Mercury

“Increasing knowledge about the risk of toxic effects caused by anthropogenic mercury accumulation in ecosystems has resulted in a growing pressure for reduction of the discharge of mercury waste. Consequently, the mercury waste problems of dental clinics have been given increased attention, and restrictions on handling and discharge of contaminated waste have been established in several countries. Major amalgam particles from trituration surplus of those produced during the carving and burnishing of new amalgam restorations are generally collected in coarse filters and sold for refinement. Minor amalgam particles released by production of new fillings or by removal of old restorations partly sediment in tubes and drains. The remaining particles are carried with the waste water stream to the local purifying plant. In Scandinavia, the industrial discharge of mercury-contaminated waste water has been reduced to a minimum. According to recent investigations, dental clinics appear to be responsible for the major amount of mercury collected in the sludge generated in purifying plants. If threshold values for heavy metal content, including mercury, are exceeded, the sludge is not allowed to be recycled as fertilizer. Installation of an approved amalgam-separating apparatus in dental clinics is now mandatory in several countries–for example, Switzerland, Germany, Sweden, and Denmark. Approval of amalgam separators is based on national testing programs, including clinical or laboratory tests demanding 95-99% separating efficiency.”

The use of base metal alloys in dentistry has gained wide popularity in recent years. However, claims of their safety have not been universally accepted. An artificial oral environment capable of reproducing three-dimensional force-movement cycles of human mastication was used to determine whether nickel, chromium, and beryllium ions were leached from base metal alloy. Twelve pairs of crowns were articulated in the following combinations: metal versus metal, metal versus enamel, metal versus porcelain, and metal versus metal without chewing as a control. In a simulated 1-year period of mastication, the results showed that nickel and beryllium metals were released both by dissolution and occlusal wear. These findings suggest that if these conditions occur in the oral cavity, the stability of base-metal alloys is subject to question. Further studies are needed to determine whether the leaching reported has long-term consequences for patients receiving base metal restorations.

Mercury has several forms and produces subtle effects at chronic low-level exposures, mercury toxicity can be a difficult diagnosis to establish.

“The toxicity of the various chemical species of mercury and its organic and inorganic compounds is well known. In the past few decades, increased concern about toxicity, often heightened by tragic mass outbreaks of mercury-induced human disease, has led to the virtual elimination of mercurials in drugs and cosmetics, increased monitoring of mercury contamination of seafood, and reduced industrial exposure. In terms of the number of exposed individuals, the most prevalent remaining source of deliberate mercury exposure is almost certainly dental amalgam.”

However, the effects on the central nervous system often appear after a long latency and remain long after the excretion in urine has dimished.

“Documented cases of oral mucosa and skin affections related to amalgam restorations are rare, although the exact incidence is unknown. Lesions of the oral mucosa may be due to specific immunologic or non-specific toxic reactions toward products generated from restorations. The immunologic reaction most probably involved in mucosal affections related to amalgam is the delayed or cell-mediated (type IV) reaction. Such reactions are seen in contact allergy, and the term “contact lesions of the oral mucosa” has been used. There is a much lower tendency of sensitization through mucous membranes than through skin, and it is questionable whether mercury released from amalgam restorations is able to sensitize a patient. A chronic toxic reaction may be established due to repeated or constant influence to toxic agents in low concentrations over long periods. Such reactions are most frequently localized to the contact zone with the toxic agent. Chronic toxic reactions may possibly be seen in areas of the oral mucosa in direct contact with amalgam fillings. Since the clinical features of these lesions do not differ from those of lesions due to contact hypersensitivity, the diagnosis is obtained by exclusion based on a negative patch test.”

