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Comparison of a chemical and enzymatic extraction of arsenic from rice and an assessment of the arsenic absorption from contaminated water by cooked rice.

Rice is a target food for arsenic speciation based analyses because of its relatively high arsenic concentration and per capita consumption rates. Improved speciation data for rice can be helpful in estimating inorganic arsenic exposures in the U.S. and in endemic populations. The inorganic arsenic exposure for cooked rice should include both the arsenic in raw rice plus the arsenic absorbed from the water used to prepare it. The amount of arsenic absorbed from water by rice during preparation was assessed using five different types of rice cooked in both contaminated drinking water and arsenic-free reagent water. The rice samples were extracted using trifluoroacetic acid (TFA) and speciated using IC-ICP-MS. The TFA procedure was able to extract 84-104% of the arsenic (As) from the five different cooked rice samples. Chromatographic recoveries ranged from 99% to 116%. The dimethylarsinic acid (DMA) and inorganic arsenic concentration ranged from 22 to 270 ng of As/g of rice and from 31 to 108 ng of As/g of rice, respectively, for samples cooked in reagent water. The overall recoveries, which relate the sum of the chromatographic species back to the total digested concentration, ranged from 89% to 117%. The absorption of arsenic by rice from the total volume of water [1:1 to 4:1 (water:rice)] used in cooking was between 89% and 105% for two different contaminated drinking water samples. A comparison of the TFA extraction to an enzymatic extraction was made using the five rice samples and NIST 1568a rice flour. The two extraction procedures produced good agreement for inorganic arsenic, DMA, and the overall recovery. Through the use of IC-ESI-MS/ MS with a parent ion of m/z 153 and fragment ions of m/z 138, 123, and 105, the structure dimethylthioarsinic acid was tentatively identified in two of the rice samples using the enzymatic extraction.

Absorption↗

The role of oxidative DNA damage in human arsenic carcinogenesis: detection of 8-hydroxy-2'-deoxyguanosine in arsenic-related Bowen's disease.

Arsenic is widely distributed in nature in the form of either metalloids or chemical compounds, which cause a variety of pathologic conditions including cutaneous and visceral malignancies. Recently, reactive oxygen species have been hypothesized to be one of the causes of arsenic-induced carcinogenesis. 8-Hydroxy-2'-deoxyguanosine is one of the major reactive oxygen species-induced DNA base-modified products that is widely accepted as a sensitive marker of oxidative DNA damage. We studied the presence of 8-hydroxy-2'-deoxyguanosine by immunohistochemistry using N45.1 monoclonal antibody in 28 cases of arsenic-related skin neoplasms and arsenic keratosis as well as in 11 cases of arsenic-unrelated Bowen's diseases. The frequency of 8-hydroxy-2'-deoxyguanosine positive cases was significantly higher in arsenic-related skin neoplasms (22 of 28; 78%) than in arsenic-unrelated Bowen's disease (one of 11; 9%) (p < 0.001 by chi2 test). 8-Hydroxy-2'-deoxyguanosine was also detected in normal tissue adjacent to the arsenic-related Bowen's disease lesions. Furthermore, arsenic was detected by neutron activation analysis in the deparaffined skin tumor samples of arsenic-related disease (four of five; 80%), whereas arsenic was not detected in control samples. Our results strongly suggest the involvement of reactive oxygen species in arsenic-induced human skin cancer. Key word: neutron activation analysis.

8-Hydroxy-2'-Deoxyguanosine↗

Urinary arsenic excretion as a biomarker of arsenic exposure in children.

