Toxicity Of Arsenic Compounds Research Articles

Determination of Arsenic Species Distribution in Arsenide Tailings and Leakage Using Geochemical and Geophysical Methods

This study describes the distribution of arsenic mobile species in the tailings of Cu–Co–Ni–arsenide using the sequential extraction and determining the contents of arsenate (AsV) and arsenite (AsIII). The object of this study is the tailings ponds of the Tuvakobalt plant, which contains waste from the hydrometallurgical arsenide ore processing of the Khovu-Aksy deposit (Republic of Tuva, Russia). A procedure of sequential extraction for arsenic was applied, and it includes the extraction of the following forms: water-soluble, potentially water-soluble and exchangeable, easily sorbed on the surface of carbonates, associated with Fe/Mn oxides/hydroxides, associated with easily oxidized minerals, and accounted for by non-oxidized arsenic minerals. This procedure, which takes into account the peculiarities of the physical and chemical composition of the waste, was supplemented by the analytical determination of the arsenite and arsenate content by using the methods of inductively coupled plasma atomic emission spectrometry (ICP-AES) combined with the hydride generation technique (HG-ICP-AES). The content of the most mobile forms of arsenic, which are water-soluble, potentially water-soluble, and exchangeable species, is equal to 56% of the total arsenic content, 23% and 33% of which are arsenite and arsenate, respectively. Unlike arsenic, the mobile forms of metals have been determined in small quantities. The largest proportion of water-soluble and exchangeable forms is formed by Mg, Ca, and Sr at 11, 9.4, and 20%, respectively (residual and redeposited carbonates). The proportion of water-soluble forms of other metals (Cu, Zn, Co, and Ni) is < 1% or 0. The main part of the metals is adsorbed on the surface of Fe and Mn hydroxides, enclosed in easily and hardly oxidized minerals. In addition to geochemical studies, the presence of leaks from the tailing ponds into ground waters was determined by using electrical resistivity tomography. The data obtained indicate a high environmental hazard of tailings and the possibility of water-soluble and highly toxic arsenic compounds entering ground waters and aquifers.

До обґрунтування переліку небезпечних високотоксичних хімічних речовин, які підлягають особливому контролю щодо обігу, зберігання, використання та утилізації. Частина ІІ (сполуки миш'яку та ціаніди)

The Aim of the Research. To identify a group of highly toxic chemicals which over the past decades are most often used in deliberate criminal and suicidal incidents, sabotage, and terrorist act; the handling, storage, use and disposal of which must be especially carefully monitored by law enforcement agencies. In this part of the article arsenic compounds and cyanide are considered. Materials and Methods. An analytical review of scientific publications was carried out using the abstract databases of scientific libraries Pub Med, Medline and text databases of scientific publishing houses Elsevier, Pub Med, Central, BMJ group as well as other VIP databases. Methods of systemic, comparative, and content analysis were used. Results and Conclusions. Scientific publications that contain information on highly toxic arsenic compounds and cyanides, which pose a threat to human life and health, were analyzed. Recently, in particular for more than a quarter of a century, they have become a real weapon in the hands of criminals, delinquents, and terrorists all over the world. Suicidal incidents, which also take place along with intentional criminal, terrorist, and sabotage acts, should not be concealed. Based on the analysis of the toxicity, clinical and morphological expression of intoxication when exposed to these chemicals, considering various routes of entry into the body, the need to include them in the List of hazardous highly toxic chemicals, the handling, storage, use, and disposal of which require stricter control of law enforcement agencies, is justified. Key Words: arsenic compounds, cyanide, health risk, acute poisoning.

Making good use of arsenic’s toxicity to control pests and diseases

The toxicity of arsenic compounds has meant that uncontrolled exposure to them raises issues of industrial health and safety and environmental contamination. Deployed under controlled conditions, however, arsenic compounds have been used to improve human health through control of syphilis (Salvarsan) and general well-being (Fowler’s solution) and, more recently, for treatment of some cancers. Animal health has been improved, too, by the use of arsenicals to treat parasites, crops have been protected from insect pests, and biological materials in museum and other collections have been preserved from insect and fungal attack. In some case, widespread dispersion of arsenical biocides has left a legacy of environmental contamination.

