Mercury

“In a total of 395 subjects with varying fish consumption habits, mercury levels in whole blood (B-Hg), and selenium levels in plasma (P-Se) were studied. Also, in subcohorts, mercury levels in blood cells (Ery-Hg; n = 79), plasma (P-Hg; n = 158) and urine (U-Hg; n = 125) were analysed. There were statistically significant associations between fish intake on the one hand, and B-Hg, Ery-Hg and P-Hg, on the other, but not so with U-Hg. In subjects who never had fish, the average B-Hg was 1.8 ng/g, in subjects who had at least two fish meals each week, 6.7 ng/g. Ery-Hg, and to a less extent P-Hg, were associated with levels of marine n-3 polyunsaturated fatty acids (PUFA) in serum phosphatidylcholine. P-Hg and U-Hg were associated with numbers of teeth with amalgam fillings. P-Se also correlated with fish intake. In subjects who never had fish, P-Se averaged 80 micrograms/l, in subjects who had at least two fish meals per week, 91 micrograms/l. There was an association between PUFA and P-Se. Further, there were statistically significant associations between P-Se on the one hand, and B-Hg, Ery-Hg and P-Hg on the other. The data clearly demonstrate the importance of fish for the exposure to methylmercury and selenium in the Swedish diet, and the impact of amalgam as a source of exposure to inorganic mercury.”

“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 exposure can reach levels considerably over known threshold limit values. Also, measurements of mercury absorption from intraoral air are presented. The vital importance of avoiding a galvanic amalgam-gold coupling is emphasized. The symptomatology of a disabled patient, who recovered after amalgam removal, has been included. It is concluded that discussion of the dental amalgam issue has suffered from the lack of an interdisciplinary approach. It would be wise to learn from the lesson of acrodynia, and consider amalgam mercury among other possible factors in neurological and immunological diseases of unclear etiology.”

“Urinary mercury (U-Hg) and plasma mercury (P-Hg) levels were higher in 244 dental personnel than in 81 matched referents (U-Hg: 1.8 and 1.1 mumol/mol creatinine, respectively; p less than .001; P-Hg: 6.7 and 6.2 nmol/l, respectively; p = .03). The amalgam in the mouth influenced mercury levels in whole blood (B-Hg), plasma, and urine. The association was nonlinear: the more amalgam, the larger the relative increase in mercury levels. The number of amalgam surfaces accounted for more of the variance in blood and urine mercury levels than did the number of fillings (e.g., U-Hg: 44% and 36%, respectively). The estimated increases in mercury level with rising amalgam load were 3.0%, 2.0%, and 0.8% per filled surface for U-Hg, P-Hg, and B-Hg, respectively (p less than .0001 in all cases). The impact of occupational exposure on U-Hg in the dental personnel corresponded to approximately 19 amalgam surfaces. Ceramo metallic restorations were associated with higher (31%) U-Hg.”

“These data raise serious doubts abour the reliability of statements from the Canadian and American Dental Associations. Experiments in primates clearly demonstrate that Hg [mercury] released from ‘silver’ tooth fillings concentrates in body tissues in amounts sufficient to alter cell function.'”

Epicutaneous patch testing of a battery of 35 dental test substances was carried out in 24 patients with visible lichenoid oral mucosal lesions and in 24 patients with burning mouth syndrome (BMS) without any visible lesions. Reactions to mercury ammonium chloride were found in 33% (8/24) of the patients with visible lesions compared to 0% (0/24) of the patients with BMS. The difference was statistically significant. In 7 of the 8 patients who reacted to mercury, total or partial regression of the lesions was observed after removal of dental amalgam. Reactions to nickel sulfate were found in 21% (5/24) of the patients with BMS compared to 3% (1/24) of the patients with lichenoid lesions. This difference was also statistically significant. Nickel is a rare component in dental restorations, but the oral mucosa is daily exposed to nickel through food and water intake. Removal of nickel from the environment of the patient can therefore be hard to accomplish.

