iaomtlibrary

“The city of New Orleans was spared the wrath of hurricane Ivan. Yet, a week later, the eye of a different kind of storm stirred at the edge of the Mississippi, a muddy and polluted river, emblematic of our self-inflicted health crisis affecting children and the elderly, from autism to Alzheimer’s disease. A unique international group of policymakers, environmental scientists, toxicologists, biochemists, journalists, academic physicians, practicing pediatricians, neurologists, and dentists gathered to make sense of the environmental impact, toxicology, basic science, public policy, and health implications of one of the least studied and perhaps greatest potential threats to our long-term health—mercury.”

“Measuring the amount of mercury present in the environment or food sources may provide an inadequate reflection of the potential for health risks if the protective effects of selenium are not also considered. Selenium’s involvement is apparent throughout the mercury cycle, influencing its transport, biogeochemical exposure, bioavailability, toxicological consequences, and remediation. Likewise, numerous studies indicate that selenium, present in many foods (including fish), protects against mercury exposure. Studies have also shown mercury exposure reduces the activity of selenium dependent enzymes. While seemingly distinct, these concepts may actually be complementary perspectives of the mercury-selenium binding interaction. Owing to the extremely high affinity between mercury and selenium, selenium sequesters mercury and reduces its biological availability. It is obvious that the converse is also true; as a result of the high affinity complexes formed, mercury sequesters selenium. This is important because selenium is required for normal activity of numerous selenium dependent enzymes. Through diversion of selenium into formation of insoluble mercury-selenides, mercury may inhibit the formation of selenium dependent enzymes while supplemental selenium supports their continued synthesis. Further research into mercury-selenium interactions will help us understand the consequences of mercury exposure and identify populations which may be protected or at greater risk to mercury’s toxic effects.”

“BACKGROUND:

Patients with certain autoimmune and allergic diseases, such as systemic lupus, multiple sclerosis, autoimmune thyroiditis or atopic eczema, often show increased lymphocyte stimulation by low doses of inorganic mercury in vitro. The patients often report clinical metal hypersensitivity, especially to nickel.

OBJECTIVE AND METHODS:

In this study we examined the health impact of amalgam replacement in mercury-allergic patients with autoimmunity. The suitability of MELISA, an optimized lymphocyte stimulation test, for the selection of susceptible patients and monitoring of sensitization was also examined. Amalgam fillings were replaced with composites and ceramic materials. Follow-up health status and lymphocyte reactivity were assessed and evaluated half a year or later following amalgam removal.

RESULTS:

Results of lymphocyte reactivity measured with MELISA indicate that in vitro reactivity after the replacement of dental amalgam decreased significantly to inorganic mercury, silver, organic mercury and lead. Out of 35 patients, 25 patients (71%) showed improvement of health. The remaining patients exhibited either unchanged health (6 patients, 17%) or worsening of symptoms (4 patients, 11%). The highest rate of improvement was observed in patients with multiple sclerosis, the lowest rate was noted in patients with eczema. The initial mercury-specific lymphocyte reactivity was significantly higher in the responder group, than in the non-responders, whose health was not improved by amalgam removal. All patients with health improvement after amalgam replacement showed reduced proliferation to inorganic mercury in follow-up MELISA. In vitro responses to phenylmercury and nickel did not differ between the groups.

CONCLUSIONS:

Mercury-containing amalgam may be an important risk factor for patients with autoimmune diseases. MELISA is a valuable tool for selection of patients for amalgam replacement and also for monitoring of metal allergies.”

