Mercury

“We were surprised that Björnberg et al. (2005) failed to mention saliva as a plausible biologic source of methylmercury in individuals who have mercury dental fillings.”

“BACKGROUND:

Data on mercury exposure of the Austrian population were inadequate. This study was performed to determine the causal factors underlying mercury exposure and selenium concentrations, and to estimate the gender-related health impacts.

METHODOLOGY:

Venous blood samples of 78 women and 81 men were drawn at the Austrian Red Cross, Vienna. Mercury contents in acid-digested whole blood samples were measured after amalgam enrichment by CV-AAS, and selenium by AAS (heated quartz-cell) after hydrid formation.

RESULTS:

The average total mercury blood content of Austrians was low (2.38+/-1.55 microgL(-1); N=152). Mercury and selenium concentrations were not different between the genders (P>0.05) but we observed discrepancies regarding the causal factors. Mercury levels in men were influenced not only by fish consumption but also by age, education level, and amalgam fillings, whereas in women, only the diet (fish/seafood, red wine consumption) determined blood mercury (P<0.05). Moreover, only the males indicated a depressive effect of dental amalgam on hematocrit (P<0.05). Regarding selenium, age and alcohol consumption led to lower concentrations in men, whereas a high-level education had the opposite effect; no determinant was found for women. For the whole study group, a significant effect of chronic disease on selenium levels could be detected (P<0.05). 18% of women and 13% of men showed marginal selenium deficiency (blood selenium<65 microgL(-1)). Selenium and mercury concentrations were not correlated.

CONCLUSIONS:

Our results indicate the need to evaluate and integrate gender-related findings in metal toxicology and trace element research, because different causal factors require different preventive measures to reduce mercury exposure and the risk of low selenium concentrations. Future research is needed on the gender- and age-related differences in fish/seafood consumption habits, the modifications of mercury toxicokinetics through sex hormones, the selenium supply in Austria, and the clinical relevance of a low selenium status.”

“Environmental factors are recognized as a cause of the increasing frequency of allergic and autoimmune diseases. In addition to external pollutants, metal ions released from dental restorations or from other body implants might trigger inflammation in susceptible subjects. In humans, genes governing metal-induced inflammation and autoimmunity are not yet known. In clinical praxis, metal-sensitive patients will present various symptoms ranging from oral mucosal changes and skin disease to excessive fatigue and autoimmune diseases. Since genetic markers of genetic susceptibility in man are not known, one has to rely on the phenototypic markers. Such biomarkers might be certain detoxification enzymes but also the presence of metal-specific memory cells in the blood. With the increasing use of metal implants in medicine and dentistry, it is important to have a proper tool for the diagnosis of metal allergy in susceptible subjects. After nickel, gold is now the second most common sensitizer. In addition to patch test, an in vitro blood test, an optimized commercially available lymphocyte transformation test (MELISA) is discussed. Both tests were used for the diagnosis of metal allergy in a selected group of 15 patients who suffered from clinical metal sensitivity in addition to other health problems. The concordance of the two tests was good but MELISA detected more metal allergies than patch test. The removal of incompatible dental material (RID) resulted in long-term health improvement in the majority of patients. We postulate that in vivo, metal ions activate T-cells, initiating systemic inflammation, which, through cytokines, affects the brain and hypothalamus-pituitary-adrenal axis. We postulate that in vivo metal ions will activate T-cells starting systemic inflammation which, through cytokines affect the brain and hypothalamus-pituitary-adrenal (HPA) axis. The treatment and rehabilitation of metal sensitive patients is based on a firm understanding and recognition of individual susceptibility. RID has to be done done with extreme caution and according to standard working protocol. If performed properly, this treatment can result in decreased systemic inflammation and improved health in sensitized patients.”

