Mercury

“Parts of the population are permanently exposed to low levels of Hg degrees and Hg(II) from dental amalgam. It was the aim (1) to investigate the internal exposure to amalgam-related mercury from the kinetics of inorganic Hg in plasma and erythrocytes after amalgam removal, and (2) to estimate the amalgam-related absorbed dose. Dietary coexposure was monitored by determination of blood organic-Hg. Postremoval steady-state Hg concentrations were measured for 18 months. Eighty-two patients had been randomized into three groups: (A) removal of the fillings; (B) removal and non-specific detoxification, and (C) a health promotion program without removal. After amalgam removal, inorganic Hg dropped rapidly in plasma and red cells, stabilizing at 27% of preremoval levels after 60 days. Concentrations of organic Hg in plasma remained unchanged, indicating no change in dietary uptake of organic Hg. The concentration of organic Hg in red cells of group A was in the early postremoval phase lower and in the late postremoval phase higher than the preremoval control (p<0.01 for low-high difference). A protracted increase in organic Hg was also found in red cells of group B after 60 days. Thus, the effect of removal on organic Hg levels in the combined group A+B was compared with the values of group C in a linear mixed effects (LME) model which showed a significant increase with time in group A+B (p=0.028). In all groups, time profiles of urinary concentration and excretion of total-Hg were very similar to those of inorganic-Hg levels in plasma. From extrapolations of blood and urine data it was estimated that the amalgam-related inhalation and ingestion of Hg species were within the limits proposed by WHO, ATSDR and EPA. The integrated daily Hg dose absorbed from amalgam was estimated up to 3 microg for an average number of fillings and at 7.4 for a high amalgam load.

CONCLUSIONS:

This is the first study on adult amalgam patients which continuously monitored the postremoval decline of inorganic Hg and the coexposure from dietary organic Hg in a randomized-controlled-trial design. The integrated daily dose of 7.4 microg absorbed from a high amalgam load is well below the tolerable dose of 30 microg (WHO, 1990). The unexpected postremoval increase in erythrocyte organic Hg, which is associated with the depletion of cellular inorganic Hg, might result from binding of organic Hg to cellular sites previously occupied by inorganic Hg.”

“We conducted a cross-sectional study in Sweden, Italy and Poland to assess environmental and occupational exposure to mercury from chloralkali (CA) plants and the potential association with biomarkers of early renal dysfunction. Questionnaire data and first-morning urine samples were collected from 757 eligible subjects. Urine samples were analysed for mercury corrected for creatinine (U-HgC), alpha-1-microglobulin (A1M), N-acetyl-beta-glucosaminidase (NAG) and albumin. Determinants of urinary mercury excretion were examined. Levels of kidney markers were compared in three U-HgC categories, and differences were tested taking age and other covariates into account. In the general population, the median U-HgC was higher in Italian (1.2 microg/gC) than in Polish (0.22 microg/gC) or Swedish (0.21 microg/gC) subjects, and no effect of living close to CA plants could be shown. Dental amalgam, chewing on amalgam, and fish consumption were positively associated with U-HgC. In subjects from the general population, no effects on the kidney markers could be detected, while in men, including workers occupationally exposed to mercury, U-HgC was positively associated with the kidney markers, especially with NAG, but to some extent also with A1M and albumin. Differences in urinary mercury and kidney markers in the general population between three studied countries could possibly be due to dietary factors, increased susceptibility to mercury at low selenium intake or co-exposure to other nephrotoxic metals.”

“Woods et al. (2007) reported on exposure to dental amalgam fillings and urinary mercury excretion in children. They stated that ‘urinary mercury concentrations are widely used as a measure of mercury exposure from dental amalgam fillings.’  We would like to point out some caveats about interpreting the results of mercury in urine.”

“Silver dental fillings contain mercury, and the U.S. government for the first time is warning that they may pose a safety concern for pregnant women and young children.”

“The aim of this study is to present data concerning hazardous waste management in the health area, with emphasis to the utilization of mercury in dentistry. The study was based on a bibliographic review regarding the use of mercury in dental fillings and its potential toxicological risks for patients and due to occupational exposure. The studies also take into consideration national and international recommendations on the use of mercury and its occupational exposure limits. The review of the literature reveals the potential toxic effects of mercury both on the environment and on human health. Given that the use of dental amalgam is still very frequent in dentistry, there is a need for safety regulations in order to minimize the risks posed by dental amalgam in dentistry proceedings based on technical guidelines for its use, discard and final disposal.”

“The aim of this study was to characterize a novel conjugative transposon Tn6009 composed of a Tn916 linked to a Staphylococcus aureus mer operon in representative Gram-positive and Gram-negative bacteria isolated in Nigeria and Portugal.

