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How Is a Chemical Added to the List? The reference concentration derived from Public Law Uncer- routes of exposure to a group of chemicals that share tainty and modifying factors are used to adjust the a common mechanism of toxicity EPA, a. We used the underlying toxicological data mechanism of action common to all members of the because we were interested in creating the broadest pos- group. For example, cholinesterase inhibition is the sible toxicological database for each chemical. The complex features of FQPA available in the broader toxicological literature.
RfCs assessments are consideration of multiple sources food, water, and residential and routes oral, inhalation, and dermal of exposure. This included the results of epidemiological Aniline and occupational studies but not individual case re- Antimony compounds ports. Our analyses include 40 of the 1,2-Epoxybutane HAPs. We then abases were reviewed and relevant information extracted calculated our hazard index-type ratio or hazard metric in the development of the METDB. Table 2 contains HM by dividing the exposure estimates by the NOA- background information for these sources.
Developmental 3 19 Endocrine 9 Exocrine 3 5. Discussion points. Our analysis does not characterize the potential References health risks of the HAPs. Even if such an assessment were possible, we would still need to validate the toxico- Clean Air Act Amendments of , Public Law Agency for Toxic Substances and Disease Registry. CRC Press trends in relevant populations. LLC, Boca Raton. Fox, M. Evaluating cumu- lative risk assessment for environmental justice: a community 7. Conclusion case-study.
Environmental Health Perspectives Suppl. International Life Sciences Institute, In: Mileson, B. Washington, DC. The upper respiratory tract. Some MeHg is also bound to plasma proteins. Matsuo et al. It should be emphasized that the exact form s in which MeHg exists in the body is still unknown. MeHg ion is hydrated in aqueous solutions. There are pH-dependent reactions giving rise to Hg-substituted oxonium ions Figure For example the cysteinate is with a linear C—Hg—S. MeHg is also readily transferred to the fetus and the fetal brain.
Evidence from rat experiments suggests that MeHg transport across the blood-brain barrier occurs via a MeHg- L -cysteine complex, which is transported by the L -system leucine preferring amino acid carrier Kerper et al. That action suggests that glutathione might play an indirect role in the transport of MeHg into endothelial cells. The MeHg-cysteine or MeHg-glutathione complex would be expected to be water soluble. That would not support the hypothesis. Source: Elinder et al Recently, Fujiyama et al. Aschner et al. A case study of family members that developed classic signs of MeHg poisoning due to the consumption of contaminated pork indicates that the cerebrum and the cerebellum are particularly sensitive to MeHg Davis et al.
Analyses of various regions of the brain of one female member upon autopsy, several years later, revealed that the extent of brain damage correlated with regional-brain Hg concentrations. The highest levels of Hg were found in the cerebrum and cerebellum. Magnetic Resonance Imaging MRI studies showed brain damage in the calcarine cortices, parietal cortices, and cerebellum of other family members. The damage in those areas is believed to underlie many of their persistent clinical signs, because those areas of the brain are responsible for coordination, balance, and sensations see Chapter 5.
Dimethylmercury is a supertoxic form of Hg Gosselin et al.
At Dartmouth College, a chemistry professor died days after several drops of dimethylmercury fell on her latex gloves. The gloves did not appear to act as a barrier, and the compound was rapidly absorbed through her skin. Mouse studies suggest that the extremely toxic dimethlymercury must be metabolized to MeHg before it can enter the brain Ostlund Elemental Hg in liquid or vapor form is not well absorbed from the GI tract less than 0.
Because elemental Hg is very lipid soluble, its diffusion across the lungs and dissolution in blood lipids is rapid Berlin The fact that it is uncharged with intermediate molecular weight and size might be another reason why it passes readily from air to blood. It is distributed throughout the body, and readily crosses the placenta and the blood-brain barrier Vimy et al.