“Thiol-reactive agents such as thimerosal have been shown to modulate the Ca2+-flux properties of IP3 (inositol 1,4,5-trisphosphate) receptor (IP3R) via an as yet unidentified mechanism [Parys, Missiaen, De Smedt, Droogmans and Casteels (1993) Pflügers Arch. 424, 516-522; Kaplin, Ferris, Voglmaier and Snyder (1994) J. Biol. Chem. 269, 28972-28978; Missiaen, Taylor and Berridge (1992) J. Physiol. (Cambridge, U.K.) 455, 623-640; Missiaen, Parys, Sienaert, Maes, Kunzelmann, Takahashi, Tanzawa and De Smedt (1998) J. Biol. Chem. 273, 8983-8986]. In the present study, we show that thimerosal potentiated IICR (IP3-induced Ca2+ release) and IP3-binding activity of IP3R1, expressed in triple IP3R-knockout R23-11 cells derived from DT40 chicken B lymphoma cells, but not of IP3R3 or [D1-225]-IP3R1, which lacks the N-terminal suppressor domain. Using a 45Ca2+-flux technique in permeabilized A7r5 smooth-muscle cells, we have shown that Ca2+ shifted the stimulatory effect of thimerosal on IICR to lower concentrations of thimerosal and thereby increased the extent of Ca2+ release. This suggests that Ca2+ and thimerosal synergetically regulate IP3R1. Glutathione S-transferase pull-down experiments elucidated an interaction between amino acids 1-225 (suppressor domain) and amino acids 226-604 (IP3-binding core) of IP3R1, and this interaction was strengthened by both Ca2+ and thimerosal. In contrast, calmodulin and sCaBP-1 (short Ca2+-binding protein-1), both having binding sites in the 1-225 region, weakened the interaction. This interaction was not found for IP3R3, in agreement with the lack of functional stimulation of this isoform by thimerosal. The interaction between the IP3-binding and transmembrane domains (amino acids 1-604 and 2170-2749 respectively) was not affected by thimerosal and Ca2+, but it was significantly inhibited by IP3 and adenophostin A. Our results demonstrate that thimerosal and Ca2+ induce isoform-specific conformational changes in the N-terminal part of IP3R1, leading to the formation of a highly IP3-sensitive Ca2+-release channel.”

“BACKGROUND:

Since the inhibition of mercury absorption by ethanol was serendipitously discovered in 1965,(1) a limited number of small number studies with both animal and human subjects have reported results consistent with this finding.

AIMS:

To investigate this phenomenon in a large scale human study with low level Hg exposed dentists.

METHODS:

Data were collected for a sample of 1171 dentists, and both cross sectional and case-control methods were utilised to examine the data.

RESULTS:

Abstainers (n = 345) had significantly higher urinary mercury concentrations (HgU) than drinkers (n = 826): 5.4 microg/l v 4.8 microg/l. Multiple linear regression showed a significant effect of ethanol dose on HgU after adjusting for potential confounders. A case-control analysis in which cases were defined as those individuals with urinary Hg concentrations of > or =15 microg/l (approximately top 5%), and controls as those with concentrations of <1.0 microg/l ( approximately bottom 5%), showed a clear protective dose-response relation; there was a decreasing risk of being a “case” (having an HgU > or =15 microg/l) with increasing ethanol consumption. The significance of the adjusted model is p<0.001, and the chi2 test for trend across ethanol consumption categories in the adjusted model is p<0.05, confirming the dose-response relation.

CONCLUSION:

We believe that this straightforward investigation provides the first specific confirmation in a large scale human study of the inhibitory effect of ethanol on urinary mercury concentration, and by inference, on mercury absorption.”

“Measuring the amount of mercury present in the environment or food sources may provide an inadequate reflection of the potential for health risks if the protective effects of selenium are not also considered. Selenium’s involvement is apparent throughout the mercury cycle, influencing its transport, biogeochemical exposure, bioavailability, toxicological consequences, and remediation. Likewise, numerous studies indicate that selenium, present in many foods (including fish), protects against mercury exposure. Studies have also shown mercury exposure reduces the activity of selenium dependent enzymes. While seemingly distinct, these concepts may actually be complementary perspectives of the mercury-selenium binding interaction. Owing to the extremely high affinity between mercury and selenium, selenium sequesters mercury and reduces its biological availability. It is obvious that the converse is also true; as a result of the high affinity complexes formed, mercury sequesters selenium. This is important because selenium is required for normal activity of numerous selenium dependent enzymes. Through diversion of selenium into formation of insoluble mercury-selenides, mercury may inhibit the formation of selenium dependent enzymes while supplemental selenium supports their continued synthesis. Further research into mercury-selenium interactions will help us understand the consequences of mercury exposure and identify populations which may be protected or at greater risk to mercury’s toxic effects.”