METHODS:

Eighty-three Gram-positive and 34 Gram-negative bacteria were screened for the presence of the Tn6009 using DNA-DNA hybridization, PCR, hybridization of PCR products, sequencing and mating experiments by established procedures.

RESULTS:

Forty-three oral and 23 urine Gram-negative and Gram-positive isolates carried the Tn6009. Sequencing was performed to verify the direct linkage between the mer resistance genes and the tet(M) gene. A Nigerian Klebsiella pneumoniae, isolated from a urinary tract infection patient, and one commensal isolate from each of the other Tn6009-positive genera, Serratia liquefaciens, Pseudomonas sp., Enterococcus sp. and Streptococcus sp. isolated from the oral and urine samples of healthy Portuguese children, were able to act as donors and conjugally transfer the Tn6009 to the Enterococcus faecalis JH2-2 recipient, resulting in tetracycline- and mercury-resistant E. faecalis transconjugants.

CONCLUSIONS:

This study reports a novel non-composite conjugative transposon Tn6009 containing a Tn916 element linked to an S. aureus mer operon carrying genes coding for inorganic mercury resistance (merA), an organic mercury resistance (merB), a regulatory protein (merR) and a mercury transporter (merT). This transposon was identified in 66 isolates from two Gram-positive and three Gram-negative genera and is the first transposon in the Tn916 family to carry the Gram-positive mer genes directly linked to the tet(M) gene.”

“When serial neurocognitive assessments are performed, 2 main factors are of importance: test-retest reliability and practice effects. With children, however, there is a third, developmental factor, which occurs as a result of maturation. Child tests recognize this factor through the provision of age-corrected scaled scores. Thus, a ready-made method for estimating the relative contribution of developmental versus practice effects is the comparison of raw (developmental and practice) and scaled (practice only) scores. Data from a pool of 507 Portuguese children enrolled in a study of dental amalgams (T. A. DeRouen, B. G. Leroux, et al., 2002; T. A. DeRouen, M. D. Martin, et al., 2006) showed that practice effects over a 5-year period varied on 8 neurocognitive tests. Simple regression equations are provided for calculating individual retest scores from initial test scores.”

In summary, there is currently a renaissance of interest in the contributions of the commensal microbiota to many aspects of health and disease from digestion to the development of the immune system and even to effects on the central nervous system (Yan and Polk, 2004; Kanauchi et al., 2005; Macdonald and Monteleone, 2005). One traditional area upon which this new perspective has yet to impinge is toxicology. The vigorous metabolism of all forms of Hg by bacterial members of the commensal microbiota is a rich example of what our small fellow travelers can marshal for their defense against the toxic agents to which we expose ourselves. Hopefully, toxicologists , especially those concerned with the widespread exposure to Hg from amalgam restorations, will begin to collaborate with microbiologists to take into account these bacterial processes (Fig. 1) in understanding the risks of amalgams and devising means to protect those with them and those having them removed.

“In conclusion, although Woods et al. (2007) used a well-structured experimental design, their conclusions are not accurate because of their handling of the experimental results and their use of basic toxicology terminology.”

“Thimerosal is an organic mercury compound that is widely used as a preservative in vaccines and other solution formulations. The use of thimerosal has caused concern about its ability to cause neurological abnormalities due to mercury accumulation during a normal schedule of childhood vaccinations. While the chemistry and the biological effects of methylmercury have been well-studied, those of thimerosal have not. Thimerosal reacted rapidly with cysteine, GSH, human serum albumin, and single-stranded DNA to form ethylmercury adducts that were detectable by mass spectrometry. These results indicated that thimerosal would be quickly metabolized in vivo because of its reactions with protein and nonprotein thiols. Thimerosal also potently inhibited the decatenation activity of DNA topoisomerase II alpha, likely through reaction with critical free cysteine thiol groups. Thimerosal, however, did not act as a topoisomerase II poison and the lack of cross-resistance with a K562 cell line with a decreased level of topoisomerase II alpha (K/VP.5 cells) suggested that inhibition of topoisomerase II alpha was not a significant mechanism for the inhibition of cell growth. Depletion of intracellular GSH with buthionine sulfoximine treatment greatly increased the K562 cell growth inhibitory effects of thimerosal, which showed that intracellular glutathione had a major role in protecting cells from thimerosal. Pretreatment of thimerosal with glutathione did not, however, change its K562 cell growth inhibitory effects, a result consistent with the rapid exchange of the ethylmercury adduct among various thiol-containing cellular reactants. Thimerosal-induced single and double strand breaks in K562 cells were consistent with a rapid induction of apoptosis. In conclusion, these studies have elucidated some of the chemistry and biological activities of the interaction of thimerosal with topoisomerase II alpha and protein and nonprotein thiols and with DNA.”