Arsenic speciation and elemental composition of rice samples from the Slovenian market

A survey of highly toxic arsenic compounds, together with some other elements was carried out on 40 polished rice samples (white, basmati and parboiled) and 10 brown rice samples from the Slovenian market. The average total As concentration was 157 ± 60 μg kg−1; highest levels were found in parboiled and brown rice and lowest in basmati. The average inorganic As concentration was 90 ± 35 μg kg−1. Dimethylarsinic acid and monomethylarsonic acid, which also exhibit high toxicity levels in some cases constitute >50% of total arsenic and might deserve more attention. Contrary to other foods, the total arsenic concentration in rice may even be a better health hazard indicator than the inorganic arsenic concentration. Elemental analysis of rice revealed large differences between polished and brown rice, especially for Mg, Mn, P, Fe and K, which were 2–4 times higher in brown rice than in polished rice.

Monitoring Arsenic Species Content in Seaweeds Produced off the Southern Coast of Korea and Its Risk Assessment

Seaweed, a popular seafood in South Korea, has abundant dietary fiber and minerals. The toxicity of arsenic compounds is known to be related to their chemical speciation, and inorganic arsenic (iAs) is more detrimental than other species. Due to the different toxicities of the various chemical forms, speciation analysis is important for evaluating arsenic exposure. In this study, total arsenic (tAs) and six arsenic species (arsenite, arsenate, monomethylarsonic acid, dimethylarsinic acid, arsenobetaine, and arsenocholine) were analyzed in 180 seaweed samples. Although there were differences between seaweed species, the concentration of tAs was detected at levels ranging from 1 to 100 µg/g, and the distribution of six arsenic species differed depending on the seaweed species. No correlation between the concentration of iAs and tAs was found in most seaweed species. Through statistical clustering, hijiki and gulfweed were seen to be the seaweeds with the highest ratios of iAs to tAs. Using the iAs concentration data from the arsenic speciation analysis, a risk assessment of seaweed intake in South Korea was conducted. The margin of exposure values showed no meaningful risk for the general population, but low levels of risk were identified for seaweed consumers, with high intakes of gulfweed and hijiki.

Expansion of the Transporter-Opsin-G protein-coupled receptor superfamily with five new protein families.

Here we provide bioinformatic evidence that the Organo-Arsenical Exporter (ArsP), Endoplasmic Reticulum Retention Receptor (KDELR), Mitochondrial Pyruvate Carrier (MPC), L-Alanine Exporter (AlaE), and the Lipid-linked Sugar Translocase (LST) protein families are members of the Transporter-Opsin-G Protein-coupled Receptor (TOG) Superfamily. These families share domains homologous to well-established TOG superfamily members, and their topologies of transmembranal segments (TMSs) are compatible with the basic 4-TMS repeat unit characteristic of this Superfamily. These repeat units tend to occur twice in proteins as a result of intragenic duplication events, often with subsequent gain/loss of TMSs in many superfamily members. Transporters within the ArsP family allow microbial pathogens to expel toxic arsenic compounds from the cell. Members of the KDELR family are involved in the selective retrieval of proteins that reside in the endoplasmic reticulum. Proteins of the MPC family are involved in the transport of pyruvate into mitochondria, providing the organelle with a major oxidative fuel. Members of family AlaE excrete L-alanine from the cell. Members of the LST family are involved in the translocation of lipid-linked glucose across the membrane. These five families substantially expand the range of substrates of transport carriers in the superfamily, although KDEL receptors have no known transport function. Clustering of protein sequences reveals the relationships among families, and the resulting tree correlates well with the degrees of sequence similarity documented between families. The analyses and programs developed to detect distant relatedness, provide insights into the structural, functional, and evolutionary relationships that exist between families of the TOG superfamily, and should be of value to many other investigators.

Analytical Methodologies for the Determination of Organoarsenicals in Edible Marine Species: A Review.

Setting regulatory limits for arsenic in food is complicated, owing to the enormous diversity of arsenic metabolism in humans, lack of knowledge about the toxicity of these chemicals, and lack of accurate arsenic speciation data on foodstuffs. Identification and quantification of the toxic arsenic compounds are imperative to understanding the risk associated with exposure to arsenic from dietary intake, which, in turn, underscores the need for speciation analysis of the food. Arsenic speciation in seafood is challenging, owing to its existence in myriads of chemical forms and oxidation states. Interconversions occurring between chemical forms, matrix complexity, lack of standards and certified reference materials, and lack of widely accepted measurement protocols present additional challenges. This review covers the current analytical techniques for diverse arsenic species. The requirement for high-quality arsenic speciation data that is essential for establishing legislation and setting regulatory limits for arsenic in food is explored.