The objective of this study was to determine the concentration changes of 13 elements in erythrocytes and plasma after the removal of dental amalgam and other metal alloys. Blood samples from 250 patients were collected, separated into erythrocytes and plasma, and analyzed by inductively coupled plasma-mass spectrometry. The 250 patients were divided into 3 groups (Negative, Zero, and Positive) depending on their estimation of quality of life in an earlier study. Magnesium in plasma, selenium and mercury in plasma, and erythrocytes showed decreased concentrations after amalgam removal in all groups (p < 0.05). Titanium in plasma, copper in plasma, and erythrocytes and zinc in plasma exhibited decreased concentrations after amalgam removal in the Negative and Positive groups (p < 0.05). Silver in plasma and gold in erythrocytes decreased in the Zero and Positive groups after amalgam removal (p < 0.05). Copper in erythrocytes and silver and gold in plasma showed higher concentrations after amalgam removal in the Negative compared to the Positive group (p < 0.05), suggesting that patients in the Negative group excrete metals slowly. Moreover, the cobalt levels in plasma were lowest in the Negative group and only this group showed a significant increase in vitamin B12 levels in blood after amalgam removal.

“Mercury (Hg) has been used for millennia in many applications, primarily in artisanal mining and as an electrode in the chlor-alkali industry. It is anthropogenically emitted as a pollutant from coal fired power plants and naturally emitted, primarily from volcanoes. Its unique chemical characteristics enable global atmospheric transport and it is deposited after various processes, ultimately ending up in one of its final sinks, such as incorporated into deep sediment or bioaccumulated, primarily in the marine environment. All forms of Hg have been established as toxic, and there have been no noted biological benefits from the metal. Throughout time, there have been notable incidents of Hg intoxication documented, and the negative health effects have been documented to those chronically or acutely exposed. Today, exposure to Hg is largely diet or occupationally dependent, however, many are exposed to Hg from their amalgam fillings. This paper puts a tentative monetary value on Hg polluted food sources in the Arctic, where local, significant pollution sources are limited, and relates this to costs for strategies avoiding Hg pollution and to remediation costs of contaminated sites in Sweden and Japan. The case studies are compiled to help policy makers and the public to evaluate whether the benefits to the global environment from banning Hg and limiting its initial emission outweigh the benefits from its continued use or lack of control of Hg emissions. The cases we studied are relevant for point pollution sources globally and their remediation costs ranged between 2,500 and 1.1 million US dollars kg(-1) Hg isolated from the biosphere. Therefore, regulations discontinuing mercury uses combined with extensive flue gas cleaning for all power plants and waste incinerators is cost effective.”

OBJECTIVES:
The impact of dental amalgam removal on the levels of anti-thyroid peroxidase (anti-TPO) and anti-thyroglobulin (anti-Tg) antibodies was studied in patients with autoimmune thyroiditis (AT) with and without mercury allergy.

METHODS:
Thirty-nine patients with AT were tested by an optimized lymphocyte proliferation test MELISA for allergy (hypersensitivity) to inorganic mercury. Patients were divided into two groups: Group I (n = 12) with no hypersensitivity to mercury and Group II (n = 27) with hypersensitivity to mercury. Amalgam fillings were removed from the oral cavities of 15 patients with hypersensitivity to mercury (Group IIA) and left in place in the remaining 12 patients (Group IIB). The laboratory markers of AT, anti-TPO and anti-Tg autoantibodies, were determined in all groups at the beginning of the study and six months later.

RESULTS:
Compared to levels at the beginning of the study, only patients with mercury hypersensitivity who underwent amalgam replacement (Group IIA) showed a significant decrease in the levels of both anti-Tg (p=0.001) and anti-TPO (p=0.0007) autoantibodies. The levels of autoantibodies in patients with or without mercury hypersensitivity (Group I and Group IIB) who did not replace amalgam did not change.

CONCLUSION:
Removal of mercury-containing dental amalgam in patients with mercury hypersensitivity may contribute to successful treatment of autoimmune thyroiditis.

