2 #40. Missing Parmeggiani, L., Mercury, Encyclopaedia of Occupational Health and Safety v.2, 3rd ed.:1332-1335 (1983).

Vol. 2 #41. Missing Summers, A.O., et.al., Increased Mercury Resistance in Monkey Gingival and Intestinal Bacterial Flora after Placement of Dental “Silver” Fillings, American Physiological Society Abstract Form (1990).

Vol. 2 #42. Nylander, M., et.al., Mercury concentrations in the human brain and kidneys in relation to exposure from dental amalgam fillings, Swed. Dent Journal., v.11:179-187 (1987).

Vol. 2 #43. Mercury, Material Safety Data Sheet, J.T. Baker Chemical Co., 1-4 (1986).

Vol. 2 #44. Warkany, J., et.al., Acrodynia and Mercury, The Journal of Pediatrics, v. 42:365-386 (1953).

Vol. 2 #45. Reeves, R.E., Summary of Scientific Evidence Questioning The Continued Use of Mercury as a Component of Dental Filling Material, 1-17

Vol. 2 #46. Goering, P.L., et.al., Symposium Overview-Toxicity Assessment of Mercury Vapor from Dental Amalgams, Fundamental and Applied Toxicology, v.19, no.3:319-329 (October 1992).

Vol. 2 #47. FDA Writ of Mandamus Petition, BIO-Probe Newsletter, v.8, issue 6:1-7 (November 1992).

Vol. 2 #48. “See-Surp” Report Conflict! Michael F. Ziff, DDS and Sam Ziff, Bio-Probe Newsletter, v.9, issue 2: 1-8 (March 1993). 49. Pamphlet promoting IntraCellular Diagnostics EXA Test, IntraCellular Diagnostics (1989).

Vol. 2 #50. Pamphlet promoting EXA,Elemental X-Ray Analysis, IntraCellular Diagnostics

(1991).

VOLUME 3

VOLUME 3 TOC CORRECTED BY DK 11/18/2008

1. Engle, J.H. et.al., Quantitation of total mercury vapor released during dental procedures, Dent Mater v.8:176-180 (May 1992).

Vol. 3 #2. Marek, M., The Release of Mercury from Dental Amalgam: The Mechanism and in vitro Testing, Journal of Dental Research v.69 no.5:1167-1174 (May 1990).

Vol. 3 #3. Marek, M., The Effect of Tin on the corrosion Behavior of the Ag-Hg Phase of Dental Amalgam and Dissolution of Mercury, Journal of Dental Research, v.69 no.12:1786-1790 (December 1990).

Vol. 3 #4. Marek, M., The Effect of the Electrode Potential on the Release of Mercury from Dental Amalgam, Journal of Dental Research v.72, no.9:1315-1319 (September 1993).

Vol. 3 #5. Marek, M., Interactions Between Dental Amalgams and the Oral Environment, Advances in Dental Research v. 6:100-109 (September 1992).

Vol. 3 #6. Lance, C., et al., Electrode Reactions on Freshly Generated Fracture Surfaces on Dental Amalgam Abstract #733, IADR, 1-9 (1993).

Vol. 3 #7. Marek, M., Mercury Vapor Emission from Fresh Fracture Surfaces of Dental Amalgam Abstract #26, IADR, 1-6 (1994).

Vol. 3 #8. Reinhardt, J.W., et.al., Mercury vapor expired after restorative treatment: preliminary study, Journal of Dental Research, v.58, no 10:2005 (1979).

Vol. 3 #9. Reinhardt, J.W., et. al., Mercury vaporization during amalgam removal, Journal Prosthetic Dentistry, v.50:62-64 (1983).

Vol. 3 #6. Engelman, M.A., DDS, Mercury Allergy Resulting from Amalgam Restorations, Cases & Comments, v.66: 122-123 (January 1962).

Vol. 3 #7. Table 2: Treatment room mercury vapor level (mg/M3) during ultraspeed removal of Amalgam Restorations: Dry cutting with central vacuum evacuation. Table 3: Treatment room mercury vapor level (mg/M3) during ultraspeed removal of amalgam restorations: Water spray and central vacuum evacuation. USAF US Air Force Vol. 57 #2 March/April 1978

Vol. 3 #8. Debre, R., et.al., Forme quadriplegique de l’acrodynie, Societe Medicale Des Hopitaux de Paris, 1074-1081 ( June 1934).

Vol. 3 #9. Teixeira, L.C., et.al., Printing of mercury distribution on the surface of dental amalgams, JADA, v.81:1159-1162 (November 1970).

Vol. 3 #10. Svare, C.W. et.al., Quantitative Measure of Mercury Vapor Emission from Setting Dental Amalgam, Journal of Dental Research, v. 52, no.4: 740-743 (August 1973).

Vol. 3 #11. Caron, G.A., et.al., Lymphocyte Transformation Induced by Inorganic and Organic Mercury, Int. Arch. Allergy v.37: 76-87 (1970).

Vol. 3 #12. Adverse Immune Effects of Dental Amalgam- New Evidence! Bio-Probe Newsletter, v.10, issue 6:1-8 (November 1994).

Vol. 3 #13. BIOCALEX 6/9 Directions for use 1-4.

Vol. 3 #14. Summers, A.O., et.al., Mercury Released from Dental “Silver” Fillings Provokes an Increases in Mercury- and Antibiotic Resistant Bacteria in Oral and Intestinal Floras of Primates, Antimicrobial Agents and Chemotherapy, v. 37, no. 4:825-834 (April 1993).

Vol. 3 #15. Endo, T., et.al., Gastrointestinal Absorption of Inorganic Mercuric Compounds in Vivo and in Situ, Toxicology and Applied Pharmacology, v.74:223-229 (1984).

Vol. 3 #16. Vroom, F. Q., et al., Mercury Vapour Intoxication, Brain , v.95:305-318 (1972).

Vol. 3 #17. Levine, S.P., et. al., Elemental mercury exposure: peripheral neurotoxicity, British Journal of industrial Medicine , v. 39:136-139 (1982).

Vol. 3 #18. Miller, J.M., et.al., Subclinical psychomotor and neuromuscular changes in workers exposed to inorganic mercury, American Industrial Hygiene Association Journal, 725-733 (October 1975).

Vol. 3 #19. L’Acrodynie, Diagnostic Differentie, 53-56. In French

Vol. 3 #20. Les Polyradiculonevrites Aigues Curables “Secondaires” Avec Dissociation Albumino-Cytologique.

Vol. 3 #21. Dahhan, S.S., et.al, Electrocardiographic Changes in Mercury Poisoning, The American Journal of Cardiology , v.14:178-183 (August 1964).

Vol. 3 #22. Ross, A.T., MD., Mercuri Polyneuropathy with Albumino-Cytologic Dissociation and Eosinophilia, JAMA:830-831 (June 1964).

Vol. 3 #23. Hirschman, S.Z., et. al., Mercury in House Paint as a Cause of Acrodynia, The New England Journal of Medicine, v.269, no. 17:889-893 (Oct 1963).

Vol. 3 #24 NUMBER MISSING

Vol. 3 #25. Marie, M.J., L’Acrodynie Paralytique Grave Avec Dissociation Albumino-Cytologique Du Liquide Rachidien, 217-231.

Vol. 3 #26. Iyer, K., et.al., Mercury Poisoning in a Dentist, Arch Neurol, v. 33:788-790 (November 1976).

Vol. 3 #27. Miyakawa, T., et.al., Experimental Organic Mercury Poisoning – Pathological Changes in Peripheral Nerves, Acta neropath.(Berl), v.15:45-55 (1970).

Vol. 3 #28. Barber, T.E., MD., Inorganic Mercury intoxication Reminiscent of Amyotrophic Lateral Sclerosis, Journal of Occupational Medicine, v.20, no.10:667-669 (1978).

Vol. 3 #29. Adams, C.R., et.al., Mercury Intoxication Simulating Amyotrophic Lateral Sclerosis, JAMA, v. 250, no. 5:642-643 (August 1983).

Vol. 3 #30. Albers, J.W. et.al., Neurological Abnormalities Associated with Remote Occupational Elemental Mercury Exposure, Annals of Neurology, v. 24, no.5:651-659 (November 1988).

Vol. 3 #31. Rupp, N.W., et. al., Significance to health of mercury used in dental practice: a review, JADA , v.82 1401-1407 (June 1971).

Vol. 3 #32. Levander, O.A., Nutritional factors in relation to heavy metal toxicants, Federation Proceedings, v.36, no.5:1683-1687 (April 1977).

Vol. 3 #33. Asbury, A.K., et.al., Assessment of Current Diagnostic Criteria for Guillain-Barre Syndrome, Annals of Neurology Supplement to v. 27:S21-S24 (1990).

Vol. 3 #34. Tolhurst, W.H., Letter to Dr. Allan H. Ropper on exposure to mercury causing Tolhurst’s polyneuropathy, (December 1994).

Vol. 3 #34A. Neurologic Consultation and Medical Reports on William Tolhurst (1991).

Vol. 3 #35. Lyttle, H.A., et.al., The Resistance and Adaptation of Selected Oral Bacteria to Mercury and its Impact on Their Growth, Journal of Dental Research, 1325- 1330 (1993).

Volume IVVolume IV 1. Pleva, J., Mercury from dental amalgams: exposure and effects, International Journal of Risk & Safety in Medicine , v.3:1-22 (1992).

Vol. 4 #2. Gay, D.D., Chewing Releases Mercury from Fillings, The Lancet (May 1979).

Vol. 4 #3. Corrosion of Dental Amalgam, Nature , Vol. 240:304-306 (Dec 1972).

Vol. 4 #4. Pleva, J. PhD., Mercury Poisoning from Dental Amalgam, Orthomolecular Psychiatry, v.12, no.3:184-193 (1983).

Vol. 4 #5. Matthes, F. T., et.al., Acute Poisoning Associated with Inhalation of Mercury Vapor, Pediatrics:675-688 (October 1958).

Vol. 4 #6. Hallee, T.J., Diffuse Lung Disease Caused by Inhalation of Mercury Vapor, American Review of Respiratory Disease, v. 99:430-436 (1969).

Vol. 4 #7. Sunderman, F.W., Perils of Mercury, Annals of Clinical and Laboratory Science, v. 18, no. 2: 89-101.

Vol. 4 #8. Taskinen, H., et.al., A possible case of mercury-related toxicity resulting from the grinding of old amalgam restorations, Scandinavian Journal Work Environ Health , v.15:302-304 (1989).

Vol. 4 #9. Teisinger, J., et.al., Pulmonary Retention and Excretion of Mercury Vapors in Man, Industrial Medicine and Surgery, 580-584 (1965).

Vol. 4 #10. Kazantzis, G., The Role of Hypersensitivity and the Immune Response in Influencing Susceptibility to Metal Toxicity, Environmental Health Perspectives, v.25:111-118 (1978).

Vol. 4 #11. Feit, H., Sources of Error in the Diagnosis of Guillain-Barre Syndrome, Muscle & Nerve, v.5:111-117 (1982).

Vol. 4 #12. Hoover, A.W., et.al, Absorption and Excretion of Mercury in Man, Arch Environ Health, v.12:506-508 (April 1966).

Vol. 4 #13. Jacobs, M.B., et.al., Absorption and Excretion of Mercury in Man, Archives of Environmental Health, v.9:454-463 (October 1964).

Vol. 4 #14. Leneman, F., The Guillain-Barre’ Syndrome, Arch Internal Medicine, v. 118:139-144 (August 1966).

Vol. 4 #15. Ropper, A.H., et.al., Guillain-Barre’ Syndrome, 22-30, 42, 53, 57-66, 175, 212-213.

Vol. 4 #16. Stopford, W., Mercury Intoxication Among Dental Personnel, JAMA , v. 250, no. 6:822 (August 1983).

Vol. 4 #17. Kennedy, D. Suggested Accurate Informed Consent for the Children’s Amalgam Trials in New England and Casa Pia, Orphan’s School in Lisbon, Portugal 2006

Vol. 4 #18. lobner, Asrari Neurotoxicity of Dental amalgam in Mediated by Zinc J Dent Res 82(3):243-/246, 2003

Vol. 4 #19. Anger, K Neurobehavioural tests and systems to assess neurotoxic exposures in the workplace and community Occup Environ Med Vol. 60 pp.531-538 2003 20. Yoshida M Susceptibility to metallothionein-Null Mice to the Behavioral Alterations Caused by Exposure to Mercury Vapor at Human-Relevant Concentration Toxicological Sciences Vol. 80 No. 1 (2004)

Vol. 4 #21. L. Barregard Mercury from dental amalgam: looking beyond the average OEM.bmjjournals.com 6 March 2006

Vol. 4 #22. Heyer, N Chronic Low-Level Mercury Exposure, BDNF Polymorphism, and Associations with Self-Reported Symptoms and Mood Toxicological Sciences Vol. 81 pp. 354-363 (2004)

Vol. 4 #23. Mutter, J. Blood Mercury and Neurobehavior Letters JAMA Aug. 10, 2005 Vol. 294 #6

Volume 5

1. Lorscheider, F.L., ADA's Attempt to Suppress and Outlaw Mercury-Free Dentistry Backfires, Mercury-Free News, v.5, no.2:9-15 (May 1992).

Vol. 5 #2. Safranek, T.J., et.al., Reassessment of the Association between Guillain-Barre’ Syndrome and Receipt of Swine Influenza Vacine in 1976-1977: Results of a Two-State Study, American Journal of Epidemiology, v.133, no. 9: 940-951 (1991).

Vol. 5 #3. Cornblath, D.R., et.al., Motor Conduction Studies in Guillain-Barre’ Syndrome: Description and Prognostic Value, Annals of Neurology , v. 23, no. 4:354-359 (April 1988).

Vol. 5 #4. Bromberg, M.B., et.al., Prognosis in Long-Term Immunosuppressive Treatment of Refractory Chronic Inflammatory Demyelinating Polyradiculoneuropathy, Journal Clin. Epidemiology, v.45, no.1:47-52 (1992).

Vol. 5 #5. Snapp, K.R., et.al., The Contribution of Dental Amalgam to Mercury in Blood, Journal Dental Research, v. 65, no. 5:780-785 (May 1989).

Vol. 5 #6. A. Abraham, et.al., The Effect of Dental Amalgam Restorations on Blood Mercury Levels, Journal Dental Research, v. 63. no. 1:71-73 (January 1984).

Vol. 5 #7. Plasmapheresis and acute Guillain-Barre’ syndrome, Neurology, v.35:1096-1104 (August 1985).

Vol. 5 #8. Donofrio, P.D., et.al., Acute Arsenic Intoxication Presenting as Guillain-Barre’ like Syndrome, Muscle & Nerve, v.12: 114-120 (February 1987).

Vol. 5 #9. Cornblath, D.R., et.al., Conduction Block in Clinical Practice, Muscle & Nerve, v.14:869-871 (September 1991).

Vol. 5 #10. Bromberg, M.B., et.al., Patterns of Sensory Nerve Conduction Abnormalities in Demyelinating and Axonal Peripheral Nerve Disorders, Muscle & Nerve, v. 16:262-266 (March 1993).

Vol. 5 #11. Masi, J.V., Corrosion of Restorative Materials: The Problem and the Promise, 1-16, (April 1994).

Vol. 5 #12. Grippo, J.O., et.al., Role of Biodental Engineering Factors (BEF) in the Etiology of Root Caries, Journal of Esthetic Dentistry, v.3, no. 2:71-76 (March 1991).

Vol. 5 #13. Meyer, C.B., Letter to Mrs. Renee Mauser regarding suspension of Dr. Hanus dental license, (1994).

Vol. 5 #14. Restoring the Normal Balance of Gastrointestinal Microorganisms, Health Talk, v. 9, no. 1:1-8 (June 1990).

Vol. 5 #15. MRI report/lab results for Dr. William Tolhurst, 9/8/1994.

Vol. 5 #16. Bloch, P., et.al., Summary of the International Conference on Mercury Hazards in Dental Practice, JADA, v.104, 489-490 (April 1982).

Vol. 5 #17. Eames, W. B., Preparation and condensation of amalgam with a low mercury-alloy ratio, The Journal of the American Dental Association, v. 58:78-83 (April 1959).

Vol. 5 #18. Hazards of Asbestos in Dentistry, Reports of Councils and Bureaus , JADA , v. 92: 777-778 (April 1976).

Vol. 5 #19. Guccione, P., et.al., Distribution of Mercury in the Rat After Long-Term Exposure to Vapors, Journal Dental Research, v. 54, no 6:1235 (December 1975).

Vol. 5 #20. No document

Vol. 5 #21. Chan, K.C., et.al., Mercury Vapor Emission from Dental Amalgam, Journal Dental Research, v.51, no.2:555-559 (March 1972).

Vol. 5 #22. Nunez, T.J., et.al., Influence of Amalgam, Alloy and Mercury on the In Vitro Growth of Streptococcus mutans: I. Biological Test System, Journal Dental Research, v.55, no.2:257-261.

Vol. 5 #23. Mathewson, R.J., et.al., Influences of Clinical Factors on Marginal Adaptation and Residual Mercury Content of Amalgam, Journal Dental Research, v54, no.1:104-109 (January 1973).

Vol. 5 #24. Dental Mercury Makers Not Required to Comply with California Disclosure Rules, BNA’s Health Law Reporter, (September 1994).

Vol. 5 #25. Concentration of Hazardous Substance, Labor Code, 119-120, (1992).

Vol. 5 #26. Product Label and Material Safety Data Sheets of Dispersalloy

Vol. 5 #27. Olsson, S., et.al., Release of Elements due to Electrochemical Corrosion of Dental Amalgam, Journal Dental Research, v.73, no.1: 33-43 (1994).

Vol. 5 #28. BBC-TV “Panorama” Does Expose on Dental Amalgam Controversy, Bio-Probe Newsletter, v.10, Issue 4:1-8 (July 1994).

Vol. 5 #29. Denton, S., The Mercury Cover-Up, Reprint from Health Consciousness Magazine, (June 1989).

Vol. 5 #30. Svare, C.W., et.al., Effect of Surface Treatment on the Corrodibility of Dental Amalgam, Journal Dental Research, v.51, no.1:44-46 (January 1972).

Vol. 5 #31. Jacobsen, H., et.al., Assessment of Microleakage Using a Conductimetric Technique, Journal Dental Research, 41-43 (January 1973).

Vol. 5 #32. Hinze, J., The Principles and Practice of Homeopathy, (1991).

Vol. 5 #33. Guillain, G., et.al., La forme acrodynique du syndrome de polyradiculo-nevrite avec dissociation albumino-cytologique du liquide cephalo-rachidien, Academie de Medecine, 527-533 (Mai 1941).

Vol. 5 #34. Socialstyrelsen Translation in English Stops Amalgam Use, Svenska Dagbladet, (May 1987).

Vol. 5 #35. Bundesinstitut for Drugs and Medical Products (former BGA) proposed changes in the Directives for use of amalgam. Translation in English

Vol. 5 #36. Reinhardt, J.W., et.al, Exhaled mercury following removal and insertion of amalgam restorations, Journal of Prosthetic Dentistry, v.49, no.5:652-656 (May 1983).

Vol. 5 #37. Workshop: biocompatibility of metals in dentistry, JADA, v. 100:469-471 (September 1984).

Vol. 5 #38. The Learned Intermediary Doctrine in Prescription Drug and Device Litigation, Swartz, Campbell & Detweiler, 10-12 (1994).

Vol. 5 #39. Hanson, M., Effects of Inorganic Mercury on the Nervous System, Bio-Probe Newsletter, v.5, issue 2:1-15 (March 1988).

Vol. 5 #40. Goodman and Gillman’s, Mercury, The Pharmacological Basis of Therapeutics, 8th ed. (1598-1602).

Vol. 5 #41. Overview of the Amalgam Issue, Amalgam, 28-30 (November 1985).

Vol. 5 #42. New Research – Amalgam Mercury Harms Dental Personnel, Bio-Probe Newsletter, v.11, issue 1:1-8 (January 1995).

Vol. VI.

1. Kawahara, H., et.al., Electron Microscopic Study of the Cytotoxicity of Cadmium and Mercury in Vitro, Journal Dental Research, v. 54, no. 1:125-130 (January 1975).

Vol. 6 #2. Frykholm, K.O., Mercury from Dental Amalgam Its Toxic and Allergic Effects and Some Comments on Occupational Hygiene, Acta Odontologica Scandinavica, v.15, supplement 22 (1957).Vol. VI3. Vimy, M.J., et.al., Estimation of Mercury Body Burden from Dental Amalgam: Computer Simulation of a Metabolic Compartmental Model, Journal Dental Research, v.65, no.12:1415-1419 (December 1986).

Vol. 6 #Vol. VI4. Chang, L. W., et.al, Mitochondrial Changes in Neurons Following Mercury Intoxication, American Association of Neuropathologists, 49th Annual Meeting (June 1973).

Vol. 6 #Vol. VI5. Heintze, U., et.al, Methylation of mercury from dental amalgam and mercuric chloride by oral streptococci in vitro, Scand Journal Dental Research, v91, no.2:150-152 (1983).

Vol. 6 #Vol. VI 6. Nagem-Filho, et.al., Tissue reaction to dispersion alloy amalgam, Journal Prosthet Dent., v.36, no. 4: 399-403 (October 1976).

Vol. 6 #Vol. VI #7. Trivedi, S.C., et.al., The response of human gingival to restorative materials, Journal Prosthet. Dent . , v. 29, no. 1:73-80 (January 1973).

Vol. 6 #Vol. VI #8. Cooper, G.P. et.al., Heavy Metals: Effects On Synaptic Transmission, Toxicology. V.5, no.3:247-266 (1984).

Vol. 6 #Vol. VI #9. Feldman, G., et.al., Tissue reactions to root filling materials, Odontologisk Revy, v.13, no.1:1-13 (1962).

Vol. 6 #Vol. VI #10. Eley, B.M., Tissue Reactions to Implanted Dental Amalgam, including Assessment by Energy Dispersive X-ray Micro-Analysis, Journal Pathology, v.138:251-269 (1982).

Vol. 6 #Vol. VI #11. Siblerud, R.L., The Relationship between Mercury from Dental Amalgam and Mental Health, American Journal of Psychotherapy, v.XLIII, no.4:575-587 (October 1989).

Vol. 6 #Vol. VI #12. Ellender, G., et.al., Toxic effects of dental amalgam implants. Optical histological and histochemical observations., Australian Dental Journal, v. 23, no.5:395-399 (October 1978).

Vol. 6 #Vol. VI #13. Siblerud, R.L., The Relationship between Mercury from Dental Amalgam and Oral Cavity Health, 6-10.

Vol. 6 #Vol. VI #14. Hahn, L.J., et.al., Dental “silver” tooth fillings: a source of mercury exposure revealed by whole-body image scan and tissue analysis, FASEB Journal, v. 3:2642-2646 (December 1989).

Vol. 6 #Vol. VI #15. Nilner, K., et.al., Effect of dental amalgam restorations on the mercury content of nerve tissues, Acta Odontol Scand, v. 43:303-307 (1985).

Vol. 6 #Vol. VI #16. Albers, J.W., et.al., Asymptomatic sensorimotor polyneuropathy in workers exposed to elemental mercury, Neurology, v. 32:1168-1174 (October 1982).

Vol. 6 #Vol. VI #17. Cross, J.D., et.al., Methyl Mercury in Blood of Dentists, The Lancet, 312-313 (August 1978).

Vol. 6 #Vol. VI #18. Ellingsen, A. A., et.al, A neurological and neurophysiological study of chloralkali workers previously exposed to mercury vapour, Acta Neurologica Scandinavica, v. 88:427-433 (1993).

Vol. 6 #Vol. VI #19. Feasby, T.E., Axonal Guillain-Barre Syndrome, Muscle & Nerve, v. 17:678-679 (June 1994).

Vol. 6 #Vol. VI #20. Cros, D., et.al, There are No Neurophysiologic Features Characteristic of “Axonal” Buillian-Barre Syndrome, Muscle & Nerve, v.17:675-677 (June 1994).

Vol. 6 #Vol. VI #21. Yuki, N., Pathogenesis of Axonal Guillain-Barre Syndrome: Hypothesis, Muscle & Nerve, v.17:680-682 (June 1994).

Vol. 6 #Vol. VI #22. Hartung, H., et.al, Immunopathogenesis and Treatment of the Guillain-Barre Syndrome-Part I, Muscle & Nerve, v.18:137-153 (February 1995).

Vol. 6 #Vol. VI #23. Hartung, H., et.al., Immunopathogenesis and Treatment of the Guillain-Barre Syndrome-Part II, Muscle & Nerve, v.18:154-164 (February 1995).

24. Stopford, W., et.al, Microenvironmental exposure to mercury vapor, Am. Ind. Hyg. Assoc, v. 39:378-384 (May 1978).

Vol. 6 #Vol. VI #25. Talley, R.L., et.al., Standards for the History, Examination, Diagnosis, and Treatment of Temporomandibular Disorders (TMD): A Position Paper, The Journal of Craniomandibular Practice, v.8, no1.:60-77, (January 1990).

Vol. 6 #Vol. VI #26. Recovery from Amyotrophic Lateral Sclerosis and From Allergy After Removal of Dental Amalgam Fillings, Dental Health Facts (May 1994).

Vol. 6 #Vol. VI #27. Resin Restorations, Textbook of operative dentistry, 423-431.

Vol. 6 #Vol. VI #28. Scientific Response to the American Dental Association’s Special Report and Statement of Confidence in Dental Amalgam, International Academy of Oral Medicine and Toxicology, 1-12. 1990

Vol. 6 #Vol. VI #29. Kennedy, D.C., Dental Personnel and the “Right to Know” (March 1990).

Vol. 6 #Vol. VI #30. Burton Goldberg Biological Dentistry, Alternative Medicine the Definitive Guide, 80-96 (1993).

Vol. VI #31. Silver Amalgam & Its Alternatives, Clinical Research Associates Newsletter, v.15, issue 2 (February 1991).

Vol. VI #32. Background and Agenda for Workshop on “Methods for Detection of Health Effects from Low Level Exposure to Methyl Mercury (MeHg) and Inorganic Mercury (Hg)”, (September 1994).

Vol. VI #34. Aten, J., et.al., Susceptibility to the induction of either autoimmunity or immunosuppression by mercuric chloride is related to the major histocompatibility complex class II haplotype, Euro. J. Immunol., v.21:611-616 (1991).

Vol. VI #35. World Update on the Mercury Amalgam Issue, Dental & Health Facts, v. 7, no.1:1-4 (February 1994).

Vol. VI #36. Vimy, M.J., Toxic Teeth: The Chronic Mercury Poisoning of Modern Man, Chemistry & Industry, 14-17 (January 1995).

Vol. VI #37. Lorscheider, F.L., et.al., Evaluation of the safety issue of mercury release from dental fillings, The Faseb Journal, v.7:1432-1433 (December 1993).

Vol. VI #38. Mercury, Pamphlet from U.S. Dept. of Labor OSHA (August 1975).

Vol. VI #39. Ziff, M.F., et. al., The Myth’s and the Fact’s, Bio-Probe Newsletter, v.3, issue 4:1-20 (September 1986).

Vol. VI #40. Ziff, M., et. al., Tracking the Elusive Mercury TLV, Precisely How Much Intra-Oral Mercury Vapor is Too Much?, Bio-Probe Newsletter, v.3, issue 6:1-24 (December 1986).

Vol. VI #41. Ziff, M.F., et.al., Dietary Mercury vs Amalgam Mercury A Red Herring?, Bio-Probe Newsletter , v.6, issue 1:1-12 (January 1989).

Vol. VI #42. Daily Intake of Mercury W.H.O. Scientists Disagree with Dentists, Bio-Probe Newsletter, v.7, issue 3:1-8 (May 1991).

Vol. VI #43. The ADA, FDA, NIDR and the 4th Amalgam War, Bio-Probe Newsletter , v.7, issue 6:1-16 (November 1991).

Vol. VI #44. Mercury Exposure Calculation, Kapsa & Meyer Attorneys.

Bibliography VII.

Volume VII #1. To the dental patient:, ADA News, January (1984).[vol.7, no.1]

ADA’s answers to the most commonly asked questions about dental amalgam are found on this page.

Volume VII #2. Odom, J.G., Ethics and Dental Amalgam Removal, JADA, v.122:69-71 (June 1991).[vol.7, no.2]

This review article examines the issue of dental amalgam removal from an ethical perspective and offers some practical advice on how to address this problem in the dental office.

Volume VII #3. When your patients ask about mercury in amalgam, JADA, v.120:395-398 (April 1990).[vol.7, no.3]

This article refreshes ADA members on the topic of the safety of dental amalgam; it’s presented in a question and answer format that attempts to simulate the questions you may hear from your patients.

Volume VII #4. ADA Membership, JADA, v. 114 (January 1987). [vol.7, no.4]

This article discusses several key resolutions relating to dental care programs which were adopted by the 1986 House of Delegates.

Volume VII #5. Dental Amalgam, ADA pamphlet (1985). [vol., 7, no.5] W186

ADA’s responses to the most frequently asked questions about dental amalgam are printed in this brochure.

Volume VII #6. Memo from Dr. Thomas J. Ginley (ADA) on Dental Amalgam (December 1990).[vol.7, no.6]

This memo refers to the 60 Minutes segment on dental amalgam. There is an enclosed commentary from the ADA Division of Legal Affairs addressing this issue and an ADA statement on dental amalgam both of which can be used to respond to member inquiries.

Volume VII #7. Truono, E.J., DDS., Special Report [vol.7, no.7]

This six-page booklet provides information ADA member dentists can use to answer the patient questions you have been hearing or will be hearing in the days ahead. The report was developed from the best available scientific evidence, presented by some of the most knowledgeable research scientists in the fields of biomaterials, dental restoration, dental epidemiology and health care ethics. It was created in response to the “60 Minutes” program.

Volume VII #8. M.S., arthritis groups get amalgam calls, ADA News, 10 (January 1991).[vol.7, no.8]

This news article discusses the reactions of the viewers that watched the “60 Minutes” report and how the M.S. Society in Chicago and Arthritis Foundation handled the phone calls from individuals who were looking for answers.

Volume VII #9. ADA amalgam information helps field patient queries, ADA News, 8 (January 1991).[vol.7, no.9]

This news article discusses the library of materials regarding the safety or effectiveness of dental amalgam compiled by the ADA and made available to dentists. The additional efforts made by the ADA in response to the “60 Minutes” program are listed.

Volume VII #10. Research addresses amalgam safety, ADA News, 6 (January 1991).[vol.7, no.10]

This news article reports on Dr. J. Rodway Mackert’s lecture at the ADA headquarters. He critiqued the University of Calgary study on dental amalgam’s effect on sheep and how it was flawed due to the implications for humans. The thrust of his talk dealt with disarming people’s fears about the safety of dental amalgam.

Volume VII #11. Dr. Loe: biased report ‘a disservice’, ADA News, 7 (January 1991).[vol.7, no.11]

In this news article Dr. Loe, director of the National Institute of Dental Research, analyzed the “60 Minutes” report.

Volume VII #12. Dentist barred for removing amalgam, ADA News (January 1991).[vol.7, no. 13] Baratz

This news article discusses the Iowa dentist who was charged with fraudulently treating a patient’s multiple sclerosis by removing her amalgam fillings. The dentist was barred from practicing dentistry for five years.

(Cont) Witness in Berger case responds, ADA News (January 1991).[vol.7, no.14]

This letter scripted by Dr. Robert S. Baratz was published in this journal. Dr. Baratz with the Tufts University School of Dental Medicine sent the letter to CBS-TV’s “60 minutes” on December 18, 1990. Dr. Baratz is a diplomat of the American Board of Oral Medicine and a professor in both the department of oral pathology at Tufts and the department of medicine and surgery with the Department of Veterans Affairs. Dr. Baratz presented his views as strictly his own, not necessarily those of Tufts University or the DVA.

Volume VII #13. ’60 Minutes’ report filled with errors: ADA, ADA News, (January 1991).[vol.7, no.15]

This news article discusses the six-page letter submitted by ADA President Eugene J. Truono addressed to “60 Minutes” Executive Producer Don Hewitt. The ADA letter protests that the “60 Minutes” report contained numerous inaccuracies, omitted important information and created serious misconceptions in the minds of viewers.

Volume VII #14. Questionable Care: What can be done about dental quackery?, JADA, v.115: 680-685 (November 1987). [vol. 7, no.16]

This article focuses on the nature and prevalence of quackery and health fraud, particularly as they relate to dentistry and dental care. Educators, dentists and other professionals who have devoted much of their lives to fighting quackery were interviewed.

Volume VII # 15.Lamm, O. et.al., Subclinical Effects of Exposure to Inorganic Mercury Revealed by Somatosensory-Evoked Potentials, Eur. Neurol. v.24:237-243 (1985).[vol. 7, no.17]

nerve ending conduction times at the periphery and an acceleration of the conduction from brain stem to cortex.

Volume VII #16. Arizona mercury decision “misguided’, ADA News (October 1989).[vol. 7, no.18]

This news article discusses the actions of the Arizona Department of Environmental Quality and U.S. Environmental Protection Agency on Pima County dental offices. The agencies shut down the dental offices until they met the required mercury levels-which amounted to a day. Greg McFarland, executive director of the Arizona State Dental Association states the agencies shut down the offices in order to demonstrate that they’re taking action. But they seem more interested in enforcing the federal requirements than they are about the validity of their testing methods.

Volume VII #17. Palmer, C., FDA panel: amalgam poses no direct hazard, ADA News, v.22, no.6:1,5 (March 1991).[vol. 7, no.19]

This news article discusses the Food and Drug Administration advisory panel’s urgent request to the agency to issue a public statement advising patients against removal of amalgam fillings.

Volume VII #18. Berry, T.G., et.al., Almost two centuries with amalgam: Where are we today?, JADA, v.125:392-399 (April 1994).[vol.7, no.20]

This review analyzes Amalgam and how it has provided a valuable and comparatively inexpensive service to patients for a longer time than any other restorative material. Despite the excitement surrounding the use of each new restorative material, each has a shortcoming that amalgam hasn’t.

Volume VII #19. Corbin, S.B., et.al., The benefits and risks of dental amalgam: Current findings reviewed, JADA, v.125:381-387 (April 1994).[vol. 7, no.21]

This article summarizes the principal findings, conclusions and recommendations from the comprehensive scientific review on dental amalgam performed by the U.S. Public Health Service. Both benefits and risks were analyzed and listed in the report.

Volume VII #20. Autoimmune Neuropathies: Guillain-Barre Syndrome, Annals of Neurology Supplement to Volume 27, S21-S24 (1990).[vol. 7, no.23]

This article defines GBS and the criteria for diagnosis as they were first published in the Annals of Neurology in 1978. Electrodiagnostic criteria are expanded and a series of comments and suggested modifications are added.

Volume VII #21. Advisory: Amalgam study, ADA, (1993).[vol.7, no.24]

This memo from the ADA Department of Professional Communications to Executive Directors, Constituent and Component Dental Societies discusses a study published on April 1, 1993 in the Journal of the American Society of Microbiology which claimed that the mercury in amalgam fillings may weaken the effectiveness of antibiotics and may jeopardize the effectiveness of the drugs to fight disease.

