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PubMed2003

Arsenic pollution in groundwater: a self-organizing complex geochemical process in the deltaic sedimentary environment, Bangladesh.

The presence of considerable concentrations of As (Sonargon: below detection limit (bdl)-1.46 mg/l; Faridpur: bdl-1.66 mg/l) and some other elements (like B, F, U) in groundwater of the Ganges-Meghna-Brahmaputra (G-M-B) rivers flood plain indicate that several millions of people are consuming contaminated water. Conditions regulating the mobilization and diagenetic behavior of arsenic in sediments are not well characterized, although understanding these conditions is essential in order to predict the modes of transfer of this contaminant from sediments to groundwater. Analyses of vertical profiles of total arsenic and iron as well as easily soluble As and reducible (reactive) iron concentrations in sediments of the Ganges and Meghna flood plains show no arsenic-enriched layer up to 36-m depth. However, arsenic content in sediments is relatively higher than mean crustal concentration, showing some peaks (Sonargaon: 27.9 mg/kg; 3 m, 31.5 mg/kg; 9 m, 27.30 mg/kg; 16 m, 37.70 mg/kg; 29.5 m, Faridpur: 19.80 mg/kg; 6 m, 26.60 mg/kg; 14.5 m, 29.40 mg/kg; 25 m) depending on the periodical differences in sedimentary cycling of arsenic, metal (hydr)oxides and organic matter. Seasonal changes have no clear or consistent effect on the groundwater arsenic concentrations; with the exception of a small-scale localized irregular change (10-16%). However, easily reducible metal oxides and hydroxides were significant factors affecting the retention of arsenic by sediments during leaching. The biogeochemical cycling of arsenic and iron is closely coupled in deltaic systems where iron oxy-hydroxides provide a carrier phase for the deposition of arsenic in sediments. Analytical results of mimic leaching experiments strongly supported the reduction (Fe oxy-hydroxides) mechanism for arsenic mobilization in alluvial aquifer of deltaic sedimentary environment of G-M-B rivers flood plain.

Arsenic↗
PubMed2002

Epidemiologic evidence of diabetogenic effect of arsenic.

It is well documented that arsenic can lead to skin lesions, atherosclerotic diseases and cancers. The association between arsenic exposure and diabetes mellitus is a relatively new finding. Up to now, there are six epidemiologic reports linking diabetes mellitus with arsenic exposure from environmental and occupational sources. Two reports in Taiwan carried out in the blackfoot disease-hyperendemic villages, one cross-sectional and one prospective follow-up of the same cohort, indicate that arsenic exposure from drinking artesian well water is associated with prevalence and incidence of diabetes mellitus in a dose-responsive pattern. The observation of the relation between arsenic exposure and diabetes mellitus is further supported by studies carried out in Sweden and Bangladesh. In Sweden, case-control analyses of death records of copper smelters and glass workers revealed a trend of increasing diabetes mellitus with increasing arsenic exposure from inhalation. In Bangladesh, prevalence of diabetes mellitus among arsenic-exposed subjects with keratosis was about five times higher than unexposed subjects. Increasing trends of diabetes mellitus with indices of arsenic exposure in drinking water seems to be independent of the presence of skin lesions associated with arsenic exposure. Although these studies consistently show an association between arsenic exposure and diabetes mellitus, the weak study designs of cross-sectional or case-control, the use of glucosuria or diabetes death as diagnostic criteria and the lack of adjustment for possible confounders in some studies, are major limitations that may reduce the strength of the evidence.

Arsenic↗
PubMed1998

Modulation of antioxidant responses by arsenic in maize.

The effects of arsenic on the expression of the antioxidant genes encoding superoxide dismutase, catalase, and glutathione S-transferase, as well as the activity of SOD and CAT enzymes, were examined at different developmental stages and in different tissues. Both CAT and SOD activities increased in response to low concentrations (0.01-0.1 mM) of arsenic in developing maize embryos. In germinating embryos both CAT and SOD activities increased in response to a wide range of arsenic concentrations (0.01-10 mM). Cat1 transcript increased in response to arsenic in developing and germinating embryos and in young leaves. Conversely, Cat2 increased at low concentrations of arsenic only in germinating embryos. Cat3 transcript levels increased in response to low concentrations of arsenic only in developing embryos. Sod3 transcript increased at low concentrations of arsenic in developing, germinating embryos and in leaves. The cytosolic Sod4 and Sod4A increased in response to arsenic in germinating embryos, while only Sod4 transcript increased in response to arsenic in leaves. Expression of Gst1 was similar to that of Cat1 in all tissues examined. These results indicate that arsenic triggers tissue and developmental stage specific defense responses of antioxidant and detoxification related genes in maize.

