Alkylmercury Compounds Research Articles

Modification of the toxic effects of methylmercury and thimerosal by testosterone and estradiol in SH-SY5Y neuroblastoma cell line.

Short-chained alkyl mercury compounds accumulate in particularly in the brain. Exposure to these compounds is associated with various neurotoxic effects. Gender-based differences are observed in neurodevelopmental disorders, and testosterone and estradiol may alter the toxic effect of the compounds. The present study aimed to investigate the toxic effects of methylmercury and thimerosal on SH-SY5Y cells in high testosterone/low estradiol and high estradiol/low testosterone containing cellular environment and estimate whether male and female brains react differently to the toxic effects of methylmercury and thimerosal. Study groups (n = 3) were designed as control: growth medium, thimerosal (T): 1.15-μM thimerosal, methylmercury (M): 2.93-μM methylmercury, high testosterone/low estradiol + thimerosal (TT): 1-μM testosterone + 0.75-μM estradiol + 1.15-μM thimerosal, high estradiol/low testosterone + thimerosal (ET): 0.1-μM testosterone + 7.5-μM estradiol + 1.15-μM thimerosal, high testosterone/low estradiol + methylmercury (TM): 1-μM testosterone + 0.75-μM estradiol + 2.93-μM methylmercury and high estradiol/low testosterone + methylmercury (EM): 0.1-μM testosterone + 7.5-μM estradiol + 2.93-μM methylmercury. While a significant decrease in glutathione levels was observed in M group, it was not seen in EM group. A significant increase in the protein carbonyl levels was detected in T group. A similar increase was observed in the TM and TT groups in which testosterone was dominant. It was determined that methylmercury, but not thimerosal, caused significant DNA damage and in TT group. The results showed that both thimerosal and methylmercury are toxic on SH-SY5Y cells and toxic effects of methylmercury are more severe than thimerosal. It has been determined that testosterone and estradiol alter the toxic effects of thimerosal and methylmercury.

Alkylation of uracil and thymine in the gas phase through interaction with alkylmercury compounds

The gas-phase interactions of uracil and thymine with alkylmercury cations, in particular [CH3Hg]+, n-BuHg+ and t-BuHg+, were studied through the use of electrospray ionization coupled to tandem mass spectrometry. We observed that the interaction of akylmercury compounds with the nucleobases (NB) gives rise to a single type of complex of general formula [RHg(NB)]+, except for t-butyl-mercury (no interaction). The subsequent MS/MS experiments show that the [RHg]+ ions (R = Me, n-Bu) exhibit a peculiar reactivity characterized by the transfer of the alkyl group to the nucleobases. Indeed, the main fragmentation process observed leads to the loss of neutral Hg, producing [(NB)R]+ ions. Only when the length of the alkyl chain increases, as in the case of reactions with [n-BuHg]+, a new fragmentation path is opened, yielding the protonated nucleobase, [(NB)H]+, with the concomitant elimination of 2 C4H4 + Hg. A thorough analysis of the mechanisms behind both dominant processes was carried out through the use of Infrared Multiple Photon Dissociation (IRMPD) in the fingerprint region, combined with an analysis of the corresponding potential energy surfaces by using high-level density functional theory (DFT) calculations.

A Simple and Robust Method for Determination of Alkylmercury in Seawater and Industrial Wastewater by Phenylation Pretreatment Combined with GC-MS.

For determination of methylmercury (MeHg) and ethylmercury (EtHg) in seawater and industrial wastewater, a simple and robust analytical method was developed based on phenylation and solvent extraction followed by GC-MS measurement. Alkylmercury compounds were directly phenylated with sodium tetraphenylborate in water and extracted into toluene. The method detection limits obtained for MeHg and EtHg in pure water were 53.3 and 33.5 ng Hg L-1, respectively, which are almost 10 times lower than the environmental quality standards for water pollution in Japan (EQSJ): 0.5 μg Hg L-1. The recoveries of alkylmercury compounds from seawater and four kinds of industrial wastewater except for EtHg from treated wastewater of an optic lens factory were satisfactory (>90%) at 1- or 4-fold concentrations of the EQSJ. Contrarily, the low recovery of EtHg from the treated wastewater (75.4 ± 4.7%) was found to be caused by the rapid decomposition of EtHg into inorganic mercury.