Volume VII #22. ADA Pamphlet on Mercury Testing Service [vol. 7, no.25]

This marketing brochure advertises a Mercury Testing Service offered by the American Dental Association to dentists and their staff.

Volume VII #23. American Dental Association, Principles of Ethics and Code of Professional Conduct, JADA, v. 117:657-661 (October 1988).[vol.7, no.26]

The purpose of the Principles and Code is to uphold and strengthen dentistry as a member of the learned professions. There are five principles listed along with corresponding codes of conduct and advisory opinions for each.

Volume VII #24. Spaeth, D., Researchers dispute mercury story, ADA News, v.25, no. 14:1,9 (August 1994). [vol. 7, no.28]

This news article cites a July 11 Reuters news service report which proclaimed “The use of mercury in dental fillings can cause brain damage not only in patients but in the dentists who handle it”. Diana Echeverria, PhD. whose research is cited in the Reuter article refutes that statement.

Volume VII #25. Langan, D.C., et.al., The use of mercury in dentistry: a critical review of the recent literature, JADA, v.115:867-880 (December 1987). [vol. 7, no. 29]

This report reviews recent scientific literature on the safety and use of mercury in dentistry. There is no evidence in the scientific literature that the minute amounts of mercury vapor that may be released from amalgam restorations cause mercury poisoning. Dental amalgam, which has been used extensively for more than 100 years has an exemplary record of safety and benefit to the dental patient.

Volume VII #26. Dentist accused of practicing medicine, ADA News, (June 1990).[vol.7, no.30]

This news article discusses the revocation of a dentist’s license by the New York State Dental Board. The dentist was charged with practicing medicine by

removing a patient’s dental amalgam in order to cure the patient of arm and leg pain.

Volume VII #27. ’60 Minutes’ visits ADA on amalgam, ADA news, v. 21, no.21 (November 1990)[vol.7, no.31]

This news article discusses the interview of CBS-TV’s correspondent Morley Safer with ADA Fifth District Trustee Heber Simmons regarding the safety of dental amalgam.

Volume VII #28. Mercury: muddled media ahead?, JADA, v.107:856 (November 1983).[vol. 7, no.32]

This editorial discusses the multitude of public media emphasizing the dangers of dental amalgam. Roger H. Scholle assures that current evidence indicates there is no reason for an individual to have amalgam restorations removed and that, in fact, the effect of such a procedure could be detrimental to the patient’s oral health.

Volume VII #29. Memo from Thomas H. Boerschinger on adoption of statement to ADA’s Code of Ethics (June 1987).[vol. 7, no.34]

This memo from Thomas H. Boerschinger, secretary, ADA Council on Ethics, Bylaws and Judicial Affairs to Presidents, Presidents-elect and Executive Directors of Constituent Dental Societies, Executive Secretaries and Secretaries of Component Dental Societies highlights the statement and advisory opinion no. 7 which was adopted to Section 1-J of the Association’s Code by the Council on Ethics, Bylaws and Judicial Affairs.

Volume VII #30. Dental Amalgam, ADA News, 12 (September 1986).[vol.7, no.35]

This news article reviews the seminar at ADA Headquarters where Dr. Sheldon Newman, a University of Colorado researcher, discussed whether mercury from amalgam poses a toxic hazard to patients or dental personnel.

Volume VII #31. Safety of dental amalgam-an update, JADA , v.119:204-205 (July 1989).[vol.7, no.36]

This article mentions several reviews of literature on mercury and amalgam. Based on these reviews and current information, amalgam is safe for patients not allergic to mercury and the occurrence of mercury allergy is extremely rare. There

is insufficient evidence to justify claims that mercury from amalgam restorations has an adverse effect on the health of the patients.

Volume VII #32. American National Standard/American Dental Association Specification No. 6 for Dental Mercury (January 1960).[vol. 7., no.37]

This is a list of requirements for the specification of mercury used in the production of dental amalgam.

Volume VII #33. Revised American Dental Association Specification No.1 for Alloy for Dental Amalgam, JADA, v.95:614 (September 1977).[vol.7, no.38]

The revised American Dental Association Specification No. 1 for Alloy for Dental Amalgam was approved by the Council on Dental Materials and Devices of the American Dental Association and is published in detail. This revision includes a modification of the chemical composition clause to permit more flexibility in composition and removal of the diametral tensile test at 15 minutes after mixing and replacing it with the one-hour compressive strength test

Volume VII #34. Addendum to American National Standards Institute/American Dental Association Specification No.1 for Alloy for Dental Amalgam, JADA , v.100 (February 1980).[vol. 7, no. 39]

The addendum to American National Standards Institute/American Dental Association Specification No. 1 for Alloy for Dental Amalgam was approved by the ADA’s Council on Dental Materials, Instruments, and Equipment. The creep limit was revised to 3%.

Volume VII #35. ADA agencies respond to House resolutions, ADA News (August 1987).[vol. 7, no.40]

Incomplete article. This article is a reprint of the third and final segment of the ADA midyear report.

Volume VII #36. Spaeth, D., Dentist’s license revoked, ADA News (February 1994).[vol.7, no.43]

This article discusses the case of Dr. Mark S. Hulet whose license was revoked by the California State Dental Board. Dr. Hulet was accused of gross negligence, incompetence, repeated negligent acts, fraud and false advertising. Dr. Hulet over a period of 10 years removed amalgam restorations from several patients after advising them that their health would improve by doing so.

Volume VII #37. News coverage spurs dental mercury debate, ADA News (November 1983).[vol.7, no.44]

This article discusses recent publicity about claims that amalgams can lead to a variety of diseases and maladies ranging from multiple sclerosis to epileptic seizures. Dr. Edgar W. Mitchell, PhD, secretary to the ADA Council on Dental Therapeutics reviews several scientific studies and concludes ‘there is simply no need to replace existing amalgams based on what we know.’

Volume VII #38. Workshop reaffirms dental amalgam safety, ADA News, (July 1984).[vol. 7, no.45]

This article highlights the presentations and conclusions that took place at the Workshop on the Biocompatibility of Metals in Dentistry.

Volume VII #39. Status Report on “Mercury Amalgam”, IAOMT (June 1995).[vol.7, no.46]

This announcement explains that The International Academy of Oral Medicine and Toxicology petitioned International Governments to cease and/or restrict the use of mercury-containing dental “fillings”. The governments of Austria, Finland, Germany and Sweden announced plans to stop or limit the use of dental mercury amalgams. Government of Canada has assented to place the mercury amalgam issue under review by regulatory authorities.

Volume VII #40. Letter from Michael Ziff regarding the issue of the safety of mercury exposure from amalgam dental fillings (September 1995).[vol.7, no.47]

This letter informs the reader that several nations have noted the medical scientific findings and have already announced plans to stop or severely limit the use of dental amalgam.

Volume VII #41. ADA responds to Bio-Probe, Bio-Probe Newsletter, v.11, issue 5 (September 1995).[vol.7, no.48]

This newsletter discusses Bio-Probe’s request for a response from the ADA regarding the ADA statement made in a court of law “The ADA owes no legal duty of care to protect the public from allegedly dangerous products used by dentists, etc.”

Volume VII #42. Asbury, A.K., More on the Chinese Experience with GBS, GBS Newsletter (1995).[vol. 7, no.49]

This newsletter article discusses the insight emerged from investigations in northern China where large numbers of Chinese suffer from GBS. GBS cases can be separated into two major subgroups, denoted as demyelinating and axonal. The distinction can be made by nerve conduction tests.

Volume VII #43. Opinion of John K. VandeKamp California Attorney General [vol.7, no.50]

A legal opinion was requested by The Honorable John W. Witt, City Prosecutor, City of San Diego from John K Van de Kamp, Attorney General (Ronald M. Weiskopf, Deputy Attorney General) on the questions: Is a dentist authorized to utilize the following in the course of the practice of dentistry: (1) urinalysis; (2) blood analysis; (3) hair analysis; (4) transcutaneous nerve stimulation; (5) electrogalvanic stimulation; (6) palpation to diagnose problems with the liver, thyroid and adrenal glands, (7) dietary recommendations; (8) prescribing Elavil to relax muscles, or (9) using oral drops to determine vitamin or mineral assimilation. The answer was affirmative where such endeavors could effectively be used to diagnose or treat a disease of the teeth, gums, jaw, alveolar process or associated structures. However, a dentist may not palpate the liver, the thyroid or the adrenal gland to discern problems therewith.

Volume VII #44. Breckenridge, M., Silver to the rescue, 12 (1995).[vol.7, no.52]

Incomplete – only page 12 is on file.

Volume VII #45. Maximum Allowable Concentrations of Mercury Compounds, Arch Environ Health, v. 19:891-905 (December 1969).[vol. 7, no.53]

This report is the result of decisions made at two meetings and is an evaluation of MAC values for mercury and its compounds. First, at the second International Symposium on Maximum Allowable Concentrations of Toxic Substances in Industrial Environments in 1963 expert groups established international values for the maximum allowable concentrations of a number of the more important compounds. Second, in 1966, the subcommittee for MAC values under the auspices of the Permanent Commission and International Association on Occupational Health, met in Vienna and responsibility was assigned for formation of groups to evaluate the scientific basis of MAC values for certain specific substances.

Volume VII #46. California State Bill Text for Bill number SB 934 (March 1991).[vol.7, no.54]

This is a copy of the Senate Bill Introduced by Senator Watson which would prohibit a dentist from using any material containing mercury to repair a patient’s oral condition or defect unless prior to using material containing mercury, the dentist obtains informed consent from the patient or the patient’s parent, guardian, conservator or other authorized person as appropriate.

Volume VII #47. California Governor Signs First-Ever “Dental Informed Consent Law”, Environmental Dental Association (October 1992).[vol. 7, no.57]

This press release discusses SB 934 which requires the Board of Dental Examiners of California to develop, distribute, and update as necessary a fact sheet describing and comparing the risks and efficacy of the various types of dental restorative materials.

Volume VII #48. California State Board Approves “Dental Materials Fact Sheet”, EDA Informed Consent, issue 7 (1993).[vol. 7, no.58]

This newsletter article discusses the Dental Materials Fact Sheet which was presented and approved at the State Board hearing May 3rd.

Volume VII #49. CDA “Bill of Rights” Celebrates First Anniversary, CDA Update, (March 1989).[vol. 7, no.59]

This article discusses the CDA Bill of Rights which was launched February 1988 and lists specific steps patients should take to be sure they receive proper dental care. On the first anniversary of the Bill of Rights, 10,000 requests for copies had been distributed.

Volume VII #50. Dental Patient Bill of Rights, California Dental Association, 1988. [vol. 7, no.60]

This brochure lists the six rights a dental consumer has and explains additional information regarding Dental Specialties, Recommended Office Procedures, Roles of the Dental Team Members and What to do in a Dental Emergency.

Volume VII #51. Koller, L.D., Immunosuppression Produced by Lead, Cadmium, and Mercury, Am. J. Vet. Res . , v. 34, no.11:1457-1458 (November 1973).[vol. 7, no.61]

For this experiment, rabbits were given lead acetate, cadmium chloride, or mercuric chloride in their drinking water for 70 days and then inoculated with pseudorabies virus. This produced immunosuppression to a viral agent.

Volume VII #52. Lee, S., Mercury toxicity in dental amalgam, Dentistry 85, v.5, no. 1:14-16,30 (February 1985).[vol. 7, no.62]

This article reviews the hazards of mercury and its use in dental amalgam. The evidence suggests that the mercury in dental amalgam is conditionally safe. For the dental professional, the potential for toxic mercury wexposure lies in an accidental spillage and/or poor mercury hygiene.

Volume VII #53. Eedy, D.J., et.al., Elevated T cell subpopulations in dental students, The Journal of Prosthetic Dentistry, v.63, no.5:593-596 (May 1990).[vol. 7, no.63]

For the study, the absolute numbers of circulating white cells and lymphocyte subpopulations were studied in 25 final-year dental students and compared with a control group of 28 medical students. The total lymphocyte count, total T cell numbers, T helper/inducer and T suppressor/cytotoxic numbers were significantly elevated in the dental students as compared with the control group.

Volume VII #54. Memo from Kip Sullivan on MDA-ADA line that mercury from amalgams is too little to harm anyone (October 1995). [vol. 7, no.64]

This memo addressed to Ed Munson, Rita VanPelt, Bob Asher, Pat Moore, Leo Cashman, Monica O’Kane, Barb Smial, Jan Forsberg, Elaine Kuretsky, Ron Rosenbaum and Gary Jacobson refutes the argument made by the MDA in that people with amalgams absorb (or “take up”) only two or three micrograms of mercury a day from their amalgams and this is less than 1% of what OSHA and the World Health Organization say is “safe.”

Volume VII #55. Dental Amalgam and Cognitive Function in Older Women” Findings From the Nun Study, JADA, v. 126:1495-1501 (November 1995).[vol. 7, no.65]

For this study, the authors determined the number and surface area of occlusal dental amalgams in a group of 129 Roman Catholic sisters who were 75-102 years of age. Findings from this study ow women with relatively homogeneous adult lifestyles and environments suggest that existing amalgams are not associated with lower performance on eight different tests of cognitive function.

Volume VII #56. Rees, J.H., et.al., Campylobacter Jejuni Infection and Guillain-Barre Syndrome, The New England Journal of Medicine, v.333, no.21:1374-1379 (November 1995).[vol. 7, no.66]

For this experiment, a prospective case-control study was performed in a cohort of patients with Guillain-Barre syndrome (96 patients) or Miller Fisher syndrome (7 patients) who were admitted to hospitals throughout England and Wales between November 1992 and April 1994. Infection with C. jejuni often precedes the Guillain-Barre syndrome and is associated with axonal degeneration, slow recovery, and severe residual disability.

Volume VII #57. The Changing Concepts of Guillain-Barre Syndrome, The New England Journal of Medicine, v. 333, no. 21:1415-1417 (November 1995).[vol. 7, no.67]

This article reviews the studies of the past 10 years which have dramatically altered the restricted viewpoint of what Guillain-Barre syndrome is. Suggestions of a primary axonal degeneration, a condition termed acute motor and sensory axonal neuropathy was discovered. Campylobacter jejuni must now be regarded as the chief precipitant of Guillain-Barre syndrome.

Volume VII #58. EMG in AIDP, Muscle & nerve , 534-539 (August 1985).[vol. 7, no.68]

Incomplete article- In our study, patients who fulfilled criteria suggestive of demyelination had an average of 2.4 electrodiagnostic studies, with less than half having only a single evaluation. By comparison, patients fulfilling the criteria for demyelination in a single nerve had an average of 1.4 studies, with 90% having a single evaluation. Patients with indeterminate evaluations had an average of 1.4 studies, with 71% of them having a single study.

Volume VII #59. Mercury, The Pharmacological Basis of Therapeutics, 8th Edition:1598-1602.[vol. 7, no.69]

This article explains about chemical forms and sources of mercury, the chemistry and mechanism of action, absorption, biotransformation, distribution, excretion and toxicity of various forms of mercury and the diagnosis and treatment of mercury poisoning.

Volume VII #60. What is the Faseb Journal? [vol. 7, no.70]

This paper defines and explains the structure of the FASEB Journal.

Volume VII #61. Colloidal Mild Silver Protein An Old Solution to the Problem of Increasing Antibiotic Resistance, Bio-Probe, (1995).[vol. 7, no.71]

This article discusses the use of Colloidal Mild Silver Protein as an antibiotic which has shown to have a greater range of chemotherapeutic effectiveness than any of the germ-based antibiotics.

Volume VII #62. Kiely, P., et.al., Inflammatory Polyarthritis Induced by Mercuric Chloride in the Brown Norway Rat, Laboratory Investigation, v. 73, no. 2:284-293 (1995).[vol. 7, no.72]

For this study, HgCl2-autoimmunity was induced in BN rats using standard methods. A self-limiting inflammatory arthritis develops in more than 82% of animals and is more severe in males. In contrast with other animal models, HgCl2-induced arthritis is associated with an apparent Th2 lymphokine response.

Volume VII #63. No Silver Lining for Dental Scare, (December 1995).[vol. 7, no.73]

This news article discusses a study completed by Don Henderson, head of cellular immunology and principal immunologist at Charing Cross and Westminster Medical School. His research shows that a significant number of people have an irrefutable effect with dental mercury. The immune system of these individuals responds to the mercury as if it were an invading enemy.

Volume VII #64. State Court Overturns Dental Board, Bio-Probe Newsletter, v.11, issue 6:1-8 (November 1995). [vol. 7, no.74]

This lead article discusses the State Court decision which overruled a State Dental Board’s disciplinary action against a mercury-free dentist. The Court stated that the Board of Dentistry provided no reasons or factual data for its decision to severely discipline the dentist and further, expressly stated that it relied upon material outside the evidentiary record. The Court also determined that the BOD violated State constitutional requirements and principles of due process of law, as well as the Board’s own rules and further held that the Board’s actions were arbitrary and capricious.

Volume VII #65. Testing Advice for Suspected Mercury Sensitive Patients[vol. 7, no.75]

This opinion letter discusses the removal of amalgam fillings is not advocated unless tests and history give a clear indication that mercury and/or other dental metals may cause adverse health effects in an individual.

Volume VII #66. Henderson, D., et.al., Lymphocyte Responses to Dental Metals Charing Cross & Westminster Medical School, (May 1995). [vol. 7, no. 76]

For this study, laboratory personnel and dental referral patients were recruited. 5 volunteers had no known prior exposure to dental metals but the other 4 volunteers and all 9 patients had been exposed to dental metals. The aims of this study were to develop an in vitro assay to detect memory T cells responsive to metal salts and to apply this assay to patients with possible hypersensitivity to mercury and other metals used in dental practice. Results from each group are not complete.

Volume VII #67. Henderson, D., Metal Specific Memory T Cell Tests, Charing Cross & Westminster Medical School, (May 1995). [vol. 7, no.77]

The results of two reports are shown on these pages in table format.

Volume VII #68. Choulos, V.B., et.al., It is more probable than not that we will soon become mad as hatters, or the legal and health effects of the us of dental amalgam, Toxic Substances and Mass Tort Litigation, San Francisco Barrister, (June 1985).[vol. 7, no.78]

This review article discusses the elements in our environments with direct impact upon our health, specifically, mercury contamination. Questions are answered related to the position of the ADA, if mercury leaches from dental amalgams, the effect of mercury exposure to the immune system, what is the judicial solution and does a person have a case if they suffer a serious illness following exposure to a toxic agent such as mercury.

Volume VII #69. Lorscheider, F.L., et.al., The dental amalgam mercury controversy-inorganic mercury and the CNS; genetic linkage of mercury and antibiotic resistances in intestinal bacteria, Toxicology, v.97:19-22 (1995).[vol. 7, no.79]

For this study, the effects of inorganic Hg exposure upon cell function in the brain and in the intestinal bacteria have recently been examined. In rats we demonstrate that ADP-ribosylation of tubulin and actin brain proteins is markedly inhibited, and that ionic Hg can thus alter a neurochemical reaction involved with maintaining neuron membrane structure. In monkeys we show that Hg, specifically from amalgam, will enrich the intestinal flora with Hg-resistant bacterial species which in turn also become resistant to antibiotics.

Volume VII #70. Tsuboi, R., et.al, Co-administration of Insulin-Like Growth Factor (IGF)-I and IGF-Binging Protein-1 Stimulates Wound Healing in Animal Models, Journal of Investigative Dermatology, v.104:199-203 (1995).[vol. 7, no.80]

For this experiment, the stimulatory effect of recombinant human insulin-like growth factor-I and recombinant human insulin-like growth factor –binding protein-1 on wound healing was assessed using diabetic db/db mice and normal rabbits. Results demonstrate that rhIG-FBP-1 enhances the stimulatory activity of rhIGF-I on wound healing and suggest the clinical utility of the co-administration of rhIGF-I and rhIGFBP-1 for wound repair.

Volume VII #71. Memo from Director-General of World Health Organization regarding Consensus Statement on Dental Amalgam (1995).[vol. 7, no.81]

This memo includes the WHO Consensus Statement on Dental Amalgam which lists 6 sections: Rationale for the use of amalgam in dentistry, alternative filling materials for amalgam, side-effects of amalgam, occupational risk to oral health personnel, environmental concerns, public opinion and mass media. Attached is also an Invitation to World-wide Partnership from FDI World Dental Federation.

Volume VII #72. Khare, S.S., et.al., Trace Element Imbalances in Amyotrophic Lateral Sclerosis, NeuroToxicology, v.11:521-532 (1990). [vol. 7, no.82]

For this experiment, concentrations of 15 elements were determined by instrumental neutron activation analysis in brain, spinal cord, blood cells, serum and nails of Amyotrophic Lateral Sclerosis patients and appropriately matched control subjects. Several significant imbalances were detected in trace element levels in ALS samples compared to control sample Hg and Se.

Volume VII #73. Ziff, S., et.al., The Truth About Dental Mercury Implants, Bio-Probe Newsletter, v.8, issue 1:1-8 (January 1992).[vol. 7, no.83]

This lead article discusses the history of the dental amalgam controversy and examines what events occurred in 1991 which included the ADA, FDA and National Institute of Dental Research becoming actively involved in the dental mercury controversy. Risk Assessment is also explained.

Volume VII #74. Ramirez,G., et.al., DMPS-Mercury Challenge Test, JPET, v.272:266-272 (1995).[vol. 7, no.84]

Incomplete article. The DMPS-Hg challenge test indicated that the body stores of mercury are larger in dental personnel in a modern dental clinic in Monterrey, Mexico than in nondental personnel who have not been occupationally exposed to mercury. The greatest increase in each group after the DMPS challenge occurred in the individual in that group who had the lowest urinary mercury excretion before DMPS administration.

Volume VII #75. Viola, P.L., et.al, The Effect of Chlorine on Mercury Vapor Intoxication. Autoradiographic Study, Med. Lavoro, v.59, n.6-7:437-444 (1968).[vol. 7, no.85]

A study was undertaken to investigate changes in the airborne concentration of mercury induced by adding chlorine vapors to the atmosphere. A comparative study was made of the intake and distribution of mercury in mice and rats exposed to mercury vapors alone and to mercury vapors in the presence of chlorine. Mice and rats intoxicated with mercury vapors alone or with mercury and chlorine vapors or with mercurous chloride showed marked differences in mercury uptake and distribution. The autoradiographic study of body distribution of inhaled Hg203

and Hg203-Cl absorbed from the intestinal tube, showed a much lower concentration in the brain and myocardium of Hg203-Cl as compared to inhaled Hg203.

Volume VII #76. Occupational Health Guideline for Inorganic Mercury, U.S. Department of Health and Human Services, 1-5 (September 1978).[vol. 7, no.86]

This guideline is intended as a source of information for employees, employers, physicians, industrial hygienists, and other occupational health professionals who may have a need for such information. It does not attempt to present all data; rather, it presents pertinent information and data in summary form.

Volume VII #77. Mercury in your dental fillings may be a health risk, report says, Toronto Star, A22 (November 1995).[vol. 7, no.87]

This news article reviews a report authored by Dr. Mark Richardson, a scientist assigned by Health Canada’s medical devices bureau to assess the safety of mercury in dental fillings.

Volume VII #78. Health Canada Dental Amalgam Risk Assessment, Bio-Probe Newsletter, v.12, issue 1:1-8 (January 1996).[vol. 7, no.88]

The lead article in this newsletter discusses the Health Canada report entitled “Assessment of Mercury Exposure and Risks from Dental Amalgam”. The report recommends the establishment of a “Tolerable Daily Intake” for mercury vapor and suggests the number of dental amalgam fillings for various age groups that will not compromise the TDI.

Volume VIII.

Vol. VIII #1. One Million ill from Amalgam?, German Newspaper (May 1996).[vol. 8, no.1]

This article originally written in German has been literally translated into English and discusses the level of mercury to be 10 to 100 times over the daily dose limit recommended by WHO.

Vol. VIII #2. Aposhian, H.V., Mercury Review, 1-47 (August 1991).[vol. 8, no.2]

This volume consists of 11 chapters and focuses on the pertinent question whether the release of mercury vapor from dental amalgams causes human disease. The second chapter is a brief review of mercury toxicology. Chapter three discusses if mercury from silver dental amalgams is absorbed and distributed throughout the body. Chapter four highlights how much mercury vapor is released and absorbed from dental amalgams. The fifth chapter discusses the estimated burdens in humans due to release of mercury from dental amalgams. Chapter six reviews other publications. Chapter seven focuses on reproductive hazards and remaining sections include summary, conclusion, recommendations and references.

Vol. VIII #3. Can dental amalgam be safely used with every patient?[vol. 8, no.3]

This page of questions and answers explains a definite no to the above question. Two other questions are listed related to why the dental profession continues to use amalgam and the Health Canada report on mercury exposure and risks released in 1995. The third question is missing the complete answer.

Vol. VIII #4. Dental Restorative Materials are effective and safe says NIH Panel, Consensus Development Conferences, (August 1991).[vol. 8, no.4]

This press release discusses the information shared by a panel of experts who convened at the 3-day technology assessment conference on the effects and side effects of dental restorative materials. The 14- member panel concluded that the amount of mercury vapor released from silver amalgam is very small and poses little risk to health. The conference was sponsored by at the National Institute of Dental Research and the NIH Office of Medical Applications of Research.

Vol. VIII #5. Effects and Side-Effects of Dental Restorative Materials, Advances in Dental Research, v.6:7-144 (September 1992).[vol. 8, no.5]

This report was prepared following the NIH Technology Assessment Conference in 1991 which consisted of 1 ½ days of presentations and discussion by the audience. The independent expert panel weighed the scientific evidence and wrote a draft statement in response to the following key questions: (1) What are the needs and benefits of tooth restorations? (2) What are the incidence and severity of side-effects associated with tooth restorative materials? (3) Do materials for tooth restorations contribute to systemic disease and reactions? (4) What are the benefit/risk ratios of different tooth restorative materials? (5) What should be the

future directions for research on materials for tooth restorations? The panel statement is published along with the studies that were presented.

Vol. VIII #6. Letter from Michael Ziff to John Ferguson on Technology Assessment Panel press conference, (August 1991).[vol. 8, no.6]

In his letter to Dr. Ferguson, Dr. Ziff implies that the expert panel’s statement was not based on valid scientific evidence. Dr. Ferguson replies to Dr. Ziff’s letter which is included as well.

Vol. VIII #7. Cover letter from Philip Neufeld, Health Canada, on Mark Richardson’s final report entitled “Assessment of Mercury Exposure and Risks from Dental Amalgam.” (August 1995). [vol. 8, no.7]

This letter is attached to a copy of Dr. Richardson’s report which was distributed upon request. The report is a review of the current scientific data. It estimates the exposure of the Canadian population to mercury from amalgam, food, and the environment. It reviews the Canadian and international literature on the health effects of mercury and recommends a Tolerable Daily Intake for mercury.

Vol. VIII #8. Is Mercury (from Fillings) a Factor in Causing Amyotrophic Lateral Sclerosis (ALS) (Lou Gehrig’s Disease).[vol. 8, no.8]

This review article discusses several studies regarding the connection between mercury/silver fillings and ALS.

Vol. VIII #9. Health Canada-Caves in to CDA and Amalgam Manufacturers, Bio-Probe Newsletter, v. 12, issue 2 (March 1996).[vol.8, no.9]

This article discusses Health Canada’s second meeting of the stakeholders for the risk assessment of dental amalgam held February 1996. As stated in this article, the focus of the meeting was to denigrate Dr. Mark Richardson’s risk assessment report as well as any and all published research challenging the safety of dental amalgam.

Vol. VIII #10. Feldman, R.G., et.al, Neurotoxic Effects of Trichloroethylene in Drinking Water, 3-23.[vol. 8, no.10]

This chapter discusses previous reports of areas with TCE contaminated water. There are studies of three groups who were exposed to TCE in drinking water in Massachusetts, Ohio and Minnesota. The descriptive data gathered on the individuals represent an effort to test a hypothesis of causation of possible effects of chronic exposure to TCE in drinking water in these people.

Vol. VIII #11. ADA Response on Amalgam Article, Lawsuit (1996). [vol. 8, no.11]

This article refutes the Bio-Probe Newsletter July 1995 article entitled “ADA Bails Out on Dental Amalgam-Leaves Dentists Hanging.” It explains that the ADA moved to be dismissed from the lawsuit in question on grounds that the plaintiff had failed to state a legal cause of action against the Association. The court agreed and granted the ADA’s motion.

Vol. VIII #12. First Results of Mercury Study Anticipated by EPA Reveal No Major Effects on Children, Den, v.27 (1996).[vol. 8, no.12]

This article discusses preliminary results from one of two studies holding up the release of a major EPA report on mercury indicate that elevated levels of the substance in infants do not appear to have significant neurotoxic effects.

Vol. VIII #13. Ho, T.W., et.al, Guillain-Barre syndrome in northern China Relationship to Campylobacter jejuni infection and anti-glycolipid antibodies, Brain , v. 118:597-605 (1995). [vol. 8, no.13]

For this report, 129 patients who underwent electrophysiological studies provided the demographic data for age and seasonal distributions. Based on electrophysiological criteria, Guillain-Barre syndrome in northern China can be divided into two predominant forms: AIDP and AMAN. The AMAN pattern was present in 65% and the AIDP form in 24%; 11% were unclassified. The frequency of C. jejuni antibodies was greater among AMAN patients than among patients with AIDP.

Vol. VIII #14. Enestrom, S., et.al, Does Amalgam Affect the Immune System? A Controversial Issue, Int. Arch. Allergy Immunol, v.106:180-203 (1995).[vol. 8, no.14]

This review paper gives a short history of dental amalgam, the composition of dental amalgam, describes the release of dental amalgam components, explains the non-dental exposure to mercury, outlines the daily retention of mercury in non-occupationally exposed individuals, how mercury is excreted, distribution and biological half-time of amalgam components, biocompatibility of amalgam components, highlights amalgam metals and the immune system: in vitro and in vivo studies, defines the immune responses to amalgam components in humans, as well as the systemic effects attributed to dental amalgam.

Vol. VIII #15. ADA Principles of Ethics and Code of Professional Conduct, (January 1995) [vol. 8, no.15].

The purpose of the Principles and Code is to uphold and strengthen dentistry as a member of the learned professions. There are five principles listed along with corresponding codes of conduct and advisory opinions for each.

Vol. VIII #16. Vol. VIII #16. Vimy, M.J., et.al, Mercury Usage in Canadian Dentistry Part 1: Critical Questions About Credibility, 1-26 (January 1996).[vol. 8, no.16]

The purpose of this document is to examine the role played by Canadian Dental Schools, dental professors and the Canadian Dental Association in the ongoing amalgam controversy in Canada; to disclose the limitation of their expertise as indicated by their experimental research publication productivity; and to review specific examples of whether they have disseminated scientifically accurate information to the media and the Canadian people. The data presented herein indicates that the Canadian dental academic community is not fulfilling its scientific responsibility-to create new knowledge.

Vol. VIII #17. Vimy, M.J., et.al, Mercury Usage in Canadian Dentistry Part 2: The CDA’s International Dental Expert Panel on Amalgam, 1-7 (February 1996).[vol. 8, no.17]

The purpose of this document is to examine the present CDA expert panel to determine their medical research expertise on the safety of mercury fillings. The data presented herein, clearly demonstrates that this CDA expert panel is not expert or qualified regarding the medical effects of mercury released from dental amalgam.

Vol. VIII #18 Tibbling, L., et.al, Immunological and Brain MRI Changes in Patients with Suspected Metal Intoxication, International Journal of Occupational Medicine and Toxicology, v. 4, no.2:1-10 (1995).[vol. 8, no.18] Stejskal

In this study, 34 patients with central nervous system and systemic symptoms suggestive of intoxication from dental amalgam were examined with magnetic resonance imaging of the brain and with a Memory Lymphocyte Immuno Stimulation Assay. A high rate of immunopathologies and objective signs of immunological reactions in the majority of the patients with MRI changes in the brain suggests that immunological mechanisms may play an important role in the development of the lesions.

Vol. VIII #19. Consequences of Mercury Vapor Exposure [vol.8, no.19]

This is a list of typical signs and symptoms, both short term and long term due to mercury vapor exposure as well as suggestions for treatment.

Vol. VIII #20. Dodes, J.E., Mercury in dental amalgam, The FASEB Journal, v.9 (November 1995).[vol. 8, no.20]

Dr. Dodes writes a letter to the editor of the FASEB Journal regarding the review article on mercury in dental silver-amalgam fillings which he believes neglected to cover several important pieces of information. There is an author’s reply included.

Vol. VIII #21. Are you at Risk from Amalgam Mercury Vapor? Dental Health Facts (January 1996). [vol.8, no.21]

This newsletter contains several brief articles about minimum risk levels for daily intake of mercury vapor, risk assessment studies, and discussion about Professor Alfred Stock’s statement made in 1926: “Dentistry should completely avoid the use of amalgam for fillings or at least not use it whenever this is possible. There is no doubt that many symptoms: tiredness, depression, irritability, vertigo, weak memory, mouth inflammations, diarrhea, loss of appetite and chronic catarrh often are caused by mercury which the body is exposed to from amalgam fillings, in small amounts, but continuously. Doctors should give this fact their serious consideration. It will then likely be found that the thoughtless introduction of amalgam as a filling material for teeth was a severe sin against humanity.”

Vol. VIII #22. Industrial Hygiene Technical Manual Appendix A, OSHA (March 1984).[vol. 8, no.22]

This chemical information table presents in concise form, useful data for mercury that may be encountered in industrial hygiene investigations. It is intended as a basic reference for industrial hygienists engaged in OSHA field activity.

Vol. VIII #23. Bonner, P., Update on Dentistry: An Interview With Dr. Gordon Christensen, Dentistry Today (February 1996).[vol. 8, no.23]

This interview discusses major issues facing the dental profession today and in the future with Dr. Gordon Christensen, co-founder of Clinical Research Associates and diplomate of the American Board of Prosthodontics. Dr Christensen is a researcher, lecturer and practitioner who devotes 100 days each year to presenting continuing education programs to his colleagues.

Vol. VIII #24. Clinical Implications of Elemental HG from Dental Amalgam: Amalgam and Mercury Hypersensitivity. [vol. 8, no.24]

This review article discusses dental amalgam Hg hypersensitivity which was a topic of the NIDR/ADA Workshop on the Biocompatibility of Metals in Dentistry. The steering committee at the workshop suggested that hypersensitivity occurred in less than 1% of the population, but did not cite any literature to support this hypothesis. Several studies highlighted in this text suggest considerably different estimates. which was a topic of the NIDR/ADA Workshop on the Biocompatibility of Metals in Dentistry. The steering committee at the workshop suggested that hypersensitivity occurred in less than 1% of the population, but did not cite any literature to support this hypothesis. Several studies highlighted in this text suggest considerably different estimates.

Vol. VIII #25. Controlling Mercury in Wastewater Discharges from Dental Clinics, National Association of Clean Water Agencies , 1-13, (January 2006) [vol. 8, no.25]

This White Paper is meant to help publicly owned treatment works and other organizations understand some of the technical issues associated with the generation of dental clinic wastewater. It was prepared by NACWA to assist those communities or states that decide to recommend or require the installation of amalgam separators.