Accurate Measurement of Total Arsenic in Rice and Oyster by Considering Arsenic Species

Toxicity due to arsenic (As) in food has been mostly assessed by the determination of total As amount. Although the toxicity depends on the chemical forms, the sample can be determined to be safe if the total As concentration is less than the maximum allowable amounts of the toxic arsenic compounds. In this work, the accuracy of total As analysis for rice and oyster samples was significantly influenced by the matrix effect and the chemical forms. The matrix effect could be effectively corrected by employing the appropriate internal standard, tellurium. The As species such as As(V), As(III), monomethylarsonic acid, dimethylarsinic acid, and arsenobetaine showed significantly different sensitivities in the inductively coupled plasma mass spectrometry analysis for rice and oyster samples. This indicates that the total As determined without any information of the chemical species and matching sensitivities of samples and standards may be inaccurate.

Arsenic species in rice and rice-based products consumed by toddlers in Switzerland

ABSTRACTInorganic arsenic (iAs) is a contaminant present in food, especially in rice and rice-based products. Toxicity of arsenic compounds (As) depends on species and oxidative state. iAs species, such as arsenite (As(III)) and arsenate (As(V)), are more bioactive and toxic than organic arsenic species, like methylarsonic acid (MMA(V)) and dimethylarsinic acid (DMA(V)) or arsenosugars and arsenobetaine. An ion chromatography-inductively coupled-plasma-mass spectroscopy method was developed to separate the four following arsenic anions: As(III), As(V), MMA(V) and DMA(V). Sample preparation was done in mild acidic conditions to ensure species preservation. The predominant arsenic species found in rice and rice-based products, except for rice drinks, was As(III), with 60–80% of the total As content, followed by DMA(V) and As(V). MMA(V) was measured only at low levels (<3%). Analyses of rice products (N = 105) intended for toddlers, including special products destined for infants and toddlers, such as dry form baby foods (N = 12) or ready-to-use form (N = 9), were done. It was found in this study that there is little or no margin of exposure. Risk assessment, using the occurrence data and indicated intake scenarios compared to reference BMDLs as established by EFSA, demonstrated toddlers with a high consumption of rice based cereals and rice drinks are at risk of high iAs exposure, for which a potential health risk cannot be excluded.

Selective arsenic removal from enargite by alkaline digestion and water leaching

Copper concentrates with elevated enargite content are not apt to be treated by the current technology of smelting/converting because of the high risk of pollution with toxic arsenic compounds. Therefore, these copper–high arsenic concentrates must be pretreated to remove the arsenic before smelting and the traditional method of pretreatment is roasting. In this work, an alternative hydrometallurgical method for selective removal of arsenic from enargite is presented. The process consists of alkaline digestion with a concentrated Na2S–NaOH solution followed by water leaching. The experimental results obtained using high grade enargite showed that the alkaline digestion is very effective for rapid and selective removal of arsenic from enargite. The copper in the solid residues remains as digenite (Cu9S5). More than 97% of the arsenic was removed in 12min of digestion at 80°C, 100% excess of Na2S and 2M of NaOH. The kinetics of the digestion reaction was analyzed by a shrinking particle kinetic model and the determined activation energy was 22.1kJ/mol for the temperature range of 70–90°C. This activation energy is consistent with a mass transfer kinetic control.

Arsenic-Based Warfare Agents: Production, Use, and Destruction

Since the beginning of time, civilizations have looked for more creative ways to dominate and defeat their enemies. The rapid development of the chemical industry just before the Second World War started the era of modern chemical weapon production based on poisons, including toxic arsenic compounds. This paper provides a detailed overview of the production, usage and destruction of this dangerous chemical weapon. Milestones include: (i) the development of knowledge concerning the synthesis and decomposition of toxic warfare agents containing arsenic compounds, (ii) increased awareness of the influence of this poison on human life and the environment, (iii) the development of modern technology for the destruction of chemical weapons, (iv) implementation of legislation which prohibits the use of chemical weapons in combat, and (v) the development of analytical methods to detect arsenic compounds in the environment that was used in warfare.The article includes events before World War I and next focuses on World War II, the Vietnam War and the two Gulf Wars. It further details the development of specific arsenical chemical weapons (e.g. Lewisite, Clark I, Clark II, Adamsite), as well as some agents used as herbicides, like Agent Blue. Special attention is paid to the disarmament times and the challenges of implementing a world-wide plan to destroy chemical weapon stockpiles.