Urinary arsenic concentration has been used generally for the determination of exposure, but much concern has been raised over the most appropriate expression for urinary arsenic levels. In this study, we examined the influence of various adjustments of expressing urinary arsenic data. All children who were less than 72 mo of age and who were potty trained were invited to participate in the present study. Urine, soil, and dust samples were collected, and arsenic measurements were made. The geometric mean of speciated urinary arsenic among children who provided first-voided urine samples on 2 consecutive mornings was 8.6 microg/l (geometric standard deviation = 1.7, n = 289). Speciated urinary arsenic was related significantly to soil arsenic in bare areas (p < .0005). Use of a single urine sample versus the average of two first-voided urine samples collected on 2 consecutive mornings did not significantly alter the relationship between environmental arsenic and urinary arsenic levels. Furthermore, none of the adjustments to urinary concentration improved the strength of correlation between urinary arsenic and soil arsenic levels. Concentration adjustments may not be necessary for urinary arsenic levels obtained from young children who provide first-void samples in the morning.

Arsenic↗

Arsenic uptake by native fern species in Thailand: effect of chelating agents on hyperaccumulation of arsenic by Pityrogramma calomelanos.

Nineteen native fern species collected from an area in Thailand with high arsenic concentration in soil and in ground water as a result of tin mining was screened for elevated arsenic concentration in fronds. Two species of fern were found to contain elevated arsenic in their fronds in nature: Pityrogramma calomelanos (108-1156 microg g(-1) dried weight) and Pteris vittata (79 microg g(-1) dried weight). Under hydroponic culture Pityrogramma calomelanos (a silver back fern) accumulated arsenic in its shoot at rate of 4616 microg(-1) (dried weight). The accumulation of arsenic in Pityrogramma calomelanos shoot doubled with the addition of an EDTA (Ethelenediamine tetraacetic acid) chelating agent. The highest accumulation occurred 6 weeks after exposure to 10 mg L(-1) arsenic as disodium hydrogen arsenate. The addition of another chelating agent, DMS (Dimercaptosuccinic acid), resulted in a 5-fold decrease in arsenic concentration in the Pityrogramma calomelanos shoot compared to control after 6 weeks of exposure to arsenic. The contrasting effect of the EDTA and DMSA chelating agent was attributed to the strong binding of the thiol group to arsenic ion. This study indicated that Pityrogramma calomelanos uptake and translocate arsenic in the form of arsenate and arsenite rather than the As-DMSA complex. Using phytoextraction efficiency calculations, it was determined that Pityrogramma calomelanos gave the highest arsenic phytoextraction efficiency at 6 weeks after exposure to arsenic in the EDTA treatment, with an efficiency of 77.8 mg As based on whole plant biomass.

Arsenic↗

Arsenic (+3 oxidation state) methyltransferase and the methylation of arsenicals.

Metabolic conversion of inorganic arsenic into methylated products is a multistep process that yields mono-, di-, and trimethylated arsenicals. In recent years, it has become apparent that formation of methylated metabolites of inorganic arsenic is not necessarily a detoxification process. Intermediates and products formed in this pathway may be more reactive and toxic than inorganic arsenic. Like all metabolic pathways, understanding the pathway for arsenic methylation involves identification of each individual step in the process and the characterization of the molecules which participate in each step. Among several arsenic methyltransferases that have been identified, arsenic (+3 oxidation state) methyltransferase is the one best characterized at the genetic and functional levels. This review focuses on phylogenetic relationships in the deuterostomal lineage for this enzyme and on the relation between genotype for arsenic (+3 oxidation state) methyltransferase and phenotype for conversion of inorganic arsenic to methylated metabolites. Two conceptual models for function of arsenic (+3 oxidation state) methyltransferase which posit different roles for cellular reductants in the conversion of inorganic arsenic to methylated metabolites are compared. Although each model accurately represents some aspects of enzyme's role in the pathway for arsenic methylation, neither model is a fully satisfactory representation of all the steps in this metabolic pathway. Additional information on the structure and function of the enzyme will be needed to develop a more comprehensive model for this pathway.

Amino Acid Sequence↗

[Investigation of chronic arsenic poisoning caused by high arsenic coal pollution].

