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PubMed2004

Arsenic and its speciation analysis using high-performance liquid chromatography and inductively coupled plasma mass spectrometry.

It is known that arsenic has different toxicological properties dependent upon both its oxidation state for inorganic compounds, as well as the different toxicity levels exhibited for organic arsenic compounds. The field of arsenic speciation analysis has grown rapidly in recent years, especially with the utilization of high-performance liquid chromatography (HPLC) coupled to inductively coupled plasma mass spectrometry (ICP-MS), a highly sensitive and robust detector system. Complete characterization of arsenic compounds is necessary to understand intake, accumulation, transport, storage, detoxification and activation of this element in the natural environment and living systems. This review describes the essential background and toxicity of arsenic in the environment, and more importantly, some currently used chromatographic applications and sample handling procedures necessary to accurately detect and quantify arsenic in its various chemical forms. Applications and work using only HPLC-ICP-MS for arsenic speciation of environmental and biological samples are presented in this review.

Arsenic↗
PubMed2006

Improved chromatographic separation of thio-arsenic compounds by reversed-phase high performance liquid chromatography-inductively coupled plasma mass spectrometry.

A new group of arsenic species, thio-arsenicals, have recently been reported in several natural samples such as molluscs, algae, and urine. These compounds are the sulfur analogues of oxo-arsenicals, a large group of naturally-occurring compounds, whereby the arsinoyl (As=O) group is substituted by an arsinothioyl group (As=S). The most common separation technique for oxo-arsenicals is anion-exchange HPLC with polymer-based columns, but under these conditions the thio-arsenicals show strong retention, resulting in unacceptably long analysis times and broad peaks. We report the development of a reversed-phase HPLC method, with ICPMS detection, which allows separation of the known thio-arsenicals within 15 min with significantly improved peak shapes. The detection limit is about 0.6 microg As/L based on 10 microL injection volume. Further, we have applied the method to the identification and quantification of thio-arsenic species in two standard reference materials, BCR 710 oyster tissue and NIES 18 human urine.

Animals↗
PubMed2005

Limitations of growth-parameters in Lemna gibba bioassays for arsenic and uranium under variable phosphate availability.

Growth behaviour of Lemna gibba L. at different phosphorus supply, and arsenic or uranium exposure levels was investigated in batch culture. Total frond count, total frond area, and dry biomass were used to observe growth at four phosphate, arsenic, and uranium concentrations. L. gibba dry biomass had a linear relationship with the total frond area (r=0.96 at P<0.001), but a non-linear relationship with the total frond count. Using total frond count led to significantly lower growth rates than did the use of total frond area in high phosphate supply, whereas the use of total frond count led to higher growth rates than did total frond area under low phosphorus conditions. The results under uranium loading were more or less a mirror of the results obtained under phosphate variation, except that the growth rates for L. gibba under uranium exposure were lower than in the phosphate experiments. At the lowest arsenic loading, the total frond count was significantly higher than the total frond area, whereas at higher arsenic loading, this was not observed because of arsenic was toxic to L. gibba. The longest roots were observed in lowest phosphate supply, and in highest uranium load. No significant influences on root length were observed with arsenic loading. The individual frond area increased with an increase in phosphate and decreased considerably with uranyl and arsenate loading. L. gibba multiplied rapidly into small and yellowish fronds under low phosphorus supply, and under high levels of arsenic and uranium exposure. L. gibba first developed the individual frond size before multiplying in a favourable environment. The effect of uranium may be attributed to an interaction between uranyl ions and phosphates that results in a precipitate of uranyl phosphates. The results revealed that L. gibba growth behaviour is very much influenced by multiple stresses in a bioassay. Therefore, growth rate calculation models should be chosen according to the parameter used, and toxicity estimation differs considerably with the growth parameter measured. Consequently, the interpretation of L. gibba bioassay results can be significantly influenced.

Araceae↗
PubMed2005

Sampling technologies and air pollution control devices for gaseous and particulate arsenic: a review.