Laying Waste to Mercury: Inexpensive Sorbents Made from Sulfur and Recycled Cooking Oils.

Mercury pollution threatens the environment and human health across the globe. This neurotoxic substance is encountered in artisanal gold mining, coal combustion, oil and gas refining, waste incineration, chloralkali plant operation, metallurgy, and areas of agriculture in which mercury‐rich fungicides are used. Thousands of tonnes of mercury are emitted annually through these activities. With the Minamata Convention on Mercury entering force this year, increasing regulation of mercury pollution is imminent. It is therefore critical to provide inexpensive and scalable mercury sorbents. The research herein addresses this need by introducing low‐cost mercury sorbents made solely from sulfur and unsaturated cooking oils. A porous version of the polymer was prepared by simply synthesising the polymer in the presence of a sodium chloride porogen. The resulting material is a rubber that captures liquid mercury metal, mercury vapour, inorganic mercury bound to organic matter, and highly toxic alkylmercury compounds. Mercury removal from air, water and soil was demonstrated. Because sulfur is a by‐product of petroleum refining and spent cooking oils from the food industry are suitable starting materials, these mercury‐capturing polymers can be synthesised entirely from waste and supplied on multi‐kilogram scales. This study is therefore an advance in waste valorisation and environmental chemistry.

Hunter-Russel syndrome should not to be used for symptoms of poisoning by methylmercury (alkylmercury compounds)

Hunter-Russel syndrome should not to be used for symptoms of poisoning by methylmercury (alkylmercury compounds)

Alkyl Mercury-Induced Toxicity: Multiple Mechanisms of Action.

There are a number of mechanisms by which alkylmercury compounds cause toxic action in the body. Collectively, published studies reveal that there are some similarities between the mechanisms of the toxic action of the mono-alkyl mercury compounds methylmercury (MeHg) and ethylmercury (EtHg). This paper represents a summary of some of the studies regarding these mechanisms of action in order to facilitate the understanding of the many varied effects of alkylmercurials in the human body. The similarities in mechanisms of toxicity for MeHg and EtHg are presented and compared. The difference in manifested toxicity of MeHg and EtHg are likely the result of the differences in exposure, metabolism, and elimination from the body, rather than differences in mechanisms of action between the two.

On the Structures, Lifetimes, and Infrared Spectra of Alkylmercury Hydrides

A series of six small alkylmercury hydrides of the general formula RHgH with R=methyl, ethyl, n-propyl, isopropyl, n-butyl, and 3-butenyl were obtained by reduction in vacuo of the corresponding mercury halide with tributyltin hydride in the presence of a radical inhibitor. These very reactive compounds, which have to be removed from the reaction mixture as they are formed, were characterized by (1)H NMR and (13)C NMR spectroscopy. The IR spectra of n-propyl-, isopropyl-, n-butyl-, and 3-butenylmercury hydride were recorded for the first time. All compounds were then studied by density functional theory calculations on the basis of a recent theoretical assessment for alkylmercury compounds performed by our group. Comparison of the experimental and theoretical results allowed the assignment of the vibrational modes in an unambiguous way, in spite of the low intrinsic stability of some of the derivatives investigated. The experimental procedure implemented for registering the IR spectra of these unstable species in the gas phase allowed us to obtain reasonable estimates of their lifetimes.

Alkyl mercury compounds: an assessment of DFT methods

A series of hybrid and pure density functionals have been assessed in order to provide a reliable description of infrared spectra of alkyl mercury compounds. The theoretical assessment also includes other physicochemical properties, as ionization energies and binding energies. The accuracy of the results was tested through the available experimental data and CCSD(T) calculations. B3LYP functional provides the smallest average error of all functionals considering the whole set of properties, and it offers very good results in IR spectra in particular, although other functionals as BP86, M06-L or mPW1PW91 can give even better results when looking at one particular property. Hybrid functionals B3PW91 and X3LYP and doublehybrid B2PLYP follow B3LYP in the list of most wellbehaved functionals.