Elemental Hg is oxidized to mercuric Hg. Eventually, the Hg ratio of red blood cells to plasma is Absorption is proportional to the water solubility of the mercuric salt.
Mercuric Hg has a high affinity for sulfhydryl groups in the red blood cells and plasma. The half-life in the blood is reported to be The highest accumulation of mercuric Hg is in the kidneys. The major fraction of inorganic Hg in rat kidney is bound to metallothionein Jakubowski et al.
In contrast MeHg has a low affinity for metallothionein Chen et al. Because of its ionic charge, mercuric Hg does not readily penetrate the blood-brain barrier or the placenta. The rate of demethylation in rats and most other species is very slow. The mechanisms involved in conversion of MeHg to mercuric Hg are controversial. The enzymes in mammalian. The inhaled vapor is highly mobile, readily crosses cell membranes, the blood-brain barrier, and the placenta.
Source: Elinder et al. Greater emphasis has been placed on investigating the possible role of a free radical mechanism Suda and Hirayama Intestinal flora, tissue macrophages, and fetal liver are all sites of tissue demethylation. Experiments in bacteria demonstrate many different mechanisms to detoxify heavy metals.
For example, some metals are actively transported out of the cell e. Organic Hg compounds are detoxified by a microbial organomercurial resistance system see Figure An organomercurial lyase catalyzes the protonolysis of the carbon-Hg bond to give a hydrocarbon and a mercuric ion Summers ; Robinson and Tuovinen ; Summers and Silver Mercuric reductase then catalyzes the reduction of mercuric Hg to elemental Hg.
Because elemental Hg is volatile, it evaporates from the bacterial culture. Organomercurial lyase has been purified from Escherichia coli Begley et al. The enzyme is encoded on the plasmid R No cofactors are required for enzyme activity, and the enzyme structure does not contain any metals. The enzyme can catalyze protonolysis of the C-Hg bond in primary, secondary, and tertiary alkyl, vinyl, allyl, and aryl organomercurial salts to the hydrocarbon and mercuric ion.
A thiol must be present for activity, cysteine being the most active thiol compound, for demethylation of organic mercurials. Enzymes similar to those found in bacteria have not been found in mammals. Demethylation of MeHg is thought to occur via a free-radical mechanism in the mammalian brain, possibly eliminating the need for those enzymes. It is also possible that the enzymes have not yet been identified. Lefevre and Daniel examined rat, mouse, and guinea-pig liver homogenates for activity that would degrade organic Hg compounds.
Although a minimum level of activity was found, phenylmercuric acetate and methoxyethylmercury chloride were degraded, but not MeHg. Fang and Fallin were able to show cleavage of phenylmercuric acetate PMA and ethylmercury chloride in the kidney and liver of rats, but no activity was seen against MeHg. Elemental Hg vapor is oxidized to mercuric mercury by catalase and hydrogen peroxide H 2 O 2 in blood and tissues Berlin H 2 O 2 production is the rate-limiting step.
When mercuric Hg is administered orally to rodents, elemental Hg vapor has been detected in the expired air, indicating that some metabolism to elemental Hg must have occurred. In humans, the major routes of excretion are via the bile and feces. Much of the biliary MeHg is reabsorbed; MeHg complexed with glutathione is eliminated via the bile. There was a 0. The extent of urinary excretion continued to increase up to 71 days after ingestion.
A maximum of 0. That amount was found days after ingestion. Using whole-body measurements, the. In humans, the whole-body half-life of MeHg was estimated to be days Aberg et al. The half-life in blood for MeHg as measured in blood and hair of humans ranged from 48 to 53 days Miettinen et al. Elimination rates for MeHg are dependent upon species, dose, sex, and animal strain Nielsen It is pertinent to note that neonatal rats and monkeys are limited in their ability to excrete MeHg into the bile Ballatori and Clarkson Therefore, it takes them longer than mature animals to excrete MeHg Thomas et al.
