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PubMed2005

Murshidabad--one of the nine groundwater arsenic-affected districts of West Bengal, India. Part II: dermatological, neurological, and obstetric findings.

INTRODUCTION: To understand the severity of related health effects of chronic arsenic exposure in West Bengal, a detailed 3-year study was carried out in Murshidabad, one of the nine arsenic-affected districts in West Bengal. METHODS: We screened 25,274 people from 139 arsenic-affected villages in Murshidabad to identify patients suffering from chronic arsenic toxicity for evidence of multisystemic features and collected biological samples such as head hair, nail, and spot urine from the patients along with the tubewell water they were consuming. RESULTS: Out of 25,274 people screened, 4813 (19%) were registered with arsenical skin lesions. A case series involving arsenical skin lesions resulting in cancer and gangrene were noted during this study. Representative histopathological pictures of skin biopsy of different types of lesions were also presented. Out of 2595 children we examined for arsenical skin lesions, 122 (4%) were registered with arsenical skin lesions, melanosis with or without keratosis. Different clinical and electrophysiological neurological features were noticed among the arsenic-affected villagers. Both the arsenic content in the drinking water and duration of exposure may be responsible in increasing the susceptibility of pregnant women to spontaneous abortions, stillbirths, preterm births, low birth weights, and neonatal deaths. Some additional multisystemic features such as weakness and lethargy, chronic respiratory problems, gastrointestinal symptoms, and anemia were also recorded in the affected population. DISCUSSION: The findings from this survey on different health effects of arsenic exposure were compared to those from previous studies carried out on arsenic-affected populations in India and Bangladesh as well as other affected countries. CONCLUSION: Multisystemic disorders, including dermal effects, neurological complications, and adverse obstetric outcomes, were observed to be associated with chronic arsenic exposure in the study population in Murshidabad, West Bengal. The magnitude of severity was related to the concentration of arsenic in water as well as duration of the exposure.

Arsenic Poisoning↗
PubMed2006

Efficacy of spirulina extract plus zinc in patients of chronic arsenic poisoning: a randomized placebo-controlled study.

BACKGROUND: Millions of people in Bangladesh, India, Taiwan, and Chile are consuming high concentration of arsenic through drinking water, and thousands of them have already developed chronic arsenic poisoning. There is no specific treatment. Some authors suggest the use of vitamins and minerals for more than 6 months. The present placebo-controlled double-blind study was conducted to evaluate effectiveness of spirulina extract plus zinc in the treatment of chronic arsenic poisoning. METHODS: Forty-one patients of chronic arsenic poisoning were randomly treated orally by either placebo (17 patients) or spirulina extract (250 mg) plus zinc (2 mg) (24 patients) twice daily for 16 weeks. Each patient was supplied with arsenic-safe drinking water by installing a locally made water filter at household level. Effectiveness of spirulina extract plus zinc was evaluated by comparing changes in skin manifestations (clinical scores), arsenic contents in urine and hair, between the placebo- and spirulina extract plus zinc-treated groups. RESULTS: The concentrations of total arsenic in water (without filtration) of placebo- and spirulina extract plus zinc-treated groups were 150.1 +/- 18.3 and 161.7 +/- 23.9 microg/l, respectively. Intake of these high concentrations of arsenic lead to increased excretion of arsenic in urine (72.1 +/- 14.5 microg/l in placebo-treated group and 78.4 +/- 19.1 microg/l in spirulina plus zinc-treated group). After 2 weeks of using filtered water, there were significant reduction of both arsenic intake through water and urinary arsenic excretion (8.3 +/- 3.6 microg/l and 18.4 +/- 7.3 microg/l in placebo group; 9.7 +/- 5.4 microg/l and 21.6 +/- 5.8 microg/l) in spirulina extract plus zinc-treated group. There was a sharp increase in urinary excretion of arsenic (138 +/- 43.6 microg/l) at 4 weeks following spirulina plus zinc administration and the effect was continued for another 2 weeks. Spirulina extract plus zinc removed 47.1% arsenic from scalp hair. Spirulina extract had no major adverse effect that required physician's attention. The clinical scores (median) for melanosis before and after treatment with placebo was not statistically significant (p > 0.05), whereas in spirulina extract plus zinc-treated group it was statistically significant (p < 0.01). In cases of keratosis, the median clinical scores before and after treatment was not statistically significant (p > 0.05) in placebo-treated group. In spirulina extract plus zinc-treated group, the clinical scores for keratosis before and after treatment was statistically significant (p < 0.05). CONCLUSIONS: Results show that spirulina extract (250 mg) plus zinc (2 mg) twice daily for 16 weeks may be useful for the treatment of chronic arsenic poisoning with melanosis and keratosis.

