Speciation of Inorganic Mercury Compounds in Solid Samples via Thermo‐desorption Experiments

2021 ◽  
Vol 44 (4) ◽  
pp. 788-796
Author(s):  
Isabelle Klöfer ◽  
Margot Bittig ◽  
Dieter Bathen
Keyword(s):  
Inorganic Mercury ◽  
Solid Samples ◽  
Mercury Compounds

scholarly journals Mercury and inorganic mercury compounds [MAK Value Documentations, 2011]

2016 ◽  
pp. 91-138 ◽  
Author(s):  
V. Meischner ◽  
G. Schriever-Schwemmer ◽  
U. Reuter ◽  
H. Greim ◽  
A. Hartwig ◽  
...  
Keyword(s):  
Inorganic Mercury ◽  
Mercury Compounds ◽  
Mak Value

I. Environmental Contamination and Biochemical Relationships

1975 ◽  
Vol 38 (5) ◽  
pp. 285-300 ◽  
Author(s):  
A. G. HUGUNIN ◽  
R. L. BRADLEY
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Methyl Mercury ◽  
Sea Water ◽  
Inorganic Mercury ◽  
Whole Body ◽  
Irreversible Damage ◽  
Mercury Compounds ◽  
The Central Nervous System ◽  
Pass Through

Mercury is naturally concentrated in geographical belts, but geological cycling has distributed the element in all strata of the earth. Natural concentrations of mercury are approximately 100 ppb in soil, 0.06 ppb in fresh water, 0.01–0.30 ppb in sea water, and 0.003–0.009 μg/m3 in air. Concentrations vary, being highest near mineral deposits. The concentration of mercury in some areas has been significantly increased by human carelessness. An epidemic among Japanese fishing families, death of Swedish wildlife, and discovery of elevated mercury levels in American fish focused attention on this problem. The discovery that certain species are capable of methylating inorganic mercury indicates pollution with any chemical form of mercury is dangerous. Alkylmercurials are the most dangerous form of mercury in the environment. Alkylmercurials are absorbed from the gastrointestinal tract, diffuse across the blood-brain carrier, and pass through the placental membrane in significantly higher proportions than other mercury compounds. The whole body half-life of methyl mercury in humans is 76 ± 3 days compared to half-lives of 37 ± 3 days for men and 48 ± 5 days for women observed for mercuric salts. Not readily broken down, sufficient concentrations of methyl mercury can cause irreversible damage to the central nervous system. Renal damage usually results from high levels of aryl- or alkoxyalkylmercurials and inorganic mercury; however, vapors of elemented mercury can damage the central nervous system. Organic mercury compounds cause chromosome changes, but the medical implications resulting from levels of mercury in food are unknown. The concentration of mercury in red blood cells and hair is indicative of the exposure to alkylmercurials. On a group basis, blood and urine concentrations of mercury may corrrelate with recent exposure to mercury.

scholarly journals Developmental toxicity from exposure to various forms of mercury compounds in medaka fish (Oryzias latipes) embryos

2016 ◽  
Author(s):  
Wu Dong ◽  
Jie Liu ◽  
Lixin Wei ◽  
Yang Jingfeng ◽  
Melissa Chernick ◽  
...  
Keyword(s):  
Developmental Toxicity ◽  
Inorganic Mercury ◽  
Oryzias Latipes ◽  
Heme Oxygenase 1 ◽  
Organic Form ◽  
Traditional Medicines ◽  
Mercury Compounds ◽  
Pericardial Edema ◽  
Eye Pigmentation ◽  
Swim Bladder Inflation

This study examined developmental toxicity of different mercury compounds, including some used in traditional medicines. Medaka (Oryzias latipes) embryos were exposed to 0.001-10 μM concentrations of MeHg, HgCl2, α-HgS (Zhu Sha), and β-HgS (Zuotai) from stage 10 (6-7 hpf) to 10 days post fertilization (dpf). Of the forms of mercury in this study, the organic form (MeHg) proved the most toxic followed by inorganic mercury (HgCl2), both producing embryo developmental toxicity. Altered phenotypes included pericardial edema with elongated or tube heart, reduction of eye pigmentation, and failure of swim bladder inflation. Both α-HgS and β-HgS were less toxic than MeHg and HgCl2. Total RNA was extracted from survivors 3 days after exposure to MeHg (0.1 μM), HgCl2 (1 μM), α-HgS (10 μM), or β-HgS (10 μM) to examine toxicity-related gene expression. MeHg and HgCl2 markedly induced metallothionein (MT) and heme oxygenase-1 (Ho-1), while α-HgS and β-HgS failed to induce either gene. Chemical forms of mercury compounds proved to be a major determinant in their developmental toxicity.