Vol. VIII #26. Stone, M.E., The Effect of Amalgam Separators on Mercury Loading to Wastewater Treatment Plants, CDA Journal, v.32, no.7 (July 2004) [vol., 8, no.26]

This article reviews the data from five studies which took place in Toronto, Ont., Minneapolis/St. Paul, Minn., Duluth, Minn., Great Lakes, Ill., and Denmark. The results of these studies demonstrate the efficacy of amalgam separators in reducing Hg influent into waste water treatment plants.

Bibliography IX.

Volume IX.

Vol. IX #1. Toxic Responses of the Immune System, Casarett and Doull’s Toxicology, 3rd

edition, 267 (1986).[vol. 9, no.1]

The partial page from this volume discusses mercury-containing compounds which have been implicated in autoimmune processes that may be classified as type II or type IV reactions.

Vol. IX #2. Popescu, H.I., et.al, Chromosome Aberrations Induced by Occupational Exposure to Mercury, Arch Environ Health, v.34, no.6:461-3 (1979).[vol. 9, no.2]

For this study, the incidence of chromosome aberrations was studied by peripheral blood incubation using a modification of the Evans’ technique in twenty-two men exposed to either vapors of metallic mercury (Group I) or organic mercury (Group II). There was no statistical difference in the incidence of chromosome aberrations between men belonging to Groups I and II.

Vol. IX #3. Nodlind, K., Effect of Metal Allergens on the DNA Synthesis of Unsensitized Guinea Pig Lymphoid Cells Cultured in vitro, Int. Archs Allergy appl Immun, v.69:12-17 (1982).[vol. 9, no.3]

In this study, the metal allergens cobalt chloride, mercuric chloride, nickel sulfate and potassium dichromate were tested regarding their effect on the DNA synthesis of lymphoid cells from unsensitized guinea pigs. Mercuric chloride and potassium dichromate were found to be inhibiting at 10-6 to 10-4 M, while cobalt chloride and nickel sulfate were less toxic and inhibiting at 10-4 to 10-3 M.

Vol. IX #4. Verschaieve, L., et.al, Mercury Chloride-and Methyl Mercury Chloride-Induced Inhibition in NOR Activity, Teratogenesis, Carcinogenesis, and Mutagenesis, v.3:447-456 (1983). [vol. 9, no.4]

For this experiment, a cytophotodensitometric analysis was performed on silver-stained interphase nuclei from human peripheral blood lymphocytes exposed to various concentrations of HgCl2, CH3HgCl, and actinomycin D. Like actinomycin D, both mercury compounds were shown to inhibit the NOR activity.

Vol. IX #5. Verschaieve, L, et.al, Comparative in vitro cytogenetic studies in mercury-exposed human lymphocytes, Mutation Research, v.157:221-226 (1985). [vol. 9, no.5]

In this study the authors examined the in vitro clastogenic capacity of HgCl2 and CH3HgCl as well as their influence on chromosome segregation by means of a computer-aided chromosome distribution study in metaphase plates. The results indicate that mercury compounds alter the chromosome segregation at lower concentrations than those observed for clastogenicity.

Vol. IX #6. Weening, J.J., et.al, Cellular Immunity and Immunoregulation in Mercury Induced Glomerulopathy, Mercury Induced Immune Complex Glomerulopathy: An Experimental Study, 36-54;64-66;70-82 (1980).[vol. 9, no.6]

Two main categories of T-cell functions were studied in relation to the pathogenesis of mercury-induced immune complex glomerulopathy. It was found that lymphocytes from mercury diseased animals were less stimulated by PHA than lymphocytes from control animals, whereas direct migration inhibition assays revealed the presence of T-cell reactivity to nuclear and Fx1A antigens. As to the immunoregulation, con A-activated suppression was found to be decreased in lymphocytes from mercury diseased animals as compared to lymphocytes from controls. Neonatal thymectomy was found to accelerate the induction of antinuclear antibodies and immune complex glomerulopathy considerably.

Vol. IX #7. Goter-Robinson, C.J., et.al, Mercuric Chloride-,Gold Sodium Thiomalate-, and D-Penicillamine-Induced Antinuclear Antibodies in Mice, Toxicology and Applied Pharmacology, v. 86:159-169 (1986).[vol. 9, no.7]

Inducibility of antinuclear antibodies by mercuric chloride was studied in various strains of mice. High response to the treatment was observed in strains A.SW, A.CA, A.TH, B10.S, DBA/1J, and P/J; strains A.BY, B10.M and C3H/HeSnJ showed a low response, while strains A/WySn, A/J, A.TL, BALB/cJ, C57BL/10SnJ, B10.A and PL/J did not produce any detectable ANA. Gold Sodium thiomalate and D-penicillamine, also induced ANA in A.SW mice while other strains tested resisted this treatment.

Vol. IX #8. Andres, P, IgA-IgG Disease in the Intestine of Brown-Norway Rats, Ingesting Mercuric Chloride, Clinical Immunology and Immunopathaology, v.30:488-494 (1984). [vol. 9, no.8]

In this study of Brown-Norway rats, oral administration of mercuric chloride induced morphological lesions of the ileum and in lesser degree of the colon, with abnormal deposits of IgA in the basement membranes of intestinal glands and of IgG in the basement membranes and in the lamina propria. IgG reactive with renal and intestinal basement membranes and with the lamina propria of a normal BN rat was found in the serum and IgG deposits were present in renal glomeruli of BN rats receiving HgCl2.

Vol. IX #9. Knoflach, P, et.al, Autoimmune Disease Induced by Oral Administration of Mercuric Chloride in Brown-Norway Rats, Toxicologic Pathology, v.14, no.2:188-193 (1986). [vol. 9, no.9]

For this study, forty Brown-Norway rats received 150 g HgCl2/100 g body weight 3 times a week by gavage or by i.m injection with 100 g twice per week.

Antibodies binding to renal, intestinal, and vascular basement membrane developed after 2 weeks; circulating immune complexes were detectable in increasing titers starting at week 3. There were linear deposits of IgG, IgM and IgA in the glomerular basement membrane and tubular basement membrane, and along the intestinal basement membrane. In addition, interstitial nephritis was observed in some animals. Kidney involvement was as severe in the orally as the i.m.-treated animals.

Vol. IX #10. Sapin, C., et.al, Induction of anti-flomercular basement membrane antibodies in the Brown-Norway rat by mercuric chloride, Clin. Exe. Immunol., v.28:173-179 (1977).[vol. 9, no.10]

In this study, anti-glomerular basement membrane antibodies were induced in the Brown-Norway rat by mercuric chloride. The existence of anti-GBM antibodies was suspected because of the immunofluorescent linear pattern. It was proved because eluted antibodies from kidneys and circulating IgG had an anti-glomerular basement membrane activity.

Vol. IX #11. Michaud, A., et.al, Involvement of Hemostasis During an Autoimmune Glomerulonephritis Induced by Mercuric Chloride in Brown Norway Rats, Thrombosis Research, v.33:77-88 (1983). [vol. 9, no.11]

For this study, mercuric chloride was found to induce in Brown Norway rats an autoimmune disease characterized by a biphasic glomerulonephritis. A transient nephritic syndrome occurs during the third and fourth weeks after the first HgCl2

injection. Related to nephritic syndrome, an hypercoagulable state develops with decreased factor XII and antithrombin III levels and increased factor V activity and fibrinogen concentration. Most of the rats were found thrombocytopenic.

Vol. IX #12. Weeden, R.P., Lead, Mercury and Cadmium Nephropathy, NeuroToxicology , v.4, no.3:134-143 (1983).[vol. 9, no.12]

This review article highlights the kidney diseases due to lead, cadmium and mercury because they illustrate the complexity of nephrotoxicity and hence, the opportunities for fruitful investigation in the future. These metals are responsible for the sporadic appearance of renal disease following long-term, low-dose exposure.

Vol. IX #13. Warfvinge, G., et.al, Histochemical visualization of mercury in the oral mucosa, salivary and lacrimal glands of BN rats with HGCl2-induced autoimmunity, Exp. Toxic, Pathol , v.46:329-334 (1994).[vol. 9, no.13]

In the present study, the authors have utilized autometallographic techniques to visualize mercury in the oral mucosa, salivary and lacrimal glands of mercury-sensitive BN and –non-sensitive LEW rats injected with HgCl2. Phenotypic analysis revealed that most mercury-laden cells were ED2+ resident macrophages and that some, but not all, of these cells expressed MHC class II antigens (RT1B).

Vol. IX #14. Kelman, G.R., Urinary mercury excretion in dental personnel, British J. Industrial Medicine, v.35, no 3:262-265 (1978).[vol.9, no.14]

This study included an investigation mad on a total of 17 AHA and 16 NHS dental clinics in Leicestershire. AHA personnel comprised 28 dentists and 34 DSAs; NHS personnel consisted of 21 dentists and 28 DSAs. In both groups of workers the DSAs had a higher mean and greater range of urinary mercury concentrations than the dentists; the NHS workers had similarly, for both dentists and DSAs, a higher mean and greater range of concentrations.

Vol. IX #15. Seaton, A., et.al, Acute mercury pneumonitis, British Journal of Industrial Medicine, v.35:258-261 (1978).[vol. 9, no.15]

In this case review, an industrial accident where mercury spilled from a manometer and affected four men repairing a condenser in a power station is analyzed. The clinical and physiological changes shown by the four patients are consistent with the known pathological effects of mercury vapour. Patient 1 recovered completely in one week. His dyspnoea lasted four days, while his cough and chest tightness persisted for a week. Patients 3 and 4 remained symptom-free from the second day of hospital admission. Patient 2 developed dry cough and mild exertional dyspnoea which is still present two years after the episode.

Vol. IX #16. Opitz, H., et.al, Demonstration of mercury in the human brain and other organs 17 years after metallic mercury exposure, Clinical Neuropathology, v.15, no.3: 139-144 (1996). [vol. 9, no.16]

This study examines a male subject 17 years after he became exposed to metallic mercury vapor at work. He died of lung cancer in 1990. In different organs (brain, kidney, and lung) which were sampled at autopsy elevated levels of mercury were documented by atomic absorption analysis. Histological examination of the tissue by the Danscher and Schroder method showed a highly positive staining in the majority of nerve cells and cells of other organs. Ultrastructurally, mercury could be demonstrated by elemental x-ray analysis within lipofuscin deposits. The lipofuscin content was increased in the mercury positive nerve cells as demonstrated by a strong positive autofluorescence.

Vol. IX #17. Chang, L.W., Mercury, Experimental and Clinical Neurotoxicology, 508-526 (1980).[vol. 9, no.17]

This chapter gives a historical background on mercury, describes its physical and chemical data, general toxicology, as well as its connection to human disease, animal disease, experimental animal studies, possible pathogenetic mechanisms, and usefulness as an experimental model.

Vol. IX #18. Chang, L.W., Neurotoxic Effects of Mercury –A review, Environmental Research, v. 14:329-373 (1977).[vol. 9, no.18]

This review analyzes significant literature concerning the neurotoxic effects of mercury, biochemical, physiological and morphological. Mercury was found to penetrate and damage the blood-brain barrier very rapidly, leading to a dysfunction of the blood-brain barrier system. Both biochemical and electron-microscopic histochemical analysis revealed that, intracellularly, mercury was bound to the membranous organelles such as mitochondria, endoplasmic reticulum, Golgi complex, nuclear envelopes and lysosomes. Studies also indicated that drastic reduction of neuronal RNA and protein synthesis occurred in mercury-intoxicated animals. Disturbance of the enzymatic systems in the glycolytic pathway in the brain was also reported in mercury-poisoned animals. Based on the findings, a working hypothesis on the pathogenetic mechanism of mercury on the nervous system is proposed.

Vol. IX #19. Lawrence, D.A., et.al, Mercury Effects on the Immune System, Metal Toxicology, 322-329 (1995).[vol. 9, no.19]

This review discusses the presence of Hg in the environment and how the redistribution and accumulation of compounds containing mercury as a result of industrialization are the underlying causes of man’s exposure to higher-than-natural amounts, and thus to their potential adverse effects on human health. The paper concludes that Cd, Pb, and Hg can produce very diverse effects on the immune system.

Vol. IX #20. Brune, D., et.al, Gastrointestinal and in vitro release of copper, cadmium, indium, mercury and zinc from conventional and copper-rich amalgams, Scand. J. Dent. Res., v. 91:66-71 (1983).[vol. 9, no.20]

For this study, particles of a conventional lathe-cut, a spherical non-gamma 2 and a copper amalgam have been gastrointestinally administered to rats for the purpose of evaluation of the dissolution resistance. The contents of copper, cadmium, indium, mercury and zinc in kidney, liver, lung or blood were measured using nuclear tracer techniques. The levels of copper and mercury released from

the copper amalgam were approximately 50 times those of the two other amalgam types.

Vol. IX #21. Toxicological Profile for Mercury, U.S. Dept. of Health & Human Services (May 1994).[vol. 9, no.21]

Chapters 1 (excerpts), 2 and 7 are included in this section. Chapter one is an introductory Public Health Statement. Chapter 2 is organized first by route of exposure- inhalation, oral and dermal; and then by health effect – death, systemic, immunological, neurological, reproductive, developmental, genotoxic, and carcinogenic effects. These data are discussed in terms of three exposure periods-acute (14 days or less), intermediate (15-364 days), and chronic (365 days or more). Chapter 7 summarizes the international, national, and state regulations and guidelines regarding mercury and compounds in air, water, and other media.

Vol. IX #22. Dental Amalgam, Dept. of Health & Human Services, (January 1993).[vol.9, no.22] DHHS

This report was created by the Subcommittee on Risk Management and submitted to the Assistant Secretary for Health and Chairman of the Committee to Coordinate Environmental Health and Related Programs for the U.S. Public Health Service. The objective was to prepare a coherent, broad-based plan for enhancing risk definition, for helping dental patients and providers put amalgam risks and benefits into perspective through targeted educational initiatives, for identifying important research questions, and for ensuring adequate Federal regulatory oversight of this product. This report outlines a plan of action that addresses each of these areas and suggests the PHS agencies that are best suited to implement the various tasks.

Vol. IX #23. Council to Recommend Stronger Patient Q & As on Amalgam, CDA News (July 1996).[vol. 9, no.23]

This newsletter article discusses the patient information sheet that the CDA’s board of governors will be asked to approve at their August meeting in Montreal. The new sheet incorporates many of the same questions and answers found in a similar document that the board approved in 1995. But it also includes new information on the safe use of amalgam in immunologically compromised patients, as well as in children and pregnant women.

Vol. IX #24. Connolly, A.M., et.al, High-titer selective serum anti--tubulin antibodies in chronic inflammatory demyelinating polyneuropathy, Neurology , v. 43:557-562 (March 1993).[vol. 9, no. 24]

In this experiment, sera was studied from 70 CIDP patients, 35 Guillain-Barre syndrome patients and 483 disease (amyotrophic lateral sclerosis, Alzheimer’s disease, multiple sclerosis, diabetes and other polyneuropathies) and normal controls for selective high-titer anti--tubulin using ELISA methodology. 42% of patients with CIDP had selective high titer IgM reactivity against -tubulin; 23% had selective high-titer IgG reactivity against -tubulin.

Vol. IX #25. Brodsky, J.B., et.al., Occupational exposure to mercury in dentistry and pregnancy outcome, JADA, v.111 (November 1985). [vol.9, no.25]

In this study, a questionnaire was mailed to a random sample of 29,524 male dentists and 30,272 female dental assistants requesting information about work, health and reproductive history. Statistical analysis of the data indicated that there were no increased rates of spontaneous abortions or congenital abnormalities in the children of men and women who were exposed to low versus high levels of mercury in a dental environment.

Vol. IX #26. Ahlqwist, M., et.al, Concentrations of blood, serum and urine components in relation to number of amalgam tooth fillings in Swedish women, Community Dentistry and Oral Epidemiology , v.22 (1994).[vol. 9, no.26]

In this experiment, 1462 women aged 38,46,50, 54 and 60 years were examined in 1968/69 in a combined medical and dental population study in Gothenburg, Sweden. Number of tooth surfaces restored with amalgam fillings was assessed. The examination was repeated in 1980/81 including a new dental examination. The results from a number of biochemical analyses of blood, serum and urine were analyzed for possible statistical relationship to number of dental amalgam fillings. Amalgam fillings were not found to be associated with impairment of the kidney function or the immunological status.

Vol. IX #27. Ahlqwist, M., et.al, Number of amalgam fillings in relation to cardiovascular disease, diabetes, cancer and early death in Swedish women, Community Dent. Oral Epidemiol, v. 21 (1993).[vol. 9, no.27]

In this experiment, 1462 women aged 38, 46, 50, 54 and 60 years were initially examined in 1968-69 in a combined medical and dental population study in Gothenburg, Sweden. Number of tooth surfaces restored with amalgam fillings was assessed. The incidences of myocardial infarction, stroke, diabetes, cancer and overall mortality were determined during a 20-7ear follow-up period. Women with few amalgam tooth fillings had increase incidence of myocardial infarction,

stroke, diabetes and early death compared with women with a large number of fillings.

Vol. IX #28. Ahlquist, M., et.al, Number of amalgam tooth fillings in relation to subjectively experienced symptoms in a study of Swedish women, Community Dent. Oral. Epidemiol, v. 16 (1988). [vol. 9, no.28]

In this study, 1024 dentulous women aged 38-72 answered a questionnaire with 30 specific questions concerning different symptoms and complaints. The answers were related to number of tooth surfaces restored with amalgam. No positive correlations were found between number of amalgam fillings and number of symptoms, nor between number of amalgam fillings and prevalence of specified single symptoms or complaints. Women with a high number of amalgam fillings reported a lower number of symptoms and complaints than women with a low number of amalgam fillings.

Vol. IX #29. Blais, P., Dental Amalgam and the Public Health, Bureau of Medical Devices, (December 1976). [vol. 9, no. 29]

This paper is a view from the Health Protection Branch and discusses the dental amalgam problem and trends of thought at the Health Protection Branch. Also included is a Product Deficiency report on Dispersalloy, a paper entitled Cadmium and Lead in Dental Amalgam, and a paper entitled Briefing information on mercury poisoning of dental professionals: result of 1983 Manitoba Studies.

Vol. IX #30. Assessment of Exposure and Risks From Components and Degradation Products of Composite Resin Dental Materials O’Connor Associates Environmental Inc., (April 1996).[vol. 9, no.30] Richardson

For this study, exposures to major components and degradation products of dental composite resin materials were estimated for the Canadian adult population. To determine if unacceptable risks might be posed by these exposures, the estimated doses were compared to available toxicological reference doses for human ingestion exposure to these individual substances. It was concluded that composite resin dental restorations containing silica as the inorganic filler present no appreciable risk with respect to long-term daily exposure to SiO2, formaldehyde or methacrylic acid.

Vol. IX #31-49 empty

Volume X.

Vol. X #1. Health Canada Position Statement on Dental Amalgam [vol. 10, no.1]

This sheet lists the considerations and recommendations of Health Canada to dentists regarding dental amalgam.

Vol. X #2. The Safety of Dental Amalgam, Health Canada. [vol. 10, no.2]

This report was created in response to public concern and to numerous inquiries as to Canada’s position on the safety of amalgam. The Medical Devices Bureau of Health Canada began a study of the issue in 1992 with the aim of developing a statement on dental amalgam. The report highlights concerns over amalgam safety, regulatory status of amalgam in Canada, mercury release from amalgam and its absorption by the body, adverse health effects attributed to amalgam, environmental concerns and policies regarding mercury, use, suitability and safety of alternative materials, the Health Canada assessment of mercury exposure and risks from amalgam, the Health Canada stakeholder committee and its recommendations and conclusions. Richardson

Vol. X #3. Report from the EU AD Hoc Working Group on Dental Amalgam- a Critique.[vol. 10, no.3]

The Norwegian Dental Patient Association reviewed a draft version of a document issued by the “EU ad hoc working group on dental amalgam” and responded with comments which compose this report.

Vol. X #4. Love, J.M., Position Statement Written in Support of “Informed Consent” Bill Pending in the Legislature of the State of Main.(February1999) [vol. 10, no4].

This position statement was submitted to the Business and Economic Development Committee on behalf of the International Academy of Oral Medicine & Toxicology.

Vol. X #5. Richardson, G.M., Dental Amalgam and Mercury Exposure: Potential Patient Risks and the Basis for Restrictions on Use (1997). [vol. 10, no.5]

This study assessed potential risk of amalgam by comparing estimated chemical intake to doses considered safe, tolerable or of minimal risk. The results indicate that no credible assessment of mercury exposure, and no regulatory or other reference (acceptable, tolerable or minimal risk) dose for mercury vapour, support the continued, unlimited placement of amalgam fillings in dental patients.

Vol. X #6. Nickel, A.A., Cancer; You have the right to know You have the Right to Choose.[vol.10, no.6]

In his letter, Dr. Nickel discusses local anesthetics used in dentistry which are broken down by the human body into aniline and how it can cause cancer in humans.

Vol. X #10. Florida Dental Board Retreats, Bio-Probe Newsletter, v.13, issue 5 (September 1997). [vol. 10, no.7]

This newsletter article discusses the decision made by the Probable Cause Panel of the Florida Board of Dentistry to dismiss charges against mercury-free dentists Dr. Michael Ziff and Dr. Milton McIlwain.

Vol. X #11. Schmitt, R.B., Witness Stand; Who Is an expert? In Some Courtrooms, The answer is ‘Nobody’, The Wall Street Journal (June 1997). [vol. 10, no.8]

This newspaper article discusses how judges are removing expert witnesses from trials and not allowing them to testify.

Vol. X #12. McGinley, L., Of Mice and Men; How Ex-Lax, Trusted for Nearly a Century, Became a Cancer Risk, The Wall Street Journal (September 1997). [vol. 10, no.9]

This newspaper article discusses the product Ex-Lax being removed from store shelves in August 1997 after a main ingredient, phenolphthalein, was linked to a potential cancer risk if used excessively.

Vol. X #13. Facsimile from James M. Love to Dr. James L. Adams regarding Dentsply website. [vol. 10, no.10]

This email attached to this memo was sent from Sam Ziff was to James Love and discusses a website maintained by Dentsply, a manufacturer of dental amalgam. Dentsply admits that amalgams present many of the risks previously denied by the ADA, the WHO, the FDA etc.

Vol. X #14. Report on the 50-State Petition, Bio-Probe Newsletter, vol. 14, issue 1 (January 1998).[vol. 10, no. 11]

This newsletter article discusses Consumers for Dental Choice, who working closely with DAMS and Citizens for Health and their state affiliates, filed petitions with all 50 dental boards on September 24, 1997.

Vol. X #15. BBC “Panorama” Vindicated on Dental Amalgam!, Bio-Probe Newsletter, vol.13, issue 1 (January 1997). [vol. 10, no. 12]

This newsletter article discusses the British Broadcasting Corporation show “Panorama” which aired a program on mercury exposure from amalgam dental fillings in July 1994. Following the program, the British Dental Association filed a complaint with the Broadcasting Complaints Commission, claiming unfair treatment by the program.

Vol. X #16. Appeals Court Reverses Civil Suit Judgment Against Huggins!, Bio-Probe Newsletter, vol.13, issue 4 (July 1997).[vol. 10, no.13]

This newsletter article discusses the District Court decision to reverse civil judgment against Dr. Hal A. Huggins. He was charged by a plaintiff with negligent misrepresentation for his publications and television appearances on the adverse health effects of mercury amalgam dental fillings.

Vol. X #17. Vimy, M.J., et.al., Mercury from Maternal “Silver” Tooth Fillings in Sheep and Human Breast Milk, Biological Trace Element Research, v.56 (1997). [vol. 10, no.14]

For this study, neonatal uptake of mercury from milk was examined in a pregnant sheep model, where radioactive mercury/silver tooth fillings were newly placed. In a parallel study, the relationship between dental history and breast milk concentration of Hg was also examined in 33 lactating women. Results from the animal studies showed that, during pregnancy, a primary fetal site of amalgam Hg concentration is the liver and after delivery, the neonatal lamb kidney receives additional amalgam Hg from mother’s milk. In lactating women with aged amalgam fillings, increased Hg excretion in breast milk and urine correlated with the number of fillings or Hg vapor concentration levels in mouth air.

Vol. X #18. Amalgam War heating Up ADA Plans Media Blitz, Mercury-Free News, vol. 4, no.2 (July 1991). [vol. 10, no.15]

This newsletter article discusses the ADA’s defensive, self-serving position regarding the scientific evidence showing that dental amalgam presents a health risk.

Vol. X #19. Vimy, Breast Milk 1997Things That “Bug” Us: Mercury, Rising Disease Rates, Microbes, and Dead Doctors, Health Realities, vol. 16, no.1 (1997).[vol. 10, no.16]

This newsletter article discusses how 1996 was a challenging year regarding the field of health and one section focuses on the incidence where Colorado tried to

be first state to deny people the right to choose to have dental amalgam “mercury” fillings removed.

Vol. X #20. Brochure for seminar on Fundamental Defects That Underlie All Oral and Medical Diseases [vol. 10, no.17].

This registration brochure advertises a seminar which occurred in June 1998 on Free Radical Therapy.

Vol. X #21. Creatine, Health Realities, vol. 16, no.1 (1998).[vol. 10, no.18]

This newsletter article discusses Creatine supplementation and the fatal results which occurred with 3 young college athletes who took the dietary supplement in conjunction with rigorous workouts to lose weight to meet the weight-class restrictions in their sports.

Vol. X #22. Aschner, M., et.al., Metallothionein induction in fetal rat brain and neonatal primary astrocycte cultures by in utero exposure to elemental mercury vapor (Hg0)1, Brain Research, vol. 778:222-232 (1997).[vol. 10, no.19]

In this study, brain metallothionein protein and mRNA levels were determined in the fetal rat following in utero exposure to elemental mercury vapor. These studies suggest that in utero exposure to Hg0 induces brain MT gene expression, and that MT mRNAs and their respective proteins are useful quantitative biochemical markers of intrauterine exposure to Hg0, a potentially cytotoxic challenge to astrocytes in the developing brain. Induction of MT by fetal/neonatal strocytes represents an attempt by these glial cells to protect against Hg cytotoxicity in maintaining cerebral homeostasis.

Vol. X #23. Email from John Morris to Robert Reeves on Scientifically Proven Facts about Mercury & Dental Amalgam (April 1998).[vol. 10, no.20]

This email consists of 47 facts and references.

Vol. X #24. Information on Amalgam Safe.[vol. 10, no.21]

These promotional materials explain what Amalgam Safe is and how it works.

Vol. X #25. Richardson, G.M., et.al., A Monte Carlo Assessment of Mercury Exposure and Risks from Dental Amalgam, Human and Ecological Risk Assessment, vol. 2, no. 4:709-761 (1996).[vol. 10, no.22]

This review paper discusses two independent models of Canadians with amalgam-filled teeth, where amalgam was estimated to contribute, on average, 50% of total Hg exposure from all sources (amalgam, air, water, food, soil) in adults and 32 to 42% for other age groups. Based on the least conservative exposure model of the two independent models developed, the average numbers of amalgam-filled teeth estimated not to compromise the TDI were: 1 filling in toddlers; 1 filling in children; 3 fillings in teens; and 4 fillings in adults and seniors.

Vol. X #26. Richardson, G.M, Mercury Exposure form Dental Amalgam: Re-evaluation of the Richardson Model, Standardization by Body Surface Area and Consideration of Recent Occupational Studies, Amalgam Part II (February 1998).[vol. 10, no.23]

This paper reviews the 1995 Richardson study which provided a characterization of risks posed by Hg exposure form dental amalgam by determining the Hazard Quotient, the ratio of estimated exposure to the reference dose. When the Hazard Quotient exceeds a value of 1.0, the potential increases with the degree to which the Hazard Quotient exceeds 1.0 in value.

Vol. X #27. Fawer, R.F., et.al., Measurement of hand tremor induced by industrial exposure to metallic mercury, British Journal of industrial Medicine, v. 40:204-208 (1983).[vol. 10, no.24]

In this study, hand tremor due to industrial exposure to metallic mercury vapour was recorded in 26 exposed and 25 non-exposed male workers by an accelerometer attached to the dorsum of the hand. The subjects were instructed to hold the hand and the forearm in the same position first without and then with a load of 1250 g supported by the hand. The changes in highest peak frequencies between rest and load were higher in the exposed men than in the controls and were related to the duration of exposure to mercury and to age.

Vol. X #28.Halbach, S., Estimation of mercury dose by a novel quantitation of elemental and inorganic species released from amalgam, Int. Arch Occup. Environ. Health, vol. 67:295-300 (1995). [vol. 10, no.25]

For this study, the dose of mercury released from fillings was estimated by a new procedure of mercury speciation which elutes the released elemental and inorganic mercury with solvents of different polarity (paraffin and saline). In vitro tests with spherical amalgam pellets have shown that mercury release into the solvents is linearily correlated to time and amalgam surface area. Doses estimated in volunteers by this method average 4.5 g/day as compared to a dose of 3.4 g/day measured conventionally in the oral air.

Vol. X #29. Appendix III Evaluation of Risks Associated with Mercury Vapor from Dental Amalgam (November 1991).[vol. 10, no.26]

In this report, subtle signs and symptoms of chronic mercury intoxication may not be found through routine physical examinations. Subtle changes described in this report require special tests not commonly used in routine examinations- that is, nerve conduction studies, measurement of alterations in EEG and measures of psychomotor functioning. Mercury concentrations in tissue for those with amalgam fillings compared with those without amalgams are reported to be twofold to threefold higher in brain tissue and nine fold higher in kidney tissue. Most data suggest that the daily mercury dose is 1 to 5 g higher for subjects with 7 to 10 amalgams than for persons with no amalgams.

Volume XI.

Volume XI.

Vol. XI #1. Battisone, G.C., et.al, Mercury excretion in military dental personnel, Oral Surgery 47-53 (January 1973).[vol. 11, no.1]

In this study, mercury levels were determined in the urine of 70 dentists and their assistants engaged in full-time restorative dentistry. 20 non-dental personnel were used as controls. The dental personnel were divided among six separate clinics having two basic designs. Compared to the controls, 65.7% of all personnel and the over-all data from three clinics showed significantly elevated levels of urinary mercury. In one clinic consisting of 23 dental units in one large room, all personnel showed significant elevations in urinary mercury.

Vol. XI #2. Harris, D., et.al, The dental working environment and the risk of mercury exposure, JADA, v. 97:811-815 (November 1978).[vol. 11, no.2]

For this experiment, a sample of 115 dental offices, those offices due for inspection of registered X-ray equipment, were visited between March and June 1976. The inspectors made a physical survey of the offices and checked such items as type and condition of floor covering and method of amalgamation used. Of the 115 offices visited, 51% were carpeted; hard flooring, usually tile, was found in 49% of the offices. Bulk mercury was used in 63.2% of office practices and encapsulated mercury was used in 36.8%.When encapsulated mercury is used, the concentration of mercury in the air is generally lower. Little if any difference could be found between tiled or carpeted offices in which bulk mercury was used.

Vol. XI #3. Borkowski, T.V., et.al., Mercury Contamination of the Dental Office and Central Air Conditioning, North Carolina Dental Journal 13-15 (Spring 1975) [vol. 11, no.3].

In this study, a mercury contamination survey was conducted at the offices of a four-man, group general dental practice. Mercury vapor measurements were made using two mercury vapor meters. Six of the nine mercury-use areas showed measurable contamination due to mercury hygiene procedures. More interesting, and potentially hazardous in terms of long-term, low-level exposures to mercury vapor, was the design of the central air conditioning and heating system.

Vol. XI #4. Cooley, R.L., et.al, Mercury Vapor Emitted During Ultraspeed Cutting of Amalgam, Journal/Indiana Dental Association , v. 57, no.2: 28-31 (March 1978).[vol.11, no.4]

The purpose of this study was to determine the potential for mercury contamination from the removal of amalgam restorations without water spray. Vapor determinations were made with a Bacharach mercury vapor sniffer. The study was conducted in three parts: dry cutting (no evacuator), dry cutting with the use of a central vacuum high volume evacuator and water spray cutting with the use of a central vacuum high volume evacuator. The dry cutting (no evacuator) of amalgam restorations with ultraspeed instrumentation resulted in a significant increase in the mercury vapor at the operator’s breathing level. The use of central vacuum evacuation significantly decreased the MVL increased observed with dry cutting and no evacuator. Water spray in conjunction with central vacuum evacuation was only slightly more effective than the central vacuum (dry cutting) alone in reducing mercury vapor reaching the operator during the removal of an amalgam restoration.

Vol. XI #5. Joselow, M.M., et.al, Absorption and Excretion of Mercury in Man, Arch Environ Health, v.17:39-43 (July 1968).[vol. 11, no.5]

In this study the occupational hazard of the use of mercury by dentists, were evaluated and determinations were made of (1) the total mercury and vapor concentrations in a group of urban dental offices; and (2) the urinary excretion of mercury by the dentists. In a small but significant proportion (14%) of these offices, mercury concentrations were found in excess of the threshold limit value, implying a lack of care in handling mercury. The average total mercury concentration was more than twice the average vapor concentration. Absorption of mercury was evidenced by higher than normal urinary mercury levels, which correlated well with both the total ambient air concentrations and estimated exposure times.

Vol. XI #6. Dzau, V.J., et.al, Aspiration of Metallic Mercury, JAMA, v. 238, no.14:1531-1532 (October 1977).[vol. 11, no.6]

This case study highlights the rupture of the mercury-filled bag of an intestinal tube which resulted in aspiration of metallic mercury 22 years ago in the patient. Immediate respiratory distress was treated with vigorous suctioning and postural drainage. Follow-up chest roentgenograms persistently showed radiopaque particles in the lungs. Signs and symptoms of chronic respiratory disease have since developed in the patient. Postmortem findings from the lungs included globules of metallic mercury surrounded by extensive fibrosis and granuloma formation, believed to be the result of local irritative effects of mercury.

Vol. XI #7. Nicholson, R.J., et.al, Dissemination of mercury during preparation and trituration of amalgam, Journal Pros. Dent, v.20, no.3:248-254 (September 1968).[vol. 11, no.7]

This study compared a standard plastic amalgam capsule with a preproportioned disposable capsule. The first phase of the research measured the mercury dissemination during the loading of a capsule and during trituration; the second phase measured dissemination of mercury during the trituration procedure only. The preliminary study could not measure the cumulative amounts of mercury suspended in air during amalgam preparation, a method of detecting and measuring leakage has been presented.

Vol. XI #8. Zeitlhofer, J., et.al, Neurologische Symptome bei Inhalationsvergiftung mit metallischem Quecksilber, Neruenarzt, v. 54, no.7:426-429 (1988).[vol. 11, no. 8]

Article in German.

Summary in English: Nineteen caisson workers had been exposed to metallic mercury vapours while digging tubes underneath the first district of Vienna. The main findings reported are clinical neurologic symptoms, psychic complaints, neurographic results and autonomic parameters. The cardiovascular reflexes were abnormal in 7 of 12 patients.

Vol. XI #9. Nixon, G.S., et.al, Mercury Hazards Associated with High Speed Mechanical Amalgamators, British Dental Journal 308-311 (1971).[vol. 11, no.9]

For this study, the possibility of leakage of mercury from capsules during high-speed amalgamation is investigated, different types of capsules are examined and it is shown that mercury losses do occur.