Adolescent↗
PubMed2006

Elevated urine arsenic: un-speciated results lead to unnecessary concern and further evaluations.

The consumption of seafood within two to three days of testing can increase total urine arsenic concentrations. Few clinicians are familiar with this fact and often misinterpret elevated results. A retrospective chart review of all cases with arsenic testing seen between 1991 and 2004 at an occupational and environmental medicine referral clinic was performed. Urine arsenic results were classified as follows: total arsenic levels; speciated results (inorganic, ionic arsenic); and whether the patient abstained from seafood prior to the collection. Laboratory detection limits for total and for ionic arsenic were < or = 2 microg/L. Fifty-four patients with urine arsenic testing were identified. The total urine arsenic concentration exceeded 40 microg/L for 28 patients. On paired, speciated testing (n = 21), mean total arsenic was 122 +/- 227 microg/L, and ionic arsenic was not detected in any of these same samples (p = 0.023). On paired testing, before and after seafood abstention (n = 12), total urine arsenic without abstention was 291 +/- 267 microg/L, and it was only 9 +/- 12 microg/L after seafood abstention (p = 0.004). The total urine arsenic elevations observed in our series were due to benign organic arsenic compounds commonly found in seafood. Laboratories should reflexively perform speciation on most samples with elevated total arsenic concentrations prior to reporting the results. Reflexive speciation could reduce unnecessary referrals, further testing, and patient anxiety.

Adolescent↗
PubMed2006

[Effects of MRP2-GSH cotransport system on hepatic arsenic metabolism in rats].

OBJECTIVE: To investigate the role of multidrug resistant protein 2 (MRP2) and glutathione (GSH) cotransport system in hepatic arsenic metabolism in rats. METHODS: Thirty healthy Wistar rats were divided randomizedly into five groups. The first group was the control group and the rats in this group were administered with normal saline. In the second, third and fourth group the rats were administered with 4, 10 and 20 mg As(+)3/kg BW of sodium arsenite respectively every other day for two weeks. The fifth group was the benzene-soluble organics (BSO) intervention group and in this group the rats were administered with 2 mmol/kg BW BSO intraperitoneally every day three days before the end of the experiment. The other treatment was the same as in other groups. All rats were sacrificed two weeks after the treatments. Arsenic contents in bile, liver and blood were detected by atomic absorption spectroscopy (AAS), and the expression of MRP2 in the membrane of hepatocyte was determined by Western-blot analysis. RESULTS: The level of total arsenic (including organic arsenic and inorganic arsenic) in bile, liver and blood in all three different dose groups was higher than those in the control groups (P < 0.05). Arsenic levels of bile and liver were increased with intragastric arsenic dose. Blood arsenic levels were not significantly different in three different dose groups. Expression of hepatic MRP2 was increased with intragastric arsenic concentration. A positive correlation between biliary arsenic concentration and MRP2 levels was found in liver (r = 0.986, P < 0.05). For the rats pretreated with BSO, the biliary arsenic was significantly higher than that in the control group but lower than that in the high dose group; the liver and blood arsenic was higher than that in the control group and in the high dose group. Expression of MRP2 pretreated with BSO was decreased. CONCLUSION: Sodium arsenite can induce expression of MRP2 and the up-regulation of MRP2 may play an important role in the bile secretion of arsenite and its metabolites. The function of MRP2 for transportation of arsenic and its metabolites is associated with the intracellular GSH level. BSO inhibits the synthesis of GSH, which weakens the function of the MRP2-GSH cotransport system and makes the liver arsenic increased.

