Chemical Form Of Mercury Research Articles

What does scientometry tell us about mercury toxicology and its biological impairments?

Mercury is a toxic pollutant that poses risks to both human and environmental health, making it a pressing public health concern. This study aimed to summarize the knowledge on mercury toxicology and the biological impairments caused by exposure to mercury in experimental studies and/or diagnosis in humans. The research was conducted on the main collection of Web of Science, employing as a methodological tool a bibliometric analysis. The selected articles were analyzed, and extracted data such as publication year, journal, author, title, number of citations, corresponding author's country, keywords, and the knowledge mapping was performed about the type of study, chemical form of mercury, exposure period, origin of exposure, tissue/fluid of exposure measurement, mercury concentration, evaluation period (age), mercury effect, model experiments, dose, exposure pathway, and time of exposure. The selected articles were published between 1965 and 2021, with Clarkson TW being the most cited author who has also published the most articles. A total of 38% of the publications were from the USA. These studies assessed the prenatal and postnatal effects of mercury, emphasizing the impact of methylmercury on neurodevelopment, including motor and cognitive evaluations, the association between mercury and autism, and an evaluation of its protective effects against mercury toxicity. In observational studies, the blood, umbilical cord, and hair were the most frequently used for measuring mercury levels. Our data analysis reveals that mercury neurotoxicology has been extensively explored, but the association among the outcomes evaluated in experimental studies has yet to be strengthened. Providing metric evidence on what is unexplored allows for new studies that may help governmental and non-governmental organizations develop guidelines and policies.

An overview of the complications of acute and chronic mercury exposures. Past, present and future

Mercury is a chemical element that has been known since prehistoric times and has been used over time as a component of paints, in the treatment of various diseases, and later in various industrial compounds. Mercury enters the body transcutaneously, by inhaling or by ingesting food contaminated with mercury. The most common cause of mercury poisoning is eating seafood, but people can get mercury poisoning from industrial processing, thermometers, dental work, and old paints. The most vulnerable are people at occupational risk due to chronic exposure, as well as fetuses in the intrauterine period. Mercury poisoning produces extremely serious effects on the nervous, renal, and gastrointestinal systems. The nature and extent of mercury poisoning depend on factors such as the route of exposure, the rate of exposure, the distribution and biotransformation of mercury in the body, the chemical form of mercury or the mercury compound. Both mercury in the blood and the urine should not exceed 10 μg/L. The critical values of mercury in the blood are >150 μg/L and the lethal ones exceed 800 μg/L. New diagnostic methods allow the rapid and accurate identification of the concentration of mercury in biological products. Treatment is based on the use of chelating agents. However, the prognosis of mercury poisoning is extremely variable, due to the potentially irreversible nature of the lesions.

Mercury and its effect on human health: a review of the literature

Mercury in human body is a free radical that can cause depletion of glutathione (GSH) and hoarding of H2O2, leading to shorten the age of erythrocytes and cause haemolysis. Approximately 90% organic form can be absorbed by the intestinal wall, while inorganic forms are only about 10%. The initial form can also penetrate the blood and placental barrier so that it can cause teratogenic effects and nervous disorders. The effects of mercury toxicity on humans depend on the chemical form of mercury, dosage, age of people exposed, length of exposure, entry into the body, fish diet and consumption of seafood. Mercury is able to bind sulfidril proteins in cells resulting in nonspecific cell injury or even cell death, cessation of microtubule formation, enzyme inhibition, oxidative stress, cessation of protein and DNA synthesis, and autoimmune responses. Classified into a very toxic metal, mercury can trigger the formation of ROS, hydrogen peroxide, lipid peroxidation, hydroxyl radicals that can inhibit enzymes, cell damage, DNA damage, protein structure damage, disruption on the body's antioxidant metabolism, especially superoxide dismutase (SOD) and glutathione peroxidase (GPx). Mercury exposure is associated with an increased risk of hypertension, myocardial infarction, coronary dysfunction, and atherosclerosis. This review is clearly in line to investigate the effect of mercury on human health based on previous research, article and other literature sources.

