Mercury, lead and lead isotope ratios in the teeth of moose (Alces alces) from Isle Royale, U.S. Upper Midwest, from 1952 to 2002.

Assessing the effect of recent reductions in atmospheric pollution on metal concentrations in wildlife in North America has been difficult because of the sparse availability of historical samples with which to establish a "pre-regulation" baseline, and because many ecosystems may be affected by local point sources which could obscure broader-scale trends. Here we report a recent 50 yr annual record of Hg, Pb and Pb isotope ratios in the teeth of a resident population of moose (Alces alces) in Isle Royale National Park, a relatively remote island in Lake Superior, Michigan, USA. During the early 1980s, concentrations of tooth Hg abruptly declined by approximately 65% compared to the previous 30 years (p<0.001), similar to a previous study of Hg in herring gull eggs in the Great Lakes region. Lead declined at the same time, and by 2002 Pb in adult moose teeth was approximately 80% lower than it had been prior to the early 1980s (p<0.001). These trends were unaffected by normalization against the geogenic elements La and Sr, which indicates that the trends in Hg and Pb had an anthropogenic cause. Temporal patterns of Pb isotope ratios suggested that the primary sources of Pb at different times in the moose were combustion of U.S. coal and leaded gasoline. Reductions in emissions from coal combustion might explain the co-incident reductions of Hg and Pb in Isle Royale moose, with elimination of alkyl Pb additives also playing a role in the continued tooth Pb reductions after 1983.

Does selenium deficiency unmask mercury toxicity in motor neurons?

OBJECTIVE: Inorganic mercury enters in particular motor neurons and has been implicated in motor neuron diseases. One way that cells protect themselves from mercury toxicity is via selenium, so we sought to determine whether the motor neurons of mice on a low selenium diet would be more susceptible to mercury toxicity. METHODS: Recently weaned mouse pups were placed on diets containing either low, normal or high levels of selenium. Twenty days later, half were exposed to mercury vapor. Ninety days after exposure, their spinal motor neurons and phrenic motor axons were examined histologically. Mercury in the spinal cord was sought using autometallography. RESULTS: Neither low nor high selenium diets combined with mercury vapor had any clinical effect on the mice. Mercury was seen within the spinal motor neurons of all exposed mice. Spinal motor neurons and phrenic motor axons however appeared normal in morphology and size across the groups. CONCLUSION: Diets low or high in selenium did not damage motor neurons with or without mercury. This suggests that changes in the selenium environment are unlikely to precipitate mercury toxicity in motor neurons.

Blood mercury following DMPS administration to subjects with and without dental amalgam.

The use of DMPS as a diagnostic tool in patients with symptoms allegedly caused by mercury from dental amalgam fillings is disputed. We have previously shown that the mercury concentrations in urine cannot be used in such a way. In the present study, we wished to evaluate the effect on blood mercury levels (B-Hg) following intravenously injected DMPS in four groups of subjects: 19 controls without amalgam experience; 21 healthy controls with amalgam fillings; 20 patients with self-reported symptoms from existing dental amalgams; and 20 patients who had removed amalgam fillings. A single dose of DMPS (2 mg/kg) was injected. Blood samples were collected prior to the injection and after 15, 30, 120 min, and after 24 h, and mercury was analyzed by cold vapor atomic absorption spectrophotometry. All groups showed an initial drop of 24 to 30% in the blood levels, approaching baseline values (2.5-5.5 microg/l) after 2 h. The subjects with no amalgam experience had the lowest mercury values. There was no significant difference between the three groups with such experience. There were no significant differences between the two groups with amalgam fillings present. Patients with symptoms allegedly caused by amalgam were not different from the control groups. There were indications that part of the urinary mercury excreted during the first 30 min originated from blood.

Copper, zinc, and selenium in human blood and urine after injection of sodium 2,3-dimercaptopropane-1-sulfonate: a study on subjects with dental amalgam.

This study investigated the effects of a single dose of intravenously administered sodium 2,3-dimercaptopropane-1-sulfonate (DMPS) on the essential elements copper, zinc, and selenium in human blood and urine. The possible role of dental amalgam was also addressed. Eighty individuals, divided in four groups according to the presence or absence of dental amalgam fillings and symptoms self-related to such fillings, were given DMPS (2 mg/kg body wt) and 500 mL Ringer's acetate intravenously. Urine and blood were collected prior to the injection, and thereafter at intervals over a 24-h period. Cu, Zn, and Se concentrations were determined by atomic absorption spectrometry methods. A statistically significant increase in the concentrations of Cu and Zn in urine was observed 30 and 120 min after the DMPS injection compared to the preinjection concentrations. The concentrations of Se were not affected. The cumulated excretion over 24 h after DMPS injection constitutes only from 0.1% to 0.7% of the body content of these elements. There was no effect of different amalgam statuses on Cu and Zn excretion. We found a temporary decrease (4-7%) in the concentrations of Cu, Zn, and Se in blood 15 and 30 min after DMPS, but this seems to be the result of dilution factors. Administration of a single dose of DMPS does not affect the body stores of the essential elements Cu, Zn, and Se.

Dental amalgam affects urinary selenium excretion.

Selenium may have a protective effect against mercury toxicity. The aim of the present study was to investigate if selenium excretion in urine was affected in persons with dental amalgam fillings. The reason for this study is that dental amalgam is the most important source of inorganic mercury exposure in the general population, although the potential toxic effects of this exposure remain a subject for debate. The chelating agent 2,3 dimercaptopropane-1-sulfonate (DMPS) was injected intravenously (2 mg/kg) to provoke metal excretion. Urine samples were subsequently collected at intervals over a 24-h period. Selenium concentration was determined by hydride-generation atomic absorption spectrometry. The study was comprised of 20 persons who claimed symptoms from dental amalgam and 21 healthy persons with amalgam fillings. There were two control groups without amalgam. One control group had amalgam replaced because of concern about illness resulting from mercury release (n = 20), whereas the other control group never had amalgam (n = 19). Individuals with amalgam excreted less selenium (36.4 microg, median value) over 24 hours than those without amalgam (47.5 microg) (p = 0.016). There was no difference in selenium excretion between groups with (42.4 microg) and without (39.4 microg) amalgam-related symptoms (p = 0.15). The findings indicate that individuals exposed to low levels of elemental mercury from dental amalgam excrete less selenium to urine than unexposed individuals.