Animals↗
PubMed1996

Implications of arsenic genotoxicity for dose response of carcinogenic effects.

Epidemiological data relating arsenic ingestion and skin and internal cancers strongly suggest a sublinear or threshold relationship. Physiological saturation of methylation-based arsenic detoxification has been proposed as one explanation for a sublinear response. We have evaluated the molecular bases for sublinearity in light of new data and hypotheses regarding arsenic genotoxicity and chemical carcinogenesis. A review of the dose-response relationships observed in arsenic genotoxicity assays is presented. With the exception of sister chromatid exchanges, sublinear dose-response relationships for arsenic-induced chromosomal aberrations were observed repeatedly in different mammalian and human cell systems. Arsenic also enhanced the clastogenicity and mutagenicity of other DNA damaging agents with a sublinear dose response. Consistent with the dose response of arsenic-induced genetic alterations, arsenic also inhibited DNA ligases I and II, enzymes which play a role in DNA repair, with a sublinear dose response. In some cases, protective effects of relatively low exposures to arsenic have been observed, again consistent with sublinearity. We discuss recent theories on the mechanism of arsenic carcinogenicity and the potential implications for dose-response modeling and risk assessment. Overall, based on available arsenic genotoxicity data, we conclude that it is likely that arsenic indirectly induces genetic damage with a sublinear dose response in humans, thus providing a biological basis for a sublinear dose-response relationship for human cancer. Furthermore, these results suggest that linear dose-response modeling from populations experiencing high arsenic exposures is likely to overpredict cancer risks at relatively low arsenic levels.

Animals↗
PubMed2006

Desorption of arsenic from drinking water distribution system solids.

Previous work has shown that arsenic can accumulate in drinking water distribution system (DWDS) solids (Lytle et al., 2004) when arsenic is present in the water. The release of arsenic back into the water through particulate transport and/or chemical release (e.g. desorption, dissolution) could result in elevated arsenic levels at the consumers' tap. The primary objective of this work was to examine the impact of pH and orthophosphate on the chemical release (i.e. desorption) of arsenic from nine DWDS solids collected from utilities located in the Midwest. Arsenic release comparisons were based on the examination of arsenic and other water quality parameters in leach water after contact with the solids over the course of 168~hours. Results showed that arsenic was released from solids and suggested that arsenic release was a result of desorption rather than dissolution. Arsenic release generally increased with increasing initial arsenic concentration in the solid and increasing pH levels (in the test range of 7 to 9). Finally, orthophosphate (3 and 5 mg PO(4)/L) increased arsenic release at all pH values examined. Based on the study results, utilities with measurable levels of arsenic present in their water should be aware that some water quality changes can cause arsenic release in the DWDS potentially resulting in elevated levels at the consumer's tap.

Arsenic↗
PubMed1990

Arsenic intake and excretion by Japanese adults: a 7-day duplicate diet study.

The amount of arsenic in the urine, faeces and in duplicate diets of two couples who had eaten customary Japanese meals were monitored for 7 days by arsine-generator atomic absorption spectrophotometry. For the four volunteers, the mean daily intake of arsenic from their diets was 182 micrograms (range 27 to 376 micrograms). The dietary arsenic was composed of 5.7% inorganic arsenic, 3.6% methylarsonic acid, 27.4% dimethylarsinic acid and 47.9% trimethylarsenic compounds. The mean amounts of arsenic eliminated daily in urine and faeces were 148 micrograms (50-416 micrograms) and 46 micrograms (0-138 micrograms), respectively. The urinary arsenic was composed of 1.4% inorganic arsenic, 3.5% methylarsonic acid, 33.6% dimethylarsinic acid and 61.4% trimethylarsenic compounds. The daily intake of arsenic influenced the total amount of arsenic excreted in the urine (r = 0.7302, P less than 0.01) and the amount eliminated in the faeces (r = 0.5900, P less than 0.01) the next day. Specifically, there was also a significant correlation between the daily intakes of trimethylarsenic compounds and dimethylarsinic acid and the amounts of these compounds found in the urine the following day (r = 0.6833, P less than 0.01 and r = 0.6630, P less than 0.01, respectively). Considering the amounts of arsenic compounds present in seafood and in other components of the diet together with the urinary elimination patterns of arsenic compounds, it seemed probable that the trimethylarsenic compounds in the urine originated largely from fish and shellfish, which contain mainly arsenobetaine. Trimethylarsenic compounds in the urine should therefore be the preferred indicator of arsenic arising from the ingestion of seafood, especially fish and shellfish. In this study, the mean daily intake of inorganic arsenic from the diet (0.18 micrograms/kg) did not exceed the FAO/WHO JECFA Tolerable Daily Intake of 2 micrograms inorganic arsenic kg.