In addition, their intestinal flora might also be less able to demethylate MeHg during this suckling period Rowland et al. If those two phenomena are true for humans, then neonates might be particularly sensitive to exposure to MeHg. GSH may be the major cellular defense against MeHg toxicity. MeHg has been measured in the breast milk of rats, humans, and guinea pigs Sundberg and Oskarsson ; Yoshida et al.
Therefore, breast milk is considered a route of excretion, but it is also an important route of exposure to suckling neonates. That percent is much lower than the percent of Hg found as MeHg in whole blood. In animals, the total Hg content of breast milk was found to be proportional to the total Hg content of the plasma Skerfving ; Sundberg and Oskarsson A small amount of elemental Hg vapor is excreted unchanged in exhaled air, sweat, saliva, feces, and urine Cherian et al.
Only small amounts of elemental Hg can be detected in the urine Stopford et al. Excretion via sweat and saliva is usually minimal. The hair-life for whole-body Hg excretion was 58 days in humans Hursh et al. Elemental Hg is also oxidized in the body to mercuric Hg, which is then excreted in the feces and urine. That is demonstrated by the observation that, after exposure to Hg. Fecal excretion of mercuric Hg occurs as the result of secretion through the small intestine epithelium and colon, and bile secretion Berlin Mercuric Hg is also excreted in the urine, sweat, lung Clarkson et al.
Urinary excretion is useful for biological monitoring of inorganic Hg.
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Absorbed inorganic Hg has been estimated to have a half-life of 40 days Rahola et al. Humans occupationally exposed to inorganic Hg excrete in their urine three forms of this element: a metallic form, a Hg-cysteine complex, and a large unidentified complex Henderson et al. Synthetic chelating or complexing agents that compete with endogenous ligands for mercuric or organic Hg increase the urinary excretion of inorganic Hg and organic Hg and reduce the body burden Aposhian ; Aposhian and Aposhian BAL is lipid soluble and must be given by deep intramuscular injection.
There is an injectable preparation of DMPS. However, because BAL redistributes Hg, increasing brain Hg concentrations when given to Hg-intoxicated animals, its continued therapeutic use is questionable Berlin DMPS was introduced into the official Soviet drug armamentarium in Klimova and to the western world in A number of reviews of DMPS and other chelating agents have appeared during the last 18 years Aposhian ; Aposhian et al. It is approved for use by the German and Chinese equivalents of.
Clarkson et al. Elsewhere, including the United States, DMPS has been used by alternative-medicine physicians concerned with dental amalgam toxicity. It was used recently to increase the urinary excretion of Hg in eight humans exposed to mercurous Hg Gonzalez-Ramirez et al. There is ample evidence from studies of humans Takizawa ; Matsuo et al.
Although the rate of demethylation of MeHg in the brain appears to be dose related, many questions remain concerning the mechanisms by which the brain biotransforms MeHg to inorganic Hg and the slow rate at which it occurs. Davis et al. Similar results were found in a Minamata patient who died 18 years after the exposure Takeuchi and Komyo Experimental studies have also reported a slow increase in the concentration of inorganic Hg in the brain in a number of species after administering MeHg and analyzing the brain for total and inorganic Hg from days to years after exposure Friberg and Mottet When monkeys were exposed daily to high doses of MeHg for long periods of time, there were significant concentrations of inorganic Hg found in the brain Lind et al.
Female monkeys Macaca fascicularis received daily doses of MeHg for up to 18 months Vahter et al. The extent to which demethylation of MeHg produces toxicity in the brain is not known. In addition, Magos et al. A possible hypothesis is that the long half-life of inorganic Hg in the brain once demethylation occurs might be responsible for the latent or long-term MeHg effects that have been reported. No direct evidence to support that hypothesis is available at this time.
In addition to the questions regarding whether inorganic or organic Hg mediates MeHg toxicity at the cellular level, questions have also been raised regarding the species responsible for the Iraqi poisonings.