Direct measurement of arsenic release requires a good sampling and analysis procedure in order to capture and detect the total amount of metals emitted. The literature is extensively reviewed in order to evaluate the efficiency of full field-scale and laboratory scale techniques for capturing particulate and gaseous emissions of arsenic from the thermo-chemical treatment of different sources of arsenic. Furthermore, trace arsenic concentrations in ambient air, national standard sampling methods and arsenic analysis methods are considered. Besides sampling techniques, the use of sorbents is also reviewed with respect to both approaches (1) to prevent the metals from exiting with the flue gas and (2) to react or combine with the metals in order to be collected in air pollution control systems. The most important conclusion is that submicron arsenic fumes are difficult to control in conventional air pollution control devices. Complete capture of the arsenic species requires a combination of particle control and vapour control devices.

Air Movements↗
PubMed2006

Arsenic in the soils of Zimapán, Mexico.

Arsenic concentrations of 73 soil samples collected in the semi-arid Zimapán Valley range from 4 to 14 700 mg As kg(-1). Soil arsenic concentrations decrease with distance from mines and tailings and slag heaps and exceed 400 mg kg(-1) only within 500 m of these arsenic sources. Soil arsenic concentrations correlate positively with Cu, Pb, and Zn concentrations, suggesting a strong association with ore minerals known to exist in the region. Some As was associated with Fe and Mn oxyhydroxides, this association is less for contaminated than for uncontaminated samples. Very little As was found in the mobile water-soluble or exchangeable fractions. The soils are not arsenic contaminated at depths greater than 100 cm below the surface. Although much of the arsenic in the soils is associated with relatively immobile solid phases, this represents a long-term source of arsenic to the environment.

Arsenic↗
PubMed2005

Exposure to arsenic and lead of children living near a copper-smelter in San Luis Potosi, Mexico: Importance of soil contamination for exposure of children.

The objective of this study was to assess the levels of soil contamination and child exposure in areas next to a primary smelter (arsenic-copper metallurgical) located in the community of Morales in San Luis Potosi, Mexico. In Morales, 90% of the soil samples studied in this work were above 400 mg/kg of lead, and above 100 mg/kg of arsenic, which are guidelines recommended by the United States Environmental Protection Agency (EPA). Bioaccessibility of these metals was studied in vitro in 10 soil samples; the median values of bioaccessibility obtained in these samples were 46.5% and 32.5% for arsenic and lead. Since the concentrations of arsenic and lead in soil were above normal values, and taking into account the bioaccessibility results, exposure to these metals was evaluated in children. Regarding lead, children aged 3-6 years had the highest mean blood lead levels; furthermore, 90% of them had concentrations above 10 microg/dl (CDC's action level). Total urinary arsenic was higher in children aged 8-9 yr; however, the percentage of children with concentrations above 50 microg/g creatinine (CDC's action level) or 100 microg/g creatinine (World Health Organization [WHO] action level) was similar among different age groups. Using the EPAs integrated exposure uptake biokinetic model for lead in children (IEUBK), we estimated that 87% of the total lead in blood is obtained from the soil/dust pathway. The exposure dose to arsenic, estimated for the children living in Morales using Monte Carlo analysis and the arsenic concentrations found in soil, was above the EPA's reference dose. With all these results, it is evident that studies are needed in order to identify adverse health effects in children living in Morales; nevertheless, it is more important to develop a risk reduction program as soon as possible.

Arsenic↗
PubMed2006

Arsenic release from glass containers by action of intravenous nutrition formulation constituents.

Pharmacopoeias prescribe tests to determine the levels of arsenic in raw materials and glass containers. In this study, glass ampoules for injectables containing individually the main components of intravenous nutrition formulations were submitted to the hydrolytic resistance test by heating at 121 degrees C for 30 min. As(V) and As(III) levels in these solutions after heating were determined by hydride generation atomic absorption spectrometry. The arsenic content of substances used in these formulations was previously determined, as well as the arsenic content of the glass containers. The results showed that raw substances as well as glass containers contain arsenic. Moreover, arsenic is released during the heating (hydrolytic resistance test). However, the amount released and the arsenic species present in solution depend on the solution composition. While As(V) was the predominant specie in glass, solutions containing reducing substances such as glucose and vitamins had As(III) in higher concentration. Therefore, arsenic is released from glass containers during the heating for sterilization, and reacts with formulation constituents depending on their reducing properties.