Adult↗
PubMed1995

An attempt to explain interindividual variability in 24-h urinary excretion of inorganic arsenic metabolites by C57 BL/6J mice.

Forty C57 BL/6J mice, injected subcutaneously with 0.5 mg/kg arsenic as sodium arsenite, were examined for 24-h urinary excretion of total arsenic metabolites, creatinine and S-adenosylmethionine (SAM) and for 24-h faecal excretion of arsenic and levels of arsenic in the blood, liver, kidneys, lung, skin, spleen and bone at 24-h post-dose. Total urinary arsenic metabolites were calculated by summing up the inorganic (Asi), monomethylated (MMA) and dimethylated (DMA) derivatives directly measured by selective arsine generation-atomic absorption spectrometry (AG-AAS) or were measured by AG-AAS following complete mineralization. Both sets of results showed interindividual differences varying by as much as 7-fold and correlated with the 24-h urinary excretion of both SAM (r = 0.84 and r = 0.86, respectively) and creatinine (r = 0.82 and r = 0.87, respectively). There was interindividual variability of about a 30-fold range in 24-h faecal excretion of arsenic which correlated inversely with 24-h urinary excretion of arsenic metabolites (r = -0.69) and 24-h urinary excretion of both creatinine (r = -0.70) and SAM (r = -0.67). Body tissue levels of arsenic were low and not related to 24-h urinary excretion of arsenic metabolites, SAM and creatinine. Taken together, the results indicate that differences in the profile of urinary arsenic excretion and in the retention of arsenic in a particular organ do not contribute to interindividual variability in 24-h urinary excretion of arsenic metabolites by C57 BL/6J mice, but that variability in faecal excretion does, at least in part. It is speculated that there is most likely a predominant contribution from a diffuse tissue retention of arsenic or from a third route of arsenic elimination, i.e. respiratory, to this phenomenon in view of the small faecal contribution.

Animals↗
PubMed2006

Arsenic burden of cooked rice: Traditional and modern methods.

Arsenic contamination of rice by irrigation with contaminated groundwater and secondarily increased soil arsenic compounds the arsenic burden of populations dependent on subsistence rice-diets. The arsenic concentration of cooked rice is known to increase with the arsenic concentration of the cooking water but the effects of cooking methods have not been defined. We tested the three major rice cooking procedures followed globally. Using low-arsenic water (As < 3 microg/L), the traditional method of the Indian subcontinent (wash until clear; cook with rice: water::1:6; discard excess water) removed up to 57% of the arsenic from rice containing arsenic 203-540 microg/kg. Approximately half of the arsenic was lost in the wash water, half in the discard water. A simple inexpensive rice cooker based on this method has been designed and used for this purpose. Despite the use of low-arsenic water, the contemporary method of cooking unwashed rice at rice:water::1:1.5-2.0 until no discard water remains did not modify the arsenic content. Preliminary washing until clear did remove 28% of the rice arsenic. The results were not influenced by water source (tubewell, dug well, pond or rain); cooking vessel (aluminium, steel, glass or earthenware); or the absolute weight of rice or volume of water. The use of low-As water in the traditional preparation of arsenic contaminated rice can reduce the ingested burden of arsenic.

Arsenic↗
PubMed2005

A survey of arsenic in foodstuffs on sale in the United Kingdom and imported from Bangladesh.