This article reports the results of an investigation on environmental arsenic pollution and chronic arsenic poisoning in a rural area. Exploitation of high arsenic coal caused drinking and irrigating water to be polluted by arsenic and burning of this coal caused severe environmental arsenic pollution including air, food, soil and drinking well water. 1548 villagers in 47 villages suffered from chronic arsenic poisoning who used this coal in daily life. The polluted air and food were mainly responsible, while the polluted drinking water and skin absorption played some part in poisoning. When arsenic level in coal is as high as 100mg/kg, we should consider the possibility of environmental arsenic pollution and chronic arsenic poisoning in exposed population. The high arsenic coal's distribution is very uneven. When controlling the disease, it is important to remember monitoring the quantity of arsenic coal outside the arsenic coal mining area.

Arsenic Poisoning↗

Arsenic species excretion after dimercaptopropanesulfonic acid (DMPS) treatment of an acute arsenic trioxide poisoning.

We studied the urinary excretion of the different arsenic species in urine samples from a young man who tried to commit suicide by ingesting about 0.6 g arsenic trioxide. He received immediate therapy with dimercaptopropanesulfonic acid (DMPS) after his delivery into the hospital. We assessed urinary arsenite (inorganic trivalent arsenic), arsenate (inorganic pentavalent arsenic), pentavalent dimethylarsinic acid (DMA) and pentavalent monomethylarsonic acid (MMA) in urine with ion-exchange chromatography and on-line hydride-technique atomic absorption spectrometry. The predominant amount of the excreted arsenic was unchanged trivalent inorganic arsenic (37.4%), followed by pentavalent inorganic arsenic (2.6%), MMA (2.1%), DMA (0.2%) and one unidentified arsenic species (0.7%, if calculated as DMA). In the first urine voiding in the clinic, the total arsenic concentration was 215 mg/l, which fell 1000-fold after 8 days of DMPS therapy. A most striking finding was the almost complete inhibition of the second methylation step in arsenic metabolism. As mechanisms for the reduced methylation efficiency, the saturation of the enzymatic process of arsenic methylation, the high dosage of antidote DMPS, which might inhibit the activity of the methyl transferases, and analytical reasons are discussed. The high dosage of DMPS is the most likely explanation. The patient left the hospital after a 12-day treatment with antidote.

Adult↗

Urinary arsenic profile affects the risk of urothelial carcinoma even at low arsenic exposure.

Arsenic exposure is associated with an increased risk of urothelial carcinoma (UC). To explore the association between individual risk and urinary arsenic profile in subjects without evident exposure, 177 UC cases and 313 age-matched controls were recruited between September 2002 and May 2004 for a case-control study. Urinary arsenic species including the following three categories, inorganic arsenic (As(III)+As(V)), monomethylarsonic acid (MMA(V)) and dimethylarsinic acid (DMA(V)), were determined with high-performance liquid chromatography-linked hydride generator and atomic absorption spectrometry. Arsenic methylation profile was assessed by percentages of various arsenic species in the sum of the three categories measured. The primary methylation index (PMI) was defined as the ratio between MMA(V) and inorganic arsenic. Secondary methylation index (SMI) was determined as the ratio between DMA(V) and MMA(V). Smoking is associated with a significant risk of UC in a dose-dependent manner. After multivariate adjustment, UC cases had a significantly higher sum of all the urinary species measured, higher percent MMA(V), lower percent DMA(V), higher PMI and lower SMI values compared with controls. Smoking interacts with the urinary arsenic profile in modifying the UC risk. Differential carcinogenic effects of the urinary arsenic profile, however, were seen more prominently in non-smokers than in smokers, suggesting that smoking is not the only major environmental source of arsenic contamination since the UC risk differs in non-smokers. Subjects who have an unfavorable urinary arsenic profile have an increased UC risk even at low exposure levels.

Adult↗

Evidence of hemoglobin binding to arsenic as a basis for the accumulation of arsenic in rat blood.