Toxicology of alkylmercury compounds.

Methylmercury is a global pollutant and potent neurotoxin whose abundance in the food chain mandates additional studies on the consequences and mechanisms of its toxicity to the central nervous system. Formulation of our new hypotheses was predicated on our appreciation for (a) the remarkable affinity of mercurials for the anionic form of sulfhydryl (-SH) groups, and (b) the essential role of thiols in protein biochemistry. The present chapter addresses pathways to human exposure of various mercury compounds, highlighting their neurotoxicity and potential involvement in neurotoxic injury and neurodegenerative changes, both in the developing and senescent brain. Mechanisms that trigger these effects are discussed in detail.

Quantification and Speciation of Mercury and Selenium in Fish Samples of High Consumption in Spain and Portugal

Mercury (Hg) and selenium (Se) determinations were carried out to evaluate human exposure to those elements through fish consumption in Spain and Portugal. Atomic fluorescence spectroscopy (AFS) was applied in a cold vapor mode for total mercury quantification and was also hyphenated to gas chromatography (GC) to achieve the speciation of organomercurial species in fish samples. The results obtained show the highest concentration of Hg in swordfish and tuna (0.47+/-0.02 and 0.31+/-0.01 microg g-1, respectively), and a much lower concentration in sardine, mackerel shad, and octopus (0.048+/-0.002, 0.033+/-0.001, and 0.024+/-0.001 microg g-1, respectively). The determination of alkyl mercury compounds revealed that 93-98% of mercury in the fish samples was in the organic form. Methylmercury (MeHg) was the only species found in the three fish species with higher mercury content. Total selenium concentration was high in sardine, swordfish, and tuna (0.43+/-0.02, 0.47+/-0.02, and 0.92+/-0.01 microg g-1, respectively), but low in mackerel shad and octopus (0.26+/-0.01 and 0.13+/-0.01 microg g-1, respectively). Speciation of selenium compounds was done by high-performance liquid chromatography in conjunction with inductively coupled plasma mass spectrometry (LC-ICP-MS). Selenomethionine (SeMet) was the only selenium compound identified in the fish samples with higher selenium content. Among the fish species studied, sardine had the most favourable Se:Hg and SeMet:MeHg molar ratios; therefore, its consumption seems to be preferable.

Control of chemicals in Sweden: an example of misuse of the “precautionary principle”