Arsenic↗
PubMed2005

Arsenic removal via electrocoagulation from heavy metal contaminated groundwater in La Comarca Lagunera México.

Arsenic contamination is an enormous worldwide problem. A large number of people dwelling in Comarca Lagunera, situated in the central part of northern México, use well water with arsenic in excess of the water standard regulated by the Secretary of Environment and Natural Resources of México (SEMARNAT), to be suitable for human health. Individuals with lifetime exposure to arsenic develop the classic symptoms of arsenic poisoning. Among several options available for removal of arsenic from well water, electrocoagulation (EC) is a very promising electrochemical treatment technique that does not require the addition of chemicals or regeneration. First, this study will provide an introduction to the fundamental concepts of the EC method. In this study, powder X-ray diffraction, scanning electron microscopy, transmission Mössbauer spectroscopy and Fourier transform infrared spectroscopy were used to characterize the solid products formed at iron electrodes during the EC process. The results suggest that magnetite particles and amorphous iron oxyhydroxides present in the EC products remove arsenic(III) and arsenic(V) with an efficiency of more than 99% from groundwater in a field pilot scale study.

Arsenic↗
PubMed2005

Effects of glutamine on adhesion molecule expression and leukocyte transmigration in endothelial cells exposed to arsenic.

This study evaluated whether glutamine (GLN) concentration was related to endothelial surface molecule expression and the migration of polymorphonuclear neutrophils (PMNs) through endothelial cells (ECs) stimulated by arsenic. Human umbilical vein endothelial cells (HUVECs) and PMNs were treated with different GLN concentrations (0, 300, 600 and 1000 microM) for 24 h. After that, we stimulated HUVECs for 3 h with 0.5 microM arsenic, and PMNs were allowed to transmigrate to ECs for 2 h. HUVEC surface expressions of cell adhesion molecules and integrin (CD11b) and interleukin (IL)-8 receptor expressions on PMNs were measured. The transendothelial migration of PMNs was also analyzed. The results showed that cell adhesion molecule (CAM) and integrin expressions in arsenic groups were higher than in those without arsenic. Among the arsenic groups, the expression of CAMs on ECs and CD11b, and IL-8 receptor on PMNs was lowest with 0 microM compared with the other GLN concentrations. Vascular CAM-1 on ECs and CD11b on PMN expression were higher with 300 microM than with 600 and 1000 microM GLN. IL-8 secretions from ECs and PMNs were higher with 300 muM than with 600 and 1000 microM GLN, and this was consistent with the expression of the IL-8 receptor on PMNs. Polymorphonuclear neutrophil transmigration was significantly higher with 300 muM GLN than with other GLN concentrations. These results suggest that ECs and PMNs were activated after arsenic stimulation. Cell adhesion molecule expressions on ECs and PMNs were suppressed in the absence of GLN. A low GLN concentration comparable to catabolic conditions resulted in higher adhesion molecule expression and greater transendothelial migration of neutrophils. Glutamine administration at levels similar to or higher than physiological concentrations reduced IL-8 and adhesion molecule expression; PMN transmigration was also decreased after stimulation with arsenic.

Arsenic↗
PubMed2006

Arsenic-induced gene expression changes in the neural tube of folate transport defective mouse embryos.