Vol. XI #10. Evans, H.L., et.al, Behavioral effects of mercury and methyl mercury, Federation Proceedings, v. 34, no.9: 1858-1867 (August 1975). [vol. 11, no.10]

In this review article, evidence from behavioral experiments are examined. A brief examination of the behavioral effects of inorganic mercury and methylmercury are highlighted. Variations in the profile of behavioral and neurological effects are discussed in terms of differences in species and differences between acute and long-term exposure.

Vol. XI #11. Berck, B. et.al, Mercury Vapor as an Atmospheric Contaminant of Dental Offices, Archives of Environmental Contamination, 229-244 (June 1974).[vol. 11, no.11]

In this study, airborne mercury from dental offices was selectively trapped by silver gauze elements in borosilicate glass absorbers, followed by heat-desorption and spectrophotometric measurement at 2537A. Mercury concentrations varied during the working day, depending on the time of sampling, the number of amalgams placed and the interval between placements. The lowest concentrations were obtained in the morning. Disturbance of residual mercury droplets on floors or working areas by sweeping or dusting, or immediately after attempted clean-up of a mercury spill, sharply increased the amount of airborne mercury.

Vol. XI #12. Mantyla, D.G., et.al, Mercury toxicity in the dental office: a neglected problem, JADA, v.92:1189-1194 (June 1976). [vol. 11, no.12]

This article discusses mercury contamination in the dental office. Guidelines for allowable mercury vapor levels, symptoms of mercury poisoning, and safeguards against contamination are highlighted. Two case studies are examined.

Vol. XI #13. Schneider, M., An environmental study of mercury contamination in dental offices, JADA, v.89:1092-98 (1974). [vol. 11, no.13]

An experiment with 284 dental workers was conducted to determine sources of uncontrolled exposure to mercury vapor. An additional objective was to assess the degree of risk of the various dental groups, by occupation, in the handling of mercury. Data obtained from analysis of collected wipe, air, and urine samples were used to evaluate the risk of absorption of mercury vapor. Dental assistants who prepare amalgam for filling tooth cavities show the greatest risk of exposure to mercury vapor. No evidence of acute exposure to mercury vapor was found for any other groups studied.

Vol. XI #14. Smith, P.J., et.al, Effects of occupational exposure to elemental mercury on short term memory, British Journal of Industrial Medicine, v.40:413-410 (1983).[vol.11, no.14]

In this study, two measures of short term memory capacity were used. The first, the Wechsler digit span forward, was too imprecise and unreliable to detect any adverse effects. The second measure, an estimate of the worker’s 50% threshold for correct serial recall, was more satisfactory and provided evidence of a statistically significant decrease in short term memory capacity associated with increasing exposure to elemental mercury. A replication study of another group of 60 workers was performed to confirm this apparent mercury related effect. Despite lower urinary mercury concentrations in this second group, a statistical association was again observed relating urine mercury to reduced short term memory capacity.

Vol. XI #15. Battistone, G.C., et.al., Mercury as an Occupational Hazard in the Practice of Dentistry, Clinical Chemistry and Chemical Toxicology of Metals, 205-208 (1977). [vol. 11, no.15]

For this study, the authors determined blood and/or urine mercury in 1853 general dentists and 208 specialists. Included among the general dentists were 86 military dentists and 64 dentists working as clinical instructors in dental schools. The data suggested that blood mercury levels in civilian dentists were related to some of their dental practice characteristics. Military dentists working in certain unique “group-practice” situations were found to have a significant problem in mercury hygiene. According to present criteria there was no evidence to indicate mercury toxicity in any of the dentists surveyed.

Vol. XI #16. Lenihan, J.M.A., et.al, Mercury Hazards in Dental Practice, British Dental Journal, (1973). [vol. 11, no. 16]

Mercury hazards were studied by environmental surveys in 62 dental practices and by measurement of mercury levels in head and body hair, finger-nails and toe-nails from 183 dentists, dental surgery assistants and other practice employees. Bodily contamination, as reflected in hair and nail mercury levels, was significantly higher in staff handling mercury than in a control group of practice employees not handling mercury- but was not significantly correlated with any of the commonly accepted indicators of hazard, such as atmospheric mercury level, mixing, handling and storing techniques or total amount of mercury used.

Vol. XI #17. Sollmann, T., Mercury, A Manual of Pharmacology and its applications to Therapeutics and Toxicology, 1319-1322 (1957). [vol. 11, no.17]

The pages from this edition discuss Chronic Mercury Poisoning, Mercury Vapor Poisoning and Calomel as Cathartic and Intestinal Antiseptic.

Vol. XI #18. Hryhorczuk, D.O., et.al., Treatment of Mercury Intoxication in a Dentist with N-Acetyl-D,L-penicillamine, Journal Toxicology-Clinical Toxicology, v.19, no.4:401-408 (1982). [vol. 11, no.18]

This case study examines a dentist with chronic elemental mercury intoxication, peripheral neuropathy, and visual disturbances who was removed from exposure and treated with two –d courses of N-acetyl-D, L-penicillamine. Treatment with this experimental chelating agent resulted in an increase in urinary mercury excretion and slight clinical improvement.

Vol. XI #19. Brune, D. et.al, Mercury vapor levels in a dental laboratory, Scand. Journal Dental Research, v.86:300-302 (1978). [vol. 11, no.19]

For this study, mercury vapor levels associated with grinding amalgam models and mulling amalgams in the palm of the hand following trituration have been measured in a dental laboratory in inhalation position. The threshold limit value of airborne mercury of .05 mg/m3 was essentially exceeded in the grinding procedure of amalgam. Levels in excess of seven times this value were recorded. During mulling the mercury vapor level fluctuated around the threshold limit value. The mean mercury concentrations did not essentially exceed the threshold limit value.

Vol. XI #20. Stevens, J.T., et.al, Mercury Vapor Levels in Dental Spaces, Military Medicine, v.140:114-116 (1975). [vol. 11, no. 20]

This study compared mercury vapor levels in the air of dental operating rooms at three naval facilities using direct mercury vapor meter readings. Highest mean mercury vapor concentrations were found in a carpeted clinic where the mean mercury vapor value exceeded the threshold limit value by .006mg/m3. Activities such as carpet vacuuming, foot stamping, and amalgam trituration caused momentary increases in concentrations up to four times the threshold limit value, returning to levels below the TLV in 30 minutes or less. A direct relationship was noted between the amount of mercury vapor in the air and the amount of mercury in urine of dental personnel.

Vol. XI #21. Timbrell, V., et.al, The respirability of aerosols produced in dentistry, Journal of Dentistry, v.2, no. 1:21-31.

Vol. XI #22. Angotzi, G., et.al, Neurobehavioral Follow-up Study of Mercury Exposure.

Vol. XI #23. Miller, S.L., et.al, Mercury vapor levels in the dental office: a survey, JADA , v.89 1084-1091 (November 1974).

Vol. XI #24. Freitas, J.F., Mercury in the dental work-place: An assessment of the health hazard and safeguards, Australian Dental Journal, 156-161 (June 1981).

Vol. XI #25. Schionning, J.D. et.al., A stereological study of dorsal root ganglion cells and nerve root fibers from rats exposed to mercury vapor, Acta Neuropathol, v. 96:185-190 (1998).

Vol. XI #26. Buchwald, H., Exposure of Dental Workers to Mercury, American Industrial Hygiene Association Journal, 492-502 (July 1972). Vol. XI #27. Chu, C.C., et.al, Chronic inorganic mercury induced peripheral neuropathy, Acta Neurologica Scandinavica, v. 98:461-465 (1998).

Vol. XI #28. Gallagher, P.J., et.al, The Role of Biotransformation in Organic Mercury Neurotoxicity, Toxicology, v.15:129-134 (1980).

Vol. XI #29. Haikel, Y., et.al., Intra-oral Air Mercury Vapor Released from Dental Amalgam Before and After Restorative Procedures: A Preliminary Study, Clinical Materials, v. 5:265-270 (1990).

Vol. XI #30. Storlazzi, E.D., et.al., The Significance of Urinary Mercury, The Journal of Industrial Hygiene and Toxicology, v.23, no.10:459-465 (December 1941).

Vol. XI #31. Bittner, A.C., et.al, Behavioral Effects of Low-Level Exposure to Hg0 Among Dental Professionals: A Cross-Study Evaluation of Psychomotor Effects, Neurotoxicology and Teratology, v.20, no.1:429-439 (1998).

Vol. XI #32. Hamm, H., et.al., The surfactant system of the adult lung: physiology and clinical perspectives, Clincal Investigator, v.70:637-653 (1992).

Vol. XI #33. DeClerck, J.P., Etude comparative des pertes de mercure au niveau des capsules d’amalgamation predosees a usage unique et au niveau d’un amalgamateur a doseur de vrac, Rev Belg Med Dent/Belg Tijdschr Tandheelkd, v. 38, no. 1:7-9 (1983).In French

Vol. XI #34. Castagnola, L. et.al., Mercury Vaporization during the working of amalgam, particularly when using pre-dosed capsules, Quintessence International, no.2: 19-26 (February 1974).

Vol. XI #35. Capdebosq, C.B., et.al, Mercury Leakage during Trituration: An evaluation of Capsules, Operative Dentistry, v. 4:39-42 (1979).

Vol. XI #36. Blitzer, M.H., et.al., Mercury leakage in commercially preloaded amalgam-mercury capsules, General Dentistry, v. 29, no. 2:144-145 (April 1981).

Vol. XI #37. Brown, J.W., et.al., Mercury Leakage During Amalgam Trituration, Journal Canad Dent Assn, v. 50, no. 3:234-236 (1984).

Vol. XI #38. Wilson, S.J., et.al., Mercury Leakage from Disposable Capsules, British Dental Journal , v.153:144-147 (August 1982).

Vol. XI #39. Perotti, R. et.al. L’amalgama: considerazioni merceologiche sull’uso di capsule pre-dosate e non, Minerva Stomatologica, v. 36:269-280 (1987).

Volume XII.

Vol. XII #1. Wirz, J., et.al, Quecksilberdampfe Aus Vor-Dosierten Amalgamkapseln, Schweiz Monatsschr Zahnmed, Vol. 13, no. 8 :958-964 (1993).[vol. 12, no.1]

Article in German. Summary in English: 12 dental amalgam capsules were tested for mercury leakage during trituration, storage, and disposal. The pertinent measurements were taken using two different measuring systems, both of which were based on the principle of optical absorption. While the results were excellent for half of the encapsulated products, some were deficient with respect to impermeability or safe handling. Overall, dental amalgam capsules of the latest product generations release lower mercury vapors.

Vol. XII #2. Glockmann, E., et.al, Messungen der Quecksilberdampfkonzentration der Raumluft wahrend der Dosierung und Trituration von Amalgam mit dem DMG 410, Stomatol DDR 40:333-334 (1990).[vol. 12, no.2]

Article in German, Summary in English: The tested mechanical amalgamators DMG10 showed sufficient tightness. After dosing and trituration of 5 and of 25 amalgam mixtures an increase of the mercury vapour concentration was measured from 0,003 mg Hg/m3 air of the room to 0,008 mg Hg/m3 air of the room and to 0,018 mg Hg/m3 air of the room in an unventilated room. A significant decrease of the mercury vapour concentration could be established within 10 minutes by ventilation of the measurement room.

Vol. XII #3. Riccio, C., et.al, Verifica sperimentale del contenuto di capsule predosate di Quattro differenti amalgami dentari, Archivio Stomatologico, v. 31, no. 3:451-460 (July 1990).[vol. 12, no.3]

Article in Italian. Summary in English: The authors examine the problem of exactness of measure of weight in amalgam capsules and precision of ratio metallic powder-mercury. They study four materials and in some cases they found big want of precision in dosing of capsules.

Vol. XII #4. Martin, M.D., et.al, Factors Contributing to Mercury Exposure in Dentists, JADA, vol. 126:1502-1511 (November 1995). [Vol. 12, no.4]

This study examined personal, professional and office characteristics of dentists to determine which factors contribute most to exposure. At low levels of occupational exposure, the personal factors, such as number of amalgams present in the dentist’s mouth, may be a more significant contributor to mercury exposure. However, in a few dental offices, the occupational exposure is unnecessarily high.

Vol. XII #5. Devine, J.A., Health Hazard Evaluation Determination Report No. 76-6-294, U.S. Dept. of Health, Education and Welfare National Institute for Occupational Safety and Health (May 1976).[vol.12, no.5]

This health hazard evaluation was conducted by the National Institute for Occupational Safety and Health on February 9, 1976 at the J.A. Devine Dental Clinic in Cheyenne, Wyoming. At the time of this evaluation, breathing zone and general room samples were taken for inorganic mercury. A direct reading instrument also was used. Concentrations of mercury during this evaluation ranged from less than .01 micrograms to .18 milligrams per cubic meter. This is in excess of the NIOSH recommended standard of .05 milligrams per cubic meter and is a potential health hazard to the employees.

Vol. XII #6. Freiman, C., Recovering Mercury, OHS Canada, (October 1999). [Vol. 12, no.6]

This article discusses steps of cleaning up mercury spills.

Vol. XII #7. Allan, M., et.al, Probability Density Functions Describing 24-hour Inhalation Rates for Use in Human Health Risk Assessments, Human and Ecological Risk Assessment, vol. 4, no.2:379-408 (1998). [vol. 12, no.7]

For this study, a Monte Carlo simulation was undertaken to estimate the amount of air inhaled over a typical 24-hour period by six age groups of Canadians. The objective of the simulation was to derive probability density functions that could be used to describe inhalation rates in probabilistic health risk assessments involving airborne contaminants. Inhalation rates were estimated separately for male and female toddlers, children, teenagers, adults and seniors. These estimates suggested that males inhale on average 8% to 27% more air than females of the same age.

Vol. XII #8. Hursch, J.B., et.al, Percutaneous Absorption of Mercury Vapor by Man, Archives of Environmental Health , vol. 44, no.2: 120-127 (March 1989). [vol. 12, no.8]

In this study, five volunteer male subjects who were 24 to 78 years of age exposed the skin of their forearm to mercury vapor at concentrations of .88-2.14 ng/cm3 for periods of 27-43 min. Approximately 216 to 844 ng was taken up by the skin at rates of .0101 to .0402 ng Hg per cm2 per min per ng Hg per cm3 air. About half of the mercury taken up was shed by desquamation of epidermal cells during several weeks. The remainder diffused into the general circulation and could be measured as systemic mercury. When the total skin area was compared to the lung as a route of entry for mercury vapor at the same concentration, the rate of uptake was estimated to be 2.2% of the rate of uptake by the lung.

Vol. XII #9. Cuzacq, G., et.al, Mercury Contamination in the Dental Office, Journal of the Massachusetts Dental Society,254-261 (Fall 1971). [vol. 12 no.9]

For this study, a random sample of 77 general practitioners and pedodontists from 33 communities was selected from the yellow pages of the 1970 Boston Telephone Directory. The mercury vapor level was measured by means of a previously calibrated cell-type Beckman Mercury Vapor Detector. Most of the readings in the reception rooms were low. In the main operatories, 22% of the dental offices showed mercury vapor concentrations in the general air above the allowable limit. Mercury vapor concentrations on the floors of the main operatories was above the TLV in 32% of the offices. 4% of the dentists excrete mercury above the allowable limit of .15 mg/ liter, 11% of the dental assistants excrete amounts of mercury exceeding this limit and 3% excrete more than .25 mg /liter. Investigators found, by holding the mercury vapor detector at the breathing level of the operator during the squeezing of the amalgam for a few seconds that the person was exposed to a concentration of mercury vapor exceeding the limit of .05 mg /m3 in 71 % of the cases, while in 40% of the cases it was higher than .1 mg /m3.

Vol. XII #10. Jones, D.W., et.al, Survey of Mercury Vapour in dental offices in Atlantic Canada, J. Canad. Dent. Assn., no. 6:378-394 (1983). [vol. 12, no.10]

This study was conducted by the Division of Dental Biomaterials Science, Dalhousie University, between July 1981 and March 1982, with a total of 375 dental operatories being surveyed. This involved some 3,750 individual mercury vapour measurements being made. Sample of hair and nails were also collected from dentists and dental assistants for analysis. The survey indicates a low level of usage of protective measures and insufficient planning for accidental spillage.

Vol. XII #11. Chopp, G.F., et.al, Mercury Vapor Related to Manipulation of Amalgam and to Floor Surface, Operative Dentistry, 23-27 (1983).[vol. 12, no.11]

For this study, a survey of 592 dental offices showed that lower concentrations of mercury vapor were associated with offices where capsules of premeasured amalgam were used rather than mercury in bulk, where closed system rather than open amalgamators were used, and where the excess mercury was not squeezed from the amalgam. The type of floor, whether of a hard surface or carpeted, did not affect the concentration of mercury vapor.

Vol. XII #12. Nixon, G.S., et.al., Mercury Levels in Dental Surgeries and Dental Personnel, British Dental Journal, 149-154 (1981). [vol. 12, no.12]

In this study, 200 dental surgeries were screened for mercury vapor; these consisted of 125 general practice surgeries and 75 community dental surgeries belonging to 5 different area health authorities. Only 10% of the surgeries had an ambient vapour concentration greater than 0.02 mg m-3; in the community dental surgeries 86.7 % had an ambient level less than 0.01 mg m-3 compared with 45.6 % of the general practice surgeries. High concentrations of mercury vapour were found in certain areas and occurred as the result of certain procedures, sometimes for very short periods.

Vol. XII #13. Scarlett, J.M., A Study of Mercury in the Hair of Dentists and Dental-Related Professionals in 1985 and Subcohort Comparison of 1972 and 1985 Mercury Hair Levels, Journal of Toxicology and Environmental Health, v. 25, no.3: 373-381 (1988).[vol. 12, no.13]

An epidemiologic study was conducted in central New York in 1985 comparing the concentration of mercury in the hair of 85 dentists to that of 23 dental-related health professionals who do not use mercury. Mercury in the hair of dentists was nominally higher than that of the control group but not significantly so. There was a significant positive linear trend in the concentration of mercury in the dentists’ hair with the number of years they had been in practice. Those dentists who wore masks when removing old mercury containing fillings showed significantly lower mercury concentrations in hair than those who did not. Mercury concentration in the hair of 23 of the above dentists analyzed in 1972 was 16.77+ 4.00 ppm, significantly higher than that of the same dentists in 1985 (5.27 + 1.85 ppm).

Vol. XII #14. Skare, I., et.al, Mercury exposure of different origins among dentists and dental nurses, Scand. J. Work. Environ. Health, v.16, no.5:340-347 (1990). [vol. 12, no.14]

Mercury exposure was studied among dental personnel with the use of urinary mercury excretion rates and questionnaires. The study covered 314 dentists and dental nurses employed in public clinics and private practices in Stockholm. On the average the occupational contribution to the total urinary mercury excretion

rate was small and of the same order as the contribution from their own amalgam fillings. There were, however, individuals showing excretion rates close to the levels at which effects on the central nervous system and the kidneys have been reported.

Vol. XII #15. Battistone, G.C., et.al, Mercury: its relation to the dentist’s health and dental practice characteristics, JADA, vol. 92: 1182-1188 (June 1976).[vol.12, no.15]

In this study, no significant correlations were found in a comparison of blood mercury levels with clinical chemical data and dental practice characteristics. In general, practitioners with high blood mercury values tended to show dental practice characteristics that were conducive to these higher levels. The data indicate that U.S. dentists practice good mercury hygiene.

Vol. XII #16. Vesely, V., et.al, Dichtigkeit von Amalgamkapseln auf Quecksilberdampfe, Schweiz. Mschr. Zahnmed., vol. 94, no. 6:511-523 (1984). [vol. 12, no.16]

Article in German. Summary in English: 12 predosed and 2 multiple-use amalgam capsules were tested for their impermeability for mercury vapors before, during and after trituration, with a highly sensitive measuring device. The 14 types of capsules were subdivided into 5 different basic types according to their buildup. With two exceptions, the predosed capsules were sufficiently impermeable in spite of significant differences. The capsules for multiple use sowed an initially high impermeability which decreased with the number of uses.

Vol. XII #17. Jorgensen, K.D., et.al., Mercury Leakage of Amalgam Capsules, Acta Odontologica Scandinavica , vol., 29:461-469 (1971).[vol. 12, no.17]

The purpose of the present study is to indicate the possibility of mercury spillage during mechanical trituration of dental amalgams and moreover to describe a simple method of detecting leaking capsules. Several types of amalgam capsules showed a very significant leakage and none was completely tight. Mixes with a relatively high proportion of mercury to alloy seem to produce more mercury spillage than relatively dry mixes.

Vol. XII #18. Newman, S.M, Mercury Leakage from Preproportioned Capsules, Journal of the Tennessee Dental Assoc., vol., 59, no.2:19-21 (April 1979). [vol. 12, no.18]

This study compares a series of preproportioned capsules for weight loss during activation and trituration. The assumption is made that the amount of mercury released into the operatory environment is directly proportional to weight loss. The preproportioned capsules studied were limited to those brands which enclose high copper-content amalgam alloys, due to the improved laboratory values

attained for these alloys. Two types of reusable capsules were also included in the study. Most preproportioned capsules are safe to use, except for Aristaloy CR and PACS.

Vol. XII #19. Reinhardt, J.W., et.al., Amalgam capsule leakage during trituration, General Dentistry, 116-117 (March 1983). [vol. 12, no.19]

Within this study, the authors have determined leakage of various disposable and reusable amalgam capsules and compared the results for the two types of capsules.Certain disposable and reusable capsules are found to leak more than others. The degree of leakage does not appear to be related to trituration time or presence of a pestle.

Vol. XII #20. Schoenmakers, H.P.L., Advantages and consequences of using pre-dosed materials.[vol. 12, no.20]

A research program initiated by ISO to evaluate some of advantages claimed for capsulated materials showed that capsules in which the liquid is released by pressure contained relatively constant amounts of the ingredients, whereas in the screw type the variation was many times greater. When the composition of the resulting mix produced by four different operators was compared the press type of capsule resulted in greater uniformity. The viscosity and crushing strength of capsulated silicate cement was next investigated and it was shown that considerable variations occurred between the results of different operators and between different laboratories using separate testing apparatus.

Vol. XII #21. Cooley, R.L., et.al, Evaluation of An Ultrasonically-Welded Pre-Dosed Amalgam Capsule for Mercury Leakage During Trituration, The Journal of the Nebraska Dental Assoc., vol. 60, no.3:18-20 (1984).[vol. 12, no.21]

In this study, two types of new, ultrasonically-sealed capsules were evaluated for mercury leakage during trituration. Ten capsules of each type were tested. A Jerome Mercury Vapor Analyzer Model 01 was used to detect any loss of mercury from the capsules. No mercury leakage was found during trituration for either of the two types of capsules tested. The ultrasonically-welded type of pre-dosed capsule effectively eliminates the problem of mercury leakage from capsules during trituration.

Vol. XII #22. Henke, K.R., et.al, Critical Review of Mercury Contamination Issues Relevant to Manometers at Natural Gas Industry Sites Topical Report: 1-91 (August 1993).[vol. 12, no.22]

This report summarizes and critically reviews the major issues that relate to elemental mercury releases at gas industry sites, including the properties of elemental mercury and mercury ionic species and compounds; mercury-related health and safety concerns; regulatory issues that are related to this topic; the transport and fate of mercury in the environment; the characterization and monitoring of sites that have been contaminated by elemental mercury spills; sample collection, preservation, analysis, and leaching tests; and remediation alternatives for contaminated sites. There are also discussions of further research that is needed on these mercury-related issues.

Vol. XII #23. Hooper, P.L., Mercury poisoning in dentistry, Wisconsin Medical Journal, vol. 79:35-36 (August 1980).[vol. 12, no.23]

This case report presents a 58-year-old dental assistant with paresthesia, fatigue and dropping dental instruments. Urinary mercury levels were in the toxic range. After a malfunctioning amalgamator was replaced, the patient’s symptoms resolved.

Vol. XII #24. Warfvinge, K., Mercury exposure of a female dentist before pregnancy, British Dental Journal, vol. 178:149-152 (1995).[vol. 12, no.24]

In this case report, a 30-year-old female dentist was exposed to mercury vapour from a leaking amalgamator for approximately one year. No toxic effect was noted. During and after the exposure urine samples were regularly taken for mercury analysis. The highest value during this period was 60 g Hg/1 urine (expressed in g/g creatinine:42). The mercury concentration in air was at most 840 g/m3 at the amalgamator. The dentist became pregnant and during pregnancy her average urine mercury concentration was 18 g/g creatinine. Ultrasound examination of the fetus at 20 weeks of gestation showed a mild bilateral hydronephrosis. At 32 weeks of gestation the hydronephrosis had resolved. The dentist gave birth to a normal-weight baby boy who at the time of writing is 2 years of age and appears clinically healthy.

Vol. XII #25. Wilson, J., Reduction of mercury Vapour in a Dental Surgery, The Lancet, (January 1978). [vol.12, no.25]

For this study, mercury vapour levels were measured at 11 standard sites in the surgery at the start of a working day and throughout the day. Mercury vapour was measured by the Model MV-2 J.W. Bacharach Mercury Sniffer, which uses the principle of ultraviolet absorption. Results show that a considerable reduction in contamination by mercury vapour can be achieved by the use of a fume cupboard.

Vol. XII #26. Sverdrup, H., et. al., A Model for Mercury Exposure Due to Metallic Mercury Spills, Indoor Air ’90 Proceedings of the 5 th International Conference on Indoor Air Quality and Climate, vol. 4:225-230 (July 1990). [vol. 12, no.26]

In this study, a simple model for ventilation modeling and generic physical principles governing vaporization of liquids were employed in a model used to assess the impact of mercury spills in buildings and homes. The study shows that the simple loss of a few thermometers found in great numbers in every hospital and home can severely contaminate a room.

Vol. XII #27. Owen, M.K., et.al., Airborne Particle Sizes and Sources Found in Indoor Air, Atmospheric Environment, vol. 26A, no.12:2149-2162 (1992). [vol. 12, no.27]

This paper summarizes the results of a literature search into the sources, sizes and concentrations of indoor particles. There are several types of indoor particles: plant and animal bioaerosols and mineral, combustion and home/personal care aerosols. These types may be produced indoors or outdoors, entering through building openings. The sources may be short term, seasonal or continuous. Particle sizes produced vary from submicrometer to larger than 10 m. The particles may be toxic or allergenic.

Vol. XII #28. Takenaka, S., et.al., Pulmonary and Systemic Distribution of Inhaled Ultrafine Silver Particles in Rats, Environmental Health Perspectives, vol.109:547-551 (August 2001). [vol. 12, no.28]

In this study are presented the results on the pulmonary and systemic distribution of EAg after inhalation at a relatively low concentration based on morphology and the ICP-MS analysis. 16 rats were exposed to ultra fine EAg particles in whole body chambers. Particle size and the tendency of particles to form agglomerates affect the distribution pathway in the lungs. In the alveolar region, inhaled fine particles are readily phagocytized by alveolar macrophages. The total elimination of fine particles from the alveolar region may take place through three major routes: a) elimination of particles through the tracheobronchial tree, with subsequent ingestion into gastrointestinal tract and excretion with the feces; b) translocation of particles into lymph nodes; and c) dissolution of particles with subsequent transfer of the material into the blood.

Vol. XII #29. Mackert, J.R., Factors Affecting Estimation of Dental Amalgam Mercury Exposure from Measurements of Mercury Vapor Levels in Intra-oral and Expired Air, J. Dent. Res., vol. 66, no. 12:1775-1780 (December 1987).[vol. 12, no.29]

This review discusses several investigations which have attempted to assess the extent of mercury exposure from dental amalgam restorations through the use of mercury vapor measurements of intra-oral or expired air. The sampling times and

flow rates of the mercury vapor analyzers used in intra-oral measurements are not comparable with physiological inhalation times or flow rates of air through the mouth during inhalation. The corrected estimates for daily dose of mercury from amalgam restorations are a factor of sixteen lower than those previously reported.

Vol. XII #30. Pohl, L., et.al., The dentist’s exposure to elemental mercury vapor during clinical work with amalgam, Acta Odontol. Scand., vol. 53:44-48 (1995).[vol. 12, no.30]

In this study, continuous measurements of mercury vapor in the breathing zone of the dentist were made under ordinary clinical conditions. Fifty old amalgam fillings were removed and replaced by new ones. The mercury vapor measurements were performed by means of atomic absorption spectrophotometry. During the cutting, filling, and polishing operations the mean mercury vapor levels in the breathing zone of the dentist were in the range of 1-2 g Hg m-3 air when proper mercury hygiene measures were taken. When only a saliva extractor was used, the cutting of amalgam fillings caused highly fluctuating mercury vapor levels, which were 2-15 times higher than the threshold limit value.

Vol. XII #31. Eley, B.M., The Fate of Amalgam Implanted in Soft Tissues-An Experimental Study, J. Dent. Res., vol. 58, no. 3: 1146-1152 (March 1979). [vol. 12, no.31]

For this study, a conventional lathe-cut amalgam was mechanically triturated, condensed and allowed to set at 37 degrees Celsius for 2 weeks. The material was implanted subcutaneously in the submandibular region of 18 female guinea-pigs for periods of up to 2 years. The soft tissue reaction to amalgam depended on whether it was finely ground or a solid mass. Finely ground amalgam was actively digested within macrophages and giant-cells with loss of mercury and the formation of fine particles of silver and sulphur. Larger masses became surrounded by a fibrous capsule.

Vol. XII #32. Nikula, K.J., et.al, Influence of Exposure Concentration or Dose on the Distribution of Particulate material in Rat and Human Lungs, Environmental Health Perspectives, vol. 109, no.4:311-318 (April 2001). [vol. 12, no.32]

In this study, the authors used morphometric techniques to examine the influence of exposure concentration on particle retention in histologic sections from rats and humans. In all three groups of rats, 82-85% of the retained particulate material was located in the alveolar and alveolar duct lumens, primarily in macrophages. In humans, 57, 68 and 91% of the retained particulate material was located in the interstitium of the lung in the nonminers, coal miners under the current standard , and coal miners under the former standard, respectively.

Vol. XII #33. Lazaridis, M., et.al, Integrated Exposure and Dose Modeling and Analysis System. 3. Deposition of Inhaled Particles in the Human Respiratory Tract, Environ. Sci. Technol., vol. 35, no. 18:3727-3734 (2001).[vol.12 , no. 33]

This paper discusses a new mechanistic dosimetry model which was developed to describe the dynamics of respirable particles in the human airways. The model predicts the evolution of size and composition distributions of inhaled particles and the deposition profile along the human lower respiratory tract: In general, model predictions are in qualitative and quantitative agreement with tracheobronchial and alveolar deposition data.

Vol. XII #34. Vincent, J.H., The Fate of Inhaled Aerosols: A Review of Observed Trends and Some Generalizations, Ann. Occup. Hyg., vol. 34, no. 6:623-637 (1990).[vol. 12, no.34]

This paper draws together the various factors which govern the fate of inhaled particulate matter, focusing primarily on insoluble material. It includes a review of some of the key relevant experimental physical data which have led to our current state of understanding about the physical processes by which particles enter the body through the nose and/or mouth during breathing and by which they may be deposited in the various regions of the respiratory tract. It goes on to review the biological and biophysical data relevant to the processes by which the lung tries to eliminate the deposited material and discusses how the knowledge gained might be used as a basis for pharmacokinetic models for describing the fate of the inhaled material. Finally, the paper suggests how the cumulative body of knowledge might be used as a starting point for dosimetric models for the assessment of risk to health associated with aerosol inhalation in the occupational environment.

Vol. XII #35. McNerney, J.J., et.al, Mercury Detection by Means of Thin Gold Films, Science, vol. 178 (August 1972). [vol. 12, no.35]

This study examines the absorption of elemental mercury vapor on a thin (several hundred angstroms) gold film which produces resistance changes in the film. The instrument for the detection of mercury based on this phenomenon is simple and rapid and requires no chemical separations other than passage of the vapor sample through a few standard dry filters. The instrument is portable and the technique is directly applicable to environmental problems and geochemical prospecting. The limit of detection of the prototype instrument is .05 nanogram of mercury.

Vol. XII #36. Mackert, J.R, Review of “Assessment of Exposure and Risks Arising from Mercury-Containing Dental Amalgam” by G. Mark Richardson, 1-20 (June 1995). [vol. 12, no.36]

Dr. J. Rodway Mackert expresses his opinion of each section in G. Mark Richardson’s report entitled “Assessment of Exposure and Risks Arising from Mercury Containing Dental Amalgam.”

Vol. XII #37. Patterson, J.E., et.al, Mercury in Human Breath from Dental Amalgams, Bull. Environ. Contam. Toxicol . , vol. 34:459-468 (1985). [vol. 12, no.37]

This study report the results of measurements of mercury vapour concentrations in the exhaled breath of 172 persons, a few of which exceed probable safe exposure limits and appear high enough to be a chronic toxicologic hazard for some people with numerous amalgam fillings. The levels of elemental mercury in breath derived from silver-tin amalgam fillings represent a significant and undesirable contribution to mans “normal” body burden of mercury.

Vol. XII #38. Olsson, S., et.al, Daily Dose Calculations from Measurements of Intra-oral Mercury Vapor, J. Dent. Res., vol. 71, no. 2:414-423 (February 1992).[vol.12, no.38]

The aims of this investigation were to interpret the conditions for measuring mercury vapor release from dental amalgams in the oral cavity based on the work by Berglund et al. (1988) and Olsson et al. (1989) to derive the equations for calculating the daily dose from obtained data of intra-oral mercury vapor release rate and to use these equations to test the daily dose equations hitherto published. It was found that most daily dose equations used have a questionable mercury distribution on inspiration, expiration, and swallowing.

Vol. XII #39. Weiner, J.A., nylander et.al, An estimation of the uptake of mercury from amalgam fillings based on urinary excretion of mercury in Swedish subjects, The Science of the Total Environment, vol. 168: 255-265 (1995). [vol. 12, no.39]

The purpose of this present work is to estimate the uptake of mercury from amalgam fillings based on urinary concentrations of mercury. It is estimated that the average uptake of mercury from amalgam fillings in Swedish subjects is within the interval 4-19 g/day.

Vol. XII #40. Carter, J.M., et.al, Mercury Emission from Capsules during Trituration, Operative Dentistry, vol. 7:42-47 (1982). [vol. 12, no.40]

For this study, seven brands of disposable capsules and three brands of reusable capsules were tested for change in weight during trituration. All lost weight but an

analysis of variance and ranking showed the differences among the disposable capsules were not statistically significant except for one which lost the most weight. There was no statistical difference between the three reusable capsules. There was a trend for the reusable capsules to lose less weight than the disposable ones.

Vol. XII #41. Capdeboscq, C.B., et.al, Mercury Leakage during Trituration: An evaluation of Disposable Capsules, Operative Dentistry, vol. 9:69-71 (1984).[vol. 12, no.41]

This study tested the leakage of 11 brands of disposable capsules for amalgam and has shown that though there was some leakage from most capsules, the amount was remarkably low.

