Mercury in soil: A method for assessing acceptable limits

Acceptable limits for mercury in soil were determined at a site with mercury contamination after measuring the soil concentration of total mercury, the species of mercury, and the intestinal absorption of mercuric sulfide by mice. The total concentration of mercury at this site ranged from 0.5 to 3,000 ppm. Of the total mercury present, 88% was identified as mercuric sulfide, 0.01% as methyl mercury, and 7% as elemental mercury. Intestinal absorption studies in mice following the intubation of²⁰³mercuric sulfide showed that 0.4% of the intubated dose was absorbed. We estimated an acceptable limit for mercury in soil at this site based on results of this study, on reports in the literature on the intestinal and pulmonary absorption of mercury species from air, water and food; and on the normal intake of total mercury in humans reported by the World Health Organization. Based on reports in the literature and results from the present studies, we suggest an acceptable limit for mercury in soil (at this site) to be 722 ppm. With a safety factor of 10 this limit would be reduced to 72 ppm.Research supported by the Oak Ridge Research Institute and the Department of Energy under contract (No. DE-AC05-84OR21492) with the Oak Ridge Research Institute.     

Ultrastructural studies on the cytotoxic effects of mercuric chloride on mouse glioma

Cytotoxic effects of mercuric chloride on cultured mammalian cells were studied by light and electron microscopy. Cell proliferation of mouse glioma was completely suppressed by treatment with 5 × 10⁻⁵ mercuric chloride. The mitotic index remained at the control level for 4 hr after treatment but decreased afterward. The amount of mercuric mercury bound to the cells increased markedly above 2 × 10⁻⁵ mercuric chloride. Electron microscopic examination revealed many kinds of changes of organelles in cells exposed to 5 × 10⁻⁵ mercuric chloride for 4 hr: Nuclei were transformed into pyknotic and irregular shapes; mitochondria lost their normal cristae and abnormal electron dense-areas were present within the matrix; polyribosomes were dispersed. Numerous electron-dense granules and vacuolations were seen in the cytoplasm, especially around the Golgi region. However, microtubules were still evident, although the amount seemed to decrease compared with control cells. Thus, the inhibition of growth by mercuric chloride may be ascribed to the degenerative changes which occur in many organelles.     

The effects of organic and inorganic lead and mercury on neurotransmitter high-affinity transport and release mechanisms.

The effects of two heavy metals upon the high-affinity transport system of certain putative neurotransmitters have been studied in adult mouse brain homogenates. Carbon-linked and free ionic forms of mercury and lead were compared. Tri-n-butyl lead acetate at concentrations as low as 10^?6, m severely inhibited the sodium-dependent, energy-requiring uptake of a variety of putative neurotransmitters. Dopamine uptake was more affected than other compounds. Ionic lead (as lead acetate) was several orders of magnitude less toxic than the covalently bound lead compound. Methylmercuric chloride and mercuric chloride had an intermediate inhibitory effect on the high-affinity transport system, significant impairment becoming apparent only at around 10^?5, m. Both metals stimulated the release of labeled compounds accumulated by high-affinity transport systems in brain homogenates. This stimulation was greater with tributyl lead acetate than with any other compound tested. The effect was independent of and additive to the stimulatory effect of the calcium ion on neurotransmitter release. Unlike calcium, heavy metals could effect release of transported compounds in the absence of depolarizing conditions. While calcium-mediated release requires over 0.3 mm Ca²⁺ to be detected, tributyl lead acetate-mediated release of several putative transmitters was apparent at 5 × 10^?6, m and mercury compounds had major releasing effects at 5 × 10^?5, m. The uptake and release of dopamine was especially strongly affected by covalently bound lead whose effects could be detected at 10^?8, m.     