Four trivalent arsenic species, inorganic arsenite (iAs(III)), monomethylarsonous acid (MMA(III)), dimethylarsinous acid (DMA(III)), and phenylarsine oxide (PhAs(III)O), have shown increasing binding affinity with the hemoglobin (Hb) of rats and humans. The binding stoichiometry was consistent with the number of reactive cysteine residues in the alpha and beta chains of Hb. Comparing the binding affinity of rat Hb and human Hb for the same trivalent arsenic species, rat Hb was 3-16 times stronger than human Hb as demonstrated by their apparent binding constants. Comparative experiments involving incubation of human and rat red blood cells (RBC) with iAs(III), MMA(III), and DMA(III) showed that 15-30-fold more arsenic species were bound to the Hb of rat RBC than that of human RBC. In vivo experiments using rats fed with an arsenic-supplemented diet showed that arsenic in RBC of the rats was predominantly found in the protein-bound form. Further characterization by nanoelectrospray mass spectrometry of the arsenic species in the RBC of these rats confirmed that most arsenic was bound to the alpha chain of Hb. Taken together, these results suggest that the stronger binding affinity of these arsenic species to rat Hb is responsible for the accumulation of arsenic in rat blood. The results provide a chemical basis to explain the previously observed intriguing difference in the retention of arsenic in the human and the rat. The techniques and approaches described can be applied to the studies of arsenic interactions with other functional proteins.

Animals↗

[Arsenic exposure of residents in areas near Shimen arsenic mine].

OBJECTIVES: To investigate the levels of arsenic exposure of residents in the arsenic polluted areas near an arsenic mine. METHODS: To analyse the arsenic levels in environmental samples and hair in the polluted areas and a control area. RESULTS: In three villages of the polluted areas, arsenic levels in soil were 84.17 to 296.19 mg/kg, in river water 0.5 to 14.5 mg/L, in well water and tap water lower than 0.05 mg/L, in rice 0.196 to 0.620 mg/kg. Arsenic intake amounted 195 to 1129 micrograms/day. In the hair, the arsenic contents were from 0.972 to 2.459 micrograms/g, increasing with aging. CONCLUSION: In the areas near Shimen arsenic mine, arsenic pollution was serious. The levels of arsenic exposure of residents were equal to or even over that of the severe cases of chronic arsenic poisoning reported domestically and abroad.

Adult↗

Methylated trivalent arsenicals as candidate ultimate genotoxic forms of arsenic: induction of chromosomal mutations but not gene mutations.

Arsenic is a prevalent human carcinogen whose mutagenicity has not been characterized fully. Exposure to either form of inorganic arsenic, As(III) or As(V), can result in the formation of at least four organic metabolites: monomethylarsonic acid, monomethylarsonous acid (MMA(III)), dimethylarsinic acid, and dimethylarsinous acid (DMA(III)). The methylated trivalent species, as well as some of the other species, have not been evaluated previously for the induction of chromosome aberrations, sister chromatid exchanges (SCE), or toxicity in cultured human peripheral blood lymphocytes; for mutagenicity in L5178Y/Tk(+/-) mouse lymphoma cells or in the Salmonella reversion assay; or for prophage-induction in Escherichia coli. Here we evaluated the arsenicals in these assays and found that MMA(III) and DMA(III) were the most potent clastogens of the six arsenicals in human lymphocytes and the most potent mutagens of the six arsenicals at the Tk(+/-) locus in mouse lymphoma cells. The dimethylated arsenicals were also spindle poisons, suggesting that they may be ultimate forms of arsenic that induce aneuploidy. Although the arsenicals were potent clastogens, none were potent SCE inducers, similar to clastogens that act via reactive oxygen species. None of the six arsenicals were gene mutagens in Salmonella TA98, TA100, or TA104; and neither MMA(III) nor DMA(III) induced prophage. Our results show that both methylated As(V) compounds were less cytotoxic and genotoxic than As(V), whereas both methylated As(III) compounds were more cytotoxic and genotoxic than As(III). Our data support the view that MMA(III) and DMA(III) are candidate ultimate genotoxic forms of arsenic and that they are clastogens and not gene mutagens. We suggest that the clastogenicity of the other arsenicals is due to their metabolism by cells to MMA(III) or DMA(III).