Vol. XII #42. Anderson, M.H., et.al, Mercury Leakage During Amalgam Trituration, Operative Dentistry , vol. 13:185-190 (1988).[vol. 12, no.42]

For this study, nine precapsulated mercury-alloy systems were tested for leakage during trituration. All tested precapsulated systems lost some weight during trituration. Most of the systems demonstrated very small leakage rates, with an occasional capsule exhibiting high leakage. Additionally, the manufacturers tended to be inconsistent in the amount of mercury/alloy dispensed into precapsulated systems, and there was a disparity between the amount of usable alloy advertised and the amount actually delivered.

Bibliography XIII.

Vol. XIII #1. Eames, W.B., Status report on amalgamators and mercury/alloy proportioners and disposable capsules, J. Am. Dent. Assoc., v.85, no.4:928-932 (1972).[vol. 13, no.1]

This report serves to update previous evaluations by describing new instruments and modifications of others.

Vol. XIII #2. Cooley, R.L., Mercury vapor emitted from disposable capsules placed in trash containers, General Dentistry, v. 33, no.6:498-500 (November 1985).[vol. 13, no.2]

For this study, a dental treatment room used primarily for dental prophylaxis was selected as the test area because of its low exposure to mercury. Two brands of predosed amalgamator capsules were evaluated. The capsules were triturated for 10 seconds, the amalgam contents discarded and the room was air-sampled for mercury emission. The capsules were evaluated in both reassembled (closed) and open (two halves unassembled) states. No mercury vapor was detected in the ambient air with either personal dosimeters or direct reading mercury detection instruments. Mercury vapor could only be detected directly over the capsules in the trash container.

Vol. XIII #3. Burgess, V.B., et.al, Mercury leakage from some disposable amalgam capsules during transport, Australian Dental Journal, v. 27, no.1:47-48 (1982).[vol. 13, no.3]

In this report, a total of 119 boxes of amalgam capsules were examined. 6 showing evidence of mercury leakage ranging from one or two globules to gross amounts of leakage. In eight of these boxes one or more capsules had completely come apart losing all of their mercury content and from this group the contents of 160 capsules were weighed. The results here indicate that in addition to mercury leakage during trituration there may be leakage when transporting the capsules.

Vol. XIII #4. Burgess, V.B., et. al., Mercury vapour associated with amalgam capsule and waste storage, Australian Dental Journal, v. 28, no.6:352-354 (December 1983).[vol. 13, no.4]

In this analysis, mercury vapour levels were measured by probe within containers and in close proximity to containers of two types of disposable amalgam capsules, of collections of used capsules in unsealed cartons, and of containers used for storage of amalgam waste. Three types of storage media for amalgam waste were tested and residue from spent capsules weighed. Vapour levels were found to be below recommended safety limits but indicate that these capsule systems require attention as a potential mercury hygiene hazard.

Vol. XIII #5. Donahue, W.J., et.al, Evaluation of the Dispersalloy Caplet System, Operative Dentistry, v.12:121-126 (1987).[vol. 13, no.5]

This report is an evaluation of the Caplet system which is a new and unique method of dispensing mercury and amalgam alloy. Advantages and disadvantages of this system in relation to mercury hygiene are compared to pre-encapsulated disposable capsules and reusable capsules loaded from bulk supplies. Mercury leakage, amalgam retention, and capsule degradation are evaluated and discussed. The best mercury hygiene, however, is available only with the use of disposable predosed capsule systems.

Vol. XIII #6. Gough, J.E., et.al, Mercury Dissemination During Amalgam Trituration, Calif. Dental Assoc. Journal , v.5, no.6 (1977).[vol. 13, no.6]

The purpose of this study was to compare mercury leakage from the newer, preproportioned amalgam with that from conventional nondisposable amalgam capsules. The study included an evaluation of the mercury vapor leakage from capsules triturated under a protective shielding hood attached to the triturator. This study indicates that, of those capsules tested, disposable capsules leak more than non-disposable capsules.

Vol. XIII #7. Chew, C.L., et.al, Long-Term Dissolution of Mercury from a Non-Mercury Releasing Amalgam, Clinical Preventive Dentistry, v. 13, no.3 (May 1991).[vol. 13, no.7]

This study was conducted to measure the long-term mercury release from a non-mercury-releasing system. Four cylindrical specimens were incubated in 10 ml of purified water at 37 degrees Celsius. Results showed that the overall mean release of mercury was 43.5 + 3.2 g/cm2/24 hr, and the amount of mercury released remained fairly constant during the duration of the experiment. This study showed that Composil releases mercury in quantities that far exceed those detected in other amalgam systems.

Vol. XIII #8. Sokal, R.R., et.al, Normality, Assumptions of Analysis of Variance, Biometry, 2 nd Edition , Chapt. 13:412-414. [vol. 13, no.8]

This chapter discusses error terms which are normally distributed. To test this assumption the authors compute normal expected frequencies from the observed data and test the departure of the observed from the expected distributions.

Vol. XIII #9. Casarett and Doull’s Toxicology The Basic Science of Poisons, Fifth Edition, 98-99; 447-450; 709-712; 870-871.[vol. 13, no.9]

The first pages of chapter five discuss Aerosols and Particles, and Absorption of Toxicants through the Skin.The pages from Chapter 15 discuss Toxic Inhalants, Gases, and Dosimetry, Particle Deposition and Clearance, and Mediators of Lung Toxicity. Chapter 23 highlights Mercury and Nickel. Pages from chapter 28 discuss Particulate Matter.

Vol. XIII #10. Kvikksolvtap ved mekanisk blanding av alloy og kvikksolv, Norske Tannlaegeforenings Tidende, v.83, no.5:180-184 (May 1973). [vol. 13, no.10]

Summary of article in English: Six different types of capsules for automatic mixing of amalgam are investigated for leakage of mercury during vibration. Measurements of mercury vapour in the air around capsules during vibration are carried out with a mercury vapour detector. Values for mercury vapour concentration never reached threshold limit value of 0,05 mg Hg/m3, even though the loss of weight for some capsules were relatively great.

Vol. XIII #11. Dunninger, P., et.al, Quecksilberdampfabgabe aus Amalgamkapseln wahrend Trituration und Lagerung, Dtsch Zahnarztl Z, v.46, no. 9:599-601 (1991).[vol. 13, no11]

Summary of article in English: Inhalation of mercury vapor is a potential hazard when handling dental amalgam. To prove the safety of modern capsule systems, we tested 21 brands of dental amalgam. Mercury vapor emission was measured at different stages during handling. Highly significant differences between capsule types were found for the measured parameters. Disposable capsules that could be reassembled showed the most favorable results.

Vol. XIII #12. Brune, D. et.al, Dust in dental laboratories. Part III: Efficiency of ventilation systems and face masks, The Journal of Prosthetic Dentistry, v. 44, no. 2:211-215 (August 1980).[vol. 13, no.12]

This study focuses on the efficiency of local exhaust systems mounted close to emission sources associated with specific operations. The effect of air speed in the suction area of the local exhaust system, which strongly influences the efficiency of air purification was closely evaluated. Use of local ventilation with a suction capacity of about 30 liters per second mounted close to work-piece (about 10 cm distance) allows the major part of dust arising from processing dental materials to attain tolerable levels in breathing air positions.

Vol. XIII #13. Foo, S.C., et.al, Neurobehavioral Effects in Occupational Chemical Exposure, Environmental Research, v. 60:267-273 (1993).[vol. 13, no.13]

This study highlights the neurobehavioral effects in 30 female workers exposed to an average of 341 mg/m3 toluene for an average of 5.7, 24 male workers exposed to solvent mixture in a factory printing plastic packaging materials, and 98 dentists exposed to metallic mercury in their work .The Z score for each group of exposed subjects was statistically poorer than that for its controls. Neurobehavioral performance was statistically related to exposure intensity for the toluene exposed workers and to years of exposure or dose for mixed solvent-and mercury-exposed subjects. The type of chemical species and pattern of exposure appear to influence whether the adverse effects will be cumulative.

Vol. XIII #14. Angotzi, G., et.al, Impairment of nervous system in workers exposed to inorganic mercury, Toxicological European Research (November 1981).[vol. 13, no.14]

For this study, impairment of nervous functions has been investigated by clinical and neurophysiological methods in 55 workers exposed to inorganic mercury intoxication and 27 controls living in the same area. A polyneuropathy, mainly of sensory type, has been found in 5 exposed workers and 2 controls; a mono of multineuropathy of sensory or motor type was present in 15 exposed and 10 control subjects. Central N.S. involvement has been ground in 7 out of 12 exposed workers examined and in 1 out of 7 controls by electronystagmography. Neurological examination demonstrated minor signs of cerebellar type in 3 instances.

Vol. XIII #15. Dickens, D., Dental Offices; Open Wide to Mercury Hazards, Job Safety and Health, 15-20 (July 1977).[vol. 13, no.15]

This report discusses symptoms of mercury poisoning, research into mercury contamination, regulation of workplace exposure, instruments for sampling, analyzing and monitoring of mercury, and safeguards against contamination.

Vol. XIII #16. Cooley, R.L., et.al., Mercury-vapor leakage from disposable capsules, General Dentistry, v. 32, no. 3:218-221 (June 1984).[vol. 13, no.16]

Five brands of pre-dosed capsules were evaluated for mercury leakage using a mercury vapor analyzer. Of the 50 capsules tested, only two allowed mercury leakage. However, all brands emitted significant levels of mercury vapor when the capsule halves were separated after trituration and not reassembled.

Vol. XIII #17. Triebig, G., et.al, Neurotoxic Effects in Mercury-Exposed Workers, Neurobehavioral Toxicology and Teratology, v.4:717-720 (1982).[vol. 13, no.17]

For this study, mercury levels in blood and urine and several nerve conduction velocities were measured in two groups of workers exposed to mercury and in a

reference group. Furthermore neuropsychiatric examination and psychological tests were performed. There was a significant mild degree of slowing of sensory CV, but no dose-effect relationship was evaluated on a group basis. The individual assessment showed in some cases hints of abnormal CV caused by mercury exposure. Significant correlations were found between duration of exposure and decrease of short-term memory. However there was no relationship in the case of the other psychological tests. Results indicate that there are no disorders of central and/or peripheral nervous system function if the valid Biological Threshold Limit Values in FRG are not exceeded.

Vol. XIII #18. Bluhm, R.E., Elemental Mercury Vapour Toxicity, Treatment, and Prognosis After Acute, Intensive Exposure in Chloralkali Plant Workers. Part I: History, Neuropsychological Findings and Chelator effects, Human & Experimental Toxicology, v. 11:201-210 (1992).[vol. 13, no.18]

This case report highlights mercury poisoning which occurred after the acute, prolonged exposure of 53 construction workers to elemental mercury. 26 of those workers were evaluated by clinical examination and tests of neuropsychological function. These observations demonstrate that acute exposure to elemental mercury and its vapour induces acute, inorganic mercury toxicity and causes long-term, probably irreversible, neurological sequelae.

Vol. XIII #19. Singer, R., et.al, Peripheral Neurotoxicity in Workers Exposed to Inorganic Mercury Compounds, Archives of Environmental Health, v.42, no. 4:181-184 (July 1987). [vol. 13, no.19]

In this study, nerve conduction velocity of the median motor, median sensory, and sural nerves was assessed in 16 workers chronically exposed to various inorganic mercury compounds. Exposed workers were compared with an unexposed control group using t test analyses. Slowing of the median motor nerve NCV was found, which was correlated with both increased levels of mercury in blood and urine, and with increased number of neurologic symptoms.

Vol. XIII #20. Langolf, G.D., et.al, Measurements of Neurological Functions in the Evaluations of Exposure to Neurotoxic Agents, Ann. Occup. Hyg . , v. 24, no. 3:293-296 (1981).[vol. 13, no.20]

This review analyzes a six-year study of effects of elemental mercury exposure to provide an illustration of behavioural testing methods.

Vol. XIII #21. Liang, Y., et.al., Psychological Effects of Low Exposure to Mercury Vapor: Application of a Computer-Administered Neurobehavioral Evaluation System, Environmental Research, v.60:320-327 (1993).[vol. 13, no.21]

This study used a computer-administered neurobehavioral evaluation system in a Chinese language version and a mood inventory of the profile of mood states to assess the psychological effects of low-level exposure to mercury vapor in a group of 88 workers exposed to mercury vapor on the average duration of 10.4 years. The results indicated that the profile of mood states posed was moving to the negative side in Hg-exposed group and most of the NES-C performances, in particular, the mental arithmetic, two-digit search, switching attention, visual choice reaction time, and finger tapping, were also significantly affected compared with those obtained from controls.

Vol. XIII #22. Cavanagh, J.B., Peripheral Neuropathy Cased by Chemical Agents, Critical Reviews in Toxicology, v.2, no. 3 (1973).[vol. 13, no.22]

This report is missing consecutive pages. The conclusion discusses the constant and reiterated theme that it is the distal parts of the nerve cell that show degenerative changes, whether this is indicated by the clinical appreciation of signs and symptoms at the ends of the limbs or whether anatomical dissection at a histological level shows a greater amount of degenerative change distally rather than proximally.

Vol. XIII #23. Weiss, B., Behavioral Toxicology of Heavy Metals, 1-49.[vol. 13, no.23]

This report discusses the toxicological effects on humans and animals of Lead, Mercury, and other heavy metals.

Vol. XIII #24. White, R.F., et.al, Neurobehavioral Effects of Toxicity Due to Metals, Solvents, and Insecticides, Clinical Neuropharmacology, v.13, no.5:392-412 (1990).[vol. 13, no.24]

This review contains a number of reports on adult cases, an overview of specific epidemiologic studies, and summaries of cases describing patterns of neuropsychological deficits associated with selected common examples of toxic exposure.

Vol. XIII #25. Kishi, R., et.al, Subjective Symptoms and Neurobehavioral Performances of Ex-Mercury Miners at an Average of 18 Years after the Cessation of Chronic Exposure to Mercury Vapor, Environmental Research, v. 62:289-302 (1993).[vol. 13, no.25]

This purpose of this study was to determine if there are any residual effects of long-term exposure to mercury vapor. Neurobehavioral tests were given to ex-mercury miners about 18 years after the cessation of mercury exposure. Matched-pair analysis showed that performances of motor coordination, simple reaction time, and short-term memory in the ex miners were significantly deteriorated

compared to those of controls. There are slight but persistent effects on neurobehavioral function, especially on motor coordination function, among mercury miners more than 10 years after the cessation of exposure.

Vol. XIII #26. Krigman, M.R., Neuropathology of Heavy Metal Intoxication, Environmental Health Perspectives, v.26:117-120 (1978).[vol. 13, no.26]

This report presents the basis for utilizing altered morphology, i.e., pathology, in defining diseases of the nervous system. The importance of recognizing the dynamics of pathologic processes is emphasized, particularly in understanding the pathogenesis of neural diseases. Demonstrative examples of the neuropathology of human heavy metal toxicity are presented. The limitations of descriptive pathology are considered, and the potentials of quantitative (morphometric) analysis for studying pathologic processes are introduced.

Vol. XIII #27. Stockstill, J.W., et.al, Prevalence of Upper Extremity Neuropathy in a Clinical Dentist Population, JADA, v.124:67-72 (August 1993).[vol. 13, no.27]

All licenses dentists in Nebraska were sent a 24-item mail questionnaire with a follow-up mailing a few months later. Final response rate was 98%. Of the 1,016 respondents, 294 reported symptoms of peripheral neuropathy, a prevalence rate of 29%. When asked to characterize the altered sensation, the most frequent response was pain followed by numbness and tingling.

Vol. XIII #28. Soleo, L., et.al, Effects of low exposure to inorganic mercury on psychological performance, British Journal of Industrial Medicine, v.47:105-109 (1990).[vol. 13, no.28]

The study groups included eight chronically exposed workers and 20 who were only occasionally exposed. Of the psychic functions explored by behavioural tests, only short term auditory memory was found to be impaired in the chronically exposed workers. The chronically exposed workers were also found to be more depressed than those in the other group. No changes of visual motor functions were observed. The personality of the occupationally exposed workers was found to be considerably changed compared with that of the control group.

Vol. XIII #29. Amler, R.W., et.al, Assessment of Mercury Neurotoxicity Through Psychometric and Neurobehavioral Testing: Session Summary, NeuroToxicology, v.17, no. 1:237-240 (1996).[vol. 13, no.29]

This is a summarization of a plenary session on the predictive value of psychometric and neurobehavioral testing of animals and humans in assessing neurotoxic effects that took place at the Twelfth International Neurotoxicology Conference. The session provided a broad view of the methods currently in use to

measure adverse effects on the nervous system, in particular those effects that might be attributed to mercury exposure.

Vol. XIII #30. Gunther, W., et.al, Repeated Neurobehavioral Investigations in Workers Exposed to Mercury in a Chloralkali Plant, NeuroToxicology, v.17:605-614 (1996).[vol. 13, no.30]

This study investigated mercury exposed workers of a chloralkali electrolysis plant with neurobehavioral methods. Four periods of investigations were carried out over the course of 7 years. Symptoms and personality traits did not covary significantly with the exposure. Finger dexterity, tapping and aiming were variables out of 13 performance measurements, which showed repeatedly a lower level of performance corresponding with increasing current exposure.

Vol. XIII #31. Fullerton, P.M., Toxic Chemicals and Peripheral Neuropathy: Clinical and Epidemiological Features, Proc. Roy. Soc. Med., v. 62:201-208 (February 1969).[vol. 13, no.31]

This report highlights the substances known to produce peripheral neuropathy which are a hazard in industry. An additional report is included entitled “Toxic Chemicals and Peripheral Neuropathy: Experimental Studies”.

Vol. XIII #32. Henderson, R., et.al, Effect of Equivalent Time-Weighted Exposures at Different Rates of Exposure to Elemental Mercury Vapour on Mercury Concentrations in the Brain, Liver, Kidney, Blood, and Urine of Rats (1975).[vol. 13, no.32]

For this study, 60 rats were exposed to mercury vapor concentrations of .1, .2 and .6 mg/m3 air for each of the three groups respectively. The animals were exposed for 90, 45 and 15 minutes for each of the three groups respectively. The results indicate that the concentration of mercury accumulated in the kidney and brain is affected by the concentration of elemental mercury vapor to which the animals were exposed be the concentrations of mercury in blood, liver, and urine were not affected by the concentration of elemental mercury vapor when the doses were equal.

Vol. XIII #33. empty

Bibliography XIV.

Vol. XIV #1. Shaikh, Z.A., et.al, Metal Transport in Cells: Cadmium Uptake by Rat Hepatocytes and Renal Cortical Epithelial Cells, Environmental Health Perspective, v.103, Supplement 1:73-75 (1995).[vol. 14, no.1]

This report summarizes recent findings on the transport of cadmium in rat hepatocytes and renal cortical epithelial cells in the presence or absence of certain essential metals. The hepatocytes were isolated by a collagenase perfusion

method from Sprague-Dawley rats. Cadmium appears to use the transport pathways intended for the essential metals, zinc, copper, calcium, etc. Furthermore, these pathways are not available to the same extent in all cell types.

Vol. XIV #2. Carter, D.E., Oxidation – Reduction Reactions of Metal Ions, Environmental Health Perspectives, v.103, Supplement 1: 17-19 (1995).[vol. 14, no.2]

This report illustrates how several metals species react in biological and environmental systems to participate in electron transfer reactions in which they change oxidation states. As different species are formed, there are significant changes in toxicity.

Vol. XIV #3. Clarkson, T.W., The Role of Biomarkers in Reproductive and Developmental Toxicology, Environmental Health Perspectives, v. 74:103-107 (1987).[vol. 14, no.3]

This study used longitudinal hair analysis to compare the methylmercury levels in a mother during pregnancy with the severity and frequency of effects in her offspring. Methylmercury concentration in hair is an excellent biomarker for fetal and adult absorbed doses. Of special importance is the ability of the hair sample to recapitulate blood levels during pregnancy. The developing nervous system is more susceptible to damage than the mature brain.

Vol. XIV #4. Fitzgerald, W.F., et.al, Mercury and Monomethylmercury: Present and Future Concerns, Environmental Health Perspectives, v.96:159-166 (1991).[vol. 14, no.4]

This report reviews many studies that have investigated the global atmospheric cycling of mercury, particularly its interactions at the air-water interface. Human exposure and health risks from methylmercury are also discussed.

Vol. XIV #5. Mokrzan, E.M., et.al, Methylmercury-Thiol Uptake into Cultured Brain Capillary Endothelial Cells on Amino Acid System L1 , Journal of Pharmacology and Experimental Therapeutics, v. 272:1277-1284 (1995).[vol. 14, no.5]

For this study, the mechanism of MeHg uptake into cultured calf brain capillary endothelial cells, an in vitro model of the blood-brain barrier, was examined. This study provides direct evidence that MeHg-L-cysteine is a substrate for the L amino acid carrier and that this is a major pathway for MeHg uptake into brain capillary endothelial cells. The uptake was saturable, stereoselective and inhibited by specific amino acids, characteristics that cannot be explained by passive mechanisms.

Vol. XIV #6. Clarkson, T.W., Molecular and Ionic Mimicry of Toxic Metals, Ann. Rev. Pharmacol. Toxicol., v. 32:545-571 (1993).[vol. 14, no.6]

This review updates the literature on both oxyanion and divalent metal competition and introduces a new extension of molecular and ionic mimicry to complexes formed by mercury that are structurally similar to and biologically mimic endogenous molecules. This review give examples that illustrate the role of molecular and ionic mimicry in the action of the toxic metals.

Vol. XIV #7. Cernichiari, E., et.al, Did Andrew Jackson Have Mercury Poisoning, JAMA, v. 283, no. 2 (January 2000).[vol. 14, no.7]

This letter to the editor refutes the report by Dr. Deppisch and colleagues by stating that Andrew Jackson’s symptoms are recognized outcomes of inorganic mercury poisoning. Dr. Deppisch replies that they hold to their contention that President Andrew Jackson did not die from calomel (mercurous chloride) poisoning.

Vol. XIV #8. Clarkson, T.W., Mercury: Major Issues in Environmental Health, Environmental Health Perspectives, v. 100:31-38 (1992).[vol. 14, no.8]

This paper discusses pathways of human exposure to methylmercury, the disposition of methylmercury, toxic action and dose-response relationships, and the treatment of methylmercury poisoning.

Vol. XIV #9. Clarkson, T., Health Effects of Metals: A role for Evolution?, Environmental Health Perspectives, v.103, Supplement 1 (January 1995).[vol. 14, no.9]

This paper discusses human exposure to metals, a role of metals in evolution, and the role of evolution in the toxicology of metals.

Vol. XIV #10. Davis, L.E., et.al, Methylmercury Poisoning: Long-term Clinical, Radiological, Toxicological, and Pathological Studies of an Affected Family, Ann. Neurol, v.35:680-688 (1994).[vol. 14, no.10]

This case report studies four children from one family in the United States who developed severe methylmercury poisoning after eating mercury-contaminated pork for 3 months in 1969. The younger the individual, the more severe the poisoning. Severely affected family members survived over 21 years.

Vol. XIV #11. Serrano, O.R., Fate, Transport and Interactions of Heavy Metals, Environmental Health Perspectives, v. 103, Supplement 1:7-8 (1995).[vol. 14, no.11]

This is a summary of a presentation about heavy metals as hazardous wastes that are potential pollutants to air, soil, water and food stuffs. The presentation was given by The Programa Universitario de Medio Ambiente at the Unites States-Mexico Conference.

Vol. XIV #12. Dental Mercury Hygiene, JADA, v.122:112 (August 1991).[vol. 14, no. 12]

This is a list of recommendations, adopted in October 1998 by the ADA Council on Scientific Affairs. They updated the recommendations published by the former ADA Council on Dental Materials, Instruments and Equipment in 1991.

Vol. XIV #13. Masters, R.D., et.al, Association of Silicofluoride Treated Water with Elevated Blood Lead, NeuroToxicology , v.21, no. 6:1091-1100 (2000).[vol. 14, no.13]

This statistical study reports on 151,225 venous blood lead tests taken from children ages 0-6 inclusive, living in 105 communities of populations from 15,000 to 75,000. For every age/race group, there was a consistently significant association of SiF treated community water and elevated blood lead. Logistic regressions above and below the median value of seven covariates show an effect of silico-fluoride on blood lead independent of those covariates.

Vol. XIV #14. Hamann, C., et.al, Prevalence of carpal tunnel syndrome and median mononeuropathy among dentists, JADA, v.132:163-170 (February 2001).[vol. 14, no.14]

This study determined the prevalence in dentists of abnormal sensory nerve conduction and/or symptoms of carpal tunnel syndrome. The dentists were screened during the ADA’s Annual Health Screening Program in 1997 and 1998 by means of standard electrodiagnostic measures in the dominant hand and a self-reported symptom questionnaire. 13% of screened dentists were diagnosed with a median mononeuropathy, but only 32% of these had symptoms consistent with CTS. When the .8-ms prolongation was used as the electrodiagnostic criterion, only 2.9% were diagnosed with CTS.

Vol. XIV #15. Stephenson, J., Biomedical Journals Ponder the Failures and Remedies of Peer Review, JAMA, v.286, no. 23:2931-2932 (December 2001). [vol. 14, no.15]

This review article discusses the soundness of the bridge between research and practice which was a topic under scrutiny by editors of biomedical journals,

researchers, and others who convened for the Fourth International Congress on Peer Review in Biomedical Publication. These individuals are looking for ways to ensure that the process of peer review provides essential quality control in the publication of new research findings.

Vol. XIV #16. Japanese Researchers Link Amalgam Fillings with Atopic Dermatitis, Dentistry Today (February 2002).[vol.14, no.16]

This news article discusses the statement made by two Japanese researchers regarding results of their research which have shown amalgam causes the chronic skin disease atopic dermatitis and other allergic dermatitis. The researchers called for the Japanese government to prohibit its use or at least inform patients of its potential side effects.

Vol. XIV #17. Mitchell, J., et. al., Peripheral Neuropathy Following Intraneural Injection of Mercury Compounds, Archives of Toxicology, v. 46:257-264 (1980).[vol. 14, no.17]

For this study, between .25-25 g of an aqueous solution of either mercuric chloride or methyl mercuric acetate was injected directly into the sciatic nerve of 28 adult Wistar rats. In most respects mercuric chloride was more toxic than methyl mercuric acetate. The large doses of mercuric chloride produced a hind limb paresis within 24 hours but no clinical signs followed injection of organic mercury. The predominant effect of mercuric chloride was on Schwann cells which showed cytoplasmic swelling and nercrosis associated with extensive segmental demyelination. Methyl mercuric acetate caused axonal degeneration in many of the large myelinated fibres but only minor alterations were observed in Schwann cells.

Vol. XIV #18. Kishi, R., et.al, Residual neurobehavioural effects associated with chronic exposure to mercury vapour, Occupational and Environmental Medicine, v. 51: 35-41 (1994).[vol. 14, no.18]

This purpose of this study was to find the residual effects of long term exposure to mercury vapour, after neurobehavioural tests were given to ex-mercury miners about 18 years after the end of mercury exposure. The duration of exposure correlated with poorer performance of hand-eye coordination, tapping and a colour card reading tests. There are slight but persistent effects on neurobehavioural function, especially on motor coordination, among mercury miners even more than 10 years after the end of exposure.

Vol. XIV #19. Hanninen, H., Behavioral Effects of Occupational Exposure to Mercury and Lead, Acta neurol. scandinav., Supplement 92, v. 66: 167-175 (1982).[vol. 14, no.19]

This review highlights the disturbances of the motor system in connection with mercury and lead exposure, deterioration of intellectual capacities, and alterations of the emotional state.

Vol. XIV #20. Dyck, P.J., et.al, Mercury, Peripheral Neuropathy, v. 2, :1249-1262 (1975).[vol. 14, no20]

This report discusses the historical background, clinical aspects, pathology, biochemistry and treatment of mercury poisoning. An illustrative case report on Mercury Neuropathy is also highlighted.

Vol. XIV #21. Fagala, G.E., et.al., Psychiatric manifestations of Mercury Poisoning, Case Sudy, J. Am. Acad. Child Adolesc. Psychiatry, v. 31, no.2:306-311 (March 1992).[vol. 14, no.21]

This case study highlights mercury poisoning in a 12-year-old girl with prominent psychiatric manifestations. Relevant literature concerning the psychiatric manifestations of mercury poisoning is discussed. The importance of considering mercury poisoning, and toxic conditions in general, in the differential diagnosis of psychiatric disorders is emphasized.

Vol. XIV #22. Barnes, J.M., Toxic Chemicals and Peripheral Neuropathy: Experimental Studies, Proceedings of the Royal Society of Medicine, v. 62, no. 1: 205-211 (January 1969). [vol. 14, no.22]

This review considers how studies on experimental animals may help to throw light on a possible aetiological relationship between the exposure of a person to a toxic chemical and the subsequent appearance of a peripheral neuropathy.

Vol. XIV #23. Ellingsen, D.G., et.al, Relation between exposure related indices and neurological and neurophysiological effects in workers previously exposed to mercury vapour, British Journal of Industrial Medicine, v.50:736-744 (1993).[vol. 14, no.23]

A cross sectional study of aspects of their neurology was carried out on 77 chloralkali workers previously exposed to mercury vapour and compared with 53 age matched referents. The chloralkali workers had been exposed for an average of 7-9 years at a concentration of 59 g Hg/m3 in the working atmosphere. The results may indicate an effect of previous exposure to mercury vapour on the nervous system, possibly in the visual pathway, cerebellum, and the peripheral sensory nerves.

Vol. XIV #24. Powell, L.V., et.al., Mercury Vapor Release during Insertion and Removal of Dental Amalgam, Operative Dentistry, v.19:70-74 (March 1994).[vol. 14, no.24]

During this study, a clinical simulation of insertion and removal of dental amalgams, showed mercury vapor levels increasing slightly, but never exceeding the TLV of .05/mg/m3. The addition of indium to dental alloy did not affect the amount of mercury vapor released under these conditions.

Vol. XIV #25. Norton, S. Toxic Responses of the Central Nervous System, Chapter 9:179-205.[vol. 14, no.25]

This report discusses Structural Toxicity, Functional Toxicity, and Types of Nervous System Toxicants.

Vol. XIV #26. Bunn, W.B., et.al, Mercury Exposure in Chloralkali Plants, American Industrial Hygiene Association Journal, v.47, no.5:249-254 (1986).[vol. 14, no.26]

The employees of two chloralkali plants were studied to correlate the signs and symptoms of mercury toxicity with levels of exposure. The workers were divided into three groups. No significant differences in the frequency of objective or subjective findings were noted among the three groups except for a lower post exposure systolic and post exposure diastolic blood pressure in the high exposure group in the second plant’s population. There was no correlation of mercury vapor exposure with subjective or objective weight loss.

Vol. XIV #27. Langworth, S., et.al., Effects of occupational exposure to mercury vapour on the central nervous system, British Journal of Industrial Medicine, v. 49:545-555 (1992).[vol. 14, no.27]

In this study, possible effects of mercury on the central nervous system were examined in a group of chloralkali workers exposed to mercury and compared with a control group, by registration of subjective symptoms, personality changes, forearm tremor, and performance on six computerized psychometric tests in the two groups. The findings indicate a slight mercury induced effect on the CNS among the chloralkali workers.

Vol. XIV #28. Kark, R.A., Clinical and neurochemical aspects of inorganic mercury intoxication, Handbook of Clinical Neurology, v.20, no. 64:367-411.[vol. 14, no.28]

This report discusses types of inorganic mercury intoxication, body burden, susceptibility and pathogenesis, and treatment and clinical evidence of mercury intoxication.

Vol. XIV #29. Stopford, W., Industrial exposure to mercury, The biogeochemistry of mercury in the environment, 367-397 (1979).[vol. 14, no.29]

This report discusses industrial uses and exposures of mercury, inorganic mercurialism in industry, organic mercury exposures in industry, treatment of mercurialism, surveillance programs for industry, and preventive measures.

Vol. XIV #30. Le Quesne, P.M., Clinical Expression of Neurotoxic Injury and Diagnostic Use of Electromyography, Environmental Health Perspectives, v.26:89-95 (1978).[vol. 14, no.30]

This report describes the clinical features of neurological damage produced by acrylamide, lead, organophosphates, hexacarbon solvents, and methylmercury. The differences in effects of these compounds are stressed. The characteristic pattern of electrophysiological changes for each group of substances are described and correlated with pathological findings.

Vol. XIV #31. Spencer, P.S., et.al., Distal Axonopathy: One Common Type of Neurotoxic Lesion, Environmental Health Perspectives, v.26:97-105 (1978).[vol. 14, no.31]

This paper discusses the morphological aspects of neurotoxicity including establishing normative data, classifying neurotoxic injuries, distal axonopathy, principles of neurotoxicity testing, developing a new test for neurotoxicity, and a comparison of neurotoxicity, human disease, and the aging process.

Vol. XIV #32. None

Bibliography XV.

Vol. XV #1 Patient Release and Report Form for Mercury Vapor Risk Factor Analysis, Dr. W. Wayne King. [vol. 15, no.1]

This is a copy of a form used by Dr. King for his patients. By signing the form the patient grants Dr. King and his associates to perform a vapor sampling technique for the evaluation of mercury vapor coming from amalgam fillings in the patient’s mouth. Dr. King used an Arizona Instrument Jerome 411 Gold Foil Mercury Vapor Analyzer and the protocol endorsed by the IAOMT for the procedure.

Vol. XV #2 Not found Huggins, H.A., How Root Canals Generate Toxins.[vol. 15, no.2]

In this paper, Dr. Huggins discusses Dr. Weston Price’s research on root canal fundamentals.

Vol. XV #3. Friedland, B., et.al, The Regulation of Dental Licensing: The Dark Ages?, American Journal of Law & Medicine, v. 17, no.3:247-270 (1991).[vol. 15, no.3]

This article examines the history and application of the traditional justifications for state licensure and their present ramifications.

Vol. XV #4. Atherton, R.W., et.al, A Study of Rat Epididymal Sperm Adenosine 3’,5’-Monophosphate-Dependent Protein Kinases: Maturation Differences and Cellular Location, Biology of Reproduction, v. 32: 155-171 (1985).[vol. 15, no.4]

In this study, the photoaffinity analog [32P]8-N3 cAMP was used to analyze the membrane sidedness of rat sperm cAMP binding proteins during epididymal maturation. Sperm epididymal maturation coincided with changes in the cAMP-dependent protein kinase subunits since cauda sperm contained more available Type II than did caput sperm. A subcellular analysis of cAMP-dependent protein kinase regulatory subunit in head and tail fractions was done for caput and cauda sperm and demonstrated that the tail fractions showed more photo-labeling of both Type I and II regulatory subunits than did the head fractions.

Vol. XV #5. DeBortoli, M.E., et.al, Amplified Expression of p21 ras Protein in Hormone-Dependent Mammary Carcinomas of Humans and Rodents, Biochemical and Biophysical Research Communications, v. 127, no.2:699-706 (March 1985).[vol. 15, no.5]

For this study, western blotting analysis was utilized to determine the amount of a ras oncogene product, p21 present in mammary carcinomas of humans and rats. The levels of p21 in hormone-dependent rat tumors was about 7-fold that of hormone-independent tumors. The majority of human breast carcinomas examined had high p21 levels, about 10-fold that of the normal breast tissue. p21 levels in the remaining tumors were 3-fold that of the normal breast tissue. The results suggest that hormone-dependency of mammary carcinomas may correlate with quantitative change in normal p21 protein.