scholarly journals The Effects of Chronic Ingestion of Mercuric Chloride on Fertility and Testosterone Levels in Male Sprague Dawley Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
John C. Heath ◽  
Y. Abdelmageed ◽  
Tim D. Braden ◽  
Hari O. Goyal
Keyword(s):  
Mercuric Chloride ◽  
Inorganic Mercury ◽  
Male Reproduction ◽  
Male Rats ◽  
Male Rat ◽  
Sprague Dawley ◽  
Testosterone Levels ◽  
Mercury Compounds ◽  
Sprague Dawley Rats ◽  
Sperm Counts

Although male infertility is well researched, the effects of inorganic mercury on male reproduction and fertility are less well known. Studies pertaining to mercury and male fertility identified reduced concentration of testosterone in the serum of male workers, a toxic influence on fertility of organic mercury compounds within concentrations at the workplace, and increased days to pregnancy. We evaluated the effect of chronic mercuric chloride (HgCl2) exposure in male rats on reproductive endpoints. Thirty-day old male Sprague Dawley rats (n=31) were exposed to 0.0, 1.0, or 2.0 mg/kg/day of HgCl2via gavage. After 60 days exposure, they were housed with nonexposed females for 21 days. A survivor analysis revealed the exposed animals took longer to impregnate the females and had a lower rate of impregnation. Further statistical analysis revealed a lower correlation between testicular testosterone levels and days to impregnate, and also lower sperm counts in the epididymis head and body of the exposed males. The results indicate that HgCl2exposure had significant adverse effects on male rat reproduction endpoints including fertility at a dose that was not clinically toxic.

scholarly journals On the methylation of inorganic mercury and the decomposition of organo-mercury compounds - a review.

1976 ◽  
Vol 24 (2) ◽  
pp. 79-97 ◽  
Author(s):  
T.M. Lexmond ◽  
F.A.M. de Haan ◽  
M.J. Frissel
Keyword(s):  
Inorganic Mercury ◽  
Anaerobic Conditions ◽  
Mercury Compounds ◽  
Laboratory Cultures ◽  
Microbial Methylation ◽  
Aerobic And Anaerobic ◽  
Aerobic And Anaerobic Conditions ◽  
Organic Mercurials

Mercury is subjected in nature to a number of turnover reactions. The conversion of inorganic to organic forms is governed by microbial methylation which may proceed at aerobic and anaerobic conditions. Decomposition of organic mercurials may follow a chemical or a microbial pathway. The reactions and mechanisms occurring in soils, water, sediments and laboratory cultures are described. 53 references. (Abstract retrieved from CAB Abstracts by CABI’s permission)

scholarly journals Developmental toxicity from exposure to various forms of mercury compounds in medaka fish (Oryzias latipes) embryos

2016 ◽  
Author(s):  
Wu Dong ◽  
Jie Liu ◽  
Lixin Wei ◽  
Yang Jingfeng ◽  
Melissa Chernick ◽  
...  
Keyword(s):  
Developmental Toxicity ◽  
Inorganic Mercury ◽  
Oryzias Latipes ◽  
Heme Oxygenase 1 ◽  
Organic Form ◽  
Traditional Medicines ◽  
Mercury Compounds ◽  
Pericardial Edema ◽  
Eye Pigmentation ◽  
Swim Bladder Inflation

This study examined developmental toxicity of different mercury compounds, including some used in traditional medicines. Medaka (Oryzias latipes) embryos were exposed to 0.001-10 μM concentrations of MeHg, HgCl2, α-HgS (Zhu Sha), and β-HgS (Zuotai) from stage 10 (6-7 hpf) to 10 days post fertilization (dpf). Of the forms of mercury in this study, the organic form (MeHg) proved the most toxic followed by inorganic mercury (HgCl2), both producing embryo developmental toxicity. Altered phenotypes included pericardial edema with elongated or tube heart, reduction of eye pigmentation, and failure of swim bladder inflation. Both α-HgS and β-HgS were less toxic than MeHg and HgCl2. Total RNA was extracted from survivors 3 days after exposure to MeHg (0.1 μM), HgCl2 (1 μM), α-HgS (10 μM), or β-HgS (10 μM) to examine toxicity-related gene expression. MeHg and HgCl2 markedly induced metallothionein (MT) and heme oxygenase-1 (Ho-1), while α-HgS and β-HgS failed to induce either gene. Chemical forms of mercury compounds proved to be a major determinant in their developmental toxicity.

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