“Thimerosal is an organomercury compound with sulfhydryl-reactive properties. The ability of thimerosal to act as a sulfhydryl group is related to the presence of mercury. Due to its antibacterial effect, thimerosal is widely used as preservatives and has been reported to cause chemically mediated side effects. In the present study, we showed that the molecular mechanism of thimerosal induced apoptosis in U937 cells. Thimerosal was shown to be responsible for the inhibition of U937 cells growth by inducing apoptosis. Treatment with 2.5-5 microM thimerosal but not thiosalicylic acid (structural analog of thimerosal devoid of mercury) for 12 h produced apoptosis, G(2)/M phase arrest, and DNA fragmentation in a dose-dependent manner. Treatment with caspase inhibitor significantly reduced thimerosal-induced caspase 3 activation. In addition, thimerosal-induced apoptosis was attenuated by antioxidant Mn (III) meso-tetrakis (4-benzoic acid) porphyrin (Mn-TBAP). These data indicate that the cytotoxic effect of thimerosal on U937 cells is attributable to the induced apoptosis and that thimerosal-induced apoptosis is mediated by reactive oxygen species generation and caspase-3 activation.”

“People in developing countries are often considered at greater risk of mercury (Hg) poisoning due to a variety of factors including a lack of awareness regarding their occupational risks. Individuals requiring urine mercury (U-Hg) analysis at the Center for Toxicological Investigations of the University of Carabobo (CITUC), between 1998 and 2002 were studied to identify demographic characteristics associated to U-Hg levels. The studied population included individuals with a history of exposure (or related exposures) to Hg processes, and was comprised of 1159 individuals (65 children, 1094 adults) ages 0.58-79 years old, mean 36.63+/-12.4. Children’s geometric mean U-Hg levels were 2.73 microg/g Creatinine (Ct) and in adults 2.55 microg/g Ct. The highest frequency of adults’ occupations were shipyard workers (35.47%), dentists (23.5%), lab technicians (11.43%), dental employees 10.42% and miners (10.2%). Chemical laboratory technicians had the highest mean U-Hg (4.46 microg/g Ct). Mean U-Hg levels in female adults (3.45 microg/g Ct) were statistically superior to levels in male adults (2.15 microg/g Ct). Two of the 172 women in reproductive age, had U-Hg levels higher than 78 microg/g Ct. Individuals from Falcon State were found to have the highest mean U-Hg (4.53 microg/g Ct). U-Hg levels higher than permissible limits were found in only 2 states (Carabobo and Bolivar) with a total of 24 cases. Although the results of this investigation were highly variable, the findings can be used to examine circumstances which influence mercury toxicity trends, and possibly used in future studies working to identify Hg exposures.”

Mercury is ubiquitous in the environment and therefore every human being, irrespective of age and location, is exposed to one form of mercury or another. The major source of environmental mercury is natural degassing of the earth’s crust, but industrial activities can raise exposure to toxic levels directly or through the use or misuse of the liquid metals or synthesized mercurial compounds. The aim of this review is to survey differences in human exposure and in the toxicology of different forms of mercury. It covers not only symptoms and signs observed in poisoned individuals by a clinician but also subclinical effects in population studies, the final evaluation of which is the domain of statisticians.

“Arachidonic acid (AA) participates in a reacylation/deacylation cycle of membrane phospholipids, the so-called Lands cycle, that serves to keep the concentration of this free fatty acid in cells at a very low level. To manipulate the intracellular AA level in U937 phagocytes, we have used several pharmacological strategies to interfere with the Lands cycle. We used inhibitors of the AA reacylation pathway, namely thimerosal and triacsin C, which block the conversion of AA into arachidonoyl-CoA, and a CoA-independent transacylase inhibitor that blocks the movement of AA within phospholipids. In addition, we used cells overexpressing group VIA phospholipase A(2), an enzyme with key roles in controlling basal fatty acid deacylation reactions in phagocytic cells. All of these different strategies resulted in the expected increase of cellular free AA but also in the induction of cell death by apoptosis. Moreover, when used in combination with any of the aforementioned drugs, AA itself was able to induce apoptosis at doses as low as 10 muM. Blocking cyclooxygenase or lipoxygenases had no effect on the induction of apoptosis by AA. Collectively, these results indicate that free AA levels within the cells may provide an important cellular signal for the onset of apoptosis and that perturbations of the mechanisms controlling AA reacylation, and hence free AA availability, may decisively affect cell survival.”