Reduction of mercuric ion and exhalation of mercury in acatalasemic and normal mice

A significant difference in the amount of exhaled mercury per hour between normal and acatalasemic mice was observed in 7 of 11 experiments for different periods of time. The total amount of mercury exhaled from acatalasemic mice was significantly higher than those of normal mice. The results confirm that the reduction of mercuric ion to metallic mercury occurs by recycling of mercury in the tissues and reoxidized metallic mercury to mercuric ion by catalase. Mercuric ion was reduced to metallic mercury in the presence of superoxide anion in vitro. The reduction rate of mercuric ion to metallic mercury in the presence of both superoxide anion and cytochrome C or nitro blue tetrazolium was higher than that in the presence of superoxide anion alone, and the reduction of mercuric ion by NADPH or NADH was also observed. The reduction of mercuric ion to metallic mercury by liver homogenates of acatalasemic mice was higher than that of normal mice.     

锌对氯化汞免疫毒性的影响及其机理

为了探讨锌对氯化汞免疫毒性的影响,采用免疫毒理学和生化毒理学方法观察氯化汞染毒的ＩＣＲ小鼠血中碳廊清率、绵阳红细胞（ＳＲＢＣ）致敏小鼠迟发型过敏反应（ＤＴＨ）、二硝基氯苯（ＤＮＣＢ）所致的迟发型皮肤过敏反应（ＤＣＨ）、血清溶血素（ＨＣ５０）和免疫脏器系数,结果显示：上述指标均明显低于对照组;预先给予醋酸锌后再给同剂量氯化汞的小鼠上述各指标均有不同程度提高;免疫器官脂质过氧化作用,汞组脂质过氧化物（     

Occupational Health and Accidents in Feldspar Mining

The percentage of whole-body mercury found in the lungs of guinea pigs exposed to mercury vapor for ten minutes was in the same range as after one hour’s exposure (25% to 33%). The highest concentrations of mercury were found in peripheral lung structures. The same distribution was found at different concentrations of mercury in the air. Only one tenth of the values were found in corresponding structures of animals injected with mercuric nitrate. Most of the mercury deposited in alveolar tissues is therefore probably deposited there directly from the air. The results are considered to indicate the following: that mercury vapor penetrates to the alveoli; that most of it is quickly transferred to the blood; and that a small fraction is deposited in the pulmonary tissues, from where it is slowly eliminated to the rest of the body.     

Effect of administration sequence of mercuric chloride and sodium selenite on their fates and toxicities in mice

Interaction of mercury and selenium was examined in mice given mercuric chloride (25 μmol/kg) intravenously with sodium selenite (25 μmol/kg, iv) according to various administration schedules. Body weight of the mice given mercuric chloride or selenite alone did not increase, but the mice given both compounds simultaneously grew as well as control mice. On the other hand, only a 1-hr shift of administration of either compound canceled the mutual detoxifying effect. The most conspicuous changes in tissue distribution of mercury and selenium and in gel filtration patterns of both elements accumulating in tissues of the mice were observed when both compounds were administered simultaneously. These experimental results indicate that the interaction of mercuric mercury with selenite in mice occurred to the greatest extent upon simultaneous administration, supporting the hypothesis that the interaction primarily occurs in the blood stream.     

Mercury intolerance in relation to superoxide dismutase, glutathione peroxidase, catalase, and the nitroblue tetrazolium responses

Through percutaneous provocation with metallic mercury and phenyl mercuric acetate in patients stating the presence of subjective psychosomatic symptoms following dental amalgam treatment, it has been possible to categorize and score two extreme groups of patients, mercury-intolerant and mercury-tolerant patients reacting and not reacting, respectively, to low doses of mercury. The intolerant patients had a high psychosomatic score and the tolerant patients had a low or null score when exposed to low doses of the two mercury compounds. Determination of the scavenger enzymes superoxide dismutase, glutathione peroxidase, and catalase showed no significant differences between the mercury-intolerant and the mercury-tolerant patients and the controls. The activity of superoxide dismutase and the quantitative psychosomatic score elicited by either metallic mercury or phenyl mercuric acetate showed a positive correlation. On the other hand, analyses of the psychosomatic score and the areas under the curves of the nitroblue tetrazolium test response showed negative correlations. The results indicate that the oxidative metabolism and, in particular, superoxide dismutase may be perturbed in mercury-intolerant patients.     