Arsenic is a highly toxic element and its presence in food composites is a matter of concern to the well being of both humans and animals. Arsenic-contaminated groundwater is often used in Bangladesh and West Bengal (India) to irrigate crops used for food and animal consumption, which could potentially lead to arsenic entering the human food chain. In this study, we used graphite furnace atomic absorption spectroscopy to determine the total arsenic concentrations in a range of foodstuffs, including vegetables, rice and fish, imported into the United Kingdom from Bangladesh. The mean and range of the total arsenic concentration in all the vegetables imported from Bangladesh were 54.5 and 5-540 microg/kg, respectively. The highest arsenic values found were for the skin of Arum tuber, 540 microg/kg, followed by Arum Stem, 168 microg/kg, and Amaranthus, 160 microg/kg. Among the other samples, freshwater fish contained total arsenic levels between 97 and 1318 microg/kg. The arsenic content of the vegetables from the UK was approximately 2- to 3-fold lower than those observed for the vegetables imported from Bangladesh. The levels of arsenic found in vegetables imported from Bangladesh in this study, in some cases, are similar to those previously recorded for vegetables grown in arsenic-affected areas of West Bengal, India, although lower than the levels reported in studies from Bangladesh. While the total arsenic content detected in our study in vegetables, imported from Bangladesh, is far less than the recommended maximum permitted level of arsenic, it does provide an additional source of arsenic in the diet. This raises the possibility that the level of arsenic intake by certain sectors of the UK population may be significantly higher then the general population and requires further investigations.

Arsenic↗
PubMed2002

Role of iron in controlling speciation and mobilization of arsenic in subsurface environment.

Widespread arsenic contamination of groundwater has been reported of late in Bangladesh and West Bengal state of India. On the basis of arsenic geochemistry, three probable mechanisms have been cited for arsenic mobility in aquifers of West Bengal and Bangladesh. First, mobilization of arsenic due to the oxidation of arsenic-bearing pyrite minerals. Second, dissolution of arsenic-contaminated iron oxy-hydroxides (FeOOH) due to onset of reducing conditions in the subsurface. Third, due to the release of arsenic sorbed to aquifer minerals by competitive exchange with phosphate ions, that migrates into aquifers due to application of fertilizer to surface soil. Based on the review of field data from the affected region, it appears that the second mechanism described above is the most probable. Two reduction processes associated with this mechanism were investigated, viz., reduction of iron oxy-hydroxide to iron (II), which results in the mobilization of arsenic, and reduction of arsenic (V) to arsenic (III), which may enhance mobility of arsenic under certain conditions. These reactions, in the opinion of some researchers, are possible in subsurface environments mainly through microbial intervention. However, through the data presented in this paper, it has been demonstrated that above red-ox reactions involving iron and arsenic are also possible through predominantly abiotic pathways. While these results do not necessarily imply that abiotic red-ox processes are dominant in all subsurface environments containing iron and arsenic, it is entirely possible that abiotic interactions as described here may be responsible for a substantial amount of transformations involving iron and arsenic in anoxic subsurface environments.

Adsorption↗
PubMed2003

Arsenic behavior in newly drilled wells.

In the present paper, inorganic arsenic species and chemical parameters in groundwater were determined to investigate the factors related to the distribution of arsenic species and their dissolution from rock into groundwater. For the study, groundwater and core samples were taken at different depths of two newly drilled wells in Huron and Lapeer Counties, Michigan. Results show that total arsenic concentrations in the core samples varied, ranging from 0.8 to 70.7 mg/kg. Iron concentration in rock was about 1800 times higher than that of arsenic, and there was no correlation between arsenic and iron occurrences in the rock samples. Arsenic concentrations in groundwater ranged from <1 to 171 microg/l. The arsenic concentration in groundwater depended on the amount of arsenic in aquifer rocks, and as well decreased with increasing depth. Over 90% of arsenic existed in the form of As(III), implying that the groundwater systems were in the reduced condition. The results such as high ferrous ion, low redox potential and low dissolved oxygen supported the observed arsenic species distribution. There was no noticeable difference in the total arsenic concentration and arsenic species ratio between unfiltered and filtered (0.45 microm) waters, indicating that the particulate form of arsenic was negligible in the groundwater samples. There were correlations between water sampling depth and chemical parameters, and between arsenic concentration and chemical parameters, however, the trends were not always consistent in both wells.