With a background in biochemistry and radiation biology, I started to get involved in the control of chemicals area by battling the use of alkyl-mercury compounds in Swedish agriculture during the years 1964–1965 (C.-G. Rosén, H. Ackefors, and R. Nilsson, 1966, Seed dressing compounds based on organic mercury—economic aspects and health hazards, Svensk Kemisk Tidskrift 78, 8–19), and subsequently I acted as the sole technical advisor to the plaintiffs for the thalidomide children in Sweden for 4 years, ending in a 100 million US dollar (present value) settlement with the producers in 1969 (H. Sjöström and R. Nilsson, 1991, Thalidomide and the Power of the Drug Companies, Penguin, London, Feltrinelli, Milano, Iwanami Shoten, Tokyo Fisher Verlag, Berlin). I joined the Swedish EPA in 1974 and became head of the toxicological unit of the Products Control Division, where I was instrumental inter alia in pushing through regulations on reductions of lead in gasoline as well as the first general restrictions in world on the use of cadmium (R. Nilsson, 1989, Cadmium—an Analysis of Swedish Regulatory Experience, Report to the OECD Chemicals Group and Management Committee, January 1989). Since 1986 responsibility for control of chemicals was largely taken over from the Swedish EPA by the newly created National Chemicals Inspectorate (KEMI), an agency that employs me in the capacity of toxicologist. In between, I have been working for the OECD Chemicals Program as well as for WHO (IPCS) in various capacities and as a consultant in risk assessment for the US chemical industry under the Superfund Program. I was also associated with the Ministries of Environment of the governments of Iran and India. With respect to the latter, part of my recommendations were incorporated in the new Indian laws and regulations on chemicals that were issued subsequent to the Bhopal disaster (R. Nilsson, 1988, Procedures and Safeguards for Notification and Handling of Hazardous Chemicals in India, Report to WHO South-East Asia Region, SEA/EH/391, April 1988). As a consequence of a decreasing role for science in regulatory affairs, and a corresponding increasing influence from politics, for the past 8 years I have devoted myself mainly to research-oriented activities in my capacity as adjunct professor of molecular toxicology and risk assessment at the Stockholm University. In international collaboration, my projects have been supported by the Directorate General for Science, Research and Development of the Commission of the European Communities, the US Chemical Manufacturers’ Association, the Coulston Foundation (Alamogordo, State of New Mexico), L’Oreal, Merck Co., and in the past to a limited extent also by my own agency, the National Swedish Chemicals Inspectorate. However, my position as member of the executive board for the International Society of Regulatory Toxicology and Pharmacology in the United States, which I held for 5 years, as well as my role as technical advisor in products liability litigation, reflects my continued interest in the “politics of chemical risk.” In this context my critical comments with respect to the current regulatory policy for control of chemicals have caused considerable concern within the Swedish regulatory establishment (R. Nilsson, M. Tasheva, and B. Jaeger, 1993. Why different regulatory decisions when the scientific information base is similar? I. Human risk assessment, Regul. Toxicol. Pharmacol. 17, 292–332; R. Nilsson, 1994, Problems in the regulation of carcinogenic chemicals in an international perspective. III. Critical assessment of regulatory approaches. Rev. Int. Contam. Ambiental, México City, 10, 99–199; R. Nilsson, 1998, Integrating Sweden into the European Union: Problems concerning chemicals control. In The Politics of Chemical Risk—Scenarios for a Regulatory Future, R. Bal and Halffman, Eds, pp. 159–171, Kluwer Academic, Dordrecht).

Selective determination of alkylmercury compounds in solid matrices after subcritical water extraction, followed by solid-phase microextraction and GC-MS

A method for the extraction and determination of methylmercury (MeHg) in solid matrices is presented. Combining the advantages of two extraction techniques—subcritical water extraction (subWE) and solid-phase microextraction (SPME)—selective separation of MeHg from soils is possible. The procedure is based on extraction with subcritical water without using organic solvents, followed by in situ aqueous-phase derivatization with sodium tetraethylborate and headspace SPME with a silica fiber coated with poly(dimethylsiloxane). The optimization of the extraction parameters is described. The identification and quantification of the extracted alkylmercury compounds from spiked soil samples is performed by GC–MS after thermal desorption. Copyright © 2000 John Wiley & Sons, Ltd.

Thimerosal positivities: patch testing to methylmercury chloride in subjects sensitive to ethylmercury chloride.

The aim of this paper was to evaluate whether methylmercury chloride (MeHgCl) aq., when patch tested in a group of thimerosal-positive subjects reacting to ethylmercury chloride (EtHgCl), might be a reliable model for the better understanding of interactions between alkylmercury compounds and the skin. 19 out of 21 consecutive patients who previously had given positive patch-test reactions to both ethylmercury chloride 0.0165% eth.(EtHgCl, 0.615 mM) and MeHgCl 0.031% aq.(1.23 mM), and negative reactions to thiosalicylic acid 0.05% (3.24 mM) aq./eth. 50/50, were repatch tested to 8 microl of MeHgCl 0.031% aq. and to 8 microl of aq. solutions containing MeHgCl mixed with cysteine, glutathione, ZnSO4, MgSO4, MnSO4, ZnCl2, MgCl2 and MnCl2, respectively. The results showed that cysteine, glutathione and Zn(II) salts were able to abolish the positive reactions, demonstrating the rôle played by both thiol groups and Zn(II) itself. Patch tests concomitantly carried out in 16 out of 19 patients to 8 microl of aqueous MeHgCl and to 8 microl of aqueous solutions containing MeHgCl and MeHgCl mixed to fragment 56-61 of metallothionein I (MT I), MT I and MT II-Zn, respectively, revealed that all the MTs tested were able to reduce or to inhibit the reactions, demonstrating the effect of the thiol groups. Due to the close chemical similarities to EtHgCl and to its water solubility, MeHgCl seems to be a suitable model for evaluating the reactivity of alkylmercury compounds in the skin. We speculate that both EtHg- and MeHg-derivatives are xenobiotics with similar reactivity. However, the lack of clinical relevance of the reactions to both alkyl compounds lead us to conclude that, since environmental exposure does not seem to play a pivotal rôle, they probably have mostly to do with compounds included in in the standard series, and are elicited by reduced function of physiological SH chelators.