In the Iraqi poisoning episode, some of the grain seeds appeared to contain phenyl Hg instead of MeHg. There is no doubt, however, that gas chromatography identified MeHg in the blood of most of the exposed population, and phenyl Hg would have been quickly converted to inorganic Hg in the blood T. Clarkson, University of Rochester, personal commun. In addition, the phenyl Hg was in the barley seeds and no barley seeds were used to make bread T. Currently, there is a general consensus that the critical organ for MeHg toxicity is the brain. Both the adult and fetal brains are susceptible to MeHg toxicity see Figure , although the developing nervous system appears to be more sensitive.
Studies of the Minamata disaster in Japan indicate that prenatal exposure causes damage throughout the fetal brain and, at high doses, results in effects in the offspring that are. Exposure of adults to MeHg resulted in focal lesions Clarkson The neurotoxicity of chronic MeHg exposure at lower levels is not immediately evident. A latent period of 1 month or more usually occurs Bakir et al. Other adverse effects e. Those effects, however, are not as well studied as the neurotoxic effects. The health effects of MeHg are discussed in more detail in Chapter 5.
The target organs of elemental Hg are the brain and kidney. The toxicity of elemental Hg is believed to be due to mercuric Hg. Inhaled elemental Hg vapor readily crosses the blood-brain barrier and is then oxidized to mercuric Hg. The latter becomes firmly bound to macro-molecules in the brain. There does not seem to be any endogenous mechanism for the rapid removal of mercuric Hg from such sites.
In humans occupationally exposed to elemental Hg vapor, signs of severe exposure include tremor, psychiatric disturbances, gingivitis, and altered behavior. The target organ of mercuric Hg toxicity is the kidney due to Hg accumulation there. Although the exact mechanism of renal toxicity is not known, it is known that mercuric Hg has a strong affinity for sulfhydryl moieties.
The formation constant for mercuric Hg and the anionic form of a sulfhydryl group, RS - , is greater than or equal to 10 10 -fold higher than that for the carboxyl or amino groups Ballatori ; Divine et al. Since there is a wide distribution of sulfhydryl groups in the body, especially in proteins, mercuric Hg is believed to cause toxicity by combining with the active centers of critical enzymes and structural proteins.
Experimental studies of the possible biochemical mechanisms of MeHg neurotoxicity have been reviewed in detail Atchison and Hare. Mitochondrial changes, induction of lipid peroxidation, microtuble disruption, and disrupted protein synthesis have all been proposed as possible mechanisms. In developmental toxicity, disruption of cell-surface recognition has also been proposed as a possible mechanism Baron et al. To date, no definitive data are available that point to any one mechanism as the proximate cause for the neurotoxic symptoms associated with MeHg exposure in adults.
Exposure of rats to MeHg has long been known to cause biochemical and ultrastructural changes in the mitochondria, but the evidence is not convincing that those changes are the primary mechanism for MeHg toxicity Denny and Atchison ; Yoshino et al. Sarafian and Verity showed that MeHg causes membrane peroxidation in nerve cells.
Because antioxidants, such as vitamin E and selenium, offer some protection in vivo against MeHg neurotoxicity Chang et al. However, lipid peroxidation does not appear to be the critical mechanism that causes cell lethality for many reasons, as summarized by Atchison and Hare MeHg disrupts protein synthesis, and disruption has been proposed as the primary mechanism of MeHg neurotoxicity. In the rat, inorganic Hg, however, was 10 times more potent an inhibitor of cell-free protein synthesis than MeHg Sugano et al.
Stimulation of protein synthesis by MeHg was also reported Burbaker et al. Mitotic arrest is one of the most sensitive indicators of MeHg exposure in mice. The ratio of late mitotic figures to total mitotic figures was significantly reduced in the cerebellum of exposed mice, indicating mitotic arrest Sager et al. Oxidative stress might also be involved in MeHg toxicity. Glutathione is the major antioxidant of the cell.