Arsenicals↗

Recent advances in arsenic carcinogenesis: modes of action, animal model systems, and methylated arsenic metabolites.

Recent advances in our knowledge of arsenic carcinogenesis include the development of rat or mouse models for all human organs in which inorganic arsenic is known to cause cancer-skin, lung, urinary bladder, liver, and kidney. Tumors can be produced from either promotion of carcinogenesis protocols (mouse skin and lungs, rat bladder, kidney, liver, and thyroid) or from complete carcinogenesis protocols (rat bladder and mouse lung). Experiments with p53(+/-) and K6/ODC transgenic mice administered dimethylarsinic acid or arsenite have shown some degree of carcinogenic, cocarcinogenic, or promotional activity in skin or bladder. At present, with the possible exception of skin, the arsenic carcinogenesis models in wild-type animals are more highly developed than in transgenic mice. Recent advances in arsenic metabolism have suggested that methylation of inorganic arsenic may be a toxification, rather than a detoxification, pathway and that trivalent methylated arsenic metabolites, particularly monomethylarsonous acid and dimethylarsinous acid, have a great deal of biological activity. Accumulating evidence indicates that these trivalent, methylated, and relatively less ionizable arsenic metabolites may be unusually capable of interacting with cellular targets such as proteins and even DNA. In risk assessment of environmental arsenic, it is important to know and to utilize both the mode of carcinogenic action and the shape of the dose-response curve at low environmental arsenic concentrations. Although much progress has been recently made in the area of arsenic's possible mode(s) of carcinogenic action, a scientific concensus has not yet been reached. In this review, nine different possible modes of action of arsenic carcinogenesis are presented and discussed-induced chromosomal abnormalities, oxidative stress, altered DNA repair, altered DNA methylation patterns, altered growth factors, enhanced cell proliferation, promotion/progression, gene amplification, and suppression of p53.

Animals↗

A new metabolic pathway of arsenite: arsenic-glutathione complexes are substrates for human arsenic methyltransferase Cyt19.

The metabolism of arsenic is generally accepted to proceed by repetitive reduction and oxidative methylation; the latter is mediated by arsenic methyltransferase (Cyt19). In human urine, the major metabolites of inorganic arsenicals such as arsenite (iAsIII) and arsenate (iAsV) are monomethylarsonic acid (MMA(V)) and dimethylarsinic acid (DMA(V)). On the other hand, in rat bile, the major metabolites of iAsIII have been reported to be arsenic-glutathione (As-GSH) complexes. In the present study we investigate whether these As-GSH complexes are substrates for arsenic methyltransferase by using human recombinant Cyt19. Analyses by high-performance liquid chromatography-inductively coupled plasma mass spectrometry suggested that arsenic triglutathione (ATG) was generated nonenzymatically from iAsIII when GSH was present at concentrations 2 mM or higher. Human recombinant Cyt19 catalyzed transfer of a methyl group from S-adenosyl-L-methionine to arsenic and produced monomethyl and dimethyl arsenicals. The methylation of arsenic was catalyzed by Cyt19 only when ATG was present in the reaction mixture. Moreover, monomethylarsonic diglutathione (MADG) was a substrate of Cyt19 for further methylation to dimethylarsinic glutathione (DMAG). On the other hand, monomethylarsonous acid (MMA(III)), a hydrolysis product of MADG, was not methylated to dimethyl arsenical by Cyt19. These results suggest that As-GSH complexes such as ATG and MADG were converted by Cyt19 to MADG and DMAG, respectively. Both MADG and DMAG were unstable in solution when the GSH concentration was lower than 1 mM, and were hydrolyzed and oxidized to MMA(V) and DMA(V), respectively. Metabolism of iAsIII to methylated arsenicals by Cyt19 was via ATG and MADG rather than by oxidative methylation of iAsIII and MMA(III).