Vol. XV #6. Owens, J.R., et.al, Synthesis and Utilization of 8-Azidoguanosine 3’-Phosphate 5’-[5’-32P]Phosphate, Journal of Biological Chemistry, v. 259, no. 23:14843-14848 (December 1984).[vol. 15, no.6]

In this study, a family of guanosine 3’,5’-phosphorylated nucleotides have been postulated to have pleiotypic regulatory properties in prokaryotes during the stringent response. To study proteins which may interact with nucleotides of this homologous series, a photoactive analog of guanosine 3’,5’-diphosphate has been synthesized. The results indicate that the 8-azidoguanosine analogs of this homologous series will prove to be effective probes for studying the protein-nucleotide interactions involved in the stringent response.

Vol. XV #7. Khatoon, S., et.al, A Comparative Analysis of cAMP-dependent Protein Kinase Regulatory Subunits in Sea Urchin and Rat Spermatozoa, J. Androl, v. 6:251-260 (1985).[vol. 15, no.7]

For this study, 8-Azido cAMP photoaffinity labeling of cAMP-dependent protein kinase regulatory subunits was done on spermatozoa from species lacking and species containing an epididymis. Spermatozoa from sea urchin and trout contained only R1, while rat caudaepididymal spermatozoa contained both R1 and R2 subunits.These data suggest that the cAMP regulation of sperm physiology may require R1 subunit in species both with and without an epididymis.

Vol. XV #8. Pfister, K.K., et.al, The Photoaffinity Probe 8-Azidoadenosine 5’-Triphosphate Selectively Labels the Heavy Chain of Chlamydomonas 12 S Dynein, Journal of Biological Chemistry, v. 259, no. 13:8499-8504 (July 1984).[vol. 15, no.8]

In this study, the authors used 8-azidoadenosine 5’-triphosphate, a photoaffinity analog of ATP, to investigate which of the dynein polypeptides contains the site of ATP hydrolysis. The results suggest that the hydrolytic site of 12 S dynein is contained in its heavy chain.

Vol. XV #9. Woody, Y.M., et.al, Photoaffinity Labeling of DNA-Dependent RNA Polymerase from Escherichia coli with 8-Azidoadenosine 5’Triphosphate, Biochemistry , v.23:2843-2848 (1984).[vol. 15, no.9] Haley

In this study, a photoaffinity analogue of adenosine 5’-triphosphate, 8-azidoadenosine 5’-triphosphate, has been used to elucidate the role of the various subunits involved in forming the active site of Escherichia coli DNA-dependent RNA polymerase. Results indicate major involvement of the ’ and subunits in the active site of RNA polymerase. The observation of a small extent of labeling of the and subunits, which was prevented by saturating levels of ATP, suggests that these subunits are in close proximity to the catalytic site.

Vol. XV #10. Haley, B.E., Development and utilization of 8-azidopurine nucleotide photoaffinity probes, Federation Proc., v. 42:2831-2836 (1983).[vol. 15, no.10]

This study included the synthesis and testing of a series of 8-azidopurine analogs as biological mimics and photoaffinity probes to present some interesting new techniques and approaches.

Vol. XV #11. Kaiser, I.I., et.al, Photoaffinity Labeling of Catechol O-Methyltransferase with 8-Azido-S-adenosylmethionine, Journal of Biological Chemistry, v.258, no. 3:1747-1751 (February 1983).[vol. 15, no.11]

For this study, an in vitro system using an enzyme extract containing ATP:L-methionine S-adenosyltransferase from Escherichia coli MRE 600 cells was used to synthesize 8-azido-S-adenosyl-L-methionine from methionine and 8-azidoadenosine 5’-triphosphate. The results indicate that the incorporation is occurring at the S-adenosylmethionine binding site in the catechol O-methyltransferase.

Vol. XV #12. Owens, J.R., et.al, Use of Photoaffinity Nucleotide Analogs to Determine the Mechanism of ATP Regulation of a Membrane-Bound, cAMP-Activated Protein Kinase, Journal of Supramolecular Structure, v. 9:57-68 (1978).[vol. 15, no.12]

In this study, using a radioactively tagged, photoaffinity analog of cAMP, 8-azidoadenosine-3’, 5’-cyclic monophosphate, and [32P] ATP, the membrane binding properties of both the regulatory and catalytic subunits of the cAMP-activated protein kinase of human erythrocyte membranes were investigated. The data indicate that the regulatory subunit contains an ATP regulatory site which inhibits 8-N3cAMP binding and the release of the catalytic subunit. These results indicate that the membrane-bound type I enzyme differs significantly from the soluble enzyme studied in other tissues. These enzymes are compartmentalized by being in different cellular locations and are regulated differently by Mg .ATP.

Vol. XV #13. Takemoto, D.J., et.al, GTPase from Rod Outer Segments: Characterization by Photoaffinity Labeling and Tryptic Peptide Mapping, Biochemical and Biophysical Research Communications, v. 102, no. 1:341-347 (September 1981).[vol. 15, no.13]

For this study, the photoaffinity label [-32P]8-N3GTP has been used to identify GTP-binding components in highly purified preparations of GTPase from bovine rod outer segments. These preparations contain two major polypeptides of 37,000 and 39,000 daltons. In the presence of photolyzing radiation, [-32P]8-N3GTP is covalently attached to the 37,000 dalton polypeptide. Tryptic peptide mapping of this polypeptide indicates that it is highly related to the 39,000 dalton species that has been previously identified as a GTP-binding component.

Vol. XV #14. King, M.M., et.al, Photoaffinity Labeling of the Subunit of Phosphorylase Kinase by 8-Azidoadenosine 5’-Triphosphate and Its 2’,3’-Dialdehyde Derivative, The Journal of Biological Chemistry, v. 257, no. 23: 14058-14065 (1982).[vol. 15, no.14]

In this study photoaffinity labeling of rabbit skeletal muscle phosphorylase kinase in the presence of micromolar concentrations of [-32P]8-azidoadenosine 5’triphosphate resulted in preferential labeling of its subunit.

Vol. XV #15. Geahlen, R.L., et.al, Interactions of a photoaffinity analog of GTP with the proteins of microtubules, Proc. Natl. Acad. Sci , v. 74, no. 10:4375-4377 (October 1977).[vol. 15, no. 15]

This study explains tubulin dimmers isolated from brain contain two GTP binding sites, a nonexchangeable site and an exchangeable site. To localize the exchangeable site, the authors used a photoaffinity analog of GTP, 8-azidoguanosine triphosphate, which supports tubulin polymerization in the absence of activating light. Photolysis of tubulin polymerized in the presence of .01 to .1 mM [,-32P]8-N3GTP resulted in covalent incorporation of radioactivity only onto the monomer. Photolysis with 8-N3GTP also prevented any further repolymerization of the tubulin wheras like treatment in the presence of GTP had no effect. Preincubation of tubulin with GTP prevented photoincorporation of [,-32P]8-N3GTP whereas preincubation with ATP did not.

Vol. XV #16. Haley, B.E., Nucleotide Photoaffinity Labeling of Protein Kinase Subunits, Methods of Enzymology, v. 200:477-487 (1991).[vol. 15, no.16]

This chapter presents a series of experimental considerations which may be used to resolve problems faced when using nucleotide potoaffinity probes to detect the subunits involved in the catalytic activity of protein kinases.

Vol. XV #17. Gunnersen, D., et.al, Detection of glutamine synthetase in the cerebrospinal fluid of Alzheimer diseased patients A potential diagnostic biochemical marker, Proc. Natl. Acad. Sci . , v.89:11949-11953 (December 1992).[vol. 15, no.17]

In this study, 8-and 2-azidoadenosine 5’-[l-32P]triphosphate were used to examine cerebrospinal fluid samples for the presence of an ATP binding protein unique to individuals with Alzheimer disease. The protein was identified as glutamine synthetase [GS] based on similar nucleotide binding properties, comigration on two dimensional gels, reaction with a polyclonal anti-GS antibody, and the presence of significant GS enzyme activity in AD CSF.

Vol. XV #18. Chavan, A.J., et.al, NAD+ Binding Site of Clostridium botulinum C3 ADP-ribosyltransferase, The Journal of Biological Chemistry, v. 267, no. 21:14866-14870 (July 1992).[vol. 15, no.18]

In this study, the use of the photoaffinity probe [-P]nicotinamide-2azidoadenine dinucleotide, helped to identify the adenine ring binding domain of the NAD+ binding site. The specificity of labeling was demonstrated by saturation effects and protection by the natural compound at physiologically relevant concentrations. Saturation of labeling was observed at 50 M. Protection experiments indicated an 80% protection of labeling by 100 M NAD+ when protein was photolyzed in the presence of 10 M probe. Trypsin or Staphylococcus aureus V8 protease digestion of the photolabeled protein, along with boronate affinity chromatography and immobilized metal affinity chromatography, was used to specifically isolate the peptide region photolabeled with the probe. The peptide corresponded to Phe9-Gly19 near the N terminus.

Vol. XV #19. Shoemaker, M.T., et.al, Identification of a Guanine Binding Domain Peptide of the GTP Binding Site of Glutamate Dehydrogenase: Isolation with Metal-Chelate Affinity Chromatography, Biochemistry, v.32, no. 7:1883-1890 (1993).[vol. 15, no.19]

In this study, photoaffinity labeling with [-32P]8N3GTP and [-32P]8N3GTP was used to identify the guanine binding domain of the GTP regulatory site within glutamate dehydrogenase. Without photolysis, 8N3GTP mimicked the regulatory properties of GTP on GDH activity with 8N3GTP exhibiting a Ki of 5 M while the Ki for GTP was about .6 M. Results suggest that Lys445 may be the residue modified by [-32P]8N3GTP.

Vol. XV #20. Bhattacharyya, A.K., et.al, Identification of the NADP(H) Binding Site of Rat Liver Microsomal 4-Reductase (Isozyme-1): Purification of a Photolabeled Peptide Corresponding to the Adenine Binding Domain, Biochemistry, v.264:16249-16255 (1995).[vol. 15, no.20]

In this study, PEG-fractionated (6.5%) detergent-solubilized preparations (40mg) containing 5R-1 activity were UV-photolyzed with [32P]-2-azido-NADP+ and subjected to preparative gel electrophoresis on 8% SDS-PAGE. The [32P]-2N3-NADP+ -labeled peptide was eluted with potassium phosphate, concentrated, and further purified by reverse-phase (C8) HPLC. Sequence analysis of the purified peptide indicated that it consisted of 11 amino acids with the sequence N-L-R-K-P-G-E-T-G-Y-K, corresponding to residues 170-180 of the rat 5R-1 sequence.

Vol. XV #21. Potter, R.L., et.al, Photoaffinity Labeling of Nucleotide Binding Sites with 8-Azidopurine Analogs: Techniques and Applications, Methods in Enzymology, v. 91:613-633 (1983).[vol. 15, no.21]

The thrust of this chapter is to cover the more practical aspects of labeling with the 8-azidopurine analogs as well as to emphasize the many types of biological questions that can best be answered utilizing these probes.

Vol. XV #22. Khatoon, S, et.al, Aberrant Guanosine Triphosphate-Beta-Tubulin Interaction in Alzheimer’s Disease, Annals of Neurology, v. 26, no.2:211-215 (August 1989).[vol. 15, no.22]

This study used [32P]8N3GTP to demonstrate that the exchangeable GTP site of the beta subunit of tubulin is available to added guanine nucleotide in normal aged brain homogenates, whereas it is variably unavailable in Alzheimer’s diseased brain. The results support the hypothesis that microtubule formation is abnormal in brains affected by Alzheimer’s disease.

Vol. XV #23. King, S.M., et.al, Strategies and Reagents for Photoaffinity Labeling of Mechanochemical Proteins, Methods in Enzymology, v. 196:449-466 (1991).[vol. 15, no.23]

The object of this chapter is to present some of the uses of nucleotide photoaffinity probes to study various aspects of the interaction of nucleotides with mechanochemical proteins. These applications of photoaffinity probes range from detecting the subunits involved in nucleotide binding to the isolation and sequencing of the active site peptides that are photolabeled.

Vol. XV #24. Trad, C.H., et.al, Identification and Characterization of a Nucleotide Binding Site of ovine Prolactin with 2-Azido-NAD, Archives of Biochemistry and Biophysics, v.304, no.1:58-64 (July 1993).[vol. 15, no.24]

In this study, photoaffinity labeling of ovine prolactin with the NAD+ photoaffinity analog ]l-32P]nicotinamide-2azidoadenine dinucleotide has been used to identify an NADH/NADPH binding site. Specificity of nucleotide interaction was demonstrated by saturation and protection of labeling at physiologically relevant concentrations. These studies demonstrate that prolactin contains an NADH/NADPH binding site which may be significant in the mechanism of action of this hormone.

Vol. XV #25. Criteria for a recommended standard…Occupational Exposure to Inorganic Mercury, U.S. Depart. Of Health, Education and Welfare, 1973.[vol. 15, no.25]

This paper reviews a study of three plants in which groups of workers were exposed to single phenylmercuric compounds. The study involved a total of 67 workers and would suggest that PMA and PMB both have a low toxicity for humans, in terms of industrial exposure, and that what absorption does take place from the air is probably in the form of mercury vapor.

Vol. XV #26. Lung function tests in four workers exposed to mercury vapour.[vol. 15, no.26]

These pages highlight a case study of four workers exposed to mercury vapour where chest radiography, pulmonary function, and serum and urinary mercury levels were tested.

Vol. XV #27. Email message from Dorothy Preslar to Stephen Morse on Campylobacter Jejuni and Guillain-barre syndrome.[vol. 15, no.27]

This email message states that a NEJM team of doctors reported research linking Campylobacter jejuni to Guillain-Barre syndrome or Miller Fisher syndrome.

Vol. XV #28. Sfikas, P.M., Can a Dentist Ethically Remove Serviceable Amalgam Restorations?, JADA, v. 127:685-687 (May 1996).[vol. 15, no.28]

This article discusses the above question and provides a positive answer under certain limited circumstances. Informed consent and dentist responsibilities are also discussed.

Bibliography XVI.

Vol. XVI A-1. Chase, H.S., Some Observations and Experiments connected with Oral Electricity, American J. Dental Science, v.12:18-23.[vol. 16, no.1]

This study compares filling materials amalgam, gold, tin, and Hill’s stopping and their ability to arrest decay in acid conditions.

Vol. XVI A-2. Excerpts from the deposition of John Renner, M.D.[vol. 16, no.2]

These pages from the deposition highlight questions and answers which took place.

Vol. XVI A-3. Workshop: Biocompatibility of Metals in Dentistry, J. American Dental Association, v.109:469-471 (1984).[vol 16, no.3]

This report summarizes the workshop, hosted by the ADA in July 1984, which reviewed existing scientific evidence and literature about metals used in dentistry and pinpointed areas of interest or concern that may warrant further research. Among the materials highlighted are Nickel, Beryllium, Cobalt, Chromium, Gold, and Mercury.

Vol. XVI A-4. An Assessment of Mercury in the Environment: The Effects of Selenium on Methyl Mercury Toxicity, National Academy of Sciences, 84-87 (1978).[vol. 16, no.4]

This is an incomplete paper. The sections shown review several studies on the protective effect of dietary selenium against mercury toxicity.

Vol. XVI A-5. Berlin, M.H., et.al, Maximum Allowable Concentrations of Mercury Compounds: Report of an International Committee, Arch. Environ. Health, v. 19:981-905 (1969).[vol. 16, no.5]

At the second International Symposium on Maximum Allowable Concentrations of Toxic Substances in Industrial Environments in 1963, a recommendation was made to have expert groups convene to establish international values for the maximum allowable concentrations of a number of the more important compounds. In 1966, the subcommittee for MAC values under the auspices of the Permanent Commission and International Association on Occupational Health met in Vienna, and responsibility was assigned for formation of groups to evaluate the scientific basis of MAC values for certain specific substances. As a consequence of decisions made at these meetings, an evaluation of MAC values for mercury and its compounds was made at a symposium at the Karolinska Institute in Stockholm, 1968. This report highlights those evaluations.

Vol. XVI A-6. . Mission Statement -International Academy of Oral Medicine and Toxicology.

Vol. XVI A-7. Approval of Dental and Dental Hygiene Schools, Florida State Laws and Rules, v. 15, 1323 (October 1994).

Vol. XVI A-8. ADA Letter from Thomas H. Boerschinger on Council of Ethics, Bylaws and Judicial Affairs adopting a statement and Advisory Opinion No. 7 to Section 1-J of the Association’s Code (June 1987).

Vol. XVI A-9. blank

Vol. XVI A-10. Clifford, J.W., Materials Reactivity Testing, Background, Basis and Procedures for the Immunological Evaluation of Systemic Sensitization to Components Which Emanate from Biomaterials.

Vol. XVI A-11. Clifford Materials Reactivity Testing Brochure, Clifford Consulting & Research, Inc.

Vol. XVI A-12. 1986 Annual Session, Journal American Dental Association, v.114:22-23 (1987). ADA withdraws liability plan endorsement

Vol. XVI A-13. Cooley, R.L., et. al, Mercury Vapor Emitted During Ultraspeed Cutting of Amalgam, J. Indiana Dent. Assn., v.57:28-31 (1978).

Vol. XVI A-14. Dorland’s Illustrated Medical Dictionary, 25th Edition (1974).

Vol. XVI A-15. The Safety of Dental Amalgam, Health Canada (1996).

Vol. XVI A-16. Critical Flaws of Richardson, G.M Report by an International Panel prepared on behalf of the Canadian Dental Association’s International Panel.’

Vol. XVI A-17. Risk Assessment/Risk Management: A Handbook for Use Within the Bureau of Chemical Hazards, Health Canada, (January 1991).

Vol. XVI A-18. Dept. of State 33-14 Disciplinary Action No. 204 Nov. 1991

Vol. XVI A-19. Sato, K. et.al, An Epidemiological Study of Mercury Sensitization, Allergology International, v.46:201-206 (1997).

Vol. XVI A-20. Richardson, G.M., Mercury Exposure from Dental Amalgam: Re-evaluation of the Richardson Model, Standardization by Body Surface Area and Consideration of Recent Occupational Studies (1998).

Vol. XVI A-21. Klaassen, C.D., Heavy Metals and Heavy-Metal Antagonists, Goodman and Gilman’s The Pharmacological Basis of Therapeutics, 6th Edition, 1615-1625 (1980)

Vol. XVI A-22. Specific Poisons: Symptoms and Treatment, The Merck Manual of Diagnosis and Therapy, 16th Edition, 2696-2697 (1992).

Vol. XVI A-23. Systemic Toxicology, Casarett and Doull’s Toxicology The Basic Science of Poisons, 3rd Edition (1986).

Vol. XVI A-24. Principles of Toxicology, Casarett and Doull’s Toxicology The Basic Science of Poisons , 5th Edition.

Vol. XVI A-25. Shaffer Hine Levy Mercury, A Textbook of Oral Pathology, w. B. sanders Co. 443-445 (1958).

Vol. XVI A-26. Material Safety Data Sheet: Mercury, Dentsply (1997).

Vol. XVI A-27. Gerstner, H.B., et.al, Clinical Toxicology of Mercury, J. Toxicology, v.2:491-526 (1977).

Vol. XVI #AS-28 Cook, T Yates P., “Fatal mercury intoxication in a dental surgery assistant.” British Dent J. 127(12):553-555, Dec Vol. 16 #A-27

Bibliography XVII

Vol. XVII A-51. Warfvinge, K., et.al, Systemic Autoimmunity Due to Mercury Vapor Exposure in Genetically Susceptible Mice: Dose-Response Studies, Toxicol. Appl. Pharmacol, v.132:299-309 (1995).[vol. 17, no.1]

In this study, six groups of genetically mercury-susceptible female SJL/N (H-2s) mice were exposed to mercury vapor at a concentration of .3-1.0 mg Hg/m3 air for .5-19 hr/day 5 days a week for 10 weeks. Mercury vapor efficiently induced an autoimmune syndrome in genetically susceptible mice, and the LOAEL for the adverse effects varied in the order ANoA<B-cell stimulation<IC deposits.

Vol. XVII A-52. Hultman, P., et.al, Activation of the immune System and Systemic Immune Complex Deposits in Brown Norway Rats with Dental Amalgam Restorations, Journal Dent. Res., v. 77, no. 6:1415-1425 (June 1998).[vol. 17, no.2]

In this study, effects on the immune system were examined by giving genetically mercury-susceptible Brown Norway (BN) rats and mercury-resistant Lewis (LE) rats silver amalgam restorations in 4 molars of the upper jaw, causing a body burden similar to that described in human amalgam-bearers. Dental amalgam restorations release substantial amounts of their elements, which accumulate in the organs and which, in genetically susceptible rats, give rise to activation of the immune system and systemic IC deposits.

Vol. XVII A-53. Schriever, W., et.al, Electromotive Forces and Electric Currents Caused by Metallic Dental Fillings, J. Dental Research, v.31, no.2:205-229 (April 1952).[vol.17, no.3]

The purpose of this investigation was to devise methods, including the necessary theory and apparatus, for determining electromotive forces, electrical resistances, and electric currents associated with metallic dental fillings in place in oral cavities under normal oral conditions. The experimental procedure is described and the scheme for dealing with the data is given. Results were computed for 78 fillings in the oral cavities of 66 subjects whose ages fell in the range 18-30 years. In conclusion the electrical resistance associated with a filling is almost entirely concentrated in and very near the metal-saliva and metal-bone fluid contacts. The electric current through any metallic filling is virtually independent of the number and kinds of other metallic fillings in that oral cavity, provided that filling is not in contact with any other metallic filling.

Vol. XVII A-54. TLVs and BEIs for Chemical Substances and Physical Agents, American Conference of Governmental Industrial Hygienists (1997).[vol. 17, no.4]

This paper highlights the policy statement on the uses of TLVs and BEIs approved by the Board of Directors of ACGIH on March 1, 1988.

Vol. XVII A-55. Aronsson, A.M., et.al, Dental amalgam and mercury, Biology of Metals, v.2:25-30 (1989).[vol. 17, no.5]

For this study, mercury concentration in intraoral air and urine of seven females with dental amalgam was measured before and after intake of one hard-boiled egg. A considerable decrease in mercury concentration in intraoral air was found. Twenty women with about equal dental amalgam status, with or without subjective symptoms related to dental amalgam were also studied. No major

differences in concentration of mercury in intraoral air and in urine were obtained for the groups in study II.

Vol. XVII A-56. National Alert A Warning about Continuing Patterns of Metallic Mercury Exposure, U.S. Agency for Toxic Substances and Disease Registry and U.S. EPA.[vol. 17, no.6]

This paper examines metallic mercury exposure incidents involving schoolchildren and religious practices. Questions and answers regarding mercury risks and exposure are included.

Vol. XVII A-57. Godfrey, M.E., Chronic Illness in Association with Dental Amalgam: Report of Two Cases, J. Advance Med, v.3, no. 4 (1990).[vol. 17, no.7]

This paper examines two case studies involving multiple symptomatology. These cases demonstrate that the presence of amalgam can, in susceptible individuals, result in chronic illness due to mercury sensitivity.

Vol. XVII A-58. Langworth, S., et.al, A Case of High Mercury Exposure from Dental Amalgam, European Journal of Oral Sciences, v.104:320-321 (1996).[vol. 17, no.8]

This case report investigates a patient who suffered from several complaints, which by herself were attributed to her amalgam fillings. Analysis of mercury in plasma and urine showed unexpectedly high concentrations. Following removal of the amalgam fillings, the urinary excretion of mercury became gradually normalized and her symptoms declined.

Vol. XVII A-59. Gonzalez-Ramirez, et.al, Sodium2,3-Dimercaptopropane-1-Sulfonate Challenge Test for Mercury in Humans: II.Urinary Mercury, Porphyrins and Neurobehavioral Changes of Dental Workers in Monterrey, Mexico, J. Pharmacol., Exper. Therap, v.272, no.1:264-274 (1995).[vol. 17, no.9]

In this study, the sodium salt of 2,3-dimercaptopropane-1-sulfonic acid challenge test was given in Monterrey, Mexico to dental and nondental personnel. Urine samples were collected and analyzed for total mercury. The urinary mercury level after DMPS administration is a better indicator of exposure and renal mercury burden than is the mercury level measured in the urine before DMPS is given.

Vol. XVII A-60. Langworth, S., et.al., Exposure to Mercury Vapor and Impact on Health in the Dental Profession in Sweden, J. Dent. Res., v. 76, no. 7:1397-1404 (1997).[vol. 17, no. 10]

The objective of the present study was to carry out detailed measurements of mercury exposure in the dental profession in Sweden, and to search for adverse

health effects from such exposure. 22 dentists and 22 dental nurses, working in teams, at six Swedish dental clinics were examined. Results confirm that exposure to mercury in dental profession in Sweden is low. The air Hg levels were mainly influenced by the method of amalgam preparation and inserting, and by the method of air evacuation during drilling and polishing.

Vol. XVII A-61.0Piikivi, L., et.al, EEG findings in chlor-alkali workers subjected to low long term exposure to mercury vapour, Br. J. Ind. Med, v.46, no. 6:370-375 (1989).[vol. 17, no.11]

For this study, the cerebral effect of long term and low exposure to mercury vapour was studied in a group of 41 workers in a chlor-alkali plant and in a group of matched referents by electroencephalography. In the computerized EEG the exposed workers had significantly slower and more attenuated EEGs than the referants. This difference was most prominent in the occipital region, became milder parietally, and was almost absent frontally.

Vol. XVII A-62. Ritchie, K.A., et.al, A pilot study of the effect of low level exposure to mercury on the health of dental surgeons, Occup. Environ. Med., v.52:813-817 (1995).[vol. 17, no.12]

This study was conducted to examine whether the computerized analysis of psychomotor responses available from Cognitive Drug Research is appropriate for measuring an effect of low level exposure to mercury in dentists. A computersized batter of psychomotor tests was given to two groups of dentists (older and trainees). The older dentists had slightly higher concentrations of urinary mercury although most were around background levels and they were all within occupational limits. The older dentists showed significantly better performance on the simple reaction time test and significantly poorer performance in the immediate word recall and delayed word recall tests.

Vol. XVII A-63. Roels, H., et.al, Comparison of renal function and psychomotor performance in workers exposed to elemental mercury, Int. Arch. Occup. Environ. Health, v. 50:77-93 (1982).[vol. 17, no.13]

In this study, renal function and psychomotor performance of a group of 43 workers exposed to mercury vapor were examined. Increased proteinuria and albuminuria were found slightly more prevalent in the Hg-exposed group than in the control workers. The scores of the psychomotor tests were less satisfactory in the Hg workers than in the control workers.

Vol. XVII A-64. Roels, H., et.al., Detection of hand tremor in workers exposed to mercury vapor: a comparative study of three methods, Environ. Res., v. 49:152-165 (1989).[vol. 17, no. 14]

This study measured hand tremors in a group of 54 male workers exposed to mercury vapor (average duration of 7.7 years) using an accelerometer test and two psychomotor tests. The hand steadiness test and eye-hand coordination test revealed preclinical alterations in postural and intentional tremors whereas the changes evidenced by the accelerometer test were not statistically significant.

Vol. XVII A-65. Vimy, M.J., et.al, Dental amalgam mercury daily dose estimated from intra-oral vapor measurements: a predictor of mercury accumulation in human tissues, J.Trace Elements in Experimental Med., v.3:111-123 (1990).[vol. 17, no.1 5]

This review paper reexamines earlier estimations of Hg daily dose from dental amalgam in order to elaborate and refine the mechanical and volumetric parameters of open-mouth Hg vapor sampling. Corrections for the sampling factors of flow rate and sampling dilution, and the respiratory factor of Hg accumulation in the closed mouth between oral inhalations, reduce our original daily dose estimates by approximately 50%.

Vol. XVII A-66. IRIS Integrated Risk Information System 3/1/97 Mercury, elemental CASRN 7439-97-6

Mercury, elemental, Integrated Risk Information System , National Center for Environmental Assessment, U.S. Environ. Protection Agency (1998).[vol. 17, no.16]

Health assessment information on a chemical substance is included in IRIS only after a comprehensive review of chronic toxicity data by U.S. EPA health scientists from several Program Offices and the Office of Research and Development. The summaries presented in Sections I and II represent a consensus reached in the review process. Background information and explanations of the methods used to derive the values given in IRIS are provided in the Background Documents.

Vol. XVII A-67. Verberk, M.M., et.al, Tremor in workers with low exposure to metallic mercury, Am. Ind. Hyg. J ., v.47, no. 8:559-562 (1986).[vol. 17, no.17]

For this study a newly developed lightweight balance-tremormeter was used in a fluorescent lamp production factory to measure postural tremor of the finger in 21 workers exposed for .5-19 years to metallic mercury. In addition, tremor was measured in an indirect way by means of a hole-tremormeter. The study indicates that exposure to metallic mercury below the current TLV (50 g/m3) may increase the tremor of the finger.

Vol. XVII A-68. Uzzell, B.P., et.al, Chronic low-level mercury exposure and neuropsychological functioning, J. of Clin and Exper Neuropsych, v. 8:581-593 (1986).[vol. 17, no.18]

In this study, the effects of chronic low-level exposure to inorganic mercury were measured through the neuropsychological performances of 13 female dental auxiliary workers with elevated head mercury levels. Chronic subtoxic levels of inorganic mercury appear to produce mild changes in short-term nonverbal recall and heightened distress generally, and particularly in categories of obsessive compulsion, anxiety and psychoticism, without alterations in general intellectual functioning, attention, verbal recall and motor skills.

Vol. XVII A-69. Guidelines for Exposure Assessment, U.S. Environmental Protection Agency (1992).[vol. 17, no. 19]

These final guidelines were issued by the U.S. Environmental Protection Agency. The guidelines are intended for risk assessors in EPA and those exposure and risk assessment consultants, contractors or other persons who perform work under Agency contract or sponsorship. The guidelines describe the general concepts of exposure assessment including definitions and associated units.

Vol. XVII A-70. Risk Assessment Guidance for Superfund, volume 1, Human Health Evaluation Manual (Part A) (1989).[vol. 17, no.20]

Chapter 6 of this manual is included in this entry. The chapter describes the procedures for conducting an exposure assessment as part of the baseline risk assessment process at Superfund sites. The procedures and information presented in this chapter represent some new approaches to exposure assessment as well as a synthesis of currently available exposure assessment guidance and information published by EPA. Throughout this chapter, relevant exposure assessment documents are referenced as sources of more detailed information supporting the exposure assessment process.

Vol. XVII A-71. Human Health Risk Assessment for Priority Substances, Canadian Environmental Protection Act, Health Canada (1994).[vol. 17, no.21]

In this report, a brief description of aspects considered in the evaluation of data relevant to assessment of “toxic” under paragraph 11(c) of CEPA is presented. This is followed by a description of the principles used in the assessment of exposure and the approach to evaluation of effects for different types of substances (“non-threshold toxicants”, threshold toxicants”, “possible threshold toxicants” and mixtures).

Vol. XVII A-72. Human Health Risk Assessment of Chemicals from Contaminated Sites Volume 1, Risk Assessment Guidance Manual, Health Canada (1994).[vol. 17, no.22]

This chapter provides an overview of the framework for human health risk assessment that is the basis of the guidance provided in Parts II, III and IV of this document. One of the primary goals of this framework is to define a risk assessment process that, within the context of existing and anticipated policies and regulations, can be used at an early stage and at various points throughout the contaminated site management process.

Vol. XVII A-73. Affidavit of G. Mark Richardson, Ph.D., Cranmer v Mindrup case no. CV97-1891.[vol. 17, no.23]

This affidavit of G. Mark Richardson, PhD, is in support of the motion filed pursuant to Daubert v. Merrill Dow Pharmaceuticals, Inc. and Frye v. United States to preclude the admissibility of or reference to Dr. John W. Osborne’s assessment of plaintiff Dixie McReynolds’s mercury exposure and absorption.

Vol. XVII A-74. Curriculum Vitae of John W. Osborne, DDS., MSD. (April 1998).[vol. 17, no.24]

This document includes personal and professional information regarding Dr. John W. Osborne.

Vol. XVII A-75. Excerpts from deposition of John W. Osborne, DDS. MSD. (May 1998).[vol. 17, no.25]

This document includes questions and answers from the deposition of Dr. John W. Osborne in the McReynolds vs. Mindrup Case no. CV97-1891.

Vol. XVII A-76. Cavalleri, A., et.al, Colour vision loss in workers exposed to elemental mercury vapour, Toxicology Letters, v.77:351-356 (1995).[vol. 17, no.26]

This study evaluated colour vision in 33 workers exposed to elemental mercury (Hg) vapour. The results were expressed as colour confusion index (CCI). The results suggest that exposure to elemental Hg inducing HgU values exceeding 50 g/g creatinine can induce a dose-related colour vision loss.

Vol. XVII A-77. Guzzi, G., et. al, Dental Amalgam and Mercury Levels in Autopsy Tissues, The American Journal of Forensic Medicine and Pathology, v. 27, no.1:42-45 (March 2006) [vol. 17, no.27]

Eighteen cadavers from routine autopsy casework were subject to a study of tissue levels of total mercury in brain, thyroid, and kidney samples by atomic absorption. All dental amalgam fillings were charted. Total mercury levels were significantly higher in subjects with a greater number of occlusal amalgam surfaces. Mercury levels were significantly higher in brain tissues compared with thyroid and kidney tissues in subjects with more than 12 occlusal amalgam fillings but not in subjects with 3 or less occlusal amalgams.

Bibliography XVIII.

Vol. 17 #B-1. Mercury, U.S. Agency for Toxic Substances and Disease Registry TP-93/10 (November 1994).

Vol. 17 #B-2. Empty

Vol. 17 #B-3 Goldwater L.J. and Jacobs, M.B., et.al, Absorption and Excretion of Mercury in Man, VII Significance of mercury in blood Arch. Environ. Health, v. 9:454-463 (1964).

Vol. 17 #B-4. Stopford, W., et.al, Microenvironmental Exposure to Mercury Vapor, Amer. Indust. Hyg. Assoc. J., v. 39:378-384 (1978).

Vol. 17 #B-5. Affidavit of F. Fuller Royal, M.D.,McRenolds v. Mindrup

Vol. 17 #B-6. Friberg, L., et.al, Mercury in the Environment: An Epidemiological and Toxicological Appraisal (1972).

Vol. 17 #B-7. Rom, W.N., Environmental and Occupational Medicine (1983).

Vol. 17 #B-8. . Hamilton & Hardy’s Industrial Toxicology, 4th Edition (1983).

Vol. 17 B-9. Hahn, L. J., et.al, Dental “silver” Tooth Fillings: A source of Mercury Exposure Revealed by Whole-Body Image Scan and Tissue Analysis, FASEB J . , v. 3:2641-6 (1989).