Bartova Dental amalgam as one 2003“BACKGROUND:

Experimental and clinical data published recently show that dental amalgam can give rise to undesirable immunological responses in susceptible individuals. In genetically susceptible strains of experimental animals, mercury and silver can induce autoimmune responses. Sera of patients sensitive to mercury were found to have a higher incidence of autoantibodies relative to controls.

OBJECTIVE:

The aim of this study was to determine possible presence of antinuclear SSB/La autoantibodies after the in vitro stimulation of peripheral blood lymphocytes with HgCl2.

METHODS:

Lymphocytes were obtained from patients with autoimmune thyroiditis and increased response to mercury in vitro. Mononuclear cells were cultivated for 6 days with 100 microl HgCl2 solution or with pure medium and the levels of antinuclear autoantibodies SSB/La were assayed by a commercial SSB/La ELISA kit.

RESULTS:

Increased production of SSB/La autoantibodies in the media following stimulation of peripheral blood lymphocytes with HgCl2 was found in all cases. Using the Student’s paired test, the results were significant on the p=0.05 significance level.

CONCLUSION:

Results imply that, in some patients with thyroiditis, mercury from dental amalgam can stimulate the production of antinuclear antibodies. Dental amalgam may be a risk factor in some patients with autoimmune disease.”

“OBJECTIVE:

To evaluate maternal and fetal hair mercury levels in relation to the placement of dental amalgam tooth restorations.

DESIGN:

Cross sectional study involving women who never had dental amalgam restorations placed, women who had amalgam restorations placed before pregnancy and women who had restorations placed during the index pregnancy.

SETTING:

North of England Maternity Hospital.

SAMPLE:

Fifty-three healthy women who delivered healthy babies at term.

METHODS:

Maternal and fetal hair was collected in a standardised manner in the first few days following delivery.

MAIN OUTCOME MEASURES:

Maternal and neonatal hair mercury concentrations.

RESULTS:

When compared with women without restorations, there was a significant increase in the maternal hair mercury concentration in women who had dental amalgam placed outside of the index pregnancy and also in women who had dental amalgam placed during the index pregnancy. The fetal hair mercury concentration was significantly higher in babies when mothers had been exposed to dental amalgam either before pregnancy or during pregnancy compared with unexposed babies. There was no difference in the maternal or fetal hair mercury levels in the groups of patients who had dental amalgam placed before or during pregnancy.

CONCLUSIONS:

Maternal and fetal hair mercury levels were significantly higher in women who previously had dental amalgam restorations placed. There was no evidence that placement of dental amalgam restorations in pregnant women who had already similar restorations increased the maternal or fetal hair mercury level.”

“There is widespread concern regarding the safety of silver-mercury amalgam dental restorations, yet little evidence to support their harm or safety. We examined whether mercury dental amalgams are adversely associated with cognitive functioning in a cross-sectional sample of healthy working adults. We studied 550 adults, 30-49 years of age, who were not occupationally exposed to mercury. Participants were representative of employees at a major urban medical center. Each participant underwent a neuropsychologic test battery, a structured questionnaire, a modified dental examination, and collection of blood and urine samples. Mercury exposure was assessed using a) urinary mercury concentration (UHg); b) the total number of amalgam surfaces; and c) the number of occlusal amalgam surfaces. Linear regression analysis was used to estimate associations between each marker of mercury exposure and each neuropsychologic test, adjusting for potential confounding variables. Exposure levels were relatively low. The mean UHg was 1.7 micro g/g creatinine (range, 0.09-17.8); the mean total number of amalgam surfaces was 10.6 (range, 0-46) and the mean number of occlusal amalgam surfaces was 6.1 (range, 0-19). No measure of exposure was significantly associated with the scores on any neuropsychologic test in analyses that adjusted for the sampling design and other covariates. In a sample of healthy working adults, mercury exposure derived from dental amalgam restorations was not associated with any detectable deficits in cognitive or fine motor functioning.”