Antioxidants↗
PubMed1998

Arsenic toxicity is enzyme specific and its affects on ligation are not caused by the direct inhibition of DNA repair enzymes.

The molecular mechanism of arsenic toxicity is believed to be due to the ability of arsenite [As(III)] to bind protein thiols. Numerous studies have shown that arsenic is cytotoxic at micromolar concentrations. Micromolar As can also induce chromosomal damage and inhibit DNA repair. The mechanism of arsenic-induced genotoxicity is very important because arsenic is a human carcinogen, but not a mutagen, and there is a need to establish recommendations for safe levels of As in the environment. We have measured the dose-response for arsenic inhibition of several purified human DNA repair enzymes, including DNA polymerase beta, DNA ligase I and DNA ligase III and have found that most enzymes, even those with critical SH groups, are very insensitive to As. Many repair enzymes are activated by millimolar concentrations of As(III) and/or As(V). Only pyruvate dehydrogenase, one of eight purified enzymes examined so far, is inhibited by micromolar arsenic. In contrast to the purified enzymes, treatment of human cells in culture with micromolar arsenic produces a significant dose-dependent decrease in DNA ligase activity in nuclear extracts from the treated cells. However, the ligase activity in extracts from untreated cells is no more sensitive to arsenic than the purified enzymes. Our results show that direct enzyme inhibition is not a common toxic effect of As and that only a few sensitive enzymes are responsible for arsenic-induced cellular toxicity. Thus, arsenic-induced co-mutagenesis and inhibition of DNA repair is probably not the result of direct enzyme inhibition, but may be an indirect effect caused by As-induced changes in cellular redox levels or alterations in signal transduction pathways and consequent changes in gene expression.

Arsenic↗
PubMed1997

Relative genotoxic potency of arsenic and its methylated metabolites.

Arsenic is one of the few identified human carcinogens that has yet to be shown to cause cancer in rodents when the standard bioassay protocols are used. The reasons for this apparent interspecies difference are unclear but may be related to differences between humans and rodents in their detoxification capabilities. Detoxification of arsenic may occur through a methylation pathway. If, in fact, methylation does detoxify arsenic, one would predict that the methylated arsenicals might be less genotoxic than the inorganic arsenicals. To evaluate the hypothesis that the inorganic arsenicals are more mutagenic than the organic arsenicals, we tested sodium arsenite, sodium arsenate, monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) for their relative mutagenic and clastogenic potentials. We used the L5178Y/TK+/- mouse lymphoma assay which allows the detection of chemicals inducing a broad spectrum of different types of genetic damage. Sodium arsenite and sodium arsenate were active at concentrations of 1-2 micrograms/ml and 10-14 micrograms/ml, respectively. MMA was active between 2500-5000 micrograms/ml; while DMA required almost 10000 micrograms/ml to induce a genotoxic response. The organic arsenicals are thus much less potent as mutagenic agents than the inorganic arsenicals. All four of these arsenicals appear to act by mechanisms that cause chromosomal mutations.

Animals↗
PubMed1998

Short-column liquid chromatography with hydride generation atomic fluorescence detection for the speciation of arsenic.