A study on chemical form of mercury in flowback fluids after well workover

A study on chemical form of mercury in flowback fluids after well workover

Mercury offloaded in Northern elephant seal hair affects coastal seawater surrounding rookery

Methylmercury (MeHg) is a potent neurotoxin that is biomagnified approximately 1-10 million-fold in aquatic carnivores such as the Northern elephant seal (Mirounga angustirostris), whose excreta and molted pelage, in turn, constitute a source of environmental MeHg contamination at the base of marine food chains. The potential for this top-down contamination is greatest in coastal areas with productive marine ecosystems that provide ideal habitats for large marine mammal colonies that can number in the thousands. This recycling of MeHg was evidenced by comparing total mercury (HgT) and MeHg concentrations in seawater, and HgT in molted pelage of M. angustirostris, at the Año Nuevo State Reserve pinniped rookery with concentrations at neighboring coastal sites in Central California. Seawater MeHg concentrations around the rookery (average = 2.5 pM) were markedly higher than those at the comparison coastal sites (average = 0.30 pM), and were as high as 9.5 pM during the M. angustirostris molting season. As a consequence, excreta and molts from this marine mammal colony, and presumably other marine predator populations, constitute a major source of MeHg at the base of the local marine food chain.

Differential Effects of Organic and Inorganic Mercury on Phenotypically Variant Breast Cancer Cell Lines

Mercury remains a major environmental contaminant world-wide. Increasing evidence supports heavy metals as estrogenic agents (metalloestrogens), yet the impact of organic and inorganic mercury is unclear. The intent of this study was to increase understanding of mercury compounds as tumor causing agents and their modes of action. Changes in cellular viability, proliferation, and apoptosis after exposure to inorganic (HgCl2) and organic (CH3Hg+) mercury, were examined using a control human breast epithelial cell line (MCF-12A) compared to the human breast cancer cell lines, MCF-7 (ER+) and MDA-MB-453 (ER-). Exposure to mercuric compounds increased cellular proliferation (2-fold), altered caspase activity and p53 expression in a compound dependent manner in MCF-12A cells. Between the two tumor lines, MDA-MB-453 cells appeared most like MCF-12A cells with regard to the mercury response. MCF-7 (ER+) cells on the other hand, were relatively resistant to the effect of both HgCl2 and CH3Hg+ as indicated by the relative lack of change in any of the parameters measured. The proliferation and viability of MCF-7 cells was not significantly affected and although 5 ppm CH3Hg+ significantly increased caspase activity, there was a net inhibition of p53 expression at the same concentration. Collectively, MCF-12A (normal epithelial) cells were most sensitive to both HgCl2 and CH3Hg+. Cellular adaption and activation of the p53/apoptosis pathway would minimize tumorigenesis which was dependent on the chemical form of mercury. These protective effects were not observed in the tumor cell lines with the MCF-7 (ER+) cells being the most resistant to the mercury effects. A significant difference between MCF-7 and MDA-MB-453 cells is expression of the estrogen receptor, suggesting potential involvement of this receptor in the effects of mercuric compounds. Further work is necessary to examine the potential role of the estrogen receptor in modulating the effects of mercuric compounds on tumor development.

Methylmercury exposure in the general population; toxicokinetics; differences by gender, nutritional and genetic factors

Mercury is an environmental toxicant that causes numerous adverse effects on human health and natural ecosystems. The factors that determine the existance of adverse effects, as well as their severity are, among others: the chemical form of mercury (elemental, inorganic, organic), dosis, age, period of exposure, pathways of exposure and environmental, nutritional and genetic factors. In the aquatic cycle of mercury, once it has been deposited, it is transformed into methylmercury due to the action of certain sulphate-reducing bacteria, which bioaccumulates in the aquatic organisms and moves into the food chain. The methylmercury content of large, long-lived fish such as swordfish, shark, tuna or marlin, is higher. Methylmercury binds to protein in fish and is therefore not eliminated by cleaning or cooking the fish. Fetuses and small children are more vulnerable to the neurotoxic effects of methylmercury from the consumption of contaminated fish. Methylmercury is absorbed in the gastrointestinal tract and crosses the blood-brain barrier and the placenta. The intake of certain dietary components such as polyunsaturated fatty acids, selenium, fiber, thiol compounds, certain phytochemicals and other nutrients can modify methylmercury bioaccesibility and its toxicity. Apart from environmental factors, genetic factors can influence mercury toxicity and explain part of the individual vulnerability.