DNA sequence and expression of a defective mer operon from Pseudomonas K-62 plasmid pMR26.

pMRB01 cloned from Pseudomonas K-62 plasmid pMR26 conferred bacterial hypersensitivity to organomercurials. DNA sequence analysis of a 2.3-kb SacI-Aor51HI fragment encompassing the whole region required for expression of the hypersensitive phenotype, revealed three open reading frames. The DNA sequence of these frames had 82.5%, 99.2% and 97.0% homology with the pDU1358 merR, merB and merD, respectively. The pMRB01 mer operon differs from the already known mer operon by the absence of the merT, merP and merA genes in this plasmid. An inverted repeat-like sequence upstream from the predicted merR was observed suggesting that this defective mer operon could be part of a transposon-like structure. Induction experiments and maxicell analysis of the mer-polypeptide showed that the lyase enzyme encoded by pMRB01 merB gene is mercurial-inducible and regulated by the transacting product of the merR gene. These results suggest that the hypersensitivity to organomercurials resulted from the expression of lyase activity encoded by the defective mer operon in the absence of reductase activity. The lyase enzyme encoded by pMRB01 merB catalyzes the protonolysis of the C-Hg bond of both arylmercury and alkylmercury compounds.

Apoptotic process of cerebellar degeneration in experimental methylmercury intoxication of rats.

This report deals with the mechanism involved in the cerebellar degeneration following experimental methylmercury poisoning of male Wistar rats. The cerebellar granule cells of animals that exhibited typical hind leg paresis were shrunken and displayed marked nuclear pyknosis. At the ultrastructural level, the nuclei of these cells were condensed and fragmented, features which are characteristic of apoptosis. In situ staining for DNA strand breaks revealed that the pyknotic nuclei were positively labeled. DNA fragmentation was confirmed by agarose gel electrophoresis; a ladder pattern of multiples of approximately 200-base pair fragments, typical of apoptosis, was observed with the cerebellar DNA of the methylmercury-treated animals. These observations suggest that the degeneration of cerebellar granule cells by alkyl mercury compounds involves an apoptotic process.