Arsenic injected intraperitoneally (i.p.) during early organogenesis to small pregnant laboratory rodents (mouse, rat, and hamster) induces several congenital defects in the progeny. Among those abnormalities consistently and predominantly observed are exencephaly and encephalocele. These severe defects of the central nervous system originate from a corrupted process of neurulation and are better known as neural tube defects (NTDs). In order to understand the mechanism of arsenate-induced NTDs, we designed studies in which highly sensitive Folr2 nullizygous mice were injected intraperitoneally with sodium arsenate at the beginning of the neural tube formation process. This specific knockout mouse and the arsenic exposure conditions were chosen as they were known to provide a high incidence of exencephaly in exposed embryos. We have applied gene expression technology to the anterior neural tube. This allowed us to study arsenic-induced changes in patterns of gene expression that may contribute to the development of neural tube defects in these mice. Using extensive data analysis approaches including hierarchical clustering and gene ontology analysis, we identified several candidate genes as well as important ontology groups that may be responsible for arsenic's teratogenicity. Changes in the expression of several genes in response to arsenic treatment in our model had previously been demonstrated by other investigators to also induce NTDs in murine model systems. These include: engrailed 1 (En-1), platelet derived growth factor receptor alpha (Pdgfralpha) and ephrinA7 (EphA7). We also found several gene ontology groups that could be implicated in arsenic's underlying teratogenicity: morphogenesis, oxidative phosporylation, redox response, and regulation of I-kappaB kinase/NF-kappaB cascade. Additionally, we revealed new target genes which may be responsible for arsenic disrupted oxidative phosphorylation.

Abnormalities, Drug-Induced↗
PubMed2005

Social implications of arsenic poisoning in Bangladesh.

Besides its toxicity, groundwater arsenic contamination creates widespread social problems for its victims and their families in Bangladesh. There is, for instance, a tendency to ostracise arsenic-affected people, arsenicosis being thought of as a contagious disease. Within the community, arsenic-affected people are barred from social activities and often face rejection, even by their immediate family members. Women with visible arsenicosis symptoms are unable to get married and some affected housewives are divorced by their husbands. Children with symptoms are not sent to school in an effort to hide the problem. This paper employs mainly qualitative methods to interpret people's understandings about the toxic impact of groundwater arsenic poisoning on their social lives. Arsenic-affected patients in southwest Bangladesh were asked to determine their 'own priorities' in measuring arsenic toxicity on their social activities and to explore their perceptions about their own survival strategies. We found that patients' experiences reveal severe negative social impacts, and a sharp difference of perceptions about arsenic and social issues between arsenicosis patients and unaffected people.

Adaptation, Psychological↗
PubMed2004

Distributions and chemical forms of arsenic after intravenous administration of dimethylarsinic and monomethylarsonic acids to rats.

The observed toxicity of arsenic is highly dependent on animal species and differences in metabolism. Rats are one of the most tolerant species, and the metabolic pathway is quite different in some aspects from those of other mammals. The distinct metabolic pathway including the preferential accumulation in red blood cells (RBCs) has been explained, whereby allowing an effective use of rats as an animal model for the arsenic metabolism. In the present study, distributions of arsenic among organs/tissues/body fluids and their chemical forms were studied after intravenous injection of arsenic in the forms of dimethylarsinic (DMA(V)) and monomethylarsonic acids (MMA(V)) to rats. DMA(V) and MMA(V) were mostly excreted into urine immediately after the injection as the intact forms, and both forms were taken up less effectively by organs/tissues than arsenite. The methylated arsenics distributed in organs/tissues were excreted directly into urine and excreted before being redistributed in RBCs. DMA(V) and MMA(V) taken up by the liver were transformed to metabolites not yet identified, accumulated transiently in the liver, and then they disappeared from the liver. The unidentified metabolites were assumed to be transformed from dimethylarsinic acid (DMA(III)) following the consecutive metabolic reactions [MMA(V) --> monomethylarsonous acid (MMA(III)) --> DMA(V) --> DMA(III)]. The unidentified metabolites were excreted not into the bile but into the bloodstream. Injections of DMA(V) and MMA(V) induced a biliary excretion of arsenic but only at 0.2-0.3% of the dose, the arsenic in the bile being their intact free forms.

Animals↗
PubMed2004

Molecular basis for arsenic-induced alteration in nitric oxide production and oxidative stress: implication of endothelial dysfunction.