Distribution and chemical form of mercury in commercial fish tissues

We analyzed total Hg concentrations in various tissue samples obtained from 7 commercially available fish species. MeHg contents were also estimated for muscle and liver samples by a selective analysis of inorganic Hg. Among the tissues, high Hg accumulations were shown in liver, muscle, heart and spleen throughout all fish species. Carnivorous fish, such as scorpion fish, sea bream and Japanese whiting, tended to show higher Hg accumulations in the muscle, with the highest Hg levels being shown by scorpion fish. Although the liver was expected to show the highest Hg accumulations among tissues throughout all fish species, the highest accumulation in the liver was observed only in scorpion fish. In contrast, the muscle level was significantly higher than the liver in Pacific saury and Japanese whiting. MeHg accumulated in fish is considered to show a sustained increase throughout the life of the fish, due to its long biological half-life. In fact, in the present study, muscle Hg levels in Japanese whiting, Japanese flying fish, and halfbeak showed good correlations with body weights. However, such correlations were not clear in scorpion fish, sea bream, Jack mackerel and Pacific saury. Selective analyses of inorganic Hg levels revealed that most of the Hg (> 95%) in fish muscle existed as MeHg, while the rates of MeHg contents in the liver varied from 56% in scorpion fish to 84% in Jack mackerel. As a result, fish muscle showed the highest MeHg accumulations in all fish species examined. These results suggest that reliable information on total Hg contents in fish muscle might be sufficient to avoid the risk of MeHg exposure caused by eating fish, even when one consumes other tissues such as fish liver.

The distribution of total and methylmercury concentrations in soils near the Idrija mercury mine, Slovenia, and the dependence of the mercury concentrations on the chemical composition and organic carbon levels of the soil

Although the mining activity of the Idrija mine in Slovenia ceased in 1995, a large amount of mining dregs containing high concentrations of mercury remains in the area. The mining dregs were transported with river flow and deposition along the Idrija River. To estimate the dispersion and change in the chemical form of mercury, a total of 28 soil core samples were taken around the river. The individual core samples were separated into layers for the analysis of their chemical composition, carbon contents, total mercury (T-Hg) and methylmercury (MeHg) concentrations. The chemical composition measured by X-ray fluorescence spectrometry was useful to estimate the dispersion of tailings: the fluvial terrace soil had a chemical composition similar to that of the tailings and could be distinguished clearly from the forest soil. The highest T-Hg concentration, 1,100 mg kg−1, was observed in the fluvial terrace soil near the mine. Although the concentration decreased gradually along with distance from the mine, concentrations higher than 200 mg kg−1 of T-Hg were still observed in the fluvial terrace soil approximately 20 km downstream from the mine. In the vertical distribution of T-Hg in the hillslope soil, a higher value was observed in the upper layers, which suggests the recent atmospheric deposition of mercury. The concentration of MeHg was the lowest at the riverside and higher in the hillslope soil, which was the opposite of the T-Hg distribution. The total organic carbon content tracked similarly with the distribution of MeHg and a linear relation with a significantly high correlation coefficient was obtained. The distinction may be related to the different dispersion process of mercury, and the organic carbon contents may be an important factor for MeHg formation.

The chemical form of mercury in fish.

The primary dietary source of neurotoxic mercury compounds is via the ingestion of methylmercury species accumulated in fish. Methylmercury from fish has been linked to neurological damage (Minamata disease) ([ 1 ][1]) and increased risk of myocardial infarction ([ 2 ][2]). Despite its importance,

Determination of acute Hg emissions from solidified/stabilized cement waste forms

The chemical form of mercury in wastes to be solidified/stabilized may lead to volatile losses from the finished solidified/stabilized monolith. Elemental mercury vapor (Hg vapor) was detected in the headspace of batch reactors that contained solidified/stabilized ordinary Portland cement doped with mercuric oxide (HgO) or liquid elemental mercury [Hg°(1)]. Vapor concentrations increased as a function of time and temperature; the headspace over the HgO samples was saturated in about one hour, while the samples containing Hg°(1) reached approx. 20% of saturation in about two hours. Increased temperatures due to cement hydrolysis lead to increased Hg vapor evolution. Mercury solidified/stabilized as mercuric sulfide (HgS, black) emitted no Hg vapor. Data for the HgO and Hg°(1) experiments was fit to a reversible first-order rate expression. Samples containing HgO displayed the greatest volatility as a result of the rapid dissolution of HgO and the subsequent formation of a strong driving force across the air-water interface. The evolution of Hg vapor from samples solidified/stabilized as Hg°(1) is limited by mass transfer resistances that kinetically limit the dissolution of Hg°(1) into the aqueous phase. The inert character of HgS (extremely low solubility and resistance to oxidative dissolution) prevents the evolution of detectable Hg in wastes solidified/stabilized as HgS. The findings of these studies may be important when considering treatment and disposal scenarios for Hg-containing wastes.