Phytosorbent Prepared from Sunflower Seed Husks Prevents Mercuric Chloride Accumulation in Kidney and Muscle of Adult Rabbits

In the present study, the effect of a melanin-containing phytosorbent, “Victoria,” on mercury accumulation in rabbits' tissues was studied. This phytosorbent is derived from black sunflower seed husks. Domestic rabbits were administered either one single nontoxic low-level dose of mercuric chloride (i.e., 50 μmlg/1 kg body weight [control group]) or combinations of mercury and the phytosorbent “Victoria” (i.e., experimental group). Mercury and phytosorbent were administered per os daily for 12 d. Mercury in tissues was determined by cold-vapor atomic absorption spectroscopy. Mercury in kidney and muscle of the experiment group was, on average, 25.8 and 4.7 times less, respectively, than in the control group. The authors concluded that the phytosorbent prevented accumulation of mercury in the kidney and muscle tissues and exerted a protective effect against mercury toxicity.     

Uptake of Mercury by the Brain

A technique has been developed for injecting metallic mercury intravenously in aqueous solution. Thirty seconds after intravenous injection of rats with 0·1 μg. metallic mercury labelled with ²⁰³Hg nearly 20% of the dose had been exhaled and the concentration in the brain was nearly as high as in the blood. After injection of mercuric ion little of the dose was exhaled, and brain uptake was much less. Oxidation of mercury in the blood was, therefore, not instantaneous, and the rapid transport of the unconverted metallic mercury to the brain and its subsequent rapid diffusion from the blood was responsible for the high level of mercury in the brain after exposure to mercury vapour. The technique might be useful for the study of the passage of highly diffusible vapours through the respiratory membranes.     

Effects of dietary mercury on mink

A study was conducted to ascertain the effects of dietary mercury on mink. Five parts per million of dietary methylmercury was lethal to adult mink in about one month. Ten parts per million of mercuric chloride in the diet for five months did not produce adverse effects. Clinical signs of methyl mercurialism were anorexia, loss of weight, incoordination, tremors, and paroxysmal convulsions. The latency period was about 24 days; survival time averaged 33 days. Pathological changes were evident in the tissues of the mink that died of mercury poisoning. Tissue mercury residue analyses showed the highest concentration of mercury in tissues from mink fed methylmercury.Supported in part by a grant-in-aid from the Mink Farmers' Research Foundation, Milwaukee, Wis. and published with the approval of the director of the Michigan Agriculture Experiment Station as journal article No. 6198.     

Distribution and Excretion of Methyl and Phenyl Mercury Salts

The distribution, metabolism, and excretion of phenyl mercury acetate (P.M.A.) and of methyl mercury dicyanidiamide (M.M.D.) has been studied in the rat during the repeated subcutaneous administration of small doses over a period of six weeks, and for several weeks after a single dose.

The results indicate that P.M.A. is absorbed unchanged into the circulation from which it is mainly removed by the liver and kidneys where it is metabolized and excreted in the faeces and urine mostly as inorganic mercury. During repeated dosage the rats reached a steady state by the end of the second week when excretion approximately balanced intake. No measurable amount of mercury was found in the central nervous system.

After repeated dosage with M.M.D. there is no clear indication of a steady state being reached after six weeks. There is an accumulation of organic mercury in all tissues, particularly in the red cells, and a progressive increase in the brain concentration. M.M.D. is more slowly released from the tissues than P.M.A. and the breakdown to inorganic mercury is low.

The control of human exposure to alkyl and aryl mercury salts is considered in the light of these experimental observations. The recommendation that the concentration of alkyl mercury salts in the atmosphere should not exceed 0·01 mg./m.³ seems justifiable, but there appears to be no reason to establish the figure for aryl mercury salts below the 0·1 mg./m.³ recommended for inorganic mercury vapour.

