Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ARSENIC”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 433 records · Page 24Linked to original sources
PubMed2006

Kinetics of arsenic methylation by freshly isolated B6C3F1 mouse hepatocytes.

The toxic and carcinogenic effects of arsenic may be mediated by both inorganic and methylated arsenic species. The methylation of arsenic(III) is thought to take place via sequential oxidative methylation and reduction steps to form monomethylarsenic (MMA) and dimethylarsenic (DMA) species, but recent evidence indicates that glutathione complexes of arsenic(III) can be methylated without oxidation. The kinetics of arsenic methylation were determined in freshly isolated hepatocytes from male B6C3F1 mice. Hepatocytes (>90% viability) were isolated by collagenase perfusion and suspended in Williams' Medium E with various concentrations of arsenic(III) (sodium m-arsenite). Aliquots of the lysed cell suspension were analyzed for arsenic species by hydride generation-atomic absorption spectrometry. The formation of MMA(III) from sodium arsenite (1 microM) was linear with respect to time for >90 min. DMA(III) formation did not become significant until 60 min. MMA(V) and DMA(V) were not consistently observed in the incubations. These results suggest that the glutathione complex mechanism of methylation plays an important role in arsenic biotransformation in mouse hepatocytes. Metabolism of arsenic(V) was not observed in mouse hepatocytes, consistent with inhibition of arsenic(V) active cellular uptake by phosphate in the medium. The formation of MMA(III) increased with increasing arsenic(III) concentrations up to approximately 2 microM and declined thereafter. The concentration dependence is consistent with a saturable methylation reaction accompanied by uncompetitive substrate inhibition of the reaction by arsenic(III). Kinetic analysis of the data suggested an apparent K(M) of approximately 3.6 microM arsenic(III), an apparent V(max) of approximately 38.9 microg MMA(III) formed/L/h/million cells, and an apparent K(I) of approximately 1.3 microM arsenic(III). The results of this study can be used in the physiologically based pharmacokinetic model for arsenic disposition in mice to predict the concentration of MMA(III) in liver and other tissues.

Animals↗
PubMed2006

Major contributors to inorganic arsenic intake in southeastern Michigan.

Accurate estimates of inorganic arsenic intake are critical for evaluating potential health risks. Intake estimates have not been critically examined in regions of the United States where people are at risk from arsenic concentrations in drinking water exceeding the maximum contaminant limit of 10 microg/l. In southeastern Michigan, approximately 8% of the population is exposed to arsenic in drinking water >10 microg/l. Four hundred and forty participants of a control group in this region, frequency matched to cases in a population-based bladder cancer case-control study, answered a questionnaire about water and food consumption and smoking history. Water samples were collected from participants' current residences and analyzed for arsenic. Water arsenic data were combined with questionnaire data and published data of inorganic arsenic concentrations in select foods and cigarettes to examine the influence of arsenic in water at home, at work, and at other places, as well as inorganic arsenic intake from food and cigarettes. Monte Carlo simulations and analyses of individual-level intake estimates were conducted to quantify the variability attributed to different parameters in this primarily elderly white male population of southeastern Michigan. The 95th percentile of total inorganic arsenic intake ranges from 11 to 24 microg/day, depending on the intake metric selected. Results indicate that arsenic in home drinking water is the largest source of inorganic arsenic, accounting for 55.1% of the variance in the intake estimates. Food intake explains 37.3% of the variance, with rice being the largest contributor. In the upper decile of intake, consumption of plain water and beverages made with water at home, and ingestion of arsenic in water at work, also contribute to intake estimates. Water used for cooking and arsenic from smoking, however, only minimally alter the intake estimates. This is due to a relatively small volume of water absorbed into cooked foods and low concentrations of arsenic in cigarettes. Results from this study will assist investigators in better characterizing exposure to inorganic arsenic.

Adult↗
PubMed2005

Occurrence of arsenic contamination in Canada: sources, behavior and distribution.