Vol. 17 B10. Hahn, L.J., et.al, Whole-Body Imaging of the Distribution of Mercury Released from Dental Fillings into Monkey Tissues, FASEB J ., v.4:3256-3260 (1990)

Vol. 17 #B-11. Bauer, J.G., et.al, The Toxicity of Mercury in Dental Amalgam, Calif. Dent. Assoc. J ., v. 10:47-61 (1982).

Vol. 17 #B-12. Cooley, R.L., et.al, Detection and Diagnosis of Bioincompatibility of Mercury, Calif. Dent. Assoc. J. , 36-43 (October 1984).

Vol. 17 #B-13. Barber, T., Inorganic Mercury Intoxication Reminiscent of Amyotrophic Lateral Sclerosis, J. of Occupational Medicine, v. 20, no. 10:667-669 (October 1978).

Vol. 17 #B-14. DAMS Dental Amalgam Mercury Syndrome http://www.flcv.com/damspr2f.htm8/1/2006

Bibliography XIX.

1. Risk Assessment Guidance for Superfund Vol. 1, Human Health Evaluation Manual (Part A), U.S. Environmental Protection Agency (1989).

2. Human Health Risk Assessment for Priority Substances, Health Canada (1994).

3. Human Health Risk Assessment of Chemicals from Contaminated Sites, vol. 1, Risk Assessment Guidance Manual, Health Canada (1994).

4. Health Risk Determination:The challenge of health protection, Health Canada (1990).

5. Integrated Risk Information System, Mercury, Elemental, U.S. Environ. Protection Agency , (1998).

6. Toxicological Profile for mercury (update), U.S. Dept. of Health & Human Svcs ., 32-37 (1993).

7. Environmental Health Criteria 118, Inorganic Mercury, World Health Organization, Table 2, 35, 84-92 (1991).

8. Richardson, G.M., et.al, A Monte Carlo Assessment of Mercury Exposure and Risks from Dental Amalgam, 709-759 (1996).

9. Richardson, G.M., Mercury Exposure from Dental Amalgam: Re-evaluation of the Richardson Model, Standardization by Body Surface Area, and Consideration of Recent Occupational Studies, Amalgam Part II (1998).

10. Richardson, G.M., Assessment of Exposure and Risks from Dental Amalgam, Final Report (1995).

11. Fawer, R.F., et.al, Measurement of hand tremor induced by industrial exposure to metallic mercury, British Journal of Industrial Medicine, v. 40:204-208 (1983).

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

13. Evaluation of Risks Associated with Mercury Vapor from Dental Amalgam, Dental Amalgam Final Report, Appendix III: 1-30 (November 1991).

14. Clarkson, T.W., The Prediction of Intake of Mercury Vapor from Amalgams, Biological Monitoring of Toxic Metals, 247-264 (1988).

15. Excerpts from the deposition of John W. Osborne, DDS, MSD.

16. Guidelines for Exposure Assessment, U.S. Environ. Protection Agency, 1-169 (May 1992).

17. Richards, J.M., et.al, Mercury Vapour Released during the Removal of Old Amalgam Restorations, British Dental Journal, v. 159, no. 7:231-232 (October 1985).

18. Nimmo, A., et.al, Particulate inhalation during the removal of amalgam restorations, J. Prosthet. Dent. , v.63, no. 2:228-233 (1990).

19. Brune, D., et.al, Levels of mercury and silver in dust from the trimming of amalgam dies, Scand. J. Dent. Res., v. 87:462-465 (1979).

20. Brune, D., et. al, Dust in dental laboratories, Part II: Measurement of particle size distributions, Journal of Prosthetic Dentistry, v.44, no. 1:82-87 (July 1980).

21. Bjorkman, L., et.al, Mercury in Saliva and Feces after Removal of Amalgam Fillings, Toxicology and Applied Pharmacology, v. 144:156-162 (1997).

22. Edlund, C., et.al, Resistance of the Normal Human Microflora to Mercury and Antimicrobials After Exposure to Mercury from Dental Amalgam Fillings, Clin. Infect. Dis. v.22:944-950 (1996).

23. Goldberg, N.B., et.al, A rabbit lung model for biocompatibility testing of inhaled dental restorative materials, American Review of Respiratory Disease, American Lung Association, v. 139, no.4 part 2, Abstract 548 (April 1989).

24. TLVs and BEIs, Threshold Limit Values and Biological Exposure Indices for Chemical Substances and Physical Agents, ACGIH , (1997).

25. Ontario’s Smog Plan, Ontario Ministry of Environment and Energy, (1998).

26. Engle, J.H., et.al, Quantitation of total mercury vapor released during dental procedures, Dent. Materials, v. 8:176-180 (May 1992).

27. Marshall, S.J., et.al, Dental Amalgam: The materials, Adv. Dent. Res ., v. 6 (September 1992).

28. Fredin, B., Mercury release from dental amalgam fillings, International Journal of Risk & Safety in Medicine, v. 4:197-208 (1994).

29. Hanawa, T., et.al, Compositions of Surface Layers Formed on Amalgams in Air, Water and Saline, Dental Materials Journal, v. 12, no2:118-126 (1993).

30. Dental Mercury Hygiene, JADA, v. 122 (August 1991).

31. Advertisement of Patterson Dental Supply, Inc., JADA, (1998).

32. Ahmad, R., et.al, Mercury Release from Amalgam: A Study in Vitro and in Vivo, Operat. Dent., v. 15: 207-218 (1990).

33. Osborne, J.W., Curriculum Vitae, (April 1998).

34. Wolff, O., Mercury Toxicity and Dental Amalgam, Neurotoxicol, v. 4, no. 3: 201-204 (1983).

35. Osborne, J.W., Exposure Assessment.

36. Reinhardt, J.W., Exhaled Mercury, The Journal of Prosthetic Dentistry, v. 49, no.5:653-656 (May 1983).

Bibliography XX.

Bibliography XX.

Vol. 20 #1. Hanson, M., et.al, The dental amalgam issue. A review, Experientia, v. 47:9-22 (1991).[vol. 20, no.1]

Using an interdisciplinary approach, the current position in the dental amalgam controversy and the potential impact of amalgam mercury on human health are reviewed. Aspects of materials science, corrosion, mercury exposure, toxicology, neurology and immunology are included. New data on mercury exposure from corroded amalgam fillings in vivo are presented. The symptomatology of a disabled patient, who recovered after amalgam removal has been included.

Vol. 20 #2. Richardson, G., M., et.al, A Monte Carlo Assessment of Mercury Exposure and Risks from Dental Amalgam, Human and Ecological Risk Assessment, v. 2, no. 4:709-761 (1996).[vol. 20, no.2]

For this study, it was estimated for Canadians with amalgam-filled teeth, based on two independent models, that Hg exposure from amalgam averaged .045 to .082 g/kg bw/day in toddlers (aged 3-4 yeas); .044 to.069 g/kg bw/day in children (aged 5-11 years); .034 to .044 g/kg bw/day in teens (aged 12-19 years); .050 to .055 g/kg bw/day in adults (aged 20-59 years); and .031 to .041 g/kg bw/day in seniors (aged 60+ years). Based on the least conservative exposure model of the two independent models developed, the average numbers of amalgam-filled teeth estimated not to compromise the TDI were: 1 filling in toddlers; 1 filling in children; 3 fillings in teens; and 4 fillings in adults and seniors. Amalgam was estimated to contribute, on average, 50% of total Hg exposure form all sources (amalgam, air, water, food, soil) in adults, and 32-42% for other age groups.

Vol. 20 #3. Fischer, R. D., Graphs on Prenatal & Perinatal Exposure to Mercury (2002).[vol. 20, no.3]

These hand-drawn graphs were created by Dr. Richard D. Fischer. Graph A shows dosage of mercury to infants (birth to age 5) from vaccinations (262.5 g). Graph B shows dosage of mercury to mother from amalgam filling during 9 month gestation (2700 g).

Vol. 20 #4. Cahill, M., Environmental Contaminants in Breast Milk, Le Leche League International, (March 1982).[vol. 20, no.4]

This paper answers questions regarding environmental contaminants found in breast milk and its effect on the baby.

Vol. 20 #5. Jensen, A.A., Chemical contaminants in human milk (1983).[vol. 20, no.5]

This review is a translated, updated, and extended version of a survey requested by a governmental committee under The National Board of Health of Denmark based on information available to the author up to September 1982.

Vol. 20 #6. Wolff, M.S., Occupationally Derived Chemicals in Breast Milk, American Journal of Industrial Medicine, v. 4:259-281 (1983).[vol. 20, no.6]

This review analyzes the contamination of breast milk by several chemicals of industrial origin. Specifically, occupational versus base population levels of chemicals in human milk

Vol. 20 #7. Sundberg, et.al, Lactational Exposure and Neonatal Kinetics of Methylmercury and Inorganic Mercury in Mice, Toxicology and Applied Pharmacology, v. 154:160-169 (1999).[vol. 20, no.7]

In this study, the concentration of mercury in milk and the distribution pattern in the sucking pup was followed over time after administration of a single iv injection of .5 mg/kg body wt of 203Hg-labeled methylmercuric chloride or mercuric chloride to lactating mice on Day 10 of lactation. Lactational exposure following a maternal methylmercury or inorganic mercury dose resulted in almost similar mercury concentrations in liver, kidneys, and plasma of the suckling, but higher concentrations in brain (as most 14 times) and also twice as high mercury body burden in the methylmercury group.

Vol. 20 #8. Berlin, M., Is Amalgam in Dental Fillings a Health Risk? Lakartidn, v. 89:2918-2923 (1992), English Translation by M. Hanson.[vol. 20, no.8]

In this paper, Berlin presents some of the facts and conclusions from the World Health Organization criteria document for inorganic mercury and adds some of his own comments and views regarding the amalgam problem in Sweden.

Vol. 20 #9. Berlin, M, Mercury in dental filling materials- environmental medicine risk analysis: a literature and knowledge review, Amalgamfragan.[vol. 20, no.9]

This review paper on risk analysis deals with new information on the toxic properties of mercury, extent, magnitude and variation of mercury exposure from amalgam, identification of health risks with amalgam, based on knowledge of the toxic properties of mercury, possibilities to estimate the magnitude of the health risks, risk evaluation and risk handling from an environmental medial aspect and

finally, the further facts which might be needed for a complete basis to decide how the risks should be handled.

Vol. 20 #10. Bengtsson, A.M., et.al, Concentrations of blood, serum and urine components in relation to number of amalgam tooth fillings in Swedish women, Community Dentistry and Oral Epidemiology, v.22 (1994).[vol. 20, no.10]

In this study 1, 462 women aged 38, 46, 50, 54 and 60 years of age were examined in 1968/69 in a combined medical and dental population study in Gothenburg, Sweden. Number of tooth surfaces restored with amalgam fillings was assessed. The examination was repeated in 1980/81 including a new dental examination. The results from a number of biochemical analyses of blood, serum and urine were analyzed for possible statistical relationship to number of dental amalgam fillings. Amalgam fillings were not found to be associated with impairment of the kidney function or the immunological status.

Vol. 20 #11. Bengtsson, A.M., et.al, Number of amalgam fillings in relation to cardiovascular disease, diabetes, cancer and early death in Swedish women, Community Dent. Oral Epidemiol ., v. 21:40-44 (1993).[vol. 20, no.11]

In this study 1, 462 women aged 38, 46, 50, 54 and 60 years of age were initially examined in 1968-69 in a combined medical and dental population study in Gothenburg, Sweden. Number of tooth surfaces restored with amalgam fillings was assessed. The incidences of myocardial infarction, stroke, diabetes, cancer and overall mortality were determined during a 20-year follow-up period. The study did not provide any evidence for a correlation between amalgam fillings and cardiovascular disease, diabetes, cancer or early death.

Vol. 20 #12. Bengtsson, A.M.,et.al, Number of amalgam tooth fillings in relation to subjectively experienced symptoms in a study of Swedish women, Community Dental Oral Epidemiol, v.16:227-231 (1988).[vol. 20, no.12]

For this study, 1024 dentulous women aged 38-72 participated in a population study of women in Gothenburg, Sweden and answered a questionnaire with 30 specific questions concerning different symptoms and complaints. No positive correlations were found between number of amalgam fillings and number of symptoms, nor between number of amalgam fillings and prevalence of specified single symptoms or complaints.

Vol. 20 #13. Lavstedt, S., et.al, Medical diagnoses and symptoms related to amalgam fillings, Tandlakeratidn, v.88:81-88 (1989).[vol. 20, no.13]

In this experiment, a connection between 14 selected symptoms together with four clinical variables have been related to the number of amalgam fillings in 1204 individuals and grouped according to number of filled tooth surfaces. After standardization for age, sex, social group, smoking and the number of remaining teeth, there was no statistically significant increase of the percentage of persons with symptoms in groups with increasing number of amalgam surfaces. Comparing persons with and without teeth, the latter showed significantly less symptoms from stomach and intestine. The mean hemoglobin value was also significantly lower among the persons without teeth. These also had a significantly higher mean systolic blood pressure.

Vol. 20 #14. Aposhian, H.V., et.al, Human Studies with the Chelating Agents, DMPS and DMSA, Clinical Toxicology, v.30, no.4:505-528 (1992).[vol. 20, no.14]

This study attempted to determine whether dental amalgams influence the human body burden of mercury. Volunteers were given the sodium salt of 2,3-dimercaptopropane-1-sulfonic acid (DMPS). The diameters of dental amalgams of the subjects were determined to obtain the amalgam score. Administration of 300 mg DMPS by mouth increase the mean urinary mercury excretion of subjects over a 9 hour period. There was a positive correlation between the amount of mercury excreted and the amalgam score. DMSA analogs have been designed and synthesized in attempts to increase the uptake by cell membranes of the DMSA prototype chelating agents. The iv administration of the monomethyl ester of DMSA, the dimethyl ester of DMSA or the zinc chelate of dimethyl DMSA increase the biliary excretion of platinum and cadmium in rats.

Vol. 20 #15. Britt, A.W, Multiple Sclerosis and Mercury in Cerebrospinal Fluid (1987).[vol. 20, no.15]

In a study in progress mercury levels in cerebrospinal fluid is measured. So far 12 unselected, consecutive patients, 3 males and 9 females (age 30-61) with neurologically verified multiple sclerosis with oligocional bands in their CSF have been completed. Duration of illness is 1.5-12 years. Of 14 controls (age 17-50), 11 have underwent investigation for headache without any pathological findings and 3 were healthy volunteers. Mean Hg concentrations in CSF for the patients was 3.0 mg/l and for the controls was .4 mg/l.

Vol. 20 #16. Haley, B., Response to the NY Daily News, Copy of Email (January 2002).[vol. 20, no.16]

This email is a copy of Dr. Haley’s response to an online article he received which appeared in the New York Daily Times concerning blood mercury levels of firemen and police workers at the 9/11 Ground Zero site.

Vol. 20 #17. Leong, C.C.W, et.al., Retrograde degeneration of neurite membrane structural integrity of nerve growth cones following in vitro exposure to mercury, NeuroReport, v.12, no.4:733-737 (March 2001).[vol. 20, no.17]

This study examined whether Hg ions could affect membrane dynamics of neurite growth cone morphology and behavior. The identified, large Pedal A (PeA) neurons from the central ring ganglia of the snail were cultured for 48 hours in 2 ml brain conditioned medium. Following neurite outgrowth, metal chloride solution of Hg, Al, Pb, Cd or Mn (10-7M) was pressure applied directly onto individual growth cones. Hg ions markedly disrupted membrane structure and linear growth rates of imaged neuritis in 77% of all nerve growth cones. The evidence and previous biochemical data strongly implicate Hg as a potential etiological factor in neurodegeneration.

Vol. 20 #18. Hanson, M., Effects of Amalgam Removal on Health (2003).[vol. 20, no.18]

In this review report, several studies regarding the effects from removing dental amalgam are discussed.

Vol. 20 #19. Gay, D.D., Chewing Releases Mercury from Fillings, The Lancet (May 1979).[vol. 20, no.19]

This study consisted of patients breathing out 10 times through a Drierite tube into a Vycor tube packed with 1 g of silver wool. Mesh. This silver trap is wrapped with nichrome heating wire. The trap is connected to a continuous-flow, long-tube absorption apparatus monitoring the 254 nm absorbance wavelength of mercury. Heating the silver wool via the nichrome wire with an activated charcoal purified air stream sweeping through the trap released the mercury absorbed onto the silver and carries it into the monitor. The instrument is calibrated with standard concentrations of mercury injected onto the silver wool. After determination of the background level, the patient chews a piece of gum for 15 min and then repeats the 10 expirations into the trap. The level of elemental mercury in the expired breath of patients with silver-mercury amalgams up to 2 years old increased almost four times after a 15 min period of chewing.

Vol. 20 #20. Orlowski, J.P., et.al, Urine Mercury Levels in Kawasaki Disease, Pediatrics , v. 66, no.4 :633-636 (October 1980).[vol. 20, no.20]

This report describes the urinary excretion of mercury in six patients seen at the Cleveland Clinic Foundation with Kawasaki disease or MLNS. Three of the six patients had urinary mercury levels higher than the established normal level for mercury in urine, and considerably higher than levels in control subjects matched by age, sex, and geographic location.

Vol. 20 #21. Vimy, M.J., et.al, Intra-oral Air Mercury Released from Dental Amalgam, J. Dent. Res . , v. 64, no.8:1069-1071 (August 1985).[vol. 20, no.21]

In this study, intra-oral air was analyzed for mercury vapor concentration in 46 subjects, 35 of whom had dental amalgam restorations. Measurements were made with a Jerome Hg detector both before and ten min after chewing stimulation. Subjects with dental amalgams had unstimulated Hg vapor concentrations that were nine times greater than basal levels in control subjects with no amalgams. Chewing stimulation in subjects with amalgams increased their Hg concentration six-fold over unstimulated Hg levels, or a 54-fold increase over levels in control subjects.

Vol. 20 #22. Dodes, J.E., Dental Silver Tooth Fillings, The FASEB Journal, v. 4, no. 5 (March 1990).[vol. 20, no.22]

Dr. Dodes criticizes an article by Hahn et. al. printed in the December 1989 issue of the FASEB Journal titled “Dental silver tooth fillings: a source of mercury exposure revealed by whole-body image scan and tissue analysis”. Dr. F.L. Lorscheider, author of FASEB Journal responds to Dr. Dodes’ allegations.

Vol. 20 #23. Letters to the Editor, J. Dent. Res. (March 1991).[vol. 20, no.23]

Several letters to the Editor are included on these pages. Most discussing daily dose estimates of mercury from dental amalgams.

Vol. 20 #24. Lorscheider, F.L., et.al, Mercury exposure from “silver” fillings, The Lancet, v.337 (May 1991).[vol. 20, no.24]

This letter to the editor discusses Hg released from silver tooth fillings concentrating in body tissues in amounts sufficient to alter cell function.

Vol. 20 #25. Vimy, M.J., et.al, Serial Measurements of Intra-oral Air Mercury: Estimation of Daily Dose from Dental Amalgam, J. Dent. Res., v.64, no. 8:1072-1075 (August 1985).[vol. 20, no.25]

For this study, serial measurements of Hg concentration in intra-oral air were made during and after chewing stimulation in 35 subjects with occlusal amalgam restorations. Hg concentrations remained elevated during 30 min of continuous chewing and declined slowly over 90 min after cessation of chewing. All subjects received an average daily Hg dose of approximately 20 g. Dental amalgam Hg makes a major contribution to total daily dose.

Vol. 20 #26. Tarnish and Corrosion, Skinner’s Science of Dental Materials.[vol. 20, no.26]

These pages discuss tarnish and corrosion of dental restorations, and th clinical significance of galvanic currents.

Vol. 20 #27. Svare, C.W., et.al, The Effect of Dental Amalgams on Mercury Levels in Expired Air, J. Dent. Res, v. 60, no. 9:1668-1671 (September 1981).[vol. 20, no.27]

In this study, the expired air of a group of 48 persons was analyzed for its mercury content before and after chewing. Expired air samples were collected in polyethylene bags and a known quantity of each was pumped into the mercury detector for measurement. The results showed that examined subjects with dental amalgams had higher pre-chewing mercury levels in their expired air than those without amalgams. After chewing, these levels were increased an average of 15.6-fold in the former and remained unchanged in the latter group.

Vol. 20 #28. Bolewska, J., et.al, Amalgam associated mercury accumulations in normal oral mucosa, oral mucosal lesions of lichen planus and contact lesions associated with amalgam, J. Oral Pathol. Med., v. 19:39-42 (1990).[vol. 20, no.28]

In this study, 43 patients with oral mucosal lesions were divided into 3 groups based on the relationship between lesions and amalgam restorations. It was found that mercury is taken up by the lesioned oral mucosal membrane and that under certain conditions mercury can also penetrate the intact oral mucosa without causing clinical or histopathologic changes.

Vol. 20 #29. Kuntz, W.D., et.al, Maternal and cord blood background mercury levels: A longitudinal surveillance, Am. J. Obstet. Gynecol., v. 143: 440-443 (1982).[vol. 20, no.29]

In this study, 57 prenatal patients with no known exposure to the element mercury of any of its compounds were observed for change in whole blood total mercury concentration from the initial prenatal clinic examination through deliver and postpartum hospitalization. On hospital admission for labor and deliver, whole blood total mercury averaged 1.15 parts per billion, compared to .79 ppb from the first prenatal clinic visit; these levels represent a 46% increase and significant difference in maternal concentration of a substance previously recognized for its peculiar ease at crossing the placental barrier.

Olstad, M.L., et.al, Correlation between Amalgam Restorations and Mercury Concentrations in Urine, J. Dent. Res ., v. 66, no. 6:1179-1182 (June 1987). [vol. 20, no. 30]

For this study, the creatinine-adjusted urinary concentration of mercury in 73 schoolchildren with a mean age of 12 years was determined. In addition, the number of amalgam restorations and their size, prevalence of allergy and days absent form school due to illness were recorded for each individual. A significant positive correlation was found between urine Hg and extent of amalgam restorations, but no correlation existed between urine Hg and allergy or between urine Hg and absence from school due to illness. No correlation was found between extent of amalgam restorations and either allergy or absence from school.

Bibliography XXI.

Bibliography XXI.

Vol. XXI #1. Bjornberg, K.A., Mercury exposure during early human development, Institute of Environ. Med., Sweden (2005).[vol. 21, no.1]

In this experiment, Hg exposure during pregnancy was studied by determination of total Hg in maternal hair and MeHg and I-Hg in maternal blood. Fetal exposure was assessed by MeHg and I-Hg in cord blood. Infant exposure was assessed by MeHg and I-Hg in infant blood and total Hg in breast milk. The concentrations of MeHg and I-Hg were determined by cold vapour atomic fluorescence spectrophotometry (CVAFS). Se concentrations in serum or whole blood were analysed by graphite furnace atomic absorption spectrophotometry (GFAAS). A substantial fraction of Hg0 passes the placenta to the fetus before being oxidized to Hg2+. Also, I-Hg accumulated in the placenta in relation to the number of amalgam fillings. MeHg in cord blood increased with increasing maternal fish consumption. It was almost twice the concentration in maternal blood.

Vol. XXI #2. Tracy, J.D., et.al, Pitfalls in the Diagnosis of Hypothyroidism in the Elderly, Geriatric Medicine Today, v. , no.8:47-50 (August 1988).[vol. 21, no.2]

This short article highlights 2 case studies and offers guidelines to assist the physician in diagnosing primary and pituitary hypothyroidism and in distinguishing hypothyroidism from nonthyroidal illness.

Vol. XXI #3. Snyder, D.K., et.al, Recognizing and Managing the Adult Hypothyroid Patient, Drug Therapy, 86-97 (August 1988).[vol. 21, no.3]

This report discusses the signs and symptoms, diagnosis, causes and therapy of hypothyroidism.

Vol. XXI #4. Endocrine.[vol. 21, no.4]

This paper lists several references from other studies and statements from those studies regarding MeHg intoxication. Pituitary and thyroid as targets

Vol. XXI #5. Understanding Diabetic Neuropathy, New England Journal of Medicine, v. 319, no.9:577-578 (September 1988).[vol. 21, no.5]

This article discusses several studies regarding diabetic neuropathy.

Vol. XXI #6. Guyton, A.C., Textbook of Medical Physiology, 6th Edition: 9, 840-841, 959-960, 968 (1981).[vol. 21, no.6]

Excerpts from this volume include topics on the organization of the human body and control of the “Internal Environment”, transport of glucose through the cell membrane, storage of glycogen in liver and muscle, release of energy from the glucose molecule by the glycolytic pathway, insulin, glucagons, and diabetes mellitus.

Vol. XXI #7. Langer, S.E., A Simple Health Test That May Change Your Life, Let’s Live , 10-14 (December 1981).[vol. 21, no.7]

This article discusses hypothyroidism, its causes, symptoms, anemias, and its effect on the cardiovascular system.

Vol. XXI #8. Barnes, B., Basal Temperature versus Basal Metabolism, J. AMA, 1072-1073 (August 1942).[vol. 21, no.8]

This incomplete article defines basal temperature and conditions necessary for determining basal metabolism. Several case studies are included.

Vol. XXI #9. Cooper, D.S., et.al, L-Thyroxine Therapy in Subclinical Hypothyroidism, A. nnals of Internal Medicine, v.1010:18-24 (1984).[vol. 21, no.9]

In this study, 33 patients with subclinical hypothyroidism were randomly assigned in a double-blind manner to receive placebo or L-thyroxine therapy and were followed for 1 year with thyroid function tests, serum lipid measurements, basal metabolic rate and systolic time interval determinations and a questionnaire on hypothyroid symptoms. In the thyroxine-treated group, serum lipids and the mean systolic time interval did not change, but the systolic time intervals became normal in the 5 patients with the most abnormal baseline values. Symptoms

improved in 8 of 14 patients receiving thyroxine and in 3 of 12 patients receiving placebo.

Vol. XXI #10. Agrawal, R., et.al, Chronic Effects of Mercuric Chloride Ingestion on Rat Adrenocortical Function, Bull. Environ. Contam. Toxicol., v.43:481-484 (1989).[vol. 21, no.10]

Sixty adult male albino rats were used in this study. Rats in groups II, III and IV received 25 ppm, 50 ppm and 100 ppm of mercuric chloride in drinking water. Rats from groups II, III and IV showed a significant increase in the adrenal weight up to 180 days. The adrenal corticosterone levels were also found to be increased significantly in rats treated with different doses of mercuric chloride in a dose and duration dependent manner. The corticosterone levels increase progressively up to 120 days for rats fed lower doses of mercuric chloride. Rats fed higher doses showed a significant reduction in plasma corticosterone at the end of 60 days followed by an increase in the levels at 120 days.

Vol. XXI #11. Nikolai, T.F., Recovery of Thyroid Function in Primary Hypothyroidism, Am. J. of Medical Sciences , v. 297, no.1:18-21 (January 1989).[vol. 21, no.11]

For this study, thyroid hormone therapy was withdrawn from 63 patients with proven primary hypothyroidism at 6 months and again at 1 and 3 years to determine if there was recovery of thyroid function. Of the 49 patients with primary hypothyroidism that was not attributable to such causes as drug therapy, surgery, iodine-131 therapy, or silent or subacute thyroiditis, only two patients recovered thyroid function. In the other 14 patients, hypothyroidism developed within 6 month postpartum. Nine of these 14 recovered thyroid function.

Vol. XXI #12. Sarasua, M.M., et.al, Human Factor XIII-Metal Ion Interactions. A Luminescence and Nuclear Magnetic Resonance Study, Journal of Biological Chemistry, v. 27, no.23:14102-14109 (December 1982).[vol. 21, no.12]

In this study, metal ion binding to a variety of forms of human blood clotting factor XIII has been explored in order to reveal significant differences in metal ion binding behavior related to the activation of the protein by thrombin or resulting from protein associative processes. In contrast to the a subunit, the b subunit of factor XIII appears to interact with metal ions minimally and without an apparent conformational response to the presence of metal ions.

Vol. XXI #13. Trakhtenberg, I.M, Chronic Effects of Mercury on Organisms, U.S. Dept. of Health, Education and Welfare, 1-333 (1974).[vol. 21, no.13]

This document includes 15 chapters covering the following topics: General survey of mercury and its distribution in the environment; Toxicodynamics of mercury and its compounds - entry route of mercury into the body; Basic industrial production, processes, and operations, connected with potential danger of mercury intoxification; Mercury in modern urban conditions; Problems of secondary contamination by mercury of the air of production sites; The micromercurialian phenomenon in mercury handlers; Modeling mercurialism and its manifestations under the effect of various concentrations of mercury; Proteinemic shifts in experimental mercurialism; The effect of mercury on conditioned reflex activity; Functional shifts in the hypophyseal adrenocontical system and the thyroid gland under the influence of mercury; Cardiotoxic effects of mercury; Changes in indices of immunobiological reactivity under the influence of low mercury concentrations; Morphological changes in organs and tissues affected by mercury; Basic principles of preventing effects of mercury on the organism; and Health measures for the prevention of mercurialism under laboratory conditions.

Vol. XXI #14. Cooley, R.L., et.al, Detection and diagnosis of bioincompatibility of mercury, CDA Journal , 36-43 (October 1984).[vol. 21, no.14]

The purpose of this paper is to explore the detection and diagnosis of bioincompatibility of mercury through patch testing, mercury vapor instruments, blood analysis, urine analysis, and to a lesser extent, analysis of hair and saliva.

Vol. XXI #15. Weiner, J.A., Aspects on Health Risks of Mercury from Dental Amalgams, Toxicology of Metals, 469-484 (1996).[vol. 21, no.15]

This chapter discusses the release and uptake of Hg from dental amalgam fillings and its effects on humans and animals.

Vol. XXI #16. Cherian, M.G., et.al, Estimation of Mercury Burdens in Rats by Chelation with Dimercaptopropane Sulfonate, Journal of Pharmacology and Experimental Therapeutics, v. 245, no.2:479-484 (1988).[vol. 21, no.16]

In this study, the chelation of mercury by 2,3-dimercaptopropane-1-sulfonate (DMPS) and its usefulness in the estimation of mercury burdens was investigated by exposing male, Sprague-Dawley rats to 203HgCl2 or 203Hg vapor. Whole body mercury levels, tissue levels and excretion of mercury were measured by radioactivity counting. After DMPS treatment there was a significant decrease of whole body mercury levels and an increase in urinary excretion. The increase in urinary excretion was directly proportional to the whole body burden of mercury at the time of dosing with DMPS in animals dosed with HgCl2 and exposed to mercury vapor. The increase in urinary excretion induced by DMPS was almost equal to the amount of mercury lost from the kidneys.

Vol. XXI #17. Clarkson, T.W., The Three Modern Faces of Mercury, Environmental Health Perspective , v. 110, supplement 1:11-23 (February 2002).[vol. 21, no.17]

This paper discusses the author’s perceptions of risk from the exposure of billions of people to methyl mercury in fish, mercury vapor from amalgam tooth fillings, and ethyl mercury in the form of thimerosal added as an antiseptic to widely used vaccines.

Vol. XXI #18 none

Vol. XXI #19. Ingalls, T.H., Epidemiology, etiology and prevention of multiple sclerosis, American Journal of Forensic Medicine and Pathology, v. 4, no.1:55-61 (March 1983).[vol.21, no.18]

This report reviews two previous studies based upon MS deaths at a national level and prolonged experience of white males who did service in World War II.

Vol. XXI #20. Use Survey, Clinical Research Associates Newsletter, v. 14, issue 12 (December 1990).[vol. 21, no.19]

This form shows data from 9,846 random newsletter subscribers on amalgam use, amalgam brand used, and attitudes about mercury use in dentistry.

Vol. XXI #21. Pendergrass, J.C., et.al, Inhibition of Brain Tubulin-GTP Interactions by Mercury: Similarity to Observations in Alzheimer’s Diseased Brain.[vol. 21, no.20]

This paper reviews data from studies which demonstrate that exposure to mercury causes the same aberrancy in non-AD brain and rat brain as observed in AD brain.

Vol. XXI #22. Westerlund, B.A., et.al, Altered Distribution Patterns of Macro-and Trace Elements in Human Tissues of Patients with Decreased levels of Blood Selenium, Nutrition Research, supplement 1: 442-450 (1985).[vol. 21, no.21]

This study selected patients with a variety of symptoms and examined the glutathione peroxidase activity in capillary blood estimated by a semi-quantitative method. Elemental composition of gingival biopsies and determination of plasma concentrations of iron, copper, zinc, selenium and mercury was identified by x-ray fluorescence technique. In inflammatory diseases, e.g. rheumatoid arthritis it was observed increased concentrations of copper and decreased concentrations of zinc and selenium in serum. Elemental profiles in blood cells were observed in patients with rheumatoid arthritis. Decreased enzyme activities in the patient group compared to controls were found. In biopsies from two patients with several symptoms, the presence of alloy metals was demonstrated in the absence

of selenium. In the erythrocytes and neutrophils increased concentrations of mercury and strontium were found.

Vol. XXI #23. Olivieri, G., et.al, Mercury Induces Cell Cytotoxicity and Oxidative Stress and Increases b-Amyloid Secretion and Tau Phosphorylation in SHSY5Y Neuroblastoma Cells, Journal of Neurochemistry, v.74:231-236 (2000).[vol. 21, no.22]

This study explored potential pathophysiological mechanisms via an in vitro model system and investigated the effects of inorganic mercury on oxidative stress, cell cytotosicity, -amyloid production and tau phosphorylation. Exposure of cells to 50 g/L HgCl2 for 30 min induces a 30% reduction in cellular glutathione levels. Melatonin preincubation protected ells form the deleterious effects of mercury, resulting in MTT reduction equaling control levels.

Vol. XXI #24. Agocs, M.M., et.al, Mercury Exposure from Interior Latex Paint, The New England Journal of Medicine, v. 323, no.16:1096-1101 (October 1990).[vol. 21, no.23]

For this experiment, 74 “exposed” persons living in 19 homes recently painted with the brand and 28 “unexposed” persons living in 10 homes not recently painted with paint containing mercury were studied to determine whether the recent use of that brand of paint containing phenylmercuric acetate was associated with elevated indoor-air and urinary mercury concentrations. Potentially hazardous exposure to mercury had occurred among persons whose homes were painted with a brand of paint containing mercury at concentrations approximately 2 ½ times the Environmental Protection Agency’s recommended limit.

And letter to editor from Lorscheider calculating exposure from amalgam as compared to the latex paint.

Vol. XXI #25. Malt, U.F., et.al, Physical and Mental Problems Attributed to Dental Amalgam Fillings: A Descriptive Study of 99 Self-Referred Patients Compared with 272 Controls, Psychosomatic Medicine, v. 59:32-41 (1997).[vol. 21, no.24]

For this study, the physical and mental symptomatology of 99 self-referred patients complaining of multiple somatic and mental symptoms attributed to dental amalgam fillings were compared with patients with known chronic medical disorders seen in alternative and ordinary medical family practices and patients with dental amalgam fillings seen in an ordinary dental practice. The dental amalgam sample reported significantly more physical symptoms from all body regions.

Vol. XXI #26. Olsson, S., et.al, Daily Dose Calculations from Measurements of Intra-oral Mercury Vapor, J. Dent. Res., v.71, no.2:414-423 (February 1992).[vol. 21, no.25]

This review article discusses measurements of intra-oral mercury vapor from amalgam fillings.