After exposure to MeHg, glutathione concentrations decline and then increase. Cells that are made resistant to MeHg toxicity had an increase in the rate of efflux of MeHg and had 4-fold higher glutathione concentrations than normal cells Miura and Clarkson Another proposed mechanism underlying MeHg toxicity is disruption of microtubules in the neuronal cytoskeleton Miura and Imura Hg binds to thiols in the tubulin, the protein monomers that form micro-.
Because the breakdown and assembly of microtubules are required for many cell functions, including cell division and migration, disruption of microtubule assembly could disrupt cellular processes. In vitro, MeHg has been shown to disrupt cell-cycle progression in primary rat brain cells Ponce et al. The developing nervous system would be particularly sensitive to those effects due to the extensive cell division and migration that occurs during its development.
The ability to exchange between thiols forms the basis of therapeutic techniques following both MeHg exposure and exposure to Hg vapor. The neurotoxic effects of combined exposure to MeHg and Hg vapor have been reported to be similar in nature but more severe than those observed following exposure to each alone Fredriksson et al Both cations exhibit a high affinity for SH groups, and association and dissociation reactions are rapid Carty and Malone Both are found in tissues bound to large and small molecular-weight thiol-containing molecules proteins, cysteine, and glutathione.
The formation of Hg thiol bonds is believed to underlie the mobility and toxicity of Hg in the body Clarkson Although the exposure patterns and toxicokinetics and toxicodynamics of the different Hg species are usually studied separately, organic Hg and elemental Hg are eventually converted in vivo to inorganic Hg. The estimated average daily intake and retention of various forms of Hg are shown in Table Estimates of the retention in the body of Hg from dental amalgams range from 3.
The ratio of MeHg to total Hg will be different among those with high fish consumption. The data in Table suggest that average exposure to Hg from dental amalgams might be considerably higher than exposure to Hg from MeHg. However, the available data are not adequate to permit a definitive comparison. MeHg is very slowly but ultimately metabolized in situ in the brain to inorganic Hg. Elemental mercury is also oxidized to inorganic Hg in the brain.
It is unclear whether MeHg toxicity at the cellular level is caused by the parent compound itself, due to the inorganic Hg that is its metabolite, or is caused indirectly by the free radicals generated by the. Inorganic Hg Compounds b. Note: Values given are the estimated average daily intake; the figures in parentheses represent the estimated amount retained in the body of an adult. Values are quoted to two significant figures.
If the ultimate toxic form of MeHg is indeed its inorganic Hg metabolite, that suggests that the dose of inorganic Hg to the brain from elemental Hg exposure particularly from dental amalgams and MeHg might be cumulative. That is the case even if oxidation of elemental Hg in the blood before absorption to the brain is considered. Risk-assessment models for MeHg, therefore, should consider additional chronic sources of exposure to Hg such as dental amalgams.
Such considerations are complicated by uncertainty about the mechanisms by which MeHg specifically exerts its neurodevelopmental toxicity. Such mechanisms might not be the same as those responsible for adult neurotoxicity. Nonetheless, the potential implications of additive toxicity from fish consumption and dental amalgams make elucidation of the mechanisms of MeHg toxicity in the brain a critical research priority. The water solubility of mercuric chloride is greater than elemental Hg. That of elemental Hg is greater than MeHg.
The solubility of the different forms of Hg might play a role in their differential toxicity. Elemental Hg and a portion of MeHg are converted to mercuric Hg in the body. The conversion of MeHg occurs at a very slow rate. Care must be taken to prevent contamination by Hg during sample preparation and analysis. MeHg is readily absorbed from the GI tract. It is bound primarily to red-blood-cell hemoglobin, but some is bound to plasma proteins.