Recently there has been increasing anxieties concerning arsenic related problems. Occurrence of arsenic contamination has been reported worldwide. In Canada, the main natural arsenic sources are weathering and erosion of arsenic-containing rocks and soil, while tailings from historic and recent gold mine operations and wood preservative facilities are the principal anthropogenic sources. Across Canada, the 24-h average concentration of arsenic in the atmosphere is generally less than 0.3 microg/m3. Arsenic concentrations in natural uncontaminated soil and sediments range from 4 to 150 mg/kg. In uncontaminated surface and ground waters, the arsenic concentration ranges from 0.001 to 0.005 mg/L. As a result of anthropogenic inputs, elevated arsenic levels, above ten to thousand times the Interim Maximum Acceptable Concentration (IMAC), have been reported in air, soil and sediment, surface water and groundwater, and biota in several regions. Most arsenic is of toxic inorganic forms. It is critical to recognize that such contamination imposes serious harmful effects on various aquatic and terrestrial organisms and human health ultimately. Serious incidences of acute and chronic arsenic poisonings have been revealed. Through examination of the available literature, screening and selecting existing data, this paper provides an analysis of the currently available information on recognized problem areas, and an overview of current knowledge of the principal hydrogeochemical processes of arsenic transportation and transformation. However, a more detailed understanding of local sources of arsenic and mechanisms of arsenic release is required. More extensive studies will be required for building practical guidance on avoiding and reducing arsenic contamination. Bioremediation and hyperaccumulation are emerging innovative technologies for the remediation of arsenic contaminated sites. Natural attenuation may be utilized as a potential in situ remedial option. Further investigations are needed to evaluate its applicability.

Arsenic↗
PubMed1998

Cutaneous manifestations of chronic arsenicism: review of seventeen cases.

BACKGROUND: Cutaneous complications arising from exposure to Chinese proprietary medicines known to contain inorganic arsenic have been rarely reported. OBJECTIVE: Our purpose was to study the nature, incidence, and sequelae of patients with chronic arsenicism and to review the literature on arsenic-induced skin diseases. METHODS: Case records of patients with cutaneous lesions related to chronic arsenicism seen from January 1990 to December 1996 were reviewed. Patients were interviewed and a complete skin and systemic examination was performed. Data on demography, history of arsenic ingestion, and type and distribution of skin lesions and visceral malignancy were collated. RESULTS: Seventeen Chinese patients (11 men, six women) were identified; their mean age was 64.5 years. Fourteen patients (82%) had exposure to Chinese proprietary medicines known to contain inorganic arsenic, and three had environmental arsenic exposure from well water. The mean age of these 14 patients was 17.6 years; mean duration of arsenic intake was 6.4 years. Seventeen patients had Bowen's disease; of these, 70% had 2 to 10 lesions. Of the 17 patients with arsenical keratoses on the palms, 76% had 2 to 10 lesions. Of the 14 patients (82%) with plantar arsenical keratoses, 64% had 11 to more than 50 lesions. Eleven patients (65%) had macular hypopigmentation. Seven patients (41%) had 11 squamous cell carcinomas (SCCs); three of the seven had more than one lesion. Fifty-five percent of SCCs arose from preexisting keratotic lesions (n = 4) or Bowen's disease (n = 2), and 45% arose de novo. One patient each (6%) had multiple basal cell carcinomas, laryngeal carcinoma, and metastatic SCC. The latency periods for the development of arsenical keratoses, Bowen's disease, and SCC were 28, 39, and 41 years, respectively. Patients with SCC were significantly older at the start of arsenic exposure and had significantly more palmar arsenical keratoses than those without SCC. CONCLUSION: Exposure to Chinese proprietary medicines containing inorganic arsenic poses a risk for the development of cutaneous and systemic malignancies. Long-term follow-up is necessary for tumor detection because of long latency periods. Surveillance programs are important to restrict the sale of Chinese proprietary medicines that may contain inorganic arsenic.

Aged↗
PubMed2003

Arsenic species and leachability in the fronds of the hyperaccumulator Chinese brake (Pteris vittata L.).

Arsenic speciation is important not only for understanding the mechanisms of arsenic accumulation and detoxification by hyperaccumulators, but also for designing disposal options of arsenic-rich biomass. The primary objective of this research was to understand the speciation and leachability of arsenic in the fronds of Chinese brake (Pteris vittata L.), an arsenic hyperaccumulator, with an emphasis on the implications for arsenic-rich biomass disposal. Chinese brake was grown for 18 weeks in a soil spiked with 50 mg As kg(-1) as arsenate (AsO4(3-)), arsenite (AsO3(3-)), dimethylarsinic acid (DMA), or methylarsonic acid (MMA). Plant samples were extracted with methanol/water (1:1) and arsenic speciation was performed using high performance liquid chromatography coupled with atomic fluorescence spectrometry. The impacts of air-drying on arsenic species and leachability in the fronds were examined in the laboratory. After 18 weeks, water-soluble arsenic in soil was mainly present as arsenate with little detectable organic species or arsenite regardless of arsenic species added to the soil. However, arsenic in the fronds was primarily present as inorganic arsenite with an average of 94%. Arsenite re-oxidation occurred in the old fronds and the excised dried tissues. Arsenic species in the fronds were slightly influenced by arsenic forms added to the soil. Air-drying of the fronds resulted in leaching of substantial amounts of arsenic. These findings can be of significance when looking at disposal options of arsenic-rich biomass from the point of view of secondary contamination.