Accumulated epidemiological studies have suggested that prolonged exposure of humans to arsenic in drinking water is associated with vascular diseases. The exact mechanism of how this occurs currently unknown. Nitric oxide (NO), formed by endothelial NO synthase (eNOS), plays a crucial role in the vascular system. Decreased availability of biologically active NO in the endothelium is implicated in the pathophysiology of several vascular diseases and inhibition of eNOS by arsenic is one of the proposed mechanism s for arsenic-induced vascular diseases. In addition, during exposure to arsenic, overproduction of reactive oxygen species (ROS) can occur, resulting in oxidative stress, which is another major risk factor for vascular dysfunction. The molecular basis for decreased NO levels and increased oxidative stress during arsenic exposure is poorly understood. In this article, evidence for arsenic-mediated alteration in NO production and oxidative stress is reviewed. The results of a cross-sectional study in an endemic area of chronic arsenic poisoning and experimental animal studies to elucidate a potential mechanism for the impairment of NO formation and oxidative stress caused by prolonged exposure to arsenate in the drinking water are also reviewed.

Animals↗
PubMed2004

Understanding arsenic carcinogenicity by the use of animal models.

Although numerous epidemiological studies have indicated that human arsenic exposure is associated with increased incidences of bladder, liver, skin, and lung cancers, limited attempts have been made to understand mechanisms of carcinogenicity using animal models. Dimethylarsinic acid (DMA), an organic arsenic compound, is a major metabolite of ingested inorganic arsenics in mammals. Recent in vitro studies have proven DMA to be a potent clastogenic agent, capable of inducing DNA damage including double strand breaks and cross-link formation. In our attempts to clarify DMA carcinogenicity, we have recently shown carcinogenic effects of DMA and its related metabolites using various experimental protocols in rats and mice: (1) a multi-organ promotion bioassay in rats; (2) a two-stage promotion bioassay by DMA of rat urinary bladder and liver carcinogenesis; (3) a 2-year carcinogenicity test of DMA in rats; (4) studies on the effects of DMA on lung carcinogenesis in rats; (5) promotion of skin carcinogenesis by DMA in keratin (K6)/ornithine decarboxylase (ODC) transgenic mice; (6) carcinogenicity of DMA in p53(+/-) knockout and Mmh/8-OXOG-DNA glycolase (OGG1) mutant mice; (7) promoting effects of DMA and related organic arsenicals in rat liver; (8) promoting effects of DMA and related organic arsenicals in a rat multi-organ carcinogenesis test; and (9) 2-year carcinogenicity tests of monomethylarsonic acid (MMA) and trimethylarsine oxide (TMAO) in rats. The results revealed that the adverse effects of arsenic occurred either by promoting and initiating carcinogenesis. These data, as covered in the present review, suggest that several mechanisms may be involved in arsenic carcinogenesis.

Animals↗
PubMed2004

Arsenic speciation in human urine: are we all the same?

We studied the arsenic speciation in human urine samples by using high-performance liquid chromatography-inductively coupled plasma-mass spectrometry (HPLC-ICP-MS). We investigated the arsenic speciation in the urine collected from nine volunteers during a 3-day period after a meal of blue mussels, Mytilus edulis. We also studied the effect of cooking on the arsenic speciation. Arsenobetaine and dimethylarsinic acid (DMAA) were the major arsenic metabolites found in the urine samples. Significant amounts of unknown metabolites were also detected. The excretion patterns of arsenic from individuals were generally similar except for two subjects. One of whom excreted high amounts of arsenobetaine even though no arsenic-rich food was eaten for 3 days before the experiment. The results reveal that we need a better understanding of the metabolism of arsenic compounds by human.

Animals↗
PubMed2005

Transplacental arsenic plus postnatal 12-O-teradecanoyl phorbol-13-acetate exposures associated with hepatocarcinogenesis induce similar aberrant gene expression patterns in male and female mouse liver.