Transplacental and Lactational Exposure to Mercury in Hamster Pups after Maternal Administration of Methyl Mercury in Late Gestation

Pregnant Syrian golden hamsters were given a single oral dose of 203Hg-labelled methyl mercury (MeHg), 1.6 mumol/kg body weight, on day 12 of gestation. The uptake, retention and tissue distribution of 203Hg in the dams and pups was studied by gamma-counting during the following three weeks. The average transplacental transfer of 203Hg was 1.1% of the administered dose per pup, corresponding to 11% of the administered dose to a whole litter. This was considerably more than in our previous studies when the dams were treated on gestational day 2 (1.3%) or 9 (4.6%). The amount of 203Hg transferred to each pup in utero was independent of the litter size. The average additional transfer of 203Hg to a litter via milk was 1.7% of the administered dose. In the pups, the content of 203Hg in the liver and brain decreased, while the content in the kidneys and pelt increased during the second and third week. The highest amount of 203Hg was generally found in the pelt, which indicated that unweaned hamster pups primarily excrete MeHg by binding to hair. The chemical form of mercury in the liver and kidneys of the pups was determined by ion-exchange separation of inorganic Hg and MeHg followed by gamma-counting. The amount of inorganic Hg in the liver of the pups remained constant throughout the experiment, while it increased in the kidneys after one week due to the demethylation of MeHg. The inorganic Hg in the liver of newborn pups was probably due to maternal demethylation of MeHg and transplacental transfer of inorganic Hg.(ABSTRACT TRUNCATED AT 250 WORDS)

Chemical form of mercury in water in a volcanic acid stream, Kashiranashigawa, in Japan

Chemical form of mercury in water in a volcanic acid stream, Kashiranashigawa, in Japan

Further study of effects of chelating agents on excretion of inorganic mercury in rats

The effects of three chelating agents, N- benzyl- D-glucamine dithiocarbamate (BGD), 2,3-dimercaptopropanol (BAL) and D-penicillamine ( D-PEN), on the excretion of mercury in rats exposed to mercuric chloride (HgCl 2), the chemical forms of mercury compound excreted in the bile and urine and the intestinal reabsorption of mercury compounds in the bile were studied. Rats were injected intraperitoneally with 203HgCl 2 (300 μg Hg and 74 kBq of 203Hg/kg) and 24 h later, they were injected intraperitoneally with a chelating agent (a quarter of an LD 50). The enhancing effect of BGD on the excretions of mercury was almost the same as that of BAL and much larger than that of D-PEN. The major chemical form of mercury in the bile and urine of rats injected with BGD after HgCl 2 treatment was Hg-BGD compounds. The chemical form of mercury in the bile and urine of rats injected with BAL after HgCl 2 treatment was mainly Hg-GSH compound. The mercury after HgCl 2 and D-PEN treatment was excreted mainly via the urine in the form of Hg- D-PEN compound. The intestinal reabsorption of mercury from the bile of rats injected with BGD or D-PEN was only 0.18% or 0.38% of the dose respectively. The intestinal reabsorption of mercury from the bile of rats injected with BAL was 27.38% of the dose. It was suggested that the Hg-GSH compound excreted in the bile after HgCl 2 and BAL treatment is partly degraded to Hg-cysteine (Cys) by the intestinal membrnois enzymes and that the ligand of Hg-Cys is replaced by BAL in the bile, resulting in the effective reabsorption of Hg-BAL compound from the intestine.

On the Chemical Form of Mercury in Edible Fish and Marine Invertebrate Tissue

Total mercury, monomethylmercury (CH3Hg), and dimethylmercury ((CH3)2Hg) in edible muscle were examined in 229 samples, representing seven freshwater and eight saltwater fish species and several species of marine invertebrates using ultraclean techniques. Total mercury was determined by hot HNO3/H2SO4/BrClldigestion, SnCl2 reduction, purging onto gold, and analysis by cold vapor atomic fluorescence spectrometry (CVAFS). Methylmercury was determined by KOH/methanol digestion using aqueous phase ethylation, cryogenic gas chromatography, and CVAFS detection. Total mercury and CH3Hg concentrations varied from 0.011 to 2.78 μg∙g−1 (wet weight basis, as Hg) for all samples, while no sample contained detectable (CH3)2Hg (<0.001 μg∙g−1 as Hg). The observed proportion of total mercury (as CH3Hg) ranged from 69 to 132%, with a relative standard deviation for quintuplicate analysis of about 10%; nearly all of this variability can be explained by the analytical variability of total mercury and CH3Hg. Poorly homogenized samples showed greater variability, primarily because total mercury and CH3Hg were measured on separate aliquots, which vary in mercury concentration, not speciation. I conclude that for all species studied, virtually ail (>95%) of the mercury present is as CH3Hg and that past reports of substantially lower CH3Hg fractions may have been biased by analytical and homogeneity variability.

