Mercury, Selenium, and Cadmium in Human Autopsy Samples from Idrija Residents and Mercury Mine Workers
ABSTRACT Total Hg and Se concentrations were determined in autopsy samples of retired Idrija mercury mine workers, Idrija residents living in a Hg-contami-nated environment, and a control group with no known Hg exposure from the environment. In selected samples we also checked the presence of MeHg. The highest Hg concentrations were found in endocrine glands and kidney cortex, regardless of the group. MeHg contributed only to a negligible degree to the total mercury concentrations in all analyzed samples. In the Hg-exposed groups the coaccumulation and retention of mercury and selenium was confirmed. Selenium coaccumulation with a Hg/Se molar ratio near 1 or higher was notable only in those tissue samples (thyroid, pituitary, kidney cortex, nucleus dentatus) where the mercury concentrations were >1 μg/g. After tissue separation of such samples the majority of these elements were found in the cell pellet. Because the general population is continuously exposed to Cd and possibly also to Pb from water, food, and/or air, in some samples the levels of these elements were also followed. In all examined control tissue samples the average values of Cd (kidney cortex, thyroid, hippocampus, cortex cerebellum, nucleus dentatus) and Pb (thyroid, hippocampus) exceeded the average values of Hg. Cd concentrations were the highest, particularly in kidney cortex and thyroids (μg/g), but no relationship between Cd and Se concentration was evident at the tissue level. Regarding the results in the control group, it is debatable which element is the more hazardous for the general population as concerns neurotoxicity.
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ABSTRACT: It is believed that mercury neurotoxicity is due to induction of oxidative stress [as determined by increased concentrations of malondialdehyde (MDA)], but we don't know if to have higher concentrations of MDA involves to have more neurological disorders. Objective: To establish association between urinary concentrations of MDA and the severity of neurological abnormalities in people exposed to mercury. Materials and methods: A cross-sectional study was done. Inclusion criteria: men between 18 and 60 years with occupational exposure to metallic mercury. The sample was taken from a database of 110 patients exposed to mercury. Information was gathered from medical records with emphasis on neurologic outcome, from the mercury concentration in urine of 24 hours and from urinary MDA analysis. For statistical analysis, nonparametric tests were used for comparisons between concentrations of MDA among those with neurological disorders vs. those without disorders and to evaluate differences in the concentrations of this substance according to the severity of these alterations; it was performed correlation analysis between urinary concentrations of MDA and urinary concentrations of mercury. Results: The concentrations of MDA in patients exposed to mercury with neurological abnormalities were not different from those without abnormalities. MDA concentrations neither were associated with the severity of clinical findings. There was no correlation between MDA and urinary mercury concentrations. Conclusion: It will be necessary to search biological samples other than urine that could reflect what occurs in CNS or look for other pathophysiological causes to explain the presence of clinical findings in these patients.Revista Ciencias de la Salud 03/2012; 10:17-28.
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ABSTRACT: Contamination of the food chain by mercury is a major concern of Public Health of our day. Kidney and nervous system are the major targets of mercury toxicity in mammals. We show here that the detailed subcellular in vivo topography of microparticles of mercury in tissues can be achieved by scanning electron microscopy (SEM) coupled with X-ray elemental microanalysis (XRM). SEM-XRM offered the fine topography of mercury in the kidney of BALB/c mice that were submitted to an intraperitoneal lethal injection of mercuric chloride (HgCl2). All of the renal mercury was seen inside blood vessels located in both cortex and medulla of the mouse kidney. This blood-born mercury was organised in spheroid particles of less than 50 nm in diameter (31.4±14.1 nm). They were seen attached either to aggregates of plasma proteins or to the surface of blood cells. No evidence of internalisation of mercury by blood, endothelial or kidney cells was found. The average kidney density of mercury microspheres was 1920±1320 particles per mmsupb2bsup. We propose SEM-XRM as an elective approach to further investigations, at the subcellular level, on the quantitative dynamics of mercury particles in the tissues.BioMetals 01/2003; 16(4). · 3.28 Impact Factor
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ABSTRACT: Reports from human case studies indicate a half-life for inorganic mercury in the brain of years - contradicting older radioisotope studies that estimated half-lives in the order of weeks to months in duration. This study systematically reviews available evidence on the retention time of inorganic mercury in humans and primates to better understand this conflicting evidence. A broad search strategy was used to capture 16,539 abstracts on the Pubmed database. Abstracts were screened to include only study types containing relevant information. 131 studies of interest were identified. Only 1 primate study made a numeric estimate for the half-life of inorganic mercury (227 - 540 days). Eighteen human mercury poisoning cases were followed up long term including autopsy. Brain inorganic mercury concentrations at death were consistent with a half-life of several years or longer. 5 radionucleotide studies were found, one of which estimated head half-life (21 days). This estimate has sometimes been misinterpreted to be equivalent to brain half-life - which ignores several confounding factors including limited radioactive half-life and radioactive decay from surrounding tissues including circulating blood. No autopsy cohort study estimated a half-life for inorganic mercury, although some noted bioaccumulation of brain mercury with age. Modeling studies provided some extreme estimates (69 days vs 22 years). Estimates from modeling studies appear sensitive to model assumptions, however predications based on a long half-life (27.4 years) are consistent with autopsy findings. In summary, shorter estimates of half-life are not supported by evidence from animal studies, human case studies, or modeling studies based on appropriate assumptions. Evidence from such studies point to a half-life of inorganic mercury in human brains of several years to several decades. This finding carries important implications for pharmcokinetic modeling of mercury and potentially for the regulatory toxicology of mercury.Toxicology and Applied Pharmacology 12/2013; · 3.98 Impact Factor