Our prior work shows that in utero arsenic exposure alone is a complete transplacental carcinogen, producing hepatocellular carcinoma in adult male offspring but not in females. In a follow-up study to potentially promote arsenic-initiated tumors, mice were exposed to arsenic (85 ppm) from gestation day 8 to 18 and then exposed to 12-O-teradecanoyl phorbol-13-acetate (TPA), a well-known tumor promoter after weaning. The dermal application of TPA (2 mug/0.1 ml acetone, twice/week for 21 weeks) after transplacental arsenic did not further increase arsenic-induced liver tumor formation in adult males but significantly increased liver tumor formation in adult females. Thus, for comparison, liver tumors and normal liver samples taken from adult male and female mice at necropsy were analyzed for aberrant gene/protein expression by microarray, real-time RT-PCR and Western blot analysis. Arsenic/TPA treatment resulted in increased expression of alpha-fetoprotein, k-ras, c-myc, estrogen receptor-alpha, cyclin D1, cdk2na, plasminogen activator inhibitor-1, cytokeratin-8, cytokeratin-18, glutathione S-transferases and insulin-like growth factor binding proteins in liver and liver tumors from both male and female mice. Arsenic/TPA also decreased the expression of BRCA1, betaine-homocysteine methyltransferase, CYP7B1, CYP2F2 and insulin-like growth factor-1 in normal and cancerous livers. Alterations in these gene products were associated with arsenic/TPA-induced liver tumors, regardless of sex. Thus, transplacental arsenic plus postnatal TPA exposure induced similar aberrant gene expression patterns in male and female mouse liver, which are persistent and potentially important to the mechanism of arsenic initiation of hepatocarcinogenesis.

Administration, Topical↗
PubMed2006

Arsenic-induced toxicity and the protective role of ascorbic acid in mouse testis.

Oxidative stress has been suggested to be a major cause of male reproductive failure. Here, we investigated whether arsenic, which impairs male reproductive functions in rodent models, acts by inducing oxidative stress. Male 8-week-old ICR mice were given drinking water containing 20 or 40 mg/l sodium arsenite with or without 0.75 or 1.5 g/l of the antioxidant ascorbic acid for 5 weeks. The arsenic-treated mice showed decreased epididymidal sperm counts and testicular weights compared to untreated mice. These effects were reversed in mice that were co-treated with ascorbic acid. Similarly, arsenic treatment lowered the activities of testicular 3beta-hydroxysteroid dehydrogenase (HSD) and 17beta-HSD, which play important roles in steroidogenesis, and this was reversed by co-treatment with ascorbic acid. The testicles of arsenic-treated mice had decreased glutathione (GSH) levels (which correlate inversely with the degree of cellular oxidative stress) and elevated levels of protein carbonyl (a marker of oxidative damage to tissue proteins). Ascorbic acid co-treatment reversed both of these effects. Thus, ascorbic acid blocks both the adverse effects of arsenic on male reproductive functions and the arsenic-induced testicular oxidative changes. These observations support the notion that arsenic impairs male reproductive function by inducing oxidative stress.

Animals↗
PubMed2005

Pilot-scale demonstration of phytofiltration for treatment of arsenic in New Mexico drinking water.

Arsenic contamination of drinking water poses serious health risks to millions of people worldwide. To reduce such risks, the United States Environmental Protection Agency recently lowered the Maximum Contaminant Level for arsenic in drinking water from 50 to 10 microgL(-1). The majority of water systems requiring compliance are small systems that serve less than 10,000 people. Current technologies used to clean arsenic-contaminated water have significant drawbacks, particularly for small treatment systems. In this pilot-scale demonstration, we investigated the use of arsenic-hyperaccumulating ferns to remove arsenic from drinking water using a continuous flow phytofiltration system. Over the course of a 3-month demonstration period, the system consistently produced water having an arsenic concentration less than the detection limit of 2 microgL(-1), at flow rates as high as 1900 L day(-1) for a total treated water volume of approximately 60,000 L. Our results demonstrate that phytofiltration provides the basis for a solar-powered hydroponic technique to enable small-scale cleanup of arsenic-contaminated drinking water.

Arsenic↗