Arsenic↗
PubMed2003

Biotransformation and accumulation of arsenic in soil amended with seaweed.

For many coastal regions of the world, it has been common practice to apply seaweed to the land as a soil improver and fertilizer. Seaweed is rich in arsenosugars and has a tissue concentration of arsenic up to 100 micro/g g(-1). These arsenic species are relatively nontoxic to humans; however, in the environment they may accumulate in the soil and decompose to more toxic arsenic species. The aim of this study was to determine the fate and biotransformation of these arsenosugars in soil using HPLC-ICP-MS analysis. Data from coastal soils currently manured with seaweeds were used to investigate if arsenic was accumulating in these soils. Long-term application of seaweed increased arsenic concentrations in these soils up to 10-fold (0.35 mg of As kg(-1) for nonagronomic peat, 4.3 mg of As kg(-1) for seaweed-amended peat). The biotransformation of arsenic was studied in microcosm experiments in which a sandy (machair) soil, traditionally manured with seaweed, was amended with Laminaria digitata and Fucus vesiculosus. In both seaweed species, the arsenic occurs in the form of arsenosugars (85%). The application of 50 g of seaweed to 1 kg of soil leads to an increase of arsenic in the soils, and the dominating species found in the soil pore water were dimethylarsinic acid (DMA(V)) and the inorganic species arsenate (As(V)) and arsenite (As(III)) after the initial appearance of arsenosugars. A proposed decomposition pathway of arsenosugars is discussed in which the arsenosugars are transformed to DMA(V) and further to inorganic arsenic without appreciable amounts of methylarsonic acid (MA(V)). Commercially available seaweed-based fertilizers contain arsenic concentration between 10 and 50 mg kg(-1). The arsenic species in these fertilizers depends on the manufacturing procedure. Some contain mainly arsenosugars while others contain mainly DMA(V) and inorganic arsenic. With the application rates suggested by the manufacturers, the application of these fertilizers is 2 orders of magnitude lower than the maximum permissible sewage sludge load for arsenic (varies from 0.025 kg ha(-1) yr(-1) in Styria, Austria, to 0.7 kg ha(-1) yr(-1) in the U.K.), while a direct seaweed application would exceed the maximum arsenic load by at least a factor of 2.

Arsenates↗
PubMed1998

Bioavailability and speciation of arsenic in carrots grown in contaminated soil.

Carrots were grown in seven experimental plots (A-G) containing mixtures of arsenic-contaminated and uncontaminated soil at concentrations ranging from 6.5 to 917 microgram g(-1) (dry mass). The carrots harvested from plots A-D (6.5-338 microgram g(-1) arsenic in the soil mixtures) showed a gradually increasing depression of growth with increasing level of contamination. At the experimental plots E-G with soil arsenic concentrations above 400 microgram g(-1) no carrots developed. Whether this effect was caused by arsenic or the concomitant copper content which ranged from 11 to 810 microgram g(-1) in the soil mixtures is unknown. The arsenic species extracted from the soils and carrots were separated and detected using anion-exchange HPLC coupled with ICP-MS. In the less contaminated soils from plots A and B arsenite (AsIII) was more abundant than arsenate (Asv) in the soil using 1 mmole 1-1 calcium nitrate as extractant. In the soils from plots C and D however, Asv dominated over AsIII whereas in the corresponding carrots Asv and AsIII were found at similar concentrations. Methylated arsenic species were sought after but not detected in any of the samples. The soil-to-carrot uptake rate (bioavailability) of arsenic was 0.47 +/- 0.06% (average +/- one standard deviation) of the arsenic content in the soils from plots A-D. In contrast to arsenic, the increasing copper content in the soils from plot A through D was not available to the carrots as the concentration of this element did not increase with increasing soil copper content. The ingestion of the potentially toxic inorganic arsenic via consumption of carrots grown in soil contaminated at 30 microgram g(-1) in arsenic (plot B) was conservatively estimated at 37 microgram week (-1). This was equivalent to only 4% of the provisional tolerable weekly intake (PTWI) for inorganic arsenic as suggested by the WHO and was therefore toxicologically safe. Consumption of carrots grown in more intensely arsenic-contaminated soils, however, would lead to a higher intake of inorganic arsenic and is therefore not recommended.