Arsenates↗
PubMed1999

A market basket survey of inorganic arsenic in food.

Dietary arsenic intake estimates based on surveys of total arsenic concentrations appear to be dominated by intake of the relatively non-toxic, organic arsenic forms found in seafood. Concentrations of inorganic arsenic in food have not been not well characterized. Accurate dietary intake estimates for inorganic arsenic are needed to support studies of arsenic's status as an essential nutrient, and to establish background levels of exposure to inorganic arsenic. In the market basket survey reported here, 40 commodities anticipated to provide at least 90% of dietary inorganic arsenic intake were identified. Four samples of each commodity were collected. Total arsenic was analysed using an NaOH digestion and inductively coupled plasma-mass spectrometry. Separate aliquots were analysed for arsenic species using an HCl digestion and hydride atomic absorption spectroscopy. Consistent with earlier studies, total arsenic concentrations (all concentrations reported as elemental arsenic per tissue wet weight) were highest in the seafoods sampled (ranging from 160 ng/g in freshwater fish to 2360 ng/g in saltwater fish). In contrast, average inorganic arsenic in seafood ranged from less than 1 ng/g to 2 ng/g. The highest inorganic arsenic values were found in raw rice (74 ng/g), followed by flour (11 ng/g), grape juice (9 ng/g) and cooked spinach (6 ng/g). Thus, grains and produce are expected to be significant contributors to dietary inorganic arsenic intake.

Arsenic↗
PubMed1997

Sequence of exposure to cadmium and arsenic determines the extent of toxic effects in male Fischer rats.

Arsenic and cadmium are both priority hazardous substances and human carcinogens. Although there is the potential for simultaneous exposure to both metals, the interactions of cadmium and arsenic are not well defined. We examined the toxicity of these metals when given alone or in alternating sequence to adult male Fischer rats. In the first study, a non-toxic dose of arsenic (22.5 micromol NaAsO2/kg, s.c.) was given 24 h before cadmium (10, 20, or 30 micromol CdCl2/kg, s.c.) and toxicity was assessed 24 h later. Arsenic pretreatment markedly reduced mortality in rats given the high dose of cadmium (9 survivors/10 treated) compared to rats given cadmium alone (2/10). Arsenic pretreatment also reduced cadmium-induced hepatotoxicity, as indicated by serum glutamic oxalacetic transaminase (SGOT) activity, and markedly reduced cadmium-induced testicular hemorrhagic necrosis. Arsenic pretreatment produced an 8-fold increase in hepatic levels of metallothionein (MT), a metal-binding protein often associated with cadmium tolerance. In the second study, a non-toxic dose of cadmium (3 micromol CdCl2/kg, s.c.) was given 24 h before arsenic (68, 79, 84, or 90 micro/mol NaAsO2/kg. s.c.) and toxicity was assessed 24 h later. Cadmium pretreatment did not alter the lethality of the high dose of arsenic and had no effect on arsenic-induced hepatotoxicity. Although cadmium pretreatment had no effect on arsenic toxicity, it produced large increases in hepatic MT (26-fold) before the arsenic challenge and greatly enhanced MT induction after the challenge. Thus, even though both arsenic and cadmium induce MT synthesis, only arsenic pretreatment protects against cadmium intoxication, and cadmium pretreatment does not effect arsenic toxicity. Thus, toxic interactions of arsenic and cadmium appear to depend on the sequence of exposure.

Animals↗
PubMedDate not supplied

Biochemical and histopathological changes in arsenic-intoxicated rats coexposed to ethanol.