Increasing concerns over human exposure to arsenic and more stringent environmental regulations require rapid determination of trace levels of individual arsenic species, which presents an analytical challenge. We describe a method that is capable of speciating nanogram-per-milliliter levels of arsenite (As(III)), arsenate (As(V)), monomethylarsonic acid (MMAA), and dimethylarsinic acid (DMAA) within 3 min. Speciation of two common inorganic species in drinking water, As(III) and As(V), is complete in 1.5 min. The method is based on a combination of fast high-performance liquid chromatography (HPLC) separation of arsenic species on 3-cm HPLC guard columns and the sensitive detection of arsenic hydride by atomic fluorescence spectrometry. Detection limits for the four arsenic species in urine samples are 0.4-0.8 ng/mL. This simple method allows for the direct speciation of arsenic present in natural water samples and in human urine samples from the general population, with no need of any sample pretreatment. Our results from the determination of arsenic species in urine and water standard reference materials are in good agreement with the certified values of total arsenic concentration. The method has been successfully applied to speciation studies of metabolism of arsenosugars following the consumption of arsenosugar-containing mussels by human volunteers. Speciation of arsenic in urine samples collected from four volunteers after the ingestion of musseles reveals significant increases of DMAA concentration, resulting from the metabolism of arsenosugars. These results suggest that the commonly used biomarkers for assessing human exposure to inorganic arsenic, which are based on the determination of urinary arsenite, arsenate, MMAA, and DMAA, are not reliable when arsenosugar-containing seafood is ingested.

Adult↗
PubMed2005

Characterizing and quantilying controls on arsenic solubility over a pH range of 1-11 in a uranium mill-scale experiment.

A mill-scale hydrometallurgical experiment (2700 m3 of effluent treated/day) was conducted for three months at the Rabbit Lake uranium mine site located in northern Saskatchewan, Canada, to determine the controls on the solubility of dissolved arsenic over a pH range of 1-11 and to develop a thermodynamic database for the dominant mineralogical controls on arsenic in the mill and the resulting mill tailings. The arsenic concentrations in the mill ranged from 526 mg/L at pH 1.0 (initial) to 1.34 mg/L at pH 10.8 (final discharge). Geochemical modeling of the chemistry data shows that arsenic solubility is controlled by the formation of scorodite (FeAsO4-2H2O) from pH 2.4 to pH 3.1, with 99.8% of dissolved arsenic precipitated as scorodite. Model results show that scorodite is unstable (releasing arsenic back in to solution) above pH 3.1 and arsenic adsorption to the surface of 2-line ferrihydrite is the dominant controlling factor in the solubility of arsenic from pH 3.2 to pH 11.0, with 99.8% of dissolved arsenic removed from solution via this mechanism. Finally, model results show -0.2% of the total dissolved arsenic adsorbs to the surface of amorphous aluminum hydroxide from pH 5.0 to pH 8.0. Minor alterations to the thermodynamic properties of arsenite and arsenate adsorption to 2-line ferrihydrite allowed the fit between measured mill-scale and modeled concentrations for the pH range of 3.2-11.0 to be optimized.

Adsorption↗
PubMed2005

Variation in arsenic speciation and concentration in paddy rice related to dietary exposure.

Ingestion of drinking water is not the only elevated source of arsenic to the diet in the Bengal Delta. Even at background levels, the arsenic in rice contributes considerably to arsenic ingestion in subsistence rice diets. We set out to survey As speciation in different rice varieties from different parts of the globe to understand the contribution of rice to arsenic exposure. Pot experiments were utilized to ascertain whether growing rice on As contaminated soil affected speciation and whether genetic variation accounted for uptake and speciation. USA long grain rice had the highest mean arsenic level in the grain at 0.26 microg As g(-1) (n = 7), and the highest grain arsenic value of the survey at 0.40 microg As g(-1). The mean arsenic level of Bangladeshi rice was 0.13 microg As g(-1) (n = 15). The main As species detected in the rice extract were AsIII, DMAV, and AsV. In European, Bangladeshi, and Indian rice 64 +/- 1% (n = 7), 80 +/- 3% (n = 11), and 81 +/- 4% (n = 15), respectively, of the recovered arsenic was found to be inorganic. In contrast, DMAV was the predominant species in rice from the USA, with only 42 +/- 5% (n = 12) of the arsenic being inorganic. Pot experiments show that the proportions of DMAV in the grain are significantly dependent on rice cultivar (p = 0.026) and that plant nutrient status is effected by arsenic exposure.

Arsenicals↗
PubMed2006

Arsenic removal from groundwater by household sand filters: comparative field study, model calculations, and health benefits.