95/02073 Research reactor fuel reaches the new world

With a background in biochemistry and radiation biology, I started to get involved in the control of chemicals area by battling the use of alkyl-mercury compounds in Swedish agriculture during the years 1964–1965 (C.-G. Rosén, H. Ackefors, and R. Nilsson, 1966, Seed dressing compounds based on organic mercury—economic aspects and health hazards, Svensk Kemisk Tidskrift 78, 8–19), and subsequently I acted as the sole technical advisor to the plaintiffs for the thalidomide children in Sweden for 4 years, ending in a 100 million US dollar (present value) settlement with the producers in 1969 (H. Sjöström and R. Nilsson, 1991, Thalidomide and the Power of the Drug Companies, Penguin, London, Feltrinelli, Milano, Iwanami Shoten, Tokyo Fisher Verlag, Berlin).I joined the Swedish EPA in 1974 and became head of the toxicological unit of the Products Control Division, where I was instrumental inter alia in pushing through regulations on reductions of lead in gasoline as well as the first general restrictions in world on the use of cadmium (R. Nilsson, 1989, Cadmium—an Analysis of Swedish Regulatory Experience, Report to the OECD Chemicals Group and Management Committee, January 1989).Since 1986 responsibility for control of chemicals was largely taken over from the Swedish EPA by the newly created National Chemicals Inspectorate (KEMI), an agency that employs me in the capacity of toxicologist. In between, I have been working for the OECD Chemicals Program as well as for WHO (IPCS) in various capacities and as a consultant in risk assessment for the US chemical industry under the Superfund Program. I was also associated with the Ministries of Environment of the governments of Iran and India. With respect to the latter, part of my recommendations were incorporated in the new Indian laws and regulations on chemicals that were issued subsequent to the Bhopal disaster (R. Nilsson, 1988, Procedures and Safeguards for Notification and Handling of Hazardous Chemicals in India, Report to WHO South-East Asia Region, SEA/EH/391, April 1988).As a consequence of a decreasing role for science in regulatory affairs, and a corresponding increasing influence from politics, for the past 8 years I have devoted myself mainly to research-oriented activities in my capacity as adjunct professor of molecular toxicology and risk assessment at the Stockholm University. In international collaboration, my projects have been supported by the Directorate General for Science, Research and Development of the Commission of the European Communities, the US Chemical Manufacturers’ Association, the Coulston Foundation (Alamogordo, State of New Mexico), L’Oreal, Merck Co., and in the past to a limited extent also by my own agency, the National Swedish Chemicals Inspectorate.However, my position as member of the executive board for the International Society of Regulatory Toxicology and Pharmacology in the United States, which I held for 5 years, as well as my role as technical advisor in products liability litigation, reflects my continued interest in the “politics of chemical risk.” In this context my critical comments with respect to the current regulatory policy for control of chemicals have caused considerable concern within the Swedish regulatory establishment (R. Nilsson, M. Tasheva, and B. Jaeger, 1993. Why different regulatory decisions when the scientific information base is similar? I. Human risk assessment, Regul. Toxicol. Pharmacol. 17, 292–332; R. Nilsson, 1994, Problems in the regulation of carcinogenic chemicals in an international perspective. III. Critical assessment of regulatory approaches. Rev. Int. Contam. Ambiental, México City, 10, 99–199; R. Nilsson, 1998, Integrating Sweden into the European Union: Problems concerning chemicals control. In The Politics of Chemical Risk—Scenarios for a Regulatory Future, R. Bal and Halffman, Eds, pp. 159–171, Kluwer Academic, Dordrecht).

95/02076 Scientifically valid leaching of coal conversion solid residues to predict environmental impact

With a background in biochemistry and radiation biology, I started to get involved in the control of chemicals area by battling the use of alkyl-mercury compounds in Swedish agriculture during the years 1964–1965 (C.-G. Rosén, H. Ackefors, and R. Nilsson, 1966, Seed dressing compounds based on organic mercury—economic aspects and health hazards, Svensk Kemisk Tidskrift 78, 8–19), and subsequently I acted as the sole technical advisor to the plaintiffs for the thalidomide children in Sweden for 4 years, ending in a 100 million US dollar (present value) settlement with the producers in 1969 (H. Sjöström and R. Nilsson, 1991, Thalidomide and the Power of the Drug Companies, Penguin, London, Feltrinelli, Milano, Iwanami Shoten, Tokyo Fisher Verlag, Berlin).I joined the Swedish EPA in 1974 and became head of the toxicological unit of the Products Control Division, where I was instrumental inter alia in pushing through regulations on reductions of lead in gasoline as well as the first general restrictions in world on the use of cadmium (R. Nilsson, 1989, Cadmium—an Analysis of Swedish Regulatory Experience, Report to the OECD Chemicals Group and Management Committee, January 1989).Since 1986 responsibility for control of chemicals was largely taken over from the Swedish EPA by the newly created National Chemicals Inspectorate (KEMI), an agency that employs me in the capacity of toxicologist. In between, I have been working for the OECD Chemicals Program as well as for WHO (IPCS) in various capacities and as a consultant in risk assessment for the US chemical industry under the Superfund Program. I was also associated with the Ministries of Environment of the governments of Iran and India. With respect to the latter, part of my recommendations were incorporated in the new Indian laws and regulations on chemicals that were issued subsequent to the Bhopal disaster (R. Nilsson, 1988, Procedures and Safeguards for Notification and Handling of Hazardous Chemicals in India, Report to WHO South-East Asia Region, SEA/EH/391, April 1988).As a consequence of a decreasing role for science in regulatory affairs, and a corresponding increasing influence from politics, for the past 8 years I have devoted myself mainly to research-oriented activities in my capacity as adjunct professor of molecular toxicology and risk assessment at the Stockholm University. In international collaboration, my projects have been supported by the Directorate General for Science, Research and Development of the Commission of the European Communities, the US Chemical Manufacturers’ Association, the Coulston Foundation (Alamogordo, State of New Mexico), L’Oreal, Merck Co., and in the past to a limited extent also by my own agency, the National Swedish Chemicals Inspectorate.However, my position as member of the executive board for the International Society of Regulatory Toxicology and Pharmacology in the United States, which I held for 5 years, as well as my role as technical advisor in products liability litigation, reflects my continued interest in the “politics of chemical risk.” In this context my critical comments with respect to the current regulatory policy for control of chemicals have caused considerable concern within the Swedish regulatory establishment (R. Nilsson, M. Tasheva, and B. Jaeger, 1993. Why different regulatory decisions when the scientific information base is similar? I. Human risk assessment, Regul. Toxicol. Pharmacol. 17, 292–332; R. Nilsson, 1994, Problems in the regulation of carcinogenic chemicals in an international perspective. III. Critical assessment of regulatory approaches. Rev. Int. Contam. Ambiental, México City, 10, 99–199; R. Nilsson, 1998, Integrating Sweden into the European Union: Problems concerning chemicals control. In The Politics of Chemical Risk—Scenarios for a Regulatory Future, R. Bal and Halffman, Eds, pp. 159–171, Kluwer Academic, Dordrecht).