     

The toxicity of three mercurials to Pteronarcys californica newport,and some possible physiological effects which influence the toxicities

There is little information available on the toxicity of mercurials to aquatic insects. The information that is available is confined to field observations or medium tolerance limit (TLm) values using only one form of mercury.The TLm values were determined for three different forms of mercury (phenylmercuric-, and methylmercuric-, and mercuric chloride) to the stonefly Pteronarcys californica. The order of toxicity of the three forms was found to be phenylmercuric chloride > methylmercuric chloride > mercuric chloride. The in vivo effect of the three forms of mercury on isolated gylceraldehyde-3-phosphate-dehydrogenase was also measured.Two possible physiological factors involved in determining the toxicity of mercury (or other metals) to aquatic insects may be the catabolic pathways being employed at any period during the year, particularly during periods of molting, and age of the instar.     

Fate and effects of mercury in marine plankton communities in experimental enclosures

The development of a North Sea coastal plankton community exposed to different degrees of mercury stress in six simultaneously filled plastic bags was followed for 44 days. Mercuric chloride was added to four bags to yield concentrations of 0.5 (one bag), 5 (two bags), and 50 μg Hg · liter^?1 (one bag) in the water. Two bags served as controls. It could be shown that a single dose of 0.5 μg Hg · liter^?1 altered the species composition of the algal community on the walls of the bag. Addition of 5 μg Hg · liter^?1 had a marked impact on the development of the phytoplankton, as well as on that of the zooplankton and decomposers. Addition of 50 μg Hg · liter^?1 caused inactivation or death of the phytoplankton and zooplankton. The toxicity of mercuric chloride to the phytoplankton depends on (a) the concentration of the mercury, and (b) the particle concentration, i.e., the surface area available for adsorption of mercury. For this second reason the ratio between numbers of living cells and inanimate particles is an important factor influening mercury toxicity in aquatic ecosystems. Methylation of the added mercury occurs in the sediment of the bags after a lag phase of 1 month. Most of the added mercury disappears from the system by volatilization to metallic mercury. The remainder is absorbed by the sediment and the walls of the bags.     

Phytosorbent prepared from sunflower seed husks prevents mercuric chloride accumulation in kidney and muscle of adult rabbits

In the present study, the effect of a melanin-containing phytosorbent, "Victoria," on mercury accumulation in rabbits' tissues was studied. This phytosorbent is derived from black sunflower seed husks. Domestic rabbits were administered either one single nontoxic low-level dose of mercuric chloride (i.e., 50 microg/1 kg body weight [control group]) or combinations of mercury and the phytosorbent "Victoria" (i.e., experimental group). Mercury and phytosorbent were administered per os daily for 12 d. Mercury in tissues was determined by cold-vapor atomic absorption spectroscopy. Mercury in kidney and muscle of the experiment group was, on average, 25.8 and 4.7 times less, respectively, than in the control group. The authors concluded that the phytosorbent prevented accumulation of mercury in the kidney and muscle tissues and exerted a protective effect against mercury toxicity.     

Chronic effects of inorganic and organic mercury onDaphnia magna: Toxicity,accumulation, and loss

The chronic toxicity of mercury (Hg) toDaphnia magna was studied under flow-through and renewed static conditions. Concentrations of mercuric chloride (HgCl₂), methyl mercuric chloride (MMC) and phenyl mercuric acetate (PMA) in flow-through tests significantly affecting survival were 1.92, between 0.26 and 0.98, and 2.25g Hg/L, respectively. Concentrations of HgCl₂, MMC, and PMA significantly impairing young production (P0.05) were 0.72, 0.04, and 1.90g Hg/L, respectively. Body accumulation of mercury was greatly influenced by the chemical form of mercury in the water. About nine times more mercury, added as MMC, was tolerated in daphnids at water concentrations permitting survival than was tolerated when added as HgCl₂. At about the same mercury concentration in water (0.26g Hg/L) daphnids accumulated 20 times more mercury when it was added as MMC than when it was added as HgCl₂. Mercury was rapidly accumulated in daphnids; however, 35 and 57% of the mercury added as MMC and HgCl₂, respectively, was lost when animals were placed in control water for four days following exposure. Different forms of mercury behaved quite differently in renewed-static and flow-through systems. The results also indicate the shortcomings of renewed-static tests with volatile and readily degradable compounds.     