The effects of arsenic and ethanol interaction on blood, liver and serum biochemical indices, and arsenic concentration in soft tissues of rats were investigated to determine the influence of these substances in inducing susceptibility to arsenic poisoning. Arsenic, intraperitoneally (100 ppm, once, daily), ethanol in drinking water (10%), or the combination were administered for a period of 6 weeks. Both the chemicals had some additive effects in marginally elevating blood zinc protoporphyrin. Glutathione (GSH) concentrations of blood and liver were reduced by both arsenic and ethanol; however, there was a more pronounced depletion of hepatic GSH concentration in animals coexposed to arsenic and ethanol. Combined arsenic plus ethanol exposure led to significantly more elevated activities of serum transaminases than in animals administered arsenic or ethanol alone. Histopathological alterations in kidneys and liver occurred following arsenic exposure. Arsenic plus ethanol produced more pronounced liver lesions, whereas kidney changes were the same as with arsenic alone. The concentrations of arsenic in kidney and liver were higher in rats exposed to arsenic plus ethanol. The results suggest that animals exposed to arsenic plus ethanol are more vulnerable to arsenic toxicity.

Alanine Transaminase↗
PubMed2004

Reduction of arsenic content in a complex galena concentrate by Acidithiobacillus ferrooxidans.

BACKGROUND: Bioleaching is a process that has been used in the past in mineral pretreatment of refractory sulfides, mainly in the gold, copper and uranium benefit. This technology has been proved to be cheaper, more efficient and environmentally friendly than roasting and high pressure moisture heating processes. So far the most studied microorganism in bioleaching is Acidithiobacillus ferrooxidans. There are a few studies about the benefit of metals of low value through bioleaching. From all of these, there are almost no studies dealing with complex minerals containing arsenopyrite (FeAsS). Reduction and/or elimination of arsenic in these ores increase their value and allows the exploitation of a vast variety of minerals that today are being underexploited. RESULTS: Arsenopyrite was totally oxidized. The sum of arsenic remaining in solution and removed by sampling represents from 22 to 33% in weight (yield) of the original content in the mineral. The rest of the biooxidized arsenic form amorphous compounds that precipitate. Galena (PbS) was totally oxidized too, anglesite (PbSO4) formed is virtually insoluble and remains in the solids. The influence of seven factors in a batch process was studied. The maximum rate of arsenic dissolution in the concentrate was found using the following levels of factors: small surface area of particle exposure, low pulp density, injecting air and adding 9 K medium to the system. It was also found that ferric chloride and carbon dioxide decreased the arsenic dissolution rate. Bioleaching kinetic data of arsenic solubilization were used to estimate the dilution rate for a continuous culture. Calculated dilution rates were relatively small (0.088-0.103 day(-1)). CONCLUSION: Proper conditions of solubilization of arsenic during bioleaching are key features to improve the percentage (22 to 33% in weight) of arsenic removal. Further studies are needed to determine other factors that influence specifically the solubilization of arsenic in the bioleaching system such as: pH, dissolved oxygen concentration, redox potentials, nature of concentrate and temperature among others. At. ferrooxidans was able to completely oxidize the minerals present during the arsenic bioleaching. Other elements present originally in the concentrate such as Zn, Sb, and Cu were also solubilized. The process of bioleaching is expected to be influenced by mechanisms that still need to be established due to the diversity of the minerals involved and by the presence of traces of metals in the concentrate. The increase in pulp density generates a decrease in the dissolved arsenic concentration. This decrease is greater in runs where air was not injected to the system. The maximum rate of arsenic dissolution in the concentrate was found using; small surface area of particle exposure, low pulp density, injecting air and adding 9 K medium to the system. The effect of addition of ferric chloride during the arsenic bioleaching resulted in a decrease of the solubilized arsenic in the system. The presence of CO2 is associated to the decrease in arsenic dissolution.

Acidithiobacillus↗
PubMed1995

[The study of biological monitoring of inorganic arsenic exposure].

This review will describe method for biological monitoring of inorganic arsenic exposure, that delineates the chemical species of arsenic measured in urine. The studies established a method for exposure-level-dependent biological monitoring of inorganic arsenic exposure. Low-level exposure could be monitored only by determining the urinary inorganic arsenic concentration. High-level exposures clearly produced increased urinary inorganic arsenic, methylated arsenic (MA), dimethylated arsenic (DMA) and the sum of urinary inorganic arsenic and its metabolites (inorganic arsenic+MA+DMA) could be determined. Urinary arsenobetaine proved to be specifically seafood-derived arsenic, which could be distinguished from occupational arsenic exposure. There is increased use of gallium arsenide and indium arsenide in the semiconductor industry today. The determination of arsenic in ambient air is difficult to carry out in semiconductor factories. Monitoring arsenic exposure by determining the arsenic in the hair appeared to be of value only when used for environmental monitoring of arsenic rather than for biological monitoring.