The influence of solid matrices on arsenic toxicity to Corophium orientale

In marine ecosystems, benthic organisms are really important because they are the first step in the transfer of contaminants from environment to biota. To this end, this study focused on biological assays with the amphipod Corophium orientale exposed to two different molecules of arsenic: arsenate (AsV), the most abundant form in sediments, and dimethyl-arsinate (DMA), expected to be moderately toxic as an intermediate in the process of detoxification. The toxicity of arsenic compounds was measured after exposure to three different matrices: water, spiked natural sediment and inert spiked quartz sand. LC50 values were calculated for each exposure, and the results confirmed the highest toxicity of AsV, in addition to underlining the importance of matrix of exposure. Water exposure was the matrix which presented the highest toxicity for inorganic arsenic (AsV LC50=3.51 mg L−1 vs DMA LC50=54.65 mg L−1), spiked natural sediment demonstrated its capability to chelate arsenate toxicity (AsV LC50=34.27 mg kg−1 vs. DMA LC50=52.19 mg kg−1) and spiked quartz sand presented intermediate values for AsV (LC50=25.26 mg kg−1), whereas for DMA a lower toxicity was registered (LC50=872.35 mg kg−1). This study can provide some useful data linked with chemical speciation of arsenic and exposure matrix, for improving the correct management of contaminated sediment.

Concomitant Induction of Heme Oxygenase‐1 Attenuates the Cytotoxicity of Arsenic Species from Lumbricus Extract in Human Liver HepG2 Cells

Heme oxygenase-1 (HO-1) is an inducible antioxidant enzyme that degrades heme to three products, biliverdin, carbon monoxide (CO), and iron ion. The present study was originally designed to characterize the HO-1 induction by Lumbricus extract as a potential cytoprotective mechanism. Through bioactivity-guided fractionation, with human HepG2 cells as the cellular detector, surprisingly, we found that arsenic was enriched in the active fractions isolated from Lumbricus extract. Arsenic speciation was further carried out by liquid chromatography with inductively coupled plasma mass spectrometry (LC/ICP-MS). Our results showed that Lumbricus extract contained two major arsenic species, arsenite (As(III) ; 53.7%) and arsenate (As(V) ; 34.2%), and six minor arsenic species. Commercial sodium arsenite (NaAsO(2) ) was used to verify the effects of Lumbricus extract on HO-1 expression and related intracellular signaling pathways. Both p38 MAP kinase and NF-E2-related factor 2 (Nrf2) pathways were found to modulate HO-1 induction by Lumbricus extract and NaAsO(2) . The cytotoxicity of arsenite was augmented by p38 MAP kinase inhibitor SB202190 and HO-1 inhibitor tin protoporphyrin IX (SnPP), whereas p38 MAP kinase inhibitor SB202190 also inhibited HO-1 induction by NaAsO(2) . These results suggest that arsenic-containing compounds are responsible for HO-1 induction by Lumbricus extract. Although the exact role of toxic arsenic compounds in the treatment of oxidative injury remains unclear, concomitant HO-1 induction may be a key mechanism to antagonize the cytotoxicity of arsenic compounds in human cells.

Second-order modeling of arsenite transport in soils

Rate limited processes including kinetic adsorption–desorption can greatly impact the fate and behavior of toxic arsenic compounds in heterogeneous soils. In this study, miscible displacement column experiments were carried out to investigate the extent of reactivity during transport of arsenite in soils. Arsenite breakthrough curves (BTCs) of Olivier and Windsor soils exhibited strong retardation with diffusive effluent fronts followed by slow release or tailing during leaching. Such behavior is indicative of the dominance of kinetic retention reactions for arsenite transport in the soil columns. Sharp decrease or increase in arsenite concentration in response to flow interruptions (stop-flow) further verified that non-equilibrium conditions are dominant. After some 40–60 pore volumes of continued leaching, 30–70% of the applied arsenite was retained by the soil in the columns. Furthermore, continued arsenite slow release for months was evident by the high levels of residual arsenite concentrations observed during leaching. In contrast, arsenite transport in a reference sand material exhibited no retention where complete mass recovery in the effluent solution was attained. A second-order model (SOM) which accounts for equilibrium, reversible, and irreversible retention mechanisms was utilized to describe arsenite transport results from the soil columns. Based on inverse and predictive modeling results, the SOM model successfully depicted arsenite BTCs from several soil columns. Based on inverse and predictive modeling results, a second-order model which accounts for kinetic reversible and irreversible reactions is recommended for describing arsenite transport in soils.

