Mercury

“Several aspects of Hg release from dental amalgam tooth fillings were examined both in vivo and in vitro. Using light microscopy, Hg globules (diameter =1-2µm) were observed on amalgam surfaces. Hg vapour was measured in exhaled air before and after 5 min of gum chewing in three groups of subjects with varying numbers of dental amalgams. Group 1 had symptoms similar to those of chronic low-dose Hg exposure, N=22; Group 2 had no apparent symptoms and were considered healthy, N=20; Group 3 were controls having no amalgam fillings; N=10. Groups 1 and 2 both demonstrated a significant 3-fold increase in Hg vapour levels after chewing, while levels in controls remained undetectable. A mouth rinse with hot water (55°C) in Group 2 resulted in a further increase in Hg vapour levels. Saliva samples (1 ml) from 17 subjects in Group 2, collected before and after chewing, showed a significant 8-fold increase in Hg concentration after chewing. In a fourth group Hg absorption by the oral mucosa was studied, Group 4, N=10. A 50% degree of absorption was found after 3 min. It is concluded that dental amalgam should be considered an unsuitable alloy resulting in long-term Hg exposure and that it is therefore toxicologically unsuitable as a dental filling material.”

“Biological monitoring of mercury in whole blood (B-Hg) or urine (U-Hg) can be used to assess exposure to mercury vapor if the kinetics and other sources of variation are taken into account. Its rapid rise postexposure makes B-Hg a good indicator of recent exposure peaks, while U-Hg (corrected for urinary flow rate) reflects average long-term exposure. However, high intraindividual variation sometimes requires the average of several U-Hg determinations. In the general population, methylmercury from fish and mercury from dental amalgam influence B-Hg and U-Hg, respectively, and must be considered if other exposures are being monitored. The quantitative relations between mercury in biological fluids and critical organs are poorly understood. Monitoring U-Hg is useful for assessing the risk of adverse effects and the need for preventive measures. At average U-Hg levels of about 50 micrograms.g creatinine-1 (28 nmol.mmol creatinine-1) the prevalence of symptoms and slight objective changes in the central nervous system and the excretion of certain urinary proteins are increased.”

“The influence of exposure to inorganic mercury on the immune system was examined in 36 workers occupationally exposed to mercury vapor, 14 individuals with skin hypersensitivity to mercury compounds, 21 subjects with health disturbances allegedly caused by dental amalgam fillings (“amalgam disease”), and 39 healthy referents. Concentrations of mercury in blood and urine and some parameters judged to mirror different effects on the immune system were determined. The latter included, white blood cell differential counts, serum immunoglobulins and autoantibodies, and in vitro production of the cytokines interleukin 1 (IL-1) and tumor necrosis factor alpha (TNF alpha). Virtually all of the immunologic parameters were within normal ranges and did not differ significantly between the groups. In the group sensitized to mercury, there was a reduction of the in vitro production of both TNF alpha and IL-1 compared with the reference group’s values. No significant correlations were noted between different mercury exposure estimates and the immunologic parameters.”

“Photoaffinity labeling with [alpha-32P]8N3GTP and [gamma-32P]8N3GTP was used to identify the guanine binding domain of the GTP regulatory site within glutamate dehydrogenase (GDH). Without photolysis, 8N3GTP mimicked the regulatory properties of GTP on GDH activity with 8N3GTP exhibiting a Ki of 5 microM while the Ki for GTP was about 0.6 microM. Under optimal photolabeling conditions saturation of photoinsertion with 1 microgram of GDH revealed an apparent Kd of 9 +/- 4 microM for [gamma-32P]8N3GTP. Photolabeling with this analog could be competitively inhibited with GTP with an apparent Kd of 12 +/- 2 microM. Other nucleotides such as ATP and NAD(P)H could not reduce the amount of photoinsertion as effectively as GTP. ADP could decrease photoinsertion, but only at much higher concentrations. NAD(P)+, GDP, AMP, and GMP had little effect on photoinsertion. Divalent cations Mg2+ and Ca2+ also reduced photoinsertion significantly while the monovalent K+ and Na+ ions had no effect. Aluminum(III)-chelate or iron(III)-chelate affinity chromatography and reversed-phase HPLC were used to purify photolabel-containing peptides generated with either trypsin or chymotrypsin. This identified a portion of the guanine binding domain within the GTP regulatory site as the region containing the sequence Ile439 to Tyr454. Photolabeling of this peptide was prevented 91% by the presence of 300 microM GTP during photolysis. Lys445 was not identified in sequence analyses of the photolabeled peptides. Also, trypsin was unable to cleave the photolabeled peptide at this site. These results suggest that Lys445 may be the residue modified by [alpha-32P]8N3GTP.”

The smoking habits of 119 subjects without silver/mercury dental fillings were compared to 115 subjects with amalgams. The amalgam group had 2.5-times more smokers per group than the non-amalgam group, which was highly significant. Because mercury decreases dopamine, serotonin, norepinephrine, and acetylcholine in the brain, and nicotine has just the opposite effect on these neurotransmitters, this may help explain why persons with dental amalgams smoke more than persons without amalgams.