Arsenates↗
PubMed2002

Arsenic-speciation in arsenate-resistant and non-resistant populations of the earthworm, Lumbricus rubellus.

Arsenic speciation was determined in Lumbricus rubellus Hoffmeister from arsenic-contaminated mine spoil sites and an uncontaminated site using HPLC-MS, HPLC-ICP-MS and XAS. It was previously demonstrated that L. rubellus from mine soils were more arsenate resistant than from the uncontaminated site and we wished to investigate if arsenic speciation had a role in this resistance. Earthworms from contaminated sites had considerably higher arsenic body burdens (maximum 1,358 mg As kg-1) compared to the uncontaminated site (maximum 13 mg As kg-1). The only organo-arsenic species found in methanol/water extracts for all earthworm populations was arsenobetaine, quantified using both HPLC-MS and HPLC-ICP-MS. Arsenobetaine concentrations were high in L. rubellus from the uncontaminated site when concentrations were expressed as a percentage of the total arsenic burden (23% mean), but earthworms from the contaminated sites with relatively low arsenic burdens also had these high levels of arsenobetaine (17% mean). As arsenic body burden increased, the percentage of arsenobetaine present decreased in a dose dependent manner, although its absolute concentration rose with increasing arsenic burden. The origin of this arsenobetaine is discussed. XAS analysis of arsenic mine L. rubellus showed that arsenic was primarily present as As(III) co-ordinated with sulfur (30% approx.), with some As(v) with oxygen (5%). Spectra for As(III) complexed with glutathione gave a very good fit to the spectra obtained for the earthworms, suggesting a role for sulfur co-ordination in arsenic metabolism at higher earthworm arsenic burdens. It is also possible that the disintegration of As(III)-S complexes may have taken place due to (a) processing of the sample, (b) storage of the extract or (c) HPLC anion exchange. HPLC-ICP-MS analysis of methanol extracts showed the presence of arsenite and arsenate, suggesting that these sulfur complexes disintegrate on extraction. The role of arsenic speciation in the resistance of L. rubellus to arsenate is considered.

Adaptation, Physiological↗
PubMedDate not supplied

Molecular aspects of arsenic stress.

Arsenic produces a variety of stress responses in mammalian cells, including metabolic abnormalities accompanied by growth inhibition and eventually apoptosis. Morphological alterations in cells exposed to arsenic often suggest underlying disruption of cytoskeletal structural elements responsible for cellular integrity, shape, and locomotion. However, specifics of the ultrastructural changes produced by arsenic remain poorly understood. Various tissues and organs differ in their sensitivity to arsenic, with the liver and skin being the most studied. Characteristic skin pathology related to arsenic exposure ranges from hyperkeratotic lesions to squamous-cell carcinomas. However, molecular events in the arsenic-exposed skin still remain to be elucidated. Although mutagenicity of arsenic has not been unequivocally established, recent evidence supports the view that oncogenic mutations do occur, and that only selected enzymes related to DNA replication and repair are affected by arsenic. Sensitivity of the mitotic spindle to arsenic, particularly its organic compounds, underlies the well-documented chromosomal aberrations in arsenic-exposed populations. Arsenite-induced stress at the molecular level shares many features with the heat shock response. This includes the differential sensitivity of the stress signal pathway elements to the magnitude of the stress, stressor-specific activation of the response elements, and the protective role of the heat shock response. Oxidative stress, the central component of heat shock response, is typical of arsenic-related effects that are, in fact, regarded as the chemical paradigm of heat stress. Similar to heat stress, arsenite induces heat shock proteins (HSPs) of various sizes. The signal cascade triggered by arsenite-like heat stress induces the activity of the mitogen-activated protein (MAP) kinases, extracellular regulated kinase (ERK), c-jun terminal kinase (JNK), and p38. Through the JNK and p38 pathways, arsenite activates the immediate early genes c-fos, c-jun, and egr-1, usually activated by various growth factors, cytokines, differentiation signals, and DNA-damaging agents. Like other oxygen radical-producing stressors, arsenic induces nitric oxide production at the level of transcriptional activation along with induction of poly(ADP)-ribosylation, NAD depletion, DNA strand breaks, and formation of micronuclei. This review presents an overview of current research on molecular aspects of arsenic stress with an emphasis on the tissue-specific events in humans. It deals with current progress on the understanding of the signal transduction pathways and mechanisms underlying the sensitivity of various species, organs, and tissues to arsenic.