Animals↗

Arsenic (+3 oxidation state) methyltransferase and the inorganic arsenic methylation phenotype.

Inorganic arsenic is enzymatically methylated; hence, its ingestion results in exposure to the parent compound and various methylated arsenicals. Both experimental and epidemiological evidences suggest that some of the adverse health effects associated with chronic exposure to inorganic arsenic may be mediated by these methylated metabolites. If iAs methylation is an activation process, then the phenotype for inorganic arsenic methylation may determine risk associated with exposure to this metalloid. We examined inorganic arsenic methylation phenotypes and arsenic (+3 oxidation state) methyltransferase genotypes in four species: three that methylate inorganic arsenic (human (Homo sapiens), rat (Rattus norwegicus), and mouse (Mus musculus)) and one that does not methylate inorganic arsenic (chimpanzee, Pan troglodytes). The predicted protein products from arsenic (+3 oxidation state) methyltransferase are similar in size for rat (369 amino acid residues), mouse (376 residues), and human (375 residues). By comparison, a 275-nucleotide deletion beginning at nucleotide 612 in the chimpanzee gene sequence causes a frameshift that leads to a nonsense mutation for a premature stop codon after amino acid 205. The null phenotype for inorganic arsenic methylation in the chimpanzee is likely due to the deletion in the gene for arsenic (+3 oxidation state) methyltransferase that yields an inactive truncated protein. This lineage-specific loss of function caused by the deletion event must have occurred in the Pan lineage after Homo-Pan divergence about 5 million years ago.

Animals↗

Multidrug-resistance mdr1a/1b double knockout mice are more sensitive than wild type mice to acute arsenic toxicity, with higher arsenic accumulation in tissues.

Arsenic is an environmental toxicant. Active extrusion via the ArsAB pump is a mechanism for arsenic detoxication in bacteria. However, how arsenic is effluxed from mammalian cells is not completely known. Our recent work shows that acquired arsenic resistance is associated with overexpression of P-glycoprotein and can be reversed by PSC833, an inhibitor for P-glycoprotein. This study utilized the mdr1a/1b(-/-) mice, which lack mdr1-type P-glycoproteins, to examine whether these mice are sensitive to arsenic toxicity and have higher arsenic accumulation in their tissues. The mdr1a/1b(-/-) and wild-type FVB mice were given arsenic as sodium arsenite (12-19 mg/kg, sc) and toxicity was examined 24 h later. The mdr1a/1b(-/-) mice were more sensitive than wild-type mice to arsenite-induced lethality, with LD(50) of 14.5 and 17 mg/kg, respectively. Histologically, arsenite produced more frequent and more severe lesions in the liver and kidney of the mdr1a/1b(-/-) mice than in wild-type mice. Serum alanine aminotransferase activity and blood urea nitrogen levels, indicative of hepatic and renal damage respectively, were increased 4 to 6-fold in the mdr1a/1b(-/-) mice as compared with 1-2-fold increases in wild-type mice. The mdr1a/1b(-/-) mice accumulated more arsenic in the liver (15.3 vs. 5.2 microg/g), kidney (7.23 vs. 3.22 microg/g), small intestine (3.98 vs. 1.57 microg/g) and brain (0.45 vs. 0.17 microg/g), as compared with wild-type mice 24 h after sodium arsenite (14 mg/kg, s.c.) administration. In summary, this study demonstrated that the mdr1a/1b(-/-) mice were more sensitive to acute arsenic toxicity and accumulated more arsenic than wild-type mice, suggesting that P-glycoproteins are involved, at least in part, in arsenic efflux in mammalians.