Vol. XXI #27. Olea, N., et.al, Estrogenicity of Resin-based Composites and Sealants Used in Dentistry, Environ. Health Perspect., v.104:298-305 (1996).[vol. 21, no.26]

This study tested some resin-based composites used in dentistry for estrogenic activity. A sealant based on bisphenol-A diglycidylether methacrylate increased cell yields, progesterone receptor expression, and pS2 secretion in human estrogen-target, serum-sensitive MCF7 breast cancer cells. Estrogenicity was due to bisphenol-A and bisphenol-A dimethacrylate, monomers found in the base paste of the dental sealant and identified by mass spectrometry.

Vol. XXI #28. Godfrey, M.E., et.al, The pathophysiology of long-term exposure to dental amalgam: A potential hazard for senile dementia.[vol. 21, no.27]

This review presents published animal and human evidence linking chronic low level exposures to mercury with the brain lesions of senile dementia.]

Vol. XXI #29. McCann, D., Sealants study merits further investigation, ADA News, (June 1996) [vol. 21, no.28]

This newspaper article discusses recent research indicating that resins leached from dental sealants may mimic the female hormone estrogen.

Vol. XXI #30. Christenson, G., Should use of Sealant & Composite Resins be suspended due to bisphenal A leach?, www.cranews.com (1996). [vol. 21, no.29]

This website discusses a report in Environmental Health Perspectives and abstracted in Science News which noted bisphenol A released from some dental resins. The paper stated that bisphenol A could cause estrogen-like effects in the body.

Bibliography XXII.

Bibliography XXII.

Vol. 22 #1 Herrstrom, P, et.al, Dental Amalgam, Low-Dose Exposure to Mercury, and Urinary Proteins in Young Swedish Men, Archives of Environmental Health, v.50, no.2:103-107 (March 1995). [vol. 22, no.1]

In this study, the association between the number of amalgam tooth surfaces, urinary mercury, and proteinuria was explored in a sample of 48 randomly selected, apparently healthy male students who were 17-22 years of age. No

significant relationship was found between any of the proteins and amalgam or urinary mercury.

Vol. 22 #2. Hujoel, P.P. et.al, Pre-existing Cardiovascular Disease and Periodontitis: A Follow-up Study, J. Dent. Res., v. 81, no.3: 186-191 (2002).[vol. 22, no.2]

The goal of this study was to search for an association between periodontitis and CHD events among individuals with pre-existing heart disease, reported in the First National Health and Nutrition Examination Survey Epidemiologic Follow-up Study. The presence of periodontitis and gingivitis did not increase CHD risk among these at-risk individuals. When limited to individuals with a self-reported prior heart attack, periodontitis was associated with a 34% decreased CHD risk.

Vol. 22 #3. Hanson, M., Oral Cancer, Lichen and Amalgam.[vol. 22, no.3]

This review article examines the connection between mercury and oral cancer, lichen and amalgam.

Vol. 22 #4. Hanson, M., Amalgam- Hazards in Your Teeth, J. Orthomolecular Psych., v.12:194-201 (1983).[vol. 22, no.4] Scanned

This paper discusses mercury release from dental amalgam, rate of corrosion, maximum permissible concentrations of Hg, inorganic and organic mercury, biological effects, and diagnosis and therapy.

Vol. 22 #5. Hanson, M., Blood Mercury.[vol. 22, no.5]

This review paper discusses blood mercury levels which have been reported and used to establish “safe levels”.

Vol. 22 #6. The Effects of Selenium on Methylmercury Toxicity [vol. 22, no. 6]

This review paper discusses the protective effects of selenium on methylmercury, effects of methylmercury on human health, developing fetuses and infants, genetic and reproductive processes, and the teratogenic and carcinogenic effects of methylmercury.

Vol. 22 #7. Summers, A.O., 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).[vol. 22, no.7]

In this study, the gingival and fecal flora were examined before and after the installation of 16 small occlusal surface dental “silver” fillings in two wild-caught adult male cynomolgous monkeys. Each monkey eliminated about 300 g Hg/day in feces and post-mortem exam revealed mercury concentrations of about 40-50 M Hg in the gingival, kidney and feces. 80% of the mercury-resistant bacterial strains from these monkeys were also resistant to one or more antibiotics, despite the fact that the monkeys were not exposed to antibiotics in their food or water. 20% of the multi-resistant bacteria examined could transfer their resistance genes to an antibiotic-sensitive laboratory strain, indicating that the mercury and antibiotic resistance genes were carried by conjugative or mobilizable plasmids.

Vol. 22 #8. Epidemiology of Contact Dermatitis in North America: 1972, Arch Dermatol., v.108:537-540 (October 1973).[vol. 22, no.8]

For this study, 1200 subjects in North America were patch tested identically with 16 allergens. Thirteen dermatologists representing ten separate centers participated in this epidemiologic study. A new list of 19 screening allergens recommended by the north American Contact Dermatitis Group has been published.

Vol. 22 #9. Ziff, M.F., Dental Amalgam: Status Quo, Political Aspects, International Situation.[vol. 22, no.9]

This presentation discusses the early years of dental amalgam, the modern era and current developments with the material.

Vol. 22 #10. Cruzan, S., FDA panel Considers Safety of Dental Amalgams, Talk Paper FDA, US. Depart. Of Health and Human Svcs . (March 1991).[vol. 22, no.10]

This paper discusses the FDA Dental Devices Panel’s opinion regarding the safety of dental amalgams.

Vol. 22 #11. Correspondence between WHO, Dr. Ziff and Ulf Bengtsson regarding WHO/FDI Consensus Statement on Dental Amalgam (July 1996).[vol. 22, no.11]

Three letters are presented which discuss the FDI World Dental Federation’s policy statement on dental amalgam and the WHO Consensus Statement

Vol. 22 #12 Blank

Vol. 22 #13. Bengtsson, U., Is There a Renewed Trend of Radioactive Compounds in Dental Materials? (2000).[vol. 22, no.13]

This review paper discusses the use of uranium and thorium in dental composites.

Vol. 22 #14. Chang, S.B., et.al, Factors Affecting Blood Mercury Concentrations in Practicing Dentists, J. Dent. Res, v.71, no.1:66-74 (January 1992).[vol. 22, no.14]

For this study, blood mercury concentrations of practicing dentists and non-dentists were determined by means of cold-vapor atomic absorption spectrophotometry. Potential sources of mercury exposure were identified in both groups through a questionnaire completed at the time of sampling. Concentrations of total and inorganic blood mercury were significantly higher in dentists than in non-dentists.

Vol. 22 #15. Chang, S.B., et.al, Examination of Blood Levels of Mercurials in Practicing Dentists Using Cold-Vapor Atomic Absorption Spectrometry, J. of Analytical Toxicology, v. 11 (July 1987).[vol. 22, no.15]

For this study, 255 practicing dentists and 24 nondental controls were asked to participate. The total, inorganic, and organic mercury contents of blood were determined by syringe-injection cold-vapor atomic absorption spectrometry. The total and inorganic mercury levels in blood are significantly different between dentists and nondental controls at the significant level of p<.05. The organomercurial levels are insignificant at the same test level.

Vol. 22 #16. Gerhard, I., et.al, Toxic Materials and Infertility: Heavy Metals and Minerals, Obstetrics and Gynecology, v.52:383-396 (1992).[vol. 22, no.16]

(English Translation) This paper reviews several studies and is meant to give an overview on the influence of elevated heavy-metal concentrations on reproduction.

Vol. 22 #17. Harold Loe research in progress in front of Gerhard, I., et.al., Diagnosis of Heavy Metal Loading by the Oral DMPS and Chewing-Gum Tests, Clinical Lab, v. 38:404-411 (1992) [vol. 22, no.17]

(English Translation) In this study, 490 women in the hormone and sterility lecture course, the heavy-metal flushing test was performed with DMPS. The following methods were used: arsenic and mercury: hydrid/atom-abosorption technique; cadmium and lead: the graphite-tube test; copper: the flame test. In all the women, an increased excretion of the heavy metals described above could be

attained with DMPS. In terms of amount, the highest concentrations computed were of mercury and copper. The largest amount released with DMPS was of mercury.

Vol. 22 #18. Schiele, R., et.al, Mobilization of Mercury Reserves in the Organism by means of DMPS (Dimaval), Occupational Medicine, Social Medicine Preventive Medicine, v. 24, no.11:249-251 (Nov. 1989)[vol. 22, no.18]

(English Translation) For this study, 30 persons were administered 300 mg DMPS and mercury excretion in 24-hour urine samples were taken. Before administration of DMPS a urinary mercury excretion of a median .95 g/24 hour with a maximum value of 4.2 g/24 hour was found. After DMPS administration, mercury excretion increased to a median value of 5.5 g/24 hour to a maximal value of 64.1 g/24 hour. In statistical comparison, mercury excretion was significantly higher for the group with amalgam fillings, before as well as after administration of the complex agent, than for the group of persons without amalgam fillings.

Vol. 22 #19. Zander, D., et.al, Studies on Human Exposure to Mercury: IV. Mercury Exposure in Male and Female Dentists and Female Dental Assistants, Central Hygiene Paper, v. 193:318-328 (1992) [vol. 22, no.19]

This study included 22 male and female dentists, 42 female dental assistants and 4 other coworkers of both sexes from a total of 15 dental practices in the Dusselfdorf-Krefeld area. The results show that male dentists, female dentists and female dental assistants are more strongly exposed to mercury than comparable people who don’t come into occupational contact with mercury. The dental assistants are clearly more strongly exposed than the dentists of either sex. This is also shown in relation to the mercury excretion computed by carrying out the Dimaval mobilization test.

Vol. 22 #20. Code of Federal Regulations (April 1996).[vol. 22, no.20]

These pages identify and classify dental devices such as diagnostic, prosthetic, surgical, and therapeutic.

Vol. 22 #21. Friedman, G.D., Primer of Epidemiology, Third Edition (1987).[vol. 22, no.21]

Excerpt from this volume include Chapter 2 “Basic Measurements in Epidemiology”, Chapter 4 “Basic Methods of Study”, Chapter 9 “Experimental Studies”, Chapter 11 “Making Sense Out of Statistical Associations” , and Chapter 12 “Introduction to Multivariate Analysis”.

Vol. 22 #22. Risk Assessment/Risk Management, A Handbook for Use Within the Bureau of Chemical Hazards (January 1991).[vol. 22, no.22]

Section I of this handbook provides a discussion of the components or facets of the term “risk”. Section II provides a narrative description of the risk assessment/risk management models which were examined by the Working Group, as well as the model which was finally accepted. Section III contains definitions for each of the risk assessment/risk management terms discussed by the Working Group. Sections IV and V contain case studies on formaldehyde and vinyl chloride respectively.

Vol. 22 #23. Letter from Dr. P. Blais to Dr. R.W. Campbell on Dental Amalgam (August 1976).

This letter references a manuscript not attached entitled “Dental Amalgam and the Public Health”. Dr. Blais discusses the potential hazards associated with the products.

Vol. 22 #24. Letter from Richard Tobin to Dr. James Brookfield regarding CDA’s position statement on dental amalgam.

In this letter, Dr. Tobin discusses his comments regarding the Canadian Dental Association’s position statement on dental amalgam and a set of questions and answers on amalgam to be used by dentists responding to inquiries form patients.

Vol. XXV.

Vol. 25 #1. Letter from IAOMT to NCDB requesting public retraction of previously published advertising restrictions (March 16, 2005; April 4, 2005).

In the letter dated March 16, the IAOMT encourages the NCDB to take a responsible and independent course by publicly withdrawing the admonishment concerning mercury amalgam published in “The Dental Forum”. The letter dated April 4 is a request to receive a response from the IAOMT regarding the March 16 letter.

Vol. 25 #2. Sharma, R.P., et.al., Metals and Neurotoxic Effects: Cytotoxicity of Selected Metallic Compounds on Chick Ganglia Cultures, J. Comp. Pathol., v.91, no.2: 235-244 (1981).

In this study, cytotoxic properties of metallic compounds were investigated in an isolated cell system by exposing 11-day-old chick embryonic nervous tissues to

various concentrations of the metallic compounds. Results indicated that all cell growth inhibition was dose-dependent with its magnitude ranging from severely toxic; moderately toxic and slightly toxic. In all instances nerve fibers were more sensitive to metallic compounds than were neuroglia and cells.

Vol. 25 #3. Kudsk, F.N., Absorption of Mercury Vapour from the Respiratory Tract in Man, Acta Pharmacol. et Toxicol . , v.23:250-262 (1965). scanned

This study examines the absorption of mercury vapour from the respiratory tract in four volunteers who breathed air with mercury concentrations ranging from 50 to 250 mg/m3. Results indicated that the last part of the air expired during maximal expiration contains only negligible amounts of mercury.

Vol. 25 #4. Aposhian, H.V., et.al, Urinary mercury after administration of 2,3-dimercaptopropane-1-sulfonic acid: correlation with dental amalgam score, FASEB Journal, v.6: 2472-2476 (April 1992).

To determine the influence of dental amalgams on the mercury body burden of humans, this study gave volunteers, with and without amalgams in their mouth, the sodium salt of 2,3-dimercaptopropane-1-sulfonic acid. Two-thirds of the mercury excreted in the urine of those with dental amalgams appears to be derived originally from the mercury vapor released from their amalgams. Linear regression analysis indicated a highly significant positive correlation between the mercury excreted in the urine 2 hours after DMPS administration and the dental amalgam scores.

Vol. 25 #5. Sandborgh-Englund, G., et.al., Mercury in Biological Fluids after Amalgam Removal, J. Dent. Res., v.77, no.4:615-624 (April 1998).

The objective of this study was to obtain data on changes in Hg levels in blood, plasma, and urine following removal of all amalgam fillings during one dental session in 12 healthy subjects. After removal, there was a considerable decline in the Hg levels of blood, plasma and urine, which slowly approached those of subjects without any history of amalgam fillings.

Vol. 25 #6. Eggleston, D.W., et.al., Correlation of dental amalgam with mercury in brain tissue, J. Prosth. Dent., v.58, no.6:704-707 (1987).

In this study, examination of the cadaver dentition and collection of brain tissue specimens from nonrandomized, sudden, unexpected death subjects was conducted as part of routine autopsy procedures at the LA County Coroner’s

Office. Data from this project demonstrate a positive correlation between the number of occlusal surfaces of dental amalgam and mercury levels in the brain.

Vol. 25 #7. Ngim, C.H., et.al, Chronic neurobehavioural effects of elemental mercury in dentists, Brit. J. Indust. Med., v.49:782-790 (1992).

For this study, neurobehavioural tests were performed by 98 dentists exposed to elemental mercury vapour and 54 controls with no history of occupational exposure to mercury. Significant differences in neurobehavioural performance tests were found in subjects exposed for a comparatively short period (5 ½ years) and at concentrations well below the current threshold limit value TWA recommended by the American Conference of Governmental Industrial Hygienists. The dentists scored consistently worse in the neurobehavioural tests.

Vol. 25 #8. Echeverria, D., et.al., Behavioral Effects of Low-Level Exposure to Hgo

Among Dentists, Neurotoxicol. Teratol., v.17, no.2:161-168 (1995). In this study, exposure thresholds for health effects associated with elemental mercury exposure were examined by comparing behavioral test scores of 19 exposed with those of 20 unexposed dentists. The pooled sum of rank scores for combinations of tests within domains were significantly associated with urinary Hg, providing evidence of subtle preclinical changes in behavior associated with Hg exposure.

Vol. 25 #9. Shapiro, I.M., et.al., Neurophysiological and Neuropsychological Function in Mercury-Exposed Dentists, The Lancet, 1147-1150 (May 1982).

In a study of the relation between cumulative exposure to mercury and chronic health impairment 298 dentists had their mercury levels measured by an X-ray fluorescence technique. Electrodiagnostic and neuropsychological findings in the dentists with more than 20 mg/g tissue mercury levels were compared with those of a control group consisting of dentists with no detectable mercury levels. 30% of the 23 high mercury dentists had polyneuropathies. The high mercury group had mild visuographic dysfunction; they also had more symptom-distress than did the control group.

Vol. 25 #10. Hu, H., Heavy Metal Poisoning, Harrison’s Principles of Internal Medicine, 14th Edition

The pages from this chapter discuss Lead and Mercury, their source, metabolism, clinical toxicology, laboratory findings and treatment

Vol. 25 #11. Echeverria, D., et.al., Neurobehavioral effects from exposure to dental amalgam Hgo: new distinctions between recent exposure and Hg body burden, FASEB Journal, v.12:971-980 (1998).

For this study, potential central nervous system toxicity associated with handling Hg-containing amalgam materials among dental personnel with very low levels of Hgo exposure was evaluated. A neurobehavioral test battery was applied to evaluate CNS functions in relation to both recent exposure and Hg body burden. The pattern of results, comparable to findings previously reported among subjects with urinary Hg>50 mg/1, presents convincing new evidence of adverse behavioral effects associated with low Hgo exposures within the range of that received by the general population.

Vol. 25 #12. Health Effects assessment Summary tables US EPA FY-1997 Subchronic and chronic toxicity (other than carcinogenicity) Mercury

Vol. 25 #13. Skare, I., et.al., Human Exposure to Mercury and Silver Released from Dental Amalgam Restorations, Archives of Environmental Health, v.49, no.5: 384-394 (September 1994).

Vol. 25 #14. Goldman LR, Shannon MW, Technical Report: Mercury in the Environment: Implications for Pediatricians. American Academy of Pediatrics: Committee on Environmental Health. Pediatrics (2001) Jul;108(1):197-205.

Vol. 25 #15. Drasch, G. Mercury burden of human fetal and infant tissues European Journal of Pediatrics Vol. 153 pp#607-610, 1994

Vol. 25 #16. Mortada WL, Sobh MA, El-Defrawy MM, Farahat SE. Urology and Nephrology Center, Mansoura University, Faculty of Science, Egypt. Mercury in dental restoration: is there a risk of nephrotoxicity? J Nephrol 2002 Mar-Apr;15(2):171-6.

Vol. 25 #17. Ngim, C., Epidemiologic Study on the Association between Body Burden Mercury Level and Idiopathic Parkinson’s Disease, Neuroepidemiology, 8:128-141 (1989).

Vol. 25 #18. Hultman, P., et al., Adverse Immunological Effects & Autoimmunity Induced by Dental Amalgam & Alloy in Mice, The FASEB Journal, v8, no.14:1183-1187 (November 1994).

Vol. 25 #19. Ehmann, et al., Brain Trace Elements in Alzheimer’s Disease, Neurotoxicology, 7(1):195-206 (Spring 1986);

Vol. 25 #20. Thompson, C.M., et.al., Regional Brain Trace-Element Studies in Alzheimer’s Disease, NeuroToxicology, v.9, no.1:1-6 (1988).

Vol. 25 #21. Vance, Trace Element Imbalances in Hair and Nails of Alzheimer’s Disease Patients, Neurotoxicology, 9(2):197-208 (Summer 1988);

Vol. 25 #22. Wenstrup, et al., Trace Element Imbalances in Isolated Subcellular Fractions of Alzheimer’s Disease Brains, Brain Res, 12;533(1): 125-31 (Nov. 1990);

Vol. 25 #23. Cornett, et al., Imbalances of Trace Elements Related to Oxidative Damage in Alzheimer’s Disease Brain, Neurotoxicology, 19(3):339-45 (June 1998);

Vol. 25 #24. Mutter, Alzheimer Disease: Mercury as a Pathogenetic Factor and Apolipoprotein E as a Moderator, Neuroendocrinol Lett. 2004; 25(5):275-283 (“Inorganic mercury (found in dental amalgam) may play a major role [in the pathogenesis of Alzheimer’s

Vol. 25 #25. Pendergrass, J.C., et.al, Inhibition of Brain Tubulin-GTP Interactions by Mercury: Similarity to Observations in Alzheimer’s Diseased Brain. Colege of Pharmacy U of Ky pp. 461-478

Vol. 25 #26. Duhr, E.F., et.al., HgEDTA Complex Inhibits GTP Interactions with the E-Site of Brain b-Tubulin, Toxicology and Applied Pharmacology v. 122:273-280 (1993).

Vol. 25 #27. Haley, B., The Relationship of the Toxic Effects of Mercury to Exacerbation of the Medical Condition Classified as Alzheimer’s Disease, The Nordic Journal of Biological Medicine (June-July 2003).

M Vol. 25 #28. In the case of McReynolds v. Mindrup, Case No. CV97-1891, Circuit Court of Jackson County, Missouri, a dental patient alleged that she was injured by mercury following the removal and replacement of her amalgam fillings. Comprehensive Daubert challenges brought the defendant dentist against the opinions of the plaintiff’s expert witnesses were also denied. On the basis of these repeated findings, it appears there is a sufficient body of scientific literature to adequately support medical testimony on the issue of causation.

M Vol. 25 #29. Barnes v. Kerr Corp., Case No. 4:99-CV-79, United States District Court for the Eastern District of Tennessee (at Knoxville) Report and Recomedation 8/9/2002 Vol. 25 #30. Barnes v. Kerr Corp., Case No. 4:99-CV-79, United States District Court for the Eastern District of Tennessee (Winchester Division.) MEMORANDUM AND ORDER

Vol. 25 #31. ADA Response on amalgam Article, Lawsuit File://Jim Love 1/11/2006

Vol. 25 #32. Barnes v. Kerr Corp., Case No. 4:99-CV-79, United States District Court for the Eastern District of Tennessee (Winchester division) Affidavit of David Barnes, DDS submitted in support of Plaintiff’s brief in opposition to defendant kerr

corporation’s motion for summary judgment

Vol. 25 #33. Westlaw Barnes v. Kerr Corp., Case No. 4:99-CV-79, United States Court of Appeals, Sixth Circuit Nos. 04-5546, 04-5663

Vol. 25 #34. Diana Echeverria, James S. Woods, Nicholas J. Heyer, Dianne Rholman, Federico M. Farin, Tingting Li, Claire E. Garabedian The association between a genetic polymorphism of coproporphyrinogen oxidase, dental mercury exposure and neurobehavioral response in humans Neurotoxicology and Teratology Volume 28, Issue 1, January-February 2006, Pages 39-48

Vol. 25 #35. J. Mutter, J. Naumann, C. Sadaghiani, H. Walach, G. Drasch Amalgam studies: Disreguarding basic principles of mercury toxicity Int. J. Hyg. Environ. Health 207 (2004); 391 - 397 Abstract:Dental amalgam, which has been used for over 150 years in dental practice, consists of about 50% metallic mercury. Studies on animal and humans show that mercury is continuously released from dental amalgam and absorbed by several body tissues. It is widely accepted that the main source of mercury vapor is dental amalgam and it contributes substantially to mercury load in human body tissues. There is still a controversy about the consequences of this additional mercury exposure from amalgam to human health. Many studies were performed to evaluate possible adverse effects. In this comment, these studies were analyzed with regard to their methodical quality by considering the newest findings on mercury toxicity and metabolism. In sum, a number of studies are methodically flawed drawing inaccurate conclusions as to the safety of dental amalgam.

Vol. 25 #36. Berlin, M mercury in dental-filling materials – an updated risk analysis in environmental medical terms 1997-2002 The Dental Material Commission Care and consideration Utrfdninger

Vol. 25 #37. Letter from Bob White of the North Carolina dental board April 8, 2005

Vol. 25 #38. April 25, 2005 Love’s Reply to Letter from Bob White of the North Carolina dental board April 8, 2005

Vol. 25 #39. May 18, 2005 Letter to Bob White of the North Carolina dental board re lack of response to April 25 letter.

Vol. 25 #40. Federal Trade Commission Denver office letter June 5, 1987 to Gary Strong re restrain of trade from Claude C. Wild III Director.

Vol. 25 #41. G. Mark Richardson a, Ronald W. Brecher b,*, Hugh Scobie c, Jane Hamblen d, John Samuelian d, Cindy Smith e Mercury vapour (Hg0): Continuing toxicological uncertainties, and establishing a Canadian reference exposure level

a Contaminated Sites Division, Health Canada, Ottawa, Ont., Canada K1A 0K9b Globaltox International, 367 Woodlawn Rd. W., Unit 6, Guelph, Ont., Canada N1H 7K9 cAMEC Earth & Environmental, 2 – 1398 Wellington Road South, London, Ont., Canada N6E 3N6 d AMEC Earth & Environmental, #3 – 15 Franklin St., Portland, ME, USA 04101 e Stantec Environmental, 49 Frederick St., Kitchener, Ont., Canada N2H 6M7 a r t i c l e i n f oArticle history:Received 25 January 2008Available online xxxxKeywords:Inorganic mercury Hg0Reference exposure levelRELa b s t r a c tThere are four published reference exposure levels (RELs) for Hg0, ranging from 0.09 lg/m3 to 1 lg/m3. All RELs were derived from the same toxicological database, predominantly of male chloralkali workers. Some key factors are apparent which make the use of that database questionable for REL derivation. Occupational studies of chloralkali workers are not an appropriate basis for a REL for Hg0. Concomitant exposure to chlorine gas (Cl2) diminishes uptake and effects of Hg0 exposure. There are gender differences in Hg0 uptake, distribution and excretion, with females at potentially greater risk from Hg0 exposure than males. Studies of chloralkali workers focused almost exclusively on adult males. Recent investigations of dental professionals (dentists, technicians, assistants) have failed to define a threshold in the dose–response relationship linking Hg0 with neurobehavioural outcomes, an observation generally ignored in Hg0 REL development. Finally, there is a growing database on genetic predisposition to ealth effects associated with Hg0 exposure. Based on these considerations, we propose a different key study for REL derivation, one that involved male and female dental professionals without concomitant Cl2 exposure. Adjusting the LOEAL to continuous exposure and applying appropriate UF values, we propose a Canadian REL for Hg0 of 0.06 lg/m3.

Volume XXVII

Vol. 27 #1. FDA Scientist details problem of five drugs By Liz Szabo and Rita Rubin USA Today

Vol. 27 #2. Scientist says FDA system ‘broken’ Rita Rubin USA Today

Vol. 27 #3. Currie, D. A case of Erythroedema or “Pink Disease” British medical Journal pp. 48-49 Jan 14, 1918RE: acrodynia

Vol. 27 # 4. McFarland R. Chronic Mercury Poisoning from a single Brief Exposure J. Occupational medicine vol. 20 #8 Aug 1978

Vol. 27 # 5. Zeiman M. et al Toxicity from vacuumed mercury: a household hazard Clinical Pediatrics Vol. 30 #2 Feb 1991

Vol. 27 # 6. WHO Mercury Policy Paper August 2005

Vol. 27 #7. Ziff, M., New Research – Amalgam causes harm Bio Probe Newsletter, v14 issue 5 (Sep. 1998).

Vol. 27 # 8. Ziff, M., Sweden acts on amalgam Bio Probe Newsletter, v14 issue 4 (July. 1998). Mercury amalgam risk to unborn babies

Vol. 27 # 9. ADA Council Mercury hygiene measures recommended ADA News Sept 7, 1991

Vol. 27 # 10. Schrier L. An overview of xenobiotic analysis the determination of Cd, Hg, Pb in human matrices by Atomic absorption Spectroscopy, Spectroscopy Vol. 9 #2 Feb 1994

Vol. 27 # 11. Fung et. al. Health implications of mercury in dental amalgam General Dentistry Sept-Oct 1987

Vol. 27 # 12. Fung y.k. et al., In vivo mercury and methyl mercury levels in patients at different intervals after amalgam restorations General Dentistry pp.89-91 April 1991

Vol. 27 # 13. ADA You owe it to your self Mercury testing service

Vol. 27 # 14. Lowery M, Dentists mull use of non-mercury tooth fillings City & Live Calgary Herald July 18, 1996

Vol. 27 # 15. Ziff, M., New study creates uproar in Germany Bio Probe Newsletter, v12 issue 4 (July. 1996). Mercury amalgam risk to unborn babies

Vol. 27 # 16. Pressey W., Letter to James Brookfield Canadian Dental association 3 June 1996 re false claims re Canadian risk assessment for amalgam mercury.

Vol. 27 # 17. Sellers, Wm. Et al. Methyl mercury in dental amalgams in the human mouth J. Nutritional & Environmental Medicine Vol. 6 pp 33-36, 1996

Vol. 27 # 18. McAuliffee History of methyl mercury serves ominous warning The Chemistry of mercury 4th International Conference on Mercury as a Global Pollutant Congress Centre Hamburg Germany Aug 4-8, 1996

Vol. 27 # 19. ADA Dental practice Parameters 12 oral health conditions Oct 1995

Vol. 27 # 20. Thursfield Case for Diagnosis and Dermato-Polyneuritis

Vol. 27 #21. Diseases of Children AMA Vol. 135 #4 April 1981

Vol. 27 # 22. Osborne J. W. Dental amalgam and Mercury vapor release Adv Dent Res Vol. 6 PP 135-138 Sep. 1992

Vol. 27 # 23. Rubin P Mercury vapor in amalgam waste discharged from Dental Office Vacuum Units Archives of Environmental Health Vol. 51 #4 1996

Vol. 27 # 24. Koch, P. Oral lichenoid lesions, mercury hypersensitivity and combined hypersensitivity to mercury and other metals: histologically-proven reproduction of the reaction by patch testing with metal salts Contact Dermatitis Vol. 33 pp. 323-328, 1995

Vol. 27 # 25. Society de Neurologie de Paris Séance de 1st pp. 248-255 Fevrier 1934 in French

Vol. 27 # 26. Janet, MF Syndrome of Guillain-Barre with signs of encephalitis cardiovascular and acrodynia Societe de Pediatrie de Paris pp. 431-441Séance du 18 Novembre 1941 in French

Vol. 27 # 27. Rogaz M., Acrodynie infantile aved encephalo-myelite terminale Societe de Pediatrie de Paris pp. 482-489 Séance du 18 Novembre 1941 in French

Vol. 27 # 28. Spillman, P., Polynevrites Dans l’Intoxication hydrargyrique aigue et subaigue Revue do Medicine pp.1008-1024 vol. 15 1895 in French

Vol. 27 # 29. Kernohan, J. Kennedy, R. J. Acrodynia American J. of Diseases of Children Vol. 36, 1928

Vol. 27 # 30. Paterson, D., Erythroedema Polyneuritis (the so called ‘pink disease’)Quarterly Journal of Medicine Vol. 17, 1923

Vol. 27 # 31. Van Bogaert Ludo, Sur L’acrodynie de l’enfant et de l’adulte Revue Francaise de Pediatrie Vol. 4, 1928 French

Vol. 27 # 32. Von E. Glanzmann Krankendemonstrationen Annales Paediatrici Vol. 167 1946 in German in Duke Univ medical Library

Vol. 27 # 33. Thursfield, H. Dermato-Polyneuritis Erythroedema Acrodynia British J of Children’s Diseases Vol. 19, 1922

Vol. 27 # 34. Wyllie, W.G. Pink Disease: It’s Morbid anatomy, with a note on Treatment Archives of Disease in Childhood Vol. 6, 1931

Vol. 27 # 35. Blackfan, K. D. et al Acrodynia J of Pediatrics Vol. 3, 1933

Vol. 27 # 36. Byfield, A.H. A Polyneuretic Syndrome Resembling Pellagra-acrodynia (?) Seen in very young children Am J. of Diseases of Children Vol. 20 #5 Nov. 1920

Vol. 27 # 37. Curtis, H.A., Mercury as a Health Hazard Archives of Disease in Childhood pp. 293-295 1987

Vol. 27 # 38. Campbell, J.S. Acute Mercurial Poisoning by Inhalation of metallic vapour in an infant pp 72-75 Vol. 58, 1948

Vol. 27 # 39. Tennant R., et al. Acute bilateral Pneumonitis associated with inhalation of mercury vapor Connecticut medical pp. 106109Feb 1961

Vol. 27 # 40. Taueg, C. Acute and chronic Poisoning from Residential exposure to elemental Mercury – Michigan, 1989-1990Clinical Toxicology Vol. 30 #1 pp. 63-7, 1992

Vol. 27 # 41. Snodgrass, W. et al. Mercury Poisoning from home gold ore processing JAMA Vol. 246 #17 Oct. 1981

Vol. 27 # 42. Swaiman, K. F. et al Mercury poisoning with central and peripheral nervous system involvment treated with Penicillamine Pediatrics Vol 48, 1971

Vol. 27 # 43. Jaffe, K. M. et al. Survival after acute mercury vapor poisoning role of intensive supportive care Am J. Dis Child Vol 137, Aug 1983

Vol. 27 # 44. Frustaci, A. et al, A. Marked elevation of myocardial trace elements in idiopathic dilated cardiomyopathy compared with secondary cardiac dysfunction J Am Coll Cardiology Vol. 33 pp.1578-1583, 1999

Vol. 27. #45 Olusegun O. Soge, Nicola K. Beck, Teresa M. White, David B. No and Marilyn C. Roberts*A novel transposon, Tn6009, composed of a Tn916 element linked with a Staphylococcus aureus mer operon Journal of Antimicrobial Chemotherapy Vol. 62, pp. 674–680, 2008

"Anne O. Summers" <summers@uga.edu> wrote:

excellent paper, great investigators/lab, very important - had heard from Marilyn that it was coming out - very important info for our current work on staph plasmid sequencing - expands the story of Hg exposure selecting/enriching populations of bacteria that are not only Hg resistant but also capable of transferring antibitotic resistance at the same time they transfer Hg resistance. thanks for asking!

Objectives: The aim of this study was to characterize a novel conjugative

transposon Tn6009 composed of a Tn916 linked to a Staphylococcus aureus mer operon in representative Gram-positive and Gram-negative bacteria isolated in Nigeria and Portugal. Methods: Eighty-three Gram-positive and 34 Gram-negative bacteria were screened for the presence of the Tn6009 using DNA–DNA hybridization, PCR, hybridization of PCR products, sequencing and mating experiments by established procedures. Results: Forty-three oral and 23 urine Gram-negative and Gram-positive isolates carried the Tn6009. Sequencing was performed to verify the direct linkage between the mer resistance genes and the tet(M) gene. A Nigerian Klebsiella pneumoniae, isolated from a urinary tract infection patient, and one commensal isolate from each of the other Tn6009-positive genera, Serratia liquefaciens, Pseudomonas sp., Enterococcus sp. and Streptococcus sp. isolated from the oral and urine samples of healthy Portuguese children, were able to act as donors and conjugally transfer the Tn6009 to the Enterococcus faecalis JH2-2 recipient, resulting in tetracycline- and mercury-resistant E. faecalis transconjugants. Conclusions: This study reports a novel non-composite conjugative transposon Tn6009 containing a Tn916 element linked to an S. aureus mer operon carrying genes coding for inorganic mercury resistance (merA), an organic mercury resistance (merB), a regulatory protein (merR) and a mercury transporter (merT). This transposon was identified in 66 isolates from two Gram-positive and three Gram-negative genera and is the first transposon in the Tn916 family to carry the Gram-positive mer genes directly linked to the tet(M) gene. Keywords: S. aureus, conjugative transposons, tet(M) Introduction The tet(M) gene codes for a ribosomal protection protein, which confers tetracycline, doxycycline and minocycline resistance. The tet(M) gene is usually associated with conjugative transposons (CTns) and has been found naturally in 50 different Gram-positive