Comparative Toxicity of Arsenic Metabolites in Human Bladder Cancer EJ-1 Cells

The human bladder is one of the primary target organs for arsenic-induced carcinogenicity, and arsenic metabolites in urine have been suspected to be directly involved in carcinogenesis. Thioarsenicals are commonly found in human and animal urine and are also considered to be highly toxic arsenic metabolites. The present study was performed to gain insight into the toxicity and accumulation of arsenic species found in urine, including arsenate (iAs(V)), arsenite (iAs(III)), monomethylarsonic acid (MMA(V)), monomethylmonothioarsonic acid (MMMTA(V)), dimethylarsinic acid (DMA(V)), dimethylarsinous acid (DMA(III)), dimethylmonothioarsinic acid, (DMMTA(V)), and dimethyldithioarsinic acid (DMDTA(V)) in human bladder cancer EJ-1 cells. The order of cytotoxicity of these arsenic compounds in EJ-1 human bladder cancer cells was DMA(III), DMMTA(V) > iAs(III) ≫ iAs(V) > MMMTA(V) > MMA(V), DMA(V), and DMDTA(V), indicating that the sulfur-containing DMMTA(V) was among the most toxic arsenic compounds similar to trivalent DMA(III). We further characterized the DNA damage, generation of highly reactive oxygen species (hROS), and expression of proteins p21 and p53 in cells after exposure to iAs(III), DMA(III), and DMMTA(V). Cellular exposure to DMMTA(V) resulted in reduced protein expression of p53 and p21, increased DNA damage, and increased intracellular hROS (hydroxyl radical). In contrast, iAs(III) significantly increased the protein expression of p21 and p53 and did not increase the hROS at the IC(50). Intracellular glutathione (GSH) was reduced by 60% after exposure to DMA(III) or DMMTA(V), suggesting that DMMTA(V) causes cell death through oxidative stress. In contrast, GSH levels increased in cells exposed to iAs(III), and hROS only increased after a long exposure to iAs(III). Our findings demonstrate that DMMTA(V) may be one of the most toxicologically potent arsenic species, relevant to arsenic-induced carcinogenicity in the urinary bladder.

Non-biological inhibition-based sensing (NIBS) demonstrated for the detection of toxic arsenic compounds

This work demonstrates the success of a recently developed technique in chemical amplification, non-biological inhibition-based sensing (NIBS), for the detection of toxic arsenic compounds. Screening for toxic arsenic compounds is especially important due to their prevalence in wastewater and water sources. The detection method presented in this work amplifies the chemical response of toxic arsenic compounds by developing a sensor chemistry where the analyte inhibits, rather than enhances, the rate of a catalytic reaction. This technique mimics the work done with enzyme inhibition; however, using non-biological molecules allows for selective detection without the shelf-life issue associated with biological molecules. Using NIBS we find that we can enhance the sensitivity of the system by two orders of magnitude with no apparent loss in selectivity. This work demonstrates the versatility of NIBS, showing that the technique can be of general use for the detection of toxic compounds.

Magnetometric evaluation of toxicities of chemicals to the lungs and cells

Because the lungs are exposed to airborne hazardous materials, alveolar macrophages (AMs) play a major role in defending against the exposure to various noxious chemical substances. In this study, we reviewed magnetometric investigations of the effects of various chemicals on the lungs and AMs. Magnetometry, using magnetite as an indicator, was used to evaluate the effects of certain chemicals on the lung and AMs. A rapid decrease of the remanent magnetic field after the cessation of external magnetization, a phenomenon called relaxation, was impaired when the lungs and macrophages were exposed to toxic substances. The delayed in vivo relaxation observed in the lungs exposed to magnetite and gallium arsenide was almost identical to the in vitro relaxation observed in the AMs exposed to the same materials. Delayed relaxation was observed in the AMs exposed to silica dust; various fibers, such as chrysotile and some man-made mineral fibers; and toxic arsenic and cadmium compounds. The extracellular release of lactate dehydrogenase activity was found in the AMs exposed to the chemicals. Relaxation is attributed to the cytoskeleton-driven rotation of phagosomes containing magnetite. While the exact mechanism of delayed relaxation due to exposure to harmful chemicals remains to be clarified, cell magnetometry appears to be useful for the safety screening of chemical substances.