Arsenic removal efficiencies of 43 household sand filters were studied in rural areas of the Red River Delta in Vietnam. Simultaneously, raw groundwater from the same households and additional 31 tubewells was sampled to investigate arsenic coprecipitation with hydrous ferric iron from solution, i.e., without contact to sand surfaces. From the groundwaters containing 10-382 microg/L As, < 0.1-48 mg/L Fe, < 0.01-3.7 mg/L P, and 0.05-3.3 mg/L Mn, similar average removal rates of 80% and 76% were found for the sand filter and coprecipitation experiments, respectively. The filtering process requires only a few minutes. Removal efficiencies of Fe, phosphate, and Mn were > 99%, 90%, and 71%, respectively. The concentration of dissolved iron in groundwater was the decisive factor for the removal of arsenic. Residual arsenic levels below 50 microg/L were achieved by 90% of the studied sand filters, and 40% were even below 10 microg/L. Fe/As ratios of > or = 50 or > or = 250 were required to ensure arsenic removal to levels below 50 or 10 microg/L, respectively. Phosphate concentrations > 2.5 mg P/L slightly hampered the sand filter and coprecipitation efficiencies. Interestingly, the overall arsenic elimination was higher than predicted from model calculations based on sorption constants determined from coprecipitation experiments with artificial groundwater. This observation is assumed to result from As(lll) oxidation involving Mn, microorganisms, and possibly dissolved organic matter present in the natural groundwaters. Clear evidence of lowered arsenic burden for people consuming sand-filtered water is demonstrated from hair analyses. The investigated sand filters proved to operate fast and robust for a broad range of groundwater composition and are thus also a viable option for mitigation in other arsenic affected regions. An estimation conducted for Bangladesh indicates that a median residual level of 25 microg/L arsenic could be reached in 84% of the polluted groundwater. The easily observable removal of iron from the pumped water makes the effect of a sand filter immediately recognizable even to people who are not aware of the arsenic problem.

Arsenic↗
PubMed2006

Leaching of arsenic from granular ferric hydroxide residuals under mature landfill conditions.

Most arsenic bearing solid residuals (ABSR) from water treatment will be disposed in nonhazardous landfills. The lack of an appropriate leaching test to predict arsenic mobilization from ABSR creates a need to evaluate the magnitude and mechanisms of arsenic release under landfill conditions. This work studies the leaching of arsenic and iron from a common ABSR, granular ferric hydroxide, in a laboratory-scale column that simulates the biological and physicochemical conditions of a mature, mixed solid waste landfill. The column operated for approximately 900 days and the mode of transport as well as chemical speciation of iron and arsenic changed with column age. Both iron and arsenic were readily mobilized under the anaerobic, reducing conditions. During the early stages of operation, most arsenic and iron leaching (80% and 65%, respectively) was associated with suspended particulate matter, and iron was lost proportionately faster than arsenic. In later stages, while the rate of iron leaching declined, the arsenic leaching rate increased greater than 7-fold. The final phase was characterized by dissolved species leaching. Future work on the development of standard batch leaching tests should take into account the dominant mobilization mechanisms identified in this work: solid associated transport, reductive sorbent dissolution, and microbially mediated arsenic reduction.

Arsenic↗
PubMed2006

Arsenic leaching from mulch made from recycled construction and demolition wood and impacts of iron-oxide colorants.

Mulch made from recycled construction and demolition (C&D) wood has been reported to contain elevated levels of arsenic from inadvertent inclusion of chromated copper arsenate (CCA)-treated wood. Such mulch is also commonly colored with iron oxide, a compound known to bind arsenic. The objectives of this study were to quantify the releases of arsenic from mulch made from C&D wood, to evaluate the impacts of an iron-oxide colorant in potentially decreasing arsenic leaching rates, and to evaluate the relative significance of additional variables on leachate concentrations. Atotal of 3 sets of mulch samples (0%, 5%, or 100% CCA-treated wood) were prepared containing a sample either with or without colorant addition. Each sample was subjected to two tests: a field leaching test and the Synthetic Precipitation Leaching Procedure (SPLP). Results showed that arsenic concentrations in the field leachate from the 0% treated wood mulches were consistently low (<0.003-0.013 mg/L) whereas leachates from 5 and 100% treated wood mulches were characterized by higher arsenic concentrations (0.059-2.23 mg/L for 5%; 0.711-22.7 mg/L for 100%). The mass of arsenic leached from the field samples during the 1-year monitoring period was between 10 and 15% of the initial mass of arsenic. The colorant reduced the leaching of arsenic by more than 20% for the field leachate and 50% for the SPLP leachate, on average. However, the study showed that the effect may not last for long periods. Besides colorant addition other factors were observed to affect the amount of arsenic leached from contaminated mulch. These include the proportion of CCA-treated wood in the mulch, time, and pH of rainfall.

