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“In a survey of 640 human subjects, a subgroup of 356 persons without recent exposure to antibiotics demonstrated that those with a high prevalence of Hg resistance in their intestinal floras were significantly more likely to also have resistance to two or more antibiotics. This observation led us to consider the possibility that mercury released from amalgam (“silver”) dental restorations might be a selective agent for both mercury- and antibiotic-resistant bacteria in the oral and intestinal floras of primates. Resistances to mercury and to several antibiotics were examined in the oral and intestinal floras of six adult monkeys prior to the installation of amalgam fillings, during the time they were in place, and after replacement of the amalgam fillings with glass ionomer fillings (in four of the monkeys). The monkeys were fed an antibiotic-free diet, and fecal mercury concentrations were monitored. There was a statistically significant increase in the incidence of mercury-resistant bacteria during the 5 weeks following installation of the amalgam fillings and during the 5 weeks immediately following their replacement with glass ionomer fillings. These peaks in incidence of mercury-resistant bacteria correlated with peaks of Hg elimination (as high as 1 mM in the feces) immediately following amalgam placement and immediately after replacement of the amalgam fillings. Representative mercury-resistant isolates of three selected bacterial families (oral streptococci, members of the family Enterobacteriaceae, and enterococci) were also resistant to one or more antibiotics, including ampicillin, tetracycline, streptomycin, kanamycin, and chloramphenicol. While such mercury- and antibiotic-resistant isolates among the staphylococci, the enterococci, and members of the family Enterobacteriaceae have been described, this is the first report of mercury resistance in the oral streptococci. Many of the enterobacterial strains were able to transfer mercury and antibiotic resistances together to laboratory bacterial recipients, suggesting that the loci for these resistances are genetically linked. Our findings indicate that mercury released from amalgam fillings can cause an enrichment of mercury resistance plasmids in the normal bacterial floras of primates. Many of these plasmids also carry antibiotic resistance, implicating the exposure to mercury from dental amalgams in an increased incidence of multiple antibiotic resistance plasmids in the normal floras of nonmedicated subjects.”

“Future human exposure to inorganic mercury will probably lead to a few individuals occupationally exposed to high levels and much larger populations exposed to low or very low levels from dental fillings or from food items containing inorganic mercury; human exposure to methylmercury will be relatively low and depending on intake of marine food. Ideally, risk assessment is based on detailed knowledge of relations between external and internal dose, organ levels, and their relation to toxic symptoms. However, human data on these toxicokinetic parameters originate mainly from individuals or smaller populations accidentally exposed for shorter periods to relatively high mercury levels, but with unknown total body burden. Thus, assessment of risk associated with exposure to low levels of mercury will largely depend on data from animal experiments. Previous investigations of the toxicokinetics of mercuric compounds almost exclusively employed parenteral administration of relatively high doses of soluble mercuric salts. However, human exposure is primarily pulmonary or oral and at low doses. The present study validates an experimental model for investigating the toxicokinetics of orally administered mercuric chloride and methylmercuric chloride in mice. Major findings using this model are discussed in relation to previous knowledge. The toxicokinetics of inorganic mercury in mice depend on dose size, administration route, and sex, whereas the mouse strain used is less important. The “true absorption” of a single oral dose of HgCl2 was calculated to be about 20% at two different dose levels. Earlier studies that did not take into account the possible excretion of absorbed mercury and intestinal reabsorption during the experimental period report 7-10% intestinal uptake. The higher excretion rates observed after oral than after intraperitoneal administration of HgCl2 are most likely due to differences in disposition of systemically delivered and retained mercury. After methylmercury administration, mercury excretion followed first-order kinetics for 2 wk, independently of administration route, strain, or sex. However, during longer experimental periods, the increasing relative carcass retention (slower rate of excretion) caused the elimination to deviate from first-order kinetics. Extensive differences in the toxicokinetics of methylmercury with respect to excretion rates, organ deposition, and blood levels were observed between males and females.”(ABSTRACT TRUNCATED AT 400 WORDS)

“Neurobehavioural tests were performed by 98 dentists (mean age 32, range 24-49) exposed to elemental mercury vapour and 54 controls (mean age 34, range 23-50) with no history of occupational exposure to mercury. The dentists were exposed to an average personal air concentration time weighted average (TWA) of 0.014 (range 0.0007-0.042) mg/m3 for a mean period of 5.5 (range 0.7-24) years and had a mean blood mercury concentration of 9.8 (range 0.6-57) micrograms/l. In neurobehavioural tests measuring motor speed (finger tapping), visual scanning (trail making), visuomotor coordination and concentration (digit symbol), verbal memory (digit span, logical memory delayed recall), visual memory (visual reproduction, immediate and delayed recall), and visuomotor coordination speed (bender-gestalt time), the performance of the dentists was significantly worse than that of the controls. The dentists scored 3.9 to 38.9% (mean 13.9%) worse in these tests. In trail making, digit span, logical memory delayed recall, visual reproduction delayed recall, and bender-gestalt time test scores were more than 10% poorer. In each of the tests in which significant differences were found and in the block design time, the performance decreased as the exposed dose (product of the TWA of air mercury concentrations and the years of exposure) increased. These results raise the question as to whether the current threshold limit value of 0.050 mg/m3 (TWA) provides adequate protection against adverse effects of mercury.”

“The significance of contact allergy in patients with various oral symptoms was studied. Positive patch-test reactions to mercury compounds were found in 21/91 patients. Of these, 18 had lichenoid lesions in oral mucosa in close contact to amalgam fillings, and three patients with contact allergy had neither amalgam fillings in their teeth nor visible oral lesions. Amalgam replacement was carried out in 15/18 symptomatic patients. The fillings were replaced with gold in three cases, composite resin fillings in six, glass ionomer in three and both gold and composite materials in three cases. In 10 patients there was complete replacement and in five it was restricted to the fillings adjacent to the mucosal lesions. After a mean follow-up period of 3.2 years a complete cure was seen in seven patients, each of whom had had all their fillings changed. A marked improvement occurred in six patients, and there was no change in two.”

“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 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.”

“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.”

“Individual variation in susceptibility to chemical toxicity may be due to differences in toxicokinetic patterns or effect modification. Well-documented interspecies genetic differences in susceptibility to chemicals had lead to studies of such variation also within species. Epidemiological evidence now suggests that common variations, particularly in the P-450 enzymes, may play a major role in determining individual susceptibility to chemically-induced disease. Physiologic factors are involved in the particular susceptibility of the fetus, the newborn, and the old. Constitutional susceptibility is also affected by acquired conditions, including chronic disease, such as diabetes mellitus. Perhaps the most complex area relates to the increase in vulnerability caused by previous or contemporary exposure to other factors, thus eliciting, e.g., synergistic effects. Although amply demonstrated by experimental studies, epidemiological or clinical confirmation is generally lacking. One hypothesis suggests that a chemical exposure may affect the reserve capacity of the body, though not resulting in any immediate adverse effect. Subsequently, the body becomes unable to compensate for an additional stress, and toxicity then develops. Epidemiological approaches are available and need to be expanded. Research in this area has potential ethical implications which should be dealt with in an open, informed forum.”