“Individuals who are xenobiotically sensitive to chemicals comprise a living indicator system that enables us to identify that group in the population that is also mercury sensitive. There is a spectrum of xenobiotic intolerance in the general population that is a function of, among other things, the spectrum of efficiency of the cytochrome P-450 system that exists in the population due to a spectrum of genetic polymorphism. Dental mercury inactivates those groups, whose function is protection of the cytochrome P-450 system. This inactivation and consequent loss of protection induces xenobiotic intolerance in individuals who are already compromised due to genetic polymorphism and who are the most susceptible individuals in the genetic population to further compromise. These compromised individuals will exhibit a variety of diagnostically confusing heterogenous symptoms. On March 15, 1991, the Food and Drug Administration convened a hearing on the “Potential Toxicity of Dental Amalgam”. I was one of the invited speakers. The following is based on the speech I delivered at that meeting. My purpose in this presentation is to
make three points:
1. Mercury from dental amalgam induces symptoms in a sensitive group of the population that has also been observed to be sensitive to xenobiotic substances. (Xenobiotic substances are substances which are foreign to the natural state of an organism. Examples of such foreign substances are petrochemical vapors, chlorinated hydrocarbons, sulfites, and metals which are not metabolically useful.)
2. This sensitive group serves as a marker that warns of the potential danger of dental mercury to the rest of the population who are also at risk but may not yet exhibit symptoms.
3. Dental mercury should be banned.”

“Saccharomyces cerevisiae and Candida albicans were incubated with 0.25, 0.5, or 0.75 micrograms of Hg (as HgCl2) per ml of Nelson’s medium in the presence of trace amounts of oxygen at 28 degrees C for 12 days. Two control media were used, one without added Hg and one without yeast inoculum. Yeast cell growth was estimated after 1, 2, 3, and 8 days of incubation. The contents of organomercury in the system and of elemental mercury released from the media and collected in traps were determined at the end of the experiments. The results were as follows. (i) C. albicans was the more mercury-resistant species, but both yeast species failed to grow in the media containing 0.75 micrograms of Hg per ml. (ii) The amounts of organomercury produced by the two species were proportional to the amount of HgCl2 added to the medium. In all cases C. albicans produced considerably larger amounts of methylmercury than S. cerevisiae. (iii) The amounts of elemental Hg produced were inversely proportional to the HgCl2 level added in the case of S. cerevisiae but were all similar in the case of C. albicans. (iv) Neither organomercury nor elemental Hg was produced in any of the control media.”

“A WHO Task Group on Environmental Health Criteria for Inorganic Mercury met in Bologna, Italy, at the County Council Headquarters (Provincia) from 25 to 30 September 1989.  The meeting was sponsored by the Italian Ministry of the Environment and organized locally by the Institute of Oncology and Environmental Sciences with the assistance of the County Council…The Task Group reviewed and revised the draft document and made an evaluation of the human health risks from exposure to inorganic mercury.”

“The pathogenesis of Alzheimer’s Disease (AD) is unknown. Using SDS-PAGE and autoradiography the authors’ laboratory has shown: (1) that the tubulin in AD brain is less photolabeled by ({sup 32}P)8N{sub 3}GTP than is tubulin from control brain and (2) that low {mu}M levels of preformed Hg{sup 2+}EDTA specifically blocked interactions of tubulin-({sup 32}P)8N{sub 3}GTP in control human brain homogenates giving a photolabeling profile identical to AD brain. Elevated levels of Hg{sup 2+} have been reported in AD brain by others. Earlier work using ({sup 32}P)8N{sub 3}GTP with Al{sup 3+} treated rat and rabbit brain showed no differences from control with regards to tubulin photolabeling. However, our latest data show that brain samples from Hg{sup 2+} fed rats display an abolished GTP-tubulin interaction similar to AD brain samples as determined by ({sup 32}P)8N{sub 3}GTP photolabeling profiles. Removal of Hg{sup 2+} from treated rats did not reverse the effect. These results suggest that certain complexed forms of Hg{sup 2+} must be considered as a potential source for the etiology of AD.”

“Exposure to mercury contamination in the dental office poses a potential hazard for dental personnel. Although many precautions for containing the poisonous metal vapors are routinely observed, dental personnel may place themselves at risk by failing to use proper cleaning techniques. Researchers from the National Institute for Occupational Safety and Health (NIOSH) have discovered that vacuum cleaners designed for the home are sometimes used to clean dental office carpets, which might be contaminated with mercury. Since ordinary vacuum cleaners increase airborne mercury concentrations, dental personnel should use a specially designed vacuuming system for mercury recovery.”