Arsenates↗
PubMed2001

Identification of dimethylarsinous and monomethylarsonous acids in human urine of the arsenic-affected areas in West Bengal, India.

A speciation technique for arsenic has been developed using an anion-exchange high-performance liquid chromatography/inductively coupled argon plasma mass spectrometer (HPLC/ICP MS). Under optimized conditions, eight arsenic species [arsenocholine, arsenobetaine, dimethylarsinic acid (DMA(V)), dimethylarsinous acid (DMA(III)), monomethylarsonic acid (MMA(V)), monomethylarsonous acid (MMA(III)), arsenite (As(III)), and arsenate (As(V))] can be separated with isocratic elution within 10 min. The detection limit of arsenic compounds was 0.14-0.33 microg/L. To validate the method, Standard Reference Material in freeze-dried urine, SRM-2670, containing both normal and elevated levels of arsenic was analyzed. The method was applied to determine arsenic species in urine samples from three arsenic-affected districts of West Bengal, India. Both DMA(III) and MMA(III) were detected directly (i.e., without any prechemical treatment) for the first time in the urine of some humans exposed to inorganic arsenic through their drinking water. Of 428 subjects, MMA(III) was found in 48% and DMA(III) in 72%. Our results indicate the following. (1) Since MMA(III) and DMA(III) are more toxic than inorganic arsenic, it is essential to re-evaluate the hypothesis that methylation is the detoxification pathway for inorganic arsenic. (2) Since MMA(V) reductase with glutathione (GSH) is responsible for conversion of MMA(V) to MMA(III) in vivo, is DMA(V) reductase with GSH responsible for conversion of DMA(V) to DMA(III) in vivo? (3) Since DMA(III) forms iron-dependent reactive oxygen species (ROS) which causes DNA damage in vivo, DMA(III) may be responsible for arsenic carcinogenesis in human.

Arsenic↗
PubMed2004

Formation and urinary excretion of arsenic triglutathione and methylarsenic diglutathione.

Taking advantage of mice deficient in gamma-glutamyl transpeptidase that are unable to metabolize glutathione (GSH), we have identified two previously unrecognized urinary metabolites of arsenite: arsenic triglutathione and methylarsenic diglutathione. Following administration of sodium arsenite to these mice, approximately 60-70% of urinary arsenic is present as one of these GSH conjugates. We did not detect the dimethyl derivative, dimethyl arsenic GSH; however, dimethyl arsenic (DMAV) represented approximately 30% of urinary arsenic. Administration of buthionine sulfoximine, an inhibitor of GSH synthesis, to wild-type mice reduced urinary arsenic excretion by more than 50%, indicating the GSH dependence of arsenic metabolism, transport, or both. Rodents deficient in three known ABC family transporters (MRP1, MRP2, and MDR1a/1b) exhibited urinary arsenic levels similar or greater than those in wild-type rodents; however, administration of MK571, an MRP inhibitor, reduced urinary arsenic excretion by almost 50%. MK571-treated mice showed approximately 50% reduction of AsIII, MMAV, and AsV as compared to untreated wild-type controls, while DMAV levels were unchanged. These findings suggest that arsenic excretion is in part dependent on GSH and on an MRP transporter other than MRP1 or 2.

Animals↗
PubMed2007

Binding of dimethylarsinous acid to cys-13alpha of rat hemoglobin is responsible for the retention of arsenic in rat blood.

