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: Measuring toxic metal body burden is particularly important in autism spectrum disorder (ASD) because evidence indicates that children with ASD have a greater susceptibility to heavy-metal intoxication than typically developing children. The more traditional laboratory tests used to measure toxic metal levels in ASD provide a snapshot of current exposure but do not necessarily provide a measure of tissue body burden. A more recent approach is to use urinary porphyrins which provide an indirect measure of toxic metal body burden. Urinary porphyrins are not a direct measure of toxic metals in the urine but a measure of tissue body burden by the level of disruption of the heme synthesis pathway caused by the presence of toxic metals in the tissues. Recent evidence suggests that the levels of mercury-associated porphyrins are different in children with ASD as compared to controls, with significantly increased levels of pentacarboxyporphyrin (5cxP), precoproporphyrins (prcP), and coproporphyrins (cP). In addition, there is a significant relationship between the severity of the child’s autism symptoms and the elevation of mercury-associated urinary porphyrins (i.e., the higher the mercury-associated porphyrins, the more severely affected the child). The mercury-associated porphyrins can be lowered with chelation therapy, and porphyrin profile testing can be used in clinical medicine in the targeted treatment of heavy-metal toxicity.01/2014: pages 1333-1348; , ISBN: 978-1-4614-4787-0
- 04/2013, Degree: PhD, Supervisor: Jayme R Meliker
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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