Arsenic↗
PubMedDate not supplied

Chemical extraction methods to assess bioavailable arsenic in soil and solid media.

Soil ingestion by children is an important pathway in assessing public health risks associated with exposure to arsenic-contaminated soils. Soil chemical methods are available to extract various pools of soil arsenic, but their ability to measure bioavailable arsenic from soil ingestion is unknown. Arsenic extracted by five commonly used soil extractants was compared with bioavailable arsenic measured in vivo by immature swine (Sus scrofa) dosing trials. Fifteen contaminated soils that contained 233 to 17 500 mg kg(-1) arsenic were studied. Soil extractants were selected to dissolve surficially adsorbed and/or readily soluble arsenic (water, 1 M sodium acetate, 0.1 M Na2HPO4/0.1 M NaH2PO4) and arsenic in Fe and Mn oxide minerals (hydroxylamine hydrochloride, ammonium oxalate). The mean percent of total arsenic extracted was: ammonium oxalate (53.6%) > or = hydroxylamine hydrochloride (51.7%) > phosphate (10.5%), acetate (7.16%) > water (0.15%). The strongest relationship between arsenic determined by soil chemical extraction and in vivo bioavailable arsenic was found for hydroxylamine hydrochloride extractant (r = 0.88, significant at the 0.01 probability level). Comparison of the amount of arsenic extracted by soil methods with bioavailable arsenic showed the following trend: ammonium oxalate, hydroxylamine hydrochloride > in vivo > phosphate, acetate > water. The amount of arsenic dissolved in the stomach (potentially bioavailable) is between surficially adsorbed (extracted by phosphate or acetate) and surficially adsorbed + nonsurficial forms in Fe and Mn oxides (extracted by hydroxylamine hydrochloride or ammonium oxalate). Soil extraction methods that dissolve some of the amorphous Fe, such as hydroxylamine hydrochloride, can be designed to provide closer estimates of bioavailable arsenic.

Animals↗
PubMed2004

Evaluation of DNA damage in patients with arsenic poisoning: urinary 8-hydroxydeoxyguanine.

The relationship between arsenic exposure and DNA damage in patients with acute or chronic arsenic poisoning was analyzed. Urinary 8-hydroxydeoxyguanine (8-OHdG) concentrations were measured as an indication of oxidative DNA damage. A remarkable increase in 8-OHdG in the urine was observed in 60% of 52 patients with acute arsenic poisoning from the accidental oral intake of the arsenic trioxide. This was two- to threefold higher than levels in normal healthy subjects (n = 248). There was a clear relationship between arsenic concentrations in urine after acute poisoning and elevated levels of 8-OHdG. Levels of urinary 8-OHdG returned to normal within 180 days after the acute arsenic poisoning event. In patients chronically poisoned by the consumption of well water with elevated levels of arsenate [As(V)], elevated 8-OHdG concentrations in urine were also observed. A significant correlation between the 8-OHdG levels and arsenic levels in the urine was observed in 82 patients with chronic poisoning. Thus, evidence of oxidative DNA damage occurred in acute arsenic poisoning by arsenite [As(III)] and in chronic arsenic poisoning by As(V). In chronic poisoning patients provided low-arsenic drinking water, evidence of DNA damage subsided between 9 months and 1 year after the high levels of arsenic intake were reduced. The initial level of arsenic exposure appeared to dictate the length of this recovery period. These data indicate that some aspects of chronic and acute arsenic poisoning may be reversible with the cessation of exposure. This knowledge may contribute to our understanding of the risk elevation from arsenic carcinogenesis and perhaps be used in a prospective fashion to assess individual risk.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2006

Concomitant administration of Moringa oleifera seed powder in the remediation of arsenic-induced oxidative stress in mouse.