The metabolism, disposition, and carcinogenicity of arsenic differ dramatically between humans and rats. To understand the molecular basis of these differences, we have characterized arsenic species in rats that were treated with inorganic arsenate (iAsV), monomethylarsonic acid (MMAV), or dimethylarsinic acid (DMAV) for up to 15 weeks. Arsenic significantly accumulated in the red blood cells (RBCs) of rats in the form of hemoglobin (Hb) complexed with dimethylarsinous acid (DMAIII), regardless of whether the rats were treated with iAsV, MMAV, or DMAV, suggesting rapid methylation of arsenic species followed by strong binding of DMAIII to rat Hb. The binding site for DMAIII was identified to be cysteine 13 in the alpha-chain of rat Hb with a stoichiometry of 1:1. Over 99% of the total arsenic (maximum 2.5-3.5 mM) in rat RBCs was bound to Hb for all rats examined (n = 138). In contrast, only 40-49% of the total arsenic (maximum approximately 10 muM) in rat plasma was bound to proteins. The ratios of the total arsenic in RBCs to that in plasma ranged from 88-423 for rats that were fed iAsV, 100-680 for rats that were fed MMAV, and 185-1393 for rats that were fed DMAV, when samples were obtained over the 15-week exposure duration. Previous studies have shown an increase in urothelial hyperplasia in rats fed DMAV. This is the first article reporting that treatment with iAsV in the drinking water also produces urothelial hyperplasia and at an even earlier time point than dietary DMAV. Dietary MMAV produced only a slight urothelial response. A correlation between the Hb-DMAIII complex and urothelial lesion severity in rats was observed. The lack of cysteine 13alpha in human Hb may be responsible for the shorter retention of arsenic in human blood. These differences in the disposition of arsenicals may contribute to the observed differences between humans and rats in susceptibility to arsenic carcinogenicity.

Amino Acid Sequence↗
PubMed2003

Toxicity and metabolism of subcytotoxic inorganic arsenic in human renal proximal tubule epithelial cells (HK-2).

Arsenic is an environmental toxicant and a human carcinogen. The kidney, a known target organ of arsenic toxicity, is critical for both in vivo arsenic biotransformation and elimination. This study investigates the potential of an immortalized human proximal tubular epithelial cell line, HK-2, to serve as a representative model for low level exposures of the human kidney to arsenic. Subcytotoxic concentrations of arsenite (< or = 10 micromol/L) and arsenate (< 100 micromol/L) were determined by leakage of LDH from cells exposed for 24 h. Threshold concentrations of arsenite (between 1 and 10 micromol/L) and arsenate (between 10 and 25 micromol/L) were found to affect MTT processing by mitochondria. Biotransformation of subcytotoxic arsenite or arsenate was determined using HPLC-ICP-MS to detect metabolites in cell culture media and cell lysates. Following 24 h, analysis of media revealed that arsenite was minimally oxidized to arsenate and arsenate was reduced to arsenite. Only arsenite was detected in cell lysates. Pentavalent methylated arsenicals were not detected in media or lysates following exposure to either inorganic arsenical. The activities of key arsenic biotransformation enzymes--MMAV reductase and AsIII methyltransferase--were evaluated to determine whether HK-2 cells could reduce and methylate arsenicals. When compared to the activities of these enzymes in other animal tissues, the specific activities of HK-2 cells were indicative of a robust capacity to metabolize arsenic. It appears this human renal cell line is capable of biotransforming inorganic arsenic compounds, primarily reducing arsenate to arsenite. In addition, even at low concentrations, the mitochondria are a primary target for toxicity.

Animals↗
PubMedDate not supplied

Spatial distributions of arsenic exposure and mining communities from NHEXAS Arizona. National Human Exposure Assessment Survey.