The molecular and electronic structures of ions and radicals derived from alkylmercury(II) compounds: an SCF-MO study

Molecular geometries and energies have been calculated by the semi-empirical MNDO method for closed shell species and by the UHF-MNDO method for neutral radicals, radical-cations and radical-anions, for R 2Hg (R = Me,Et), RHgX(X = Cl, Br, I)and their radical-cations, fragment ions and radicals (including RHg·, ·CH 2HgCH 3, ·CH 2HgX, and CH 3·CHHgX) and (HgMe 2) −. The radical-cations (R 2Hg) + have structures in which the organic substituents are nearly planar at the α-carbon; (CH 3HgX) + all have structures of C 3 v symmetry, but while (CH 3HgCl) + has a 2 E ground state, both (CH 3HgBr) + and (CH 3HgI) + have 2 A 1 ground states.

Studies on the role of gastrointestinal tract contents in the methylation of inorganic mercury compounds.

The toxic action of the mercury compounds and their bioavailability depends on the chemical structure of the compound. It is well known that mercury compounds can be transformed into metallic mercury or to alkyl mercury compounds in the environment. This transformation caused by microorganisms was observed in the soil and human feces. Therefore, the idea that inorganic mercury ingested in small quantities with daily meals can be partly transformed into alkyl mercury compounds can not be rejected without prior experiments. Result of such studies should be of special importance, because of the exceptionally high toxicity of methylmercury ion (MeHg) and its delayed neurotoxic action especially when in utero exposure is concerned. This study aimed at the investigation of the fate of inorganic mercury compounds influenced by the contents of the gastrointestinal tract.

Optimisation of an atmospheric pressure helium microwave-induced plasma coupled with capillary gas chromatography for the determination of alkyllead and alkylmercury compounds

This paper describes the optimisation of a microwave-induced plasma (MIP) spectrometer for the determination and speciation of organometallic compounds. The MIP was interfaced to a gas chromatograph by threading a capillary column down a heated transfer line directly into the plasma torch. Both simplex and univarite search methods were investigated for the optimisation of the system for the organometallic compounds. For both the mercury and lead compounds the most critical parameter was found to be the plasma gas flow-rate. The calibration graphs obtained for liquid standards of these compounds were linear over three orders of magnitude and detection limits of about 1 pg were obtained without background correction or the use of scavenger gases.