Contamination of ground water by arsenic has become a cause of global public health concern. In West Bengal, India, almost 6 million people are endemically exposed to inorganic arsenic by drinking heavily contaminated groundwater through hand-pumped tube wells. No safe, effective and specific preventive or therapeutic measures for treating arsenic poisoning are available. We recently reported that some of the herbal extracts possess properties effective in reducing arsenic concentration and in restoring some of the toxic effects of arsenic in animal models. Moringa oleifera Lamarack (English: Horseradish-tree, Drumstick-tree, Hindi: Saijan, Sanskrit: Shigru) belongs to the Moringaceae family, is generally known in the developing world as a vegetable, a medicinal plant and a source of vegetable oil. The objective of the present study was to determine whether Moringa oleifera (M. oleifera) seed powder could restore arsenic induced oxidative stress and reduce body arsenic burden. Exposure to arsenic (2.5 mg/kg, intraperitoneally for 6weeks) led to a significant increase in the levels of tissue reactive oxygen species (ROS), metallothionein (MT) and thiobarbituric acid reactive substance (TBARS) which were accompanied by a decrease in the activities in the antioxidant enzymes such as superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx) in mice. Arsenic exposed mice also exhibited liver injury as reflected by reduced acid phosphatase (ACP), alkaline phosphatase (ALP) and aspartate aminotransferase (AST) activities and altered heme synthesis pathway as shown by inhibited blood delta-aminolevulinic acid dehydratase (delta-ALAD) activity. Co-administration of M. oleifera seed powder (250 and 500 mg/kg, orally) with arsenic significantly increased the activities of SOD, catalase, GPx with elevation in reduced GSH level in tissues (liver, kidney and brain). These changes were accompanied by approximately 57%, 64% and 17% decrease in blood ROS, liver metallothionein (MT) and lipid peroxidation respectively in animal co-administered with M. oleifera and arsenic. Another interesting observation has been the reduced uptake of arsenic in soft tissues (55% in blood, 65% in liver, 54% in kidneys and 34% in brain) following administration of M. oleifera seed powder (particularly at the dose of 500 mg/kg). It can thus be concluded from the present study that concomitant administration of M. oleifera seed powder with arsenic could significantly protect animals from oxidative stress and in reducing tissue arsenic concentration. Administration of M. oleifera seed powder thus could also be beneficial during chelation therapy with a thiol chelator.

Animals↗
PubMed2006

Magnitude of arsenic pollution in the Mekong and Red River Deltas--Cambodia and Vietnam.

Large alluvial deltas of the Mekong River in southern Vietnam and Cambodia and the Red River in northern Vietnam have groundwaters that are exploited for drinking water by private tube-wells, which are of increasing demand since the mid-1990s. This paper presents an overview of groundwater arsenic pollution in the Mekong delta: arsenic concentrations ranged from 1-1610 microg/L in Cambodia (average 217 microg/L) and 1-845 microg/L in southern Vietnam (average 39 microg/L), respectively. It also evaluates the situation in Red River delta where groundwater arsenic concentrations vary from 1-3050 microg/L (average 159 microg/L). In addition to rural areas, the drinking water supply of the city of Hanoi has elevated arsenic concentrations. The sediments of 12-40 m deep cores from the Red River delta contain arsenic levels of 2-33 microg/g (average 7 microg/g, dry weight) and show a remarkable correlation with sediment-bound iron. In all three areas, the groundwater arsenic pollution seem to be of natural origin and caused by reductive dissolution of arsenic-bearing iron phases buried in aquifers. The population at risk of chronic arsenic poisoning is estimated to be 10 million in the Red River delta and 0.5-1 million in the Mekong delta. A subset of hair samples collected in Vietnam and Cambodia from residents drinking groundwater with arsenic levels >50 microg/L have a significantly higher arsenic content than control groups (<50 microg/L). Few cases of arsenic related health problems are recognized in the study areas compared to Bangladesh and West Bengal. This difference probably relates to arsenic contaminated tube-well water only being used substantially over the past 7 to 10 years in Vietnam and Cambodia. Because symptoms of chronic arsenic poisoning usually take more than 10 years to develop, the number of future arsenic related ailments in Cambodia and Vietnam is likely to increase. Early mitigation measures should be a high priority.

Arsenic↗
PubMed2003

The metabolism of inorganic arsenic oxides, gallium arsenide, and arsine: a toxicochemical review.