Alanine Transaminase↗

Evaluation of two new arsenic field test kits capable of detecting arsenic water concentrations close to 10 microg/L.

Millions of people worldwide are exposed to arsenic-contaminated drinking water. Arsenic field test kits may offer a cost-effective approach for measuring these exposures in the field, although the accuracy of some kits used in the past has been poor. In this study, arsenic concentrations were measured in 136 water sources in western Nevada using two relatively new arsenic test kits and compared to laboratory measurements using atomic fluorescence spectroscopy (AFS). Spearman's rank correlation coefficients comparing the Quick Arsenic and Hach EZ kits to laboratory measurements were 0.96 (p < 0.001) and 0.95 (p < 0.001), respectively. When analyzed in seven exposure categories (0-9, 10-19, 20-49, 50-99, 100-199, 200-499, and > or = 500 microg/L), test kit and AFS measurements were in the same category in 71% (Quick Arsenic) and 62% (Hach EZ) of samples, and within one category of each other in 99% (Quick Arsenic) and 97% (Hach EZ) of samples. Both kits identified all water samples with high arsenic concentrations (> 15 microg/L) as being above the United States Environmental Protection Agency's drinking water standard and the World Health Organization's guideline value for arsenic of 10 microg/L. These results suggestthatthese easily portable kits can be used to identify water sources with high arsenic concentrations and may provide an important tool for arsenic surveillance and remediation programs.

Arsenic↗

Arsenic levels in fingernails as a biological indicator of exposure to arsenic.

The analysis of urine, blood, and hair has been used previously to monitor occupational exposure to arsenic (As). Although arsenic is normally present in human fingernails (usually as a result of dietary factors), this study evaluated the potential use of levels of arsenic in fingernails as a biological indicator of occupational exposure to this element. Air samples and fingernail clippings were obtained from individuals with no exposure and high, medium, and low exposure. A washing technique, previously developed to remove exogenous arsenic from hair, was modified to wash the fingernail samples collected in this study. It was demonstrated that 98% of exogenous arsenic was removed from these nails. A high correlation coefficient (r = 0.89) was observed in a comparison of the mean air arsenic concentrations of each exposure group with corresponding arsenic levels in fingernails. From the data collected, an equation was derived to estimate the air arsenic exposure level for a worker from the arsenic content of fingernails: air arsenic concentration (micrograms As/m3) = 1.79 x fingernail arsenic level (micrograms As/g nail)-5.9.

Air Pollutants, Occupational↗

Phytoremediation of arsenic-contaminated groundwater by the arsenic hyperaccumulating fern Pteris vittata L.

Arsenic concentrations in a much larger fraction of U.S. groundwater sources will exceed the maximum contaminant limit when the new 10 microg L(-1) EPA standard for drinking water takes effect in 2006. Thus, it is important to develop remediation technologies that can meet this new standard. Phytoremediation of arsenic-contaminated groundwater is a relatively new idea. In this research, an arsenic-hyperaccumulating fern, commonly known as Chinese Brake fern (Pteris vittata L.), was grown hydroponically to examine its effectiveness in arsenic removal from what is believed to be herbicide-contaminated groundwater. One plant grown in 600 mL of groundwater effectively reduced the arsenic concentration from 46 to less than 10 microg L(-1) in 3 days. Re-used plants continued to take up arsenic from the groundwater, albeit at a slower rate (from 46 to 20 microg L(-1) during the same time). Young fern plants were more efficient in removing arsenic than were older fern plants of similar size. The addition of a supplement of phosphate-free Hoagland nutrition to the groundwater had little effect on arsenic removal, but the addition of phosphate nutrition significantly reduced its arsenic affinity and, thus, inhibited the arsenic removal. This study suggested that Chinese Brake has some potential to remove arsenic from groundwater.

Arsenic↗