A total of 142 women and 76 men with self-diagnosed oral galvanism who were referred from dentists and medical doctors for clinical evaluation during the last 2 yr are described from the perspective of general medicine. No case of clinically suspected mercury intoxication was found. Mean concentration of mercury in whole blood (B-Hg) was 17.3 nmol/l, and no value exceeded 50 nmol/l. Amalgam burden and B-Hg were not associated with clinical signs or symptoms except for a significantly lower mean value of B-Hg in patients with psychologic main symptoms than in those without (mean 15.4 vs. 18.1 nmol/l). It was possible to make one or several diagnoses in all 218 cases as reasonable alternatives to the concept of oral galvanism. Mental disorder was the main diagnosis in 93 cases (42.7%), including 41 cases of generalized anxiety disorder and 12 cases of panic disorder. A total of 87 patients (40%) did not work because of medical reasons or unemployment. Amalgam removal was recommended in a total of 65 cases (29%), mainly on psychologic indications, but in 22 cases because of oral conditions. The clinical conditions behind the concept of oral galvanism seem to be explicable in terms of general medicine, and no generalized toxic effect of amalgam fillings need be suspected.

The incidence of osteomyelitis of the jaws has decreased dramatically, except for a few subsets of individuals. This has been due, in no small part, to the availability of bacteriocidal antimicrobial therapy. The pathogenesis of osteomyelitis of the jaws is predominately due to odontogenic microorganisms rather than the classic skin contaminant, Staphylococcus. This causative relationship relegates the classification of osteomyelitis of the bimaxillary skeleton to predominately that of contiguous foci. These may be regionally progressive, secondary to microvascular compromise brought about by inherent flaws in regional anatomic calcified tissue vascular perfusion as well as by inflammatory metaplastic processes. Diagnosis is based on the presence of painful sequestra and suppurative areas of tooth-bearing jaw bone unresponsive to debridement and conservative therapy. This is usually accompanied by regional or systemic compromise of the immune response, microvascular decompensation, or both. Treatment of both acute and chronic forms of the disease, as outlined in Table 5, is successful if surgically supported. Sustained bacteriocidal antibiotic therapy is pertinent, especially in the face of potentially refractory virulent microorganisms and compromised regional vascular penetrance. The use of adjunctive hyperbaric oxygen therapy also may be included in the more refractory forms of osteomyelitis of the jaws to enhance the local and regional immune response of the jaws as well as to produce microvascular neoangiogenesis for reperfusion support. With resolution of infection, hard and soft tissue reconstruction may be necessary to augment the reparative process.

“Mercury and mercury compounds are widely used in modern society, but only sparse data are available on their carcinogenicity. Methylmercury chloride causes kidney tumors in male mice. Mercury chloride has shown some carcinogenic activity in male rats, but the evidence for female rats and male mice is equivocal. Other mercury compounds and metallic mercury have not been tested adequately in experimental animals. Epidemiologic data are available for chloralkali workers, dentists and dental nurses, and nuclear weapons workers, three groups occupationally exposed to low levels of mercury and its compounds, but those highly exposed in the past, such as miners, or populations which have suffered massive environmental exposure have not been adequately studied. However, the sparse epidemiologic data point toward the possibility of a risk of lung, kidney, and central nervous system tumors. Better data are needed on the carcinogenicity of mercury and mercury compounds in humans and experimental animals.”

“Dentistry has been portrayed as a high-risk profession in recent reports. A look at several areas of concern, however, shows that the field is no more hazardous than any other profession–and less than most.”

“Mercury levels (micrograms/mg dry weight) in dental plaque from amalgam and enamel surfaces in human subjects with amalgam restorations were (range, mean, SD) 0.5-1.31, 0.72, 0.34 and 0.01-0.54, 0.2, 0.19, respectively. The levels of mercury in plaque from amalgam surfaces were significantly higher than those from plaque on enamel (p < 0.001). No mercury was detected in plaque from subjects without amalgam restorations. The mean level of mercury in a 24-hour collection of plaque was 2 micrograms (median, 1.8 micrograms), an amount close to those calculated by other workers (1.2-1.7 micrograms) for the amount of mercury liberated in the mouth from amalgam restorations in 24 h. Freshly prepared amalgam liberated relatively large amounts of mercury into culture broth in the first 24 h of exposure; subsequently, the levels declined except in the presence of Streptococcus mutans. In vitro, biofilms of Streptococcus mutans facilitated the release of mercury from freshly prepared amalgam, in what appeared to be a cyclical fashion. Amalgam aged for two years did not release mercury, even when supporting the growth of an S. mutans biofilm. The resistance of aged amalgam was attributed to the presence of a passive tarnish layer. The mercury released by the biofilm had an effect on the composition of the biofilm. The biofilms on fresh amalgam had significantly lower levels of carbohydrate (p < 0.001-p < 0.01) and protein (p < 0.001-p < 0.02) than did biofilms on aged amalgam and on control stainless steel wires.”