Solubility of mimetite Pb5(AsO4)3Cl at 5 - 55°C

Environmetal context.The mobility of toxic arsenic compounds in the environment can be controlled by the solubility of certain minerals. To predict and model the fate and behaviour of these contaminants, the solubility and related thermodynamic properties of the lead and arsenic mineral mimetite were determined. The data obtained in this study will be used to optimise and increase the effectiveness of remediation procedures that are already applied to contaminated sites. Abstract.The solubility of the synthesised mimetite was measured in a series of dissolution experiments at 5–55°C and at pH values between 2.00 and 2.75. The solubility product logKSP for the reaction Pb5(AsO4)3Cl ↔ 5Pb2+ + 3AsO43– + Cl– at 25°C is –76.35 ± 1.01. The free energy of formation ΔGf,2980 calculated from this measured solubility product equals –2634.3 ± 5.9 kJ mol–1. The temperature dependence of the logKSP is non-linear, indicating that the enthalpy of the reaction depends on the temperature. The enthalpy of the formation of mimetite ΔHf0, is –2965.9 ± 4.7 kJ mol–1, the entropy, ΔS0, is 39.5 J mol–1 K–1, and the heat capacity, ΔCp,f0 is –6172 ± 105 J mol–1 K–1. Hydrochemical modelling indicates that regardless of the composition of the background solution, Pb5(AsO4)3Cl is most stable at neutral to weakly alkaline pH.