Effect of Chemical Form of Mercury on the Performance of Dosed Soils in Standard Leaching Protocols: EP and TCLP

ABSTRACT Application of the EP (Extraction Procedure) and TCLP (Toxicity Characteristic Leaching Procedure) to a variety of mercury-contaminated soils and solid wastes from U.S. Department of Energ...

Experimental ecosystems: Comparative study of two methods of contamination of the water column by mercury compounds in relation to bioaccumulation of the metal by rooted macrophytes(Ludwigia notons).

Abstract In the context of work on bioaccumulation and transfer of mercury compounds within a multicompartment model (water, natural sediment, rooted macrophytes) a study was set up to select from several methods of water column contamination the one which best matched our experimental objectives. After some theoretical considerations based on a simulation using simple mathematical models, an experiment was carried out to compare two methods of water column contamination, with specific reference to the bioaccumulation of total mercury by one species of rooted macrophyte (Ludwigia natans): these were: 1) continuous additions of Hg in order to maintain a constant concentration in the water, and 2) twice daily additions of a constant quantity of Hg into all experimental units. For a better appreciation of the effect of each method, the experimental protocol considered several factors: photoperiod, temperature, chemical form of mercury and length of observation period. In view of the overall objectives of our...

Mercury-selenium interactions in relation to histochemical staining of mercury in the rat liver

Selenium has been suggested to enhance the histochemical staining of mercury when sections of tissue are subjected to the silver-enhancement method. In the present study, histochemical staining patterns of mercury in tissue sections of rat livers were compared with the actual content of organic and inorganic Hg in the livers, in both the presence and the absence of Se. Rats were injected intravenously with 5 micrograms of Hg g-1 body weight as methyl [203Hg] mercury chloride (MeHg) or as [203Hg]mercuric chloride (Hg2+). After 2 h, half the rats received an additional intraperitoneal injection of 2 micrograms of Se g-1 body weight as sodium [75Se]selenite. All the rats were killed 1 h later. Homogenized liver samples were prepared for mercury analysis by two different methods: alkaline digestion and ultrasonic disintegration. Quantitative chemical analysis based on benzene extraction of the radioactively labelled Hg compounds showed that the chemical form of mercury, either organic or inorganic, was preserved from its administration to its deposition in the liver. Light and electron microscopy demonstrated that no silver enhancement of Hg occurred when MeHg alone was present in the sections of tissue, whereas MeHg accompanied by Se induced a moderate deposition of silver grains. In contrast, sections containing Hg2+ alone yielded some staining, and the addition of Se increased the staining dramatically. The results of the present study show that acute selenite pretreatment is a prerequisite for the histochemical demonstration of methyl mercury, and greatly increases the staining of inorganic mercury when applying the silver-enhancement method.

The effect of various dietary fibres on tissue concentration and chemical form of mercury after methylmercury exposure in mice.

The whole-body retention of mercury after exposure of BALB/c mice to methylmercury was measured in animals fed fibre-free, 5% pectin, 5% cellulose or 5, 15 or 30% wheat bran diets. The rate of elimination of mercury was dependent on the diet fed, with dietary bran increasing the rate of elimination. The incorporation of 15 or 30% bran in the diet of the mice decreased the total mercury concentration in the brain, blood and small intestine, although the effects were significant only in those animals on 30% bran diet. The fibres had little effect on mercury levels in other tissues. The proportion of mercury found in the mercuric form was significantly greater in liver, kidneys and gut of mice fed bran. The results suggest that dietary bran may reduce the levels of mercury in the brain after methylmercury exposure and may therefore reduce the neurotoxic effects of the organomercurial. We suggest that wheat bran exerts its effects on mercury retention and brain level via a modification of the metabolic activity of the gut microflora.

Content and Chemical Form of Mercury and Selenium in Lake Ontario Salmon and Trout

The content and chemical form of mercury and selenium were determined in the edible tissue of salmon (coho, chinook) and trout (lake, brown) taken offshore from Lake Ontario near Rochester, New York. For all fish species, total mercury content ranged from 0.3 to 0.8 μg/g (fresh-weight), which is similar to concentrations commonly found in canned tuna. Most of the total mercury (63 to 79 percent) was present as methylmercury, the remainder being divalent inorganic mercury. For all species, 6 to 45 percent of the total selenium content was present as selenate (SeVI), the remainder being selenite (SeIV) and selenide (Se-11). On a molar basis, total selenium content usually exceeded that of total mercury. Samples of smoked and unsmoked brown trout fillets were also examined. Based on the results of this study there is no immediate human health hazard from mercury and selenium. However, there is a need to report specific chemical forms of these metals in Lake Ontario salmonid fishes so that elevated concentrations can be better evaluated.