Uptake and loss of inorganic mercury in the Eastern oyster (Crassostrea virginica)

Eastern oysters (Crassostrea virginica) were found to accumulate significant levels of mercury on exposure to relatively low concentrations of mercuric chloride. Accumulation occurred in two distinct phases which may be described as a two compartment system in which accumulation is logarithmic in the first phase and linear in the second. Mercury, during the initial phase, showed a minimum outward concentration flux of 0.025 hr^–1 indicating reversibility of accumulation prior to the change in phase. However, mercury was not excreted at the end of the second phase following exposure to 10, 40, 80, and 100g/1 for 256 hr.     

Effects of endogenous and exogenous thiols on the distribution of mercurial compounds in mouse tissues

The distribution of mercury, a well known environmental contaminant, has been evaluated in detail in several species of animals; however, limited information is available in the mouse. Considerable species differences exist in the distribution of various forms of mercury. In the current study, methylmercuric chloride or mercuric chloride were injected ip in mice at two dose levels. The concentration of mercury in various organs was determined by cold-vapor atomic absorption spectrometry. After the administration of methylmercury, the concentration of mercury increased in brain up to 3 days, despite a declining mercury content in blood. The first-order rate of mercury uptake in brain was independent of the dose of methylmercury. In blood, methylmercury was largely confined to erythrocytes. Mercury concentrations in liver and kidney correlated with those in the blood. Mercuric chloride was distributed equally between erythrocytes and plasma in blood. Mice receiving mercuric chloride did not have appreciable levels of mercury in the brain throughout the sampling period. Coadministration of L-cysteine with mercuric chloride reduced mercury levels in the liver with no effect on brain concentrations. Glutathione depletion by diethylmaleate increased mercury concentration in brain after methylmercury treatment, whereas a decrease in kidney mercury concentration was observed. The results suggested that thiol compounds may not facilitate the entry of mercuric ion into the brain but can alter the distribution in other organs.     

Monothiols and Vitamins are Ideal Therapeutic Agents for Mercury Elimination from Nervous and Non-Nervous Tissues of Fish

Use of mercury and its compounds in various industries and agriculture is increasing its concentration in aquatic environment and affecting the organisms living therein. Among these, the fishes are commercially important for humans as an important source of protein. The fish meat transfers good amount of mercury to man, therefore, its elimination is quit essential both from fishes and the consumers. As a step in this direction, the present study has been designed to detoxify the fishes from mercury. For this purpose a freshwater fish (Channa punctatus) was treated with mercuric chloride (0.5 ppm) for 96 h and thereafter, detoxicated with vitamin B complex, glutathione and N-acetyl-DL-homocysteine thiolactone used either alone or in various combinations for another 96 h. One group of 96-h mercury treated animals were kept in tap water and sacrificed after 192 h. This group was considered as mercury washed group and it served as control to all therapeutic groups. Mercury treated fish showed a highest concentration of the metal in kidney followed by liver, gills, brain and muscles. In mercury washed group, metal was removed significantly from all the non-nervous tissues, but in brain about 52% further increase was observed. The results obtained from theraputic studies were quite exciting as 50–80% mercury was mobilized from all tissues including brain within 96 h of treatment.     

Effect of Selenium Pretreatment in Chronic Mercury Intoxication in Rats

Effect of selenium pretreatment (0.2 mg/kg/day, as sodium selenite), 4 h prior to mercury treatment (0.4 mg/kg/day, as mercuric chloride), administered intraperitoneally, was examined after daily exposure for 20 days’ in rats. Liver, kidney and brain tissues were assayed for malondialdehyde (MDA) level, glutathione (GSH) content and mercury concentration. Mercury induced MDA levels, which was also observed in selenium pretreated animals. Significant reduction in GSH levels was observed in mercury alone and selenium pretreated animals. Mercury accumulation was in the order of kidney, liver and brain. Selenium pretreatment resulted in further enhancement in mercury accumulation in liver and kidney.