Arsenic pollution: a global synthesis

List of Figures. List of Tables. Series Editors' Preface. Acknowledgements. List of Abbreviations. Glossary. 1. Introduction . 1.1. Background. 1.2. The Nature of Arsenic Pollution. 1.3. History of Natural Arsenic Contamination. 1.4. Arsenic Pollution. 1.5. Risk, Perception and Social Impacts. 1.6. Water-supply Mitigation. 1.7. Structure and Scope of the Book. 2. Hydrogeochemistry of Arsenic . 2.1. Introduction. 2.2. The Chemistry of Normal and Arsenic-Rich Groundwaters. 2.3. Adsorption and Desorption of Arsenic. 2.4. The Role of Sulphur in Strongly Reducing Groundwater. 2.5. Arsenic and Microbial Activity. 2.6. Arsenic Mobilisation Mechanisms. 2.7. Associations of Arsenic with other Trace Elements. 2.8. Arsenic Pollution and Mining. 2.9. Summary. Annexe 2.1. Analysis of Arsenic in Natural Waters. 3. The Hydrogeology of Arsenic . 3.1. Introduction. 3.2. Arsenic in Rocks and Sediments. 3.3. Arsenic in River Water and Sediment. 3.4. Geo-environmental Associations of Arsenic in Groundwater. 3.5. Geochemical Processes in their Geological Context. 3.6. Behaviour of Arsenic in Aquifers. 3.7. Case Histories of Arsenic-affected Aquifers. 3.8. Implications of Long-term Pumping of Arsenic Contaminated Groundwater. 3.9. Summary and Conclusions. 4. Soils and Agriculture . 4.1. Introduction. 4.2. Arsenic in Soils. 4.3. Irrigation with Arsenic-contaminated Water. 4.4. Arsenic Uptake by plants. 4.5. Options for Arsenic Management. 4.6. Research and Development Needs. 5. Health Effects of Arsenic in Drinking Water and Food. 5.1. Introduction. 5.2. A Short History of the Health Effects of Chronic Arsenic Poisoning. 5.3. Toxicity of Arsenic Compounds. 5.4. Environmental Exposure to Arsenic. 5.5. Acute Arsenic Poisoning. 5.6. Dermatological Manifestations. 5.7. Carcinogenic effects. 5.8. Systemic Non-carcinogenic Effects. 5.9. Social and Psychological Effects. 5.10. Effect of Other Toxic and Trace Elements. 5.11. Geographical differences in Health Effects. 5.12. Case History of Arsenic Exposure in Murshidabad District, West Bengal. 5.13. Diagnosis and Treatment of Arsenicosis. 5.14. Removing Exposure to Arsenic. 5.15. Summary and Recommendations. 6. Water-supply Mitigation . 6.1. Introduction. 6.2. Approaches to Water-supply Mitigation. 6.3. Surveys of Arsenic Affected Areas. 6.4. Exploiting Safe Groundwater Sources. 6.5. Developing Surface Water Sources. 6.6. Arsenic in Water Distribution Networks. 6.7. Socio-economic Aspects of Mitigation. 6.8. Policy and Planning Initiatives. 6.9. Monitoring and Evaluation of Water-supply Mitigation Programmes. 6.10. Summary. Annexe 6.1. Arsenic Survey Procedures. 7. Removing Arsenic from Drinking Water . 7.1. Introduction. 7.2. Water Quality Issues. 7.3. Methods of Arsenic Removal. 7.4. Aquifer Clean-up. 7.5. Disposing of Waste from Treatment Processes. 7.6. Examples and Operational Experience of Arsenic Removal Technologies. 7.7. Costs of Arsenic Removal. 7.8. Guidance for Selecting Treatment Methods and Technologies. 7.9. Case Study of Water Treatment Requirements in Bangladesh. 7.10. Future Needs. 8. Arsenic in Asia . 8.1. Introduction. 8.2. South Asia. 8.3. Southeast Asia. 8.4. China. 8.5. East Asia. 8.6. Western, Central and Northern Asia. 8.7. Suspect Terrain and Research Needs. Annexe 8.1. The British Geological Survey Court Case. 9. Arsenic in North America and Europe. 9.1. Introduction. 9.2. United States of America and Canada. 9.3. Mexico. 9.4. Europe. 9.5. Suspect Terrain and Research Needs. 10. Arsenic in South and Central America, Africa, Australia and Oceania . 10.1. Introduction. 10.2. South and Central America. 10.3. Africa. 10.4. Australasia. 10.5. Arsenic in the Ocean Basins. 10.6. Suspect Terrain and Research Needs. 11. Synthesis, Conclusions and Recommendations. 11.1. Scale and Impact of Arsenic Pollution. 11.2. Chemistry, Cause and Prediction. 11.3. Agricultural Impacts, Prospects and Needs. 11.4. Water-supply Mitigation. 11.5. Sustainability Issues. 11.6. Geographical Perspectives. 11.7. The Politics of Arsenic Pollution and Mitigation. 11.8. Ten Priority Actions. Notes. References. Index

Cellular uptake, subcellular distribution and toxicity of arsenic compounds in methylating and non-methylating cells

Arsenic is a known human carcinogen, inducing tumors of the skin, urinary bladder, liver and lung. Inorganic arsenic, existing in highly toxic trivalent and significantly less toxic pentavalent forms, is methylated to mono- and di-methylated species mainly in the liver. Due to the low toxicity of pentavalent methylated species, methylation has been regarded as a detoxification process for many years; however, recent findings of a high toxicity of trivalent methylated species have indicated the contrary. In order to elucidate the role of speciation and methylation for the toxicity and carcinogenicity of arsenic, systematic studies were conducted comparing cellular uptake, subcellular distribution as well as toxic and genotoxic effects of organic and inorganic pentavalent and trivalent arsenic species in both non-methylating (urothelial cells and fibroblasts) and methylating cells (hepatocytes). The membrane permeability was found to be dependent upon both the arsenic species and the cell type. Uptake rates of trivalent methylated species were highest and exceeded those of their pentavalent counterparts by several orders of magnitude. Non-methylating cells (urothelial cells and fibroblasts) seem to accumulate higher amounts of arsenic within the cell than the methylating hepatocytes. Cellular uptake and extrusion seem to be faster in hepatocytes than in urothelial cells. The correlation of uptake with toxicity indicates a significant role of membrane permeability towards toxicity. Furthermore, cytotoxic effects are more distinct in hepatocytes. Differential centrifugation studies revealed that elevated concentrations of arsenic are present in the ribosomal fraction of urothelial cells and in nucleic and mitochondrial fractions of hepatic cells. Further studies are needed to define the implications of the observed enrichment of arsenic in specific cellular organelles for its carcinogenic activity. This review summarizes our recent research on cellular uptake, distribution and toxicity of arsenic compounds in methylating and non-methylating cells.