This review covers the toxicology of mercury and its compounds. Special attention is paid to those forms of mercury of current public health concern. Human exposure to the vapor of metallic mercury dates back to antiquity but continues today in occupational settings and from dental amalgam. Health risks from methylmercury in edible tissues of fish have been the subject of several large epidemiological investigations and continue to be the subject of intense debate. Ethylmercury in the form of a preservative, thimerosal, added to certain vaccines, is the most recent form of mercury that has become a public health concern. The review leads to general discussion of evolutionary aspects of mercury, protective and toxic mechanisms, and ends on a note that mercury is still an "element of mystery."

The Toxicology of Mercury and Its Chemical Compounds

Food systems need to produce enough of the essential trace element Se to provide regular adult intakes of at least 40 microg/d to support the maximal expression of the Se enzymes, and perhaps as much as 300 microg/d to reduce risks of cancer. Deprivation of Se is associated with impairments in antioxidant protection, redox regulation and energy production as consequences of suboptimal expression of one or more of the Se-containing enzymes. These impairments may not cause deficiency signs in the classical sense, but instead contribute to health problems caused by physiological and environmental oxidative stresses and infections. At the same time, supranutritional intakes of Se, i.e. intakes greater than those required for selenocysteine enzyme expression, appear to reduce cancer risk. The lower, nutritional, level is greater than the typical intakes of many people in several parts of the world, and few populations have intakes approaching the latter, supranutritional, level. Accordingly, low Se status is likely to contribute to morbidity and mortality due to infectious as well as chronic diseases, and increasing Se intakes in all parts of the world can be expected to reduce cancer rates.

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Selenium in global food systems.

The three modern "faces" of mercury are our perceptions of risk from the exposure of billions of people to methyl mercury in fish, mercury vapor from amalgam tooth fillings, and ethyl mercury in the form of thimerosal added as an antiseptic to widely used vaccines. In this article I review human exposure to and the toxicology of each of these three species of mercury. Mechanisms of action are discussed where possible. Key gaps in our current knowledge are identified from the points of view both of risk assessment and of mechanisms of action.

The three modern faces of mercury.

Note: This article was originally published with an incorrect version of the Acknowledgments, which appeared on p. 218 of the print version. The correct version of the Acknowledgments appeared on pp. 1–2. The corrected article is available below.

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Human Health Risk Assessment for Aluminium, Aluminium Oxide, and Aluminium Hydroxide

Literature regarding the biochemistry of aluminum and eight similar ions is reviewed. Close and hitherto unknown similarities were found. A hypothetical model is presented for the metabolism, based on documented direct observations of Al3+ and analogies from other ions. Main characteristics are low intestinal absorption, rapid urinary excretion, and slow tissue uptake, mostly in skeleton and reticuloendothelial cells. Intracellular Al3+ is probably first confined in the lysosomes but then slowly accumulates in the cell nucleus and chromatin. Large, long-lived cells, e.g., neurons, may be the most liable to this accumulation. In heterochromatin, Al3+ levels can be found comparable to those used in leather tannage. It is proposed that an accumulation may take place at a subcellular level without any significant increase in the corresponding tissue concentration. The possible effects of this accumulation are discussed. As Al3+ is neurotoxic, the brain metabolism is most interesting. The normal and the lethally toxic brain levels of Al3+ are well documented and differ only by a factor of 3-10. The normal brain uptake of Al3+ is estimated from data on intestinal uptake of Al3+ and brain uptake of radionuclides of similar ions administered intravenously. The uptake is very slow, 1 mg in 36 years, and is consistent with an assumption that Al3+ taken up by the brain cannot be eliminated and is therefore accumulated. The possibility that Al3+ may cause or contribute to some specific diseases, most of them related to aging, is discussed with the proposed metabolic picture in mind.

Metabolism and possible health effects of aluminum.

Serum selenium as well as serum zinc, copper, magnesium, calcium and manganese were investigated in a control group of adult males and in 11 groups of patients in various disease states Not only the change of each trace element but also the possible association between elements was studied in the various groups All patients were fasting when sampled and studied only after the acute phase of the disease was corrected Trace metal determinations were performed by atomic absorption spectrophometry (Mg, Ca, Cu, Zn) and by neutron activation analysis (Se, Mn) All patients showed low serum zinc when compared to controls Cirrhotic patients had a low serum selenium level as well as low calcium, magnesium and zinc Emphysemia and cancer patients had an elevated serum copper concentration while copper and manganese levels were elevated in congestive heart failure, infection and pschoses To our knowledge this is the first time low serum selenium values have been demonstrated to be associated with the low serum zinc, calcium and magnesium levels found in cirrhotic patients

Serum levels of selenium, calcium, copper magnesium, manganese and zinc in various human diseases.

Evidence of aluminum absorption from the gastrointestinal tract and bone deposition by aluminum carbonate ingestion with normal renal function.

Optimized procedures have been developed for the determination of total selenium, trimethylselenonium (TMSe) ion, and selenite (SeO/sub 3//sup 2/minus//) ion in urine and serum and for total selenoamino acids in urine by anion exchange chromatography and molecular neutron activation analysis. For urine samples containing greater than 40 ng of Se/mL, determination for TMSe and SeO/sub 3//sup 2/minus// ion can be performed. For urine samples containing nondetectable SeO/sub 3//sup 2/minus// ion whose concentration differential between the total selenium and TMSe is greater than or equal to 40 ng of Se/mL, total selenoamino acids can be determined by derivatization and anion exchange chromatography. For urine samples whose differential between total selenium and TMSe + SeO/sub 3//sup 2 -/ is greater than 80 ng of Se/mL, a precipitation/coprecipitation technique employing Ba(NO/sub 3/)/sub 2/ and (NH/sub 4/)/sub 2/SO/sub 4/ must be performed prior to the subsequent steps. The procedures were evaluated for over 100 specimens from normal and diseased subjects.

Determination of selenium metabolites in biological fluids using instrumental and molecular neutron activation analysis.

Determination of trace aluminum in urine by neutron activation analysis.

A simple and rapid method for the determination of trace aluminum in urine and bone using atomic absorption with graphite furnace atomization is described. Direct atomization of raw urine and nitric acid dissolved bone resulted in aluminum values that were systematically higher for bone and variable for urine, as compared to a neutron activation analysis procedure. This was the result of calcium and phosphate interference of the aluminum signal. The optimum procedure involves digestion of bone or urine at 60/sup 0/C with concentrated nitric acid and a solution containing CaCl/sub 2/ and K/sub 2/HPO/sub 4/ to negate the effects of varying calcium and phosphate contents in the samples. The residue was brought up to volume and injected into the graphite furnace. Detection limits (2 sigma) of 20 ppB are reported. The precision of the method is 3 percent RSD when measured at the 600-pg analytical level.

Comparison between neutron activation analysis and graphite furnace atomic absorption spectrometry for trace aluminum determination in biological materials.

A. J. Blotcky

Papers

Serum levels of selenium, calcium, copper magnesium, manganese and zinc in various human diseases.

Evidence of aluminum absorption from the gastrointestinal tract and bone deposition by aluminum carbonate ingestion with normal renal function.

Determination of selenium metabolites in biological fluids using instrumental and molecular neutron activation analysis.

Determination of trace aluminum in urine by neutron activation analysis.

Comparison between neutron activation analysis and graphite furnace atomic absorption spectrometry for trace aluminum determination in biological materials.