Animals↗
PubMed2001

Total arsenic accumulation in edible pods and seeds of Phaseolus vulgaris.

The main objective of this study was to evaluate whether arsenic accumulated in the edible pods and seeds of Phaseolus vulgaris, cv. Helda, above the Spanish maximum recommended concentration for food crops, 1 mg kg(-1) on a fresh weight basis. Only organic arsenicals were used because they are: a) the only arsenic species allowed for agricultural applications and b) more mobile than inorganic species. Selection of French beans, a sensitive plant to arsenic, was based on the fact that arsenic upward translocation is higher in sensitive than in tolerant plants. A 2 x 3 factorial experiment was conducted with two organic arsenic species: methylarsonic acid (MAA) or dimethylarsinic acid (DMAA) and three arsenic concentrations: 0.2, 0.5, or 1.0 mg L(-1). Arsenic phytotoxicity was primarily determined by soluble arsenic concentration. Experimental results showed that the low bean plant tolerance to arsenic is possibly due to the high arsenic upward transport to shoots, which could result in profound negative metabolic consequences. Even under extremely adverse conditions, arsenic residues in edible beans were below the maximum statutory limit set by the Spanish legislation. It can be concluded that the major danger of organic arsenical herbicides is that of decreased productivity rather than high arsenic uptake by consumers.

Animals↗
PubMed2002

Arsenic-related chromosomal alterations in bladder cancer.

BACKGROUND: Previous studies have demonstrated that ingestion of arsenic in drinking water is a strong risk factor for several forms of cancer, including bladder cancer. It is not known whether arsenic-related cancers are genetically similar to cancers in unexposed individuals or what mechanisms of carcinogenesis may underlie their formation. This study was designed to compare chromosomal alterations in bladder cancers of arsenic-exposed individuals to provide insight into the mechanism of how arsenic may induce or promote cancer. METHODS: A case-case study was conducted in Argentina and Chile examining chromosomal alterations in bladder tumor DNA in 123 patients who had been exposed to arsenic in their drinking water. Patients were placed into one of four arsenic exposure categories according to their average 5-year peak arsenic exposure. Patients were also classified as ever smokers or never smokers. Comparative genomic hybridization was used to identify chromosomal alterations throughout the genome. All statistical tests were two-sided. RESULTS: The total number of chromosomal alterations was higher in individuals exposed to higher arsenic levels (5.7 +/- 5.1, 5.6 +/- 5.1, 7.3 +/- 7.4, and 9.1 +/- 6.5 [mean +/- standard deviation] chromosomal alterations per tumor with increasing arsenic exposure; P(trend) =.02, adjusted for stage and grade). The trend was stronger in high-grade (G2-G3) tumors (6.3 +/- 5.5, 8.3 +/- 4.7, 10.3 +/- 7.8, and 10.5 +/- 6.4 alterations per tumor; P(trend) =.01) than it was in low-grade (G1) tumors (3.5 +/- 3.1, 1.1 +/- 1.1, 2.5 +/- 2.5, and 3.6 +/- 3.2 alterations per tumor; P(trend) =.79). The mean number of chromosomal alterations also increased with tumor stage and grade (P(trend)<.001) independently of arsenic exposure but was not associated with smoking history. Deletion of part or all of chromosome 17p (P(trend)<.001) showed the strongest association with arsenic exposure. CONCLUSIONS: Bladder tumors in patients with higher levels of arsenic exposure showed higher levels of chromosomal instability. Most of the chromosomal alterations associated with arsenic exposure were also associated with tumor stage and grade, raising the possibility that bladder tumors from arsenic-exposed patients may behave more aggressively than tumors from unexposed patients.

Argentina↗