Within the context of the National Human Exposure Assessment Survey (NHEXAS), metals were evaluated in the air, soil, dust, water, food, beverages, and urine of a single respondent. Potential doses were calculated for five metals including arsenic. In this paper, we seek to validate the potential dose calculations through spatial analysis of the data. Others report elevated arsenic concentrations in biological and environmental samples from residents of mining towns, particularly Ajo, Arizona. These reports led us to expect potential arsenic doses above the 90th percentile of the NHEXAS exposure distribution to be from residents of mining communities. Arsenic dose was calculated using media concentrations, time activity patterns, and published exposure factors. Of the 179 homes evaluated, 54 were in mining communities; 11 of these were considered separately for reasons of population bias. Of the 17 homes with the greatest potential arsenic doses, almost half (47%) were in mining communities. We evaluated the potential doses by media from nonmining and mining areas using the nonparametric Mann-Whitney U test. Statistically significant (p = 0.05) differences were found between mining (n = 43) and nonmining sites (n = 122) for total exposure and for each of the following media: house dust, yard soil, outdoor air, beverage consumed, and water consumed. No differences were found in either food or indoor air of mining and nonmining areas. We eliminated outliers and repeated the test for all media; significance increased. Dietary, organic arsenic from fish consumption contributed to elevated arsenic exposure among people from nonmining communities and acted as an initial confounder. When controlling for fish consumption, we were able to validate our potential dose model using arsenic, particularly in Ajo. Further, we identified three mining communities lacking elevated arsenic exposure. Additional work is needed speciating the arsenic and evaluating health risks. The utilization of Geographic Information System facilitated spatial this project and paves the way for more sophisticated future spatial analyses.

Adult↗
PubMed2001

An evaluation of extraction techniques for arsenic species from freeze-dried apple samples.

The extraction of arsenic from freeze-dried apples and subsequent determination of individual arsenic species by HPLC-ICP-MS is described. Solvent extraction with sonication using various aqueous and aqueous/solvent mixtures was initially evaluated by measuring total arsenic extracted by ICP-MS. A two step procedure using overnight treatment with alpha-amylase enzyme followed by sonication for 6 h with 40:60 acetonitrile-water was found to provide good extraction efficiency. The concentration of arsenic extracted was compared with the concentration of total arsenic in the samples determined using ICP-MS after microwave digestion in order to calculate extraction efficiency. Individual arsenic species in the extracts were measured using HPLC-ICP-MS. The three most abundant arsenic species found were arsenite, arsenate and dimethylarsinic acid. Total arsenic concentrations in the freeze-dried apple samples ranged from 8.2 to 80.9 micrograms kg-1 As, dry mass. By HPLC-ICP-MS, the relative amount of inorganic arsenic in the samples ranged from 73 to 90% of the sum of the arsenic species detected in each sample.

Arsenicals↗
PubMed1999

Arsenic-induced oxidative stress and its reversibility following combined administration of N-acetylcysteine and meso 2,3-dimercaptosuccinic acid in rats.

1. The present study examined whether arsenic induces oxidative stress in liver, brain and erythrocytes (RBC) based on the investigation of certain selected parameters. It also explored the possibility that combined administration of N-acetylcysteine (NAC) and meso 2,3-dimercaptosuccinic acid (DMSA) was capable of achieving better reversibility in the parameters indicative of arsenic-induced oxidative stress than individual treatment with either of these drugs. 2. Male rats were exposed to 100 p.p.m. sodium arsenite in their drinking water for 12 weeks (equivalent to 12 mg/kg As). The arsenic was then removed and rats were given NAC (1 mmol/kg per day), DMSA (1 mmol/kg per day) or a combination of the two, orally, once daily for 5 days. Animals not given arsenic and those given arsenic but not NAC or DMSA served as negative and positive controls, respectively. 3. Twelve weeks of arsenic exposure was found to deplete glutathione (GSH) levels, increase oxidized glutathione (GSSG) and promote malondialdehyde (MDA) production in both liver and brain samples. In addition to a significant reduction in RBC delta-aminolevulinic acid dehydratase (ALAD) activity and GSH levels, a marked elevation in MDA production may also contribute to arsenic-induced oxidative stress. 4. Treatment with either NAC or DMSA alone partially reversed arsenic-induced alterations in hepatic GSH and MDA, while only brain MDA levels responded favourably to these drugs. Only DMSA appeared to restore blood ALAD, while RBC MDA levels responded favourably to both drugs. Treatment with DMSA also produced an effective depletion of blood and hepatic arsenic concentrations. In the liver, most of these parameters were more effectively reversed by combined treatment with NAC and DMSA compared with the effects of either drug alone. 5. These results provide in vivo evidence of arsenic-induced oxidative stress in liver, brain and RBC and indicate that these effects can be mitigated by pharmacological intervention that encompasses combined treatment with NAC and DMSA.

3,4-Methylenedioxyamphetamine↗