“The mercury concentrations in blood (HgB) and urine (HgU) samples, and in exhaled air (HgAir) were measured in 147 individuals from an urban Norwegian population, using cold vapour atomic absorption spectrometry. The study aimed to estimate the mercury exposure from the dental restorations, by correlating the data to the presence of amalgam restorations. Mean values were HgB = 24.8 nmol/l, HgU = 17.5 nmol/l and HgAir = 0.8 micrograms/m3. HgU correlated with HgAir, and both HgU and HgAir with the number of amalgam restorations, amalgam restored surfaces and amalgam restored occlusal surfaces. HgB showed poor correlation to HgU and HgAir and the presence of amalgam restorations. A differentiation of the mercury absorption due to exposure from dental amalgams and from the dietary intake, necessitates measurements of both organic and inorganic mercury in the plasma, and in the erythrocytes. The results suggest that individuals with many amalgam restorations, i.e., more than 36 restored surfaces, absorb 10-12 micrograms Hg/day.”

“There is considerable controversy as to whether dental amalgams may cause systemic health effects in humans because they liberate elemental mercury. Most such amalgams contain as much as 50% metallic mercury. To determine the influence of dental amalgams on the mercury body burden of humans, we have given volunteers, with and without amalgams in their mouth, the sodium salt of 2,3-dimercaptopropane-1-sulfonic acid (DMPS), a chelating agent safely used in the Soviet Union and West Germany for a number of years. The diameters of dental amalgams of the subjects were determined to obtain the amalgam score. Administration of 300 mg DMPS by mouth increased the mean urinary mercury excretion of the amalgam group from 0.70 to 17.2 micrograms and that of the nonamalgam group from 0.27 to 5.1 micrograms over a 9-h period. 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 h after DMPS administration and the dental amalgam scores. DMPS can be used to increase the urinary excretion of mercury and thus increase the significance and reliability of this measure of mercury exposure or burden, especially in cases of micromercurialism.”

To study amalgam-related toxicity in a primary target cell type, human oral fibroblasts were grown in a low-serum medium containing 1.25% fetal bovine serum and exposed to Hg2+, a corrosion product of amalgam. A 1-h exposure to various concentrations of Hg2+ resulted in a dose-dependent loss of colony forming efficiency. Removal of the low-molecular-weight thiol cysteine from the medium increased the toxicity of Hg2+ almost 50-fold in comparison with complete medium or medium without fetal bovine serum. Accordingly, fetal bovine serum was not found to contain detectable levels of low-molecular-weight thiols. The levels of cellular free protein thiols were shown to be depleted Hg2+ at significantly lower concentrations of the metal ion than those required to decrease the levels of the major cellular low-molecular weight thiol glutathione. These decreases were dependent on the exposure conditions, i.e. the presence of serum and thiols, in a manner similar to the effect on colony forming efficiency. Other functions commonly related to cell viability, including the accumulation of the vital dye neutral red, the cytosolic retention of deoxyglucose and the mitochondrial reduction of tetrazolium were also inhibited by Hg2+, albeit at higher concentrations. Finally, the depletion of cellular glutathione, by pre-exposure of the cells to the glutathione synthesis inhibitor buthionine sulfoximine, somewhat increased the toxicity of Hg2+ and potentiated the depletion of protein thiols. Taken together, the toxicity of Hg2+ in human oral fibroblasts was demonstrated in several assays of which colony forming efficiency was the most sensitive, cell killing by this agent was related to its high affinity for protein thiols, whereas glutathione showed a significant, but limited, ability to protect the cells from Hg2+ toxicity.

Mercury from dental amalgams does not seem to cause dose-related intoxications. However, animal studies have shown that high-dose exposure to mercury may support various types of immunologic reactions. Ten patients claiming that their symptoms were caused and aggravated by amalgam therapy were selected for a study of the effects of removal of one amalgam restoration followed by placing of a composite filling. Clinical symptoms and the result of laboratory tests were recorded. Six patients had contact allergies to metals, three of them to mercury ammonium chloride. The comparison of pre- and post-experimental test results showed significant reductions in p-IgE and dU-albumin and significant increases in p-C3d and dU-beta 2-microglobulin. There was no laboratory evidence of a direct toxic effect by mercury on the patients. The observed response by some of the studied factors to the low acute exposure to amalgam may imply that an activation of the immune system occurred.