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Hg in blood reflects recent exposure to MeHg and inorganic Hg. The half-life in blood for humans averages 50 days but can vary substantially. Because neonates have an immature transport system, they do not excrete MeHg as rapidly as adults. Hair measurements have the advantage of providing a historical record of MeHg exposure but do not accurately reflect exposure to inorganic Hg. It is excreted mainly via the bile and feces as MeHg and mercuric Hg.
Complexing with GSH is involved. Urine MeHg concentrations do not accurately reflect MeHg exposure. For elemental and inorganic Hg, the half-life in blood is months. The whole-body half-life is slightly longer, but that does not take into account Hg in the brain, which is cleared very slowly. Excretion occurs primarily via urine and feces and, to a small extent, saliva, bile, sweat, and lungs.
Dimercaprol BAL , used in the past for chelation, is contraindicated because it redistributes Hg to the brain. MeHg readily crosses the blood-brain barrier. The rapid uptake of MeHg in the brain has been proposed to be due to lipid solubility, but evidence in rats suggests that the transport is due to the formation of MeHg-cysteine complexes. MeHg accumulates in the brain where it is slowly converted to inorganic Hg. Whether CNS damage is due to MeHg per se, to its biotransformation to inorganic Hg, or to both is still controversial. The mechanisms and cellular site for the biotransformation in humans are not well understood.
Both free-radical and enzymatic biotransformation has been proposed. The critical organ for MeHg toxicity is the brain. Both adult and fetal brains are vulnerable. For elemental Hg, the critical organs are the brain and kidney. Both MeHg and elemental Hg are converted to mercuric Hg in the brain, where it is trapped.
The biological mechanisms for removing mercuric Hg from the brain are limited. The critical organ for mercuric Hg toxicity is the kidney, where it accumulates. There is emerging evidence that the cardiovascular and immune systems might be major sites of MeHg toxicity see Chapter 5. The high affinity of MeHg and mercuric Hg for sulfhydryl groups is believed to be a major mechanism that underlies their toxicity. If those sulfhydryl groups are in the active center of critical enzymes, severe inhibition of essential biochemical pathways occurs.
The toxicology of the three species of Hg — elemental Hg, mercuric Hg and MeHg — are intertwined, because MeHg and elemental Hg are transformed to inorganic Hg in the brain. Risk-assessment models for MeHg in humans are complicated because of inadequate data regarding the cumulative neurotoxic effects of MeHg per se and its biotransformation product mercuric Hg, which has a very long half-live in the brain.
As data become available, exposure to elemental Hg from dental amalgams should be considered in risk assessment of MeHg. Exposure to other chemical forms of Hg should also be considered. Retention of inorganic Hg in the brain for years following early MeHg intake is possibly related to the latent or long-term neurotoxic effects reported.
The long half-life of inorganic Hg in the brain following MeHg intake should be considered in risk assessment of MeHg. The mechanisms, including any enzymes, involved in the biotransformation of MeHg to mercuric Hg in human tissues need to be investigated, especially at the subcellular level. The effects of Hg on signaling pathways and the conformation of enzymes and structural proteins should be further elucidated, because the development and function of the brain would be particularly sensitive to such effects.
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Bruce, R. Dart, K. Hurlbut, D. Levine, W. Zheng, Q. Fernando, D. Carter, and M. Maiorino, D. Gonzalez-Ramirez, M. Zuniga-Charles, Z. Xu, K. Hurlbut, P. Junco-Munoz, R. Dart, and M. Mobilization of heavy metals by newer, therapeutically useful chelating agents. Toxicology 97 Aposhian, M. Maiorino, Z. Xu, and H. Sodium 2,3-dimercaptopropanesulfaonte DMPS treatment does not redistribute lead or mercury to the brain of rats. Toxicology 1 Arenholt-Bindslev, D. Mercury levels and discharge in waste water from dental clinics. Water Air Soil Pollut. Aschner, M. Eberle, and H.
Interactions of methylmercury with rat primary astrocyte cultures: Methylmercury efflux.
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