The aim of this review is to compare the metabolism, chemistry, and biological effects to determine if either of the industrial arsenicals (arsine and gallium arsenide) act like the environmental arsenic oxides (arsenite and arsenate). The metabolism of the arsenic oxides has been extensively investigated in the past 4 years and the differences between the arsenic metabolites in the oxidation states +III versus +V and with one or two methyl groups added have shown increased importance. The arsenic oxide metabolism has been compared with arsine (oxidation state -III) and arsenide (oxidation state between 0 to -III). The different metabolites appear to have different strengths of reaction for binding arsenic (III) to thiol groups, their oxidation-reduction reactions and their forming an arsenic-carbon bond. It is unclear if the differences in parameters such as the presence or absence of methyl metabolites, the rates of AsV reduction compared to the rates of AsIII oxidation, or the competition of phosphate and arsenate for cellular uptake are large enough to change biological effects. The arsine rate of decomposition, products of metabolism, target organ of toxic action, and protein binding appeared to support an oxidized arsenic metabolite. This arsine metabolite was very different from anything made by the arsenic oxides. The gallium arsenide had a lower solubility than any other arsenic compound and it had a disproportionate intensity of lung damage to suggest that the GaAs had a site of contact interaction and that oxidation reactions were important in its toxicity. The urinary metabolites after GaAs exposure were the same as excreted by arsenic oxides but the chemical compounds responsible for the toxic effects of GaAs are different from the arsenic oxides. The review concludes that there is insufficient evidence to equate the different arsenic compounds. There are several differences in the toxicity of the arsenic compounds that will require substantial research.

Animals↗
PubMed1998

Inorganic and methylated arsenic compounds induce cell death in murine macrophages via different mechanisms.

We demonstrate in this study the cytotoxic effects of inorganic arsenicals, arsenite and arsenate, and organic arsenic compounds, monomethylarsonic acid (MAA), dimethylarsinic acid (DMAA), and trimethylarsine oxide (TMAO), which are metabolites of inorganic arsenicals in human bodies, using murine macrophages in vitro. Inorganic arsenicals, both arsenite and arsenate, are strongly toxic to macrophages, and the concentration that decreased the number of surviving cells to 50% of that in untreated controls (IC50) was 5 or 500 microM, respectively. These inorganic arsenicals mainly caused necrotic cell death with partially apoptotic cell death; about 80% of dead cells were necrotic, and 20% were apoptotic. The inorganic arsenicals also induced marked release of an inflammatory cytokine, tumor necrosis factor alpha (TNF alpha), at cytotoxic doses. This strong cytotoxicity of an inorganic arsenical, arsenite, might be mediated via active oxygen and protease activation because it was inhibited by the addition of some antioxidant reagents, such as superoxide dismutase (SOD), catalase, and GSH, or by a peptide inhibitor of interleukin-1 beta-converting enzyme (ICE). It is likely that these immunotoxic effects of inorganic arsenicals may evoke both immunosuppression and inflammation, and they may be central factors causing carcinogenesis and severe inflammatory responses, such as hepatomegaly and splenomegaly, in chronic arsenicosis patients who daily ingested arsenic-contaminated well water. In contrast, the cytotoxic effects of methylated arsenic compounds were lower than those of inorganic arsenicals. The IC50 value of DMAA was about 5 mM, and MAA and TMAO had no toxicity even at concentrations over 10 mM. Additionally, these methylated chemicals suppressed the TNFalpha release from macrophages. DMAA induced mainly apoptotic cell death in macrophages as indicated by cellular morphological changes, condensed nuclei, terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL), and DNA fragmentation. However, the cytotoxicity of DMAA might be induced via a different mechanism from that of inorganic arsenicals because it was not abolished by the additions of SOD, catalase, or ICE inhibitor. Conversely, GSH enhanced the toxicity of DMAA. These data suggest that methylation of inorganic arsenicals in mammals plays an important role in suppression of both severe immunosuppression and inflammatory responses caused by inorganic arsenicals.

Animals↗
PubMed2006

Effect of fasting on the pattern of urinary arsenic excretion.

Millions of people in some of the poorest regions of the world are exposed to high levels of arsenic through drinking contaminated water. It has been reported that development of cancer caused by arsenic exposure in such populations is dependent on dietary and nutritional factors which can modulate arsenic metabolism. Many people in arsenic exposed regions of Bangladesh and India practice fasting for at least one month every year when they refrain from consumption of food and fluid during daylight hours. How such practices may modulate arsenic metabolism has not been previously investigated. This study investigated this issue by determining total arsenic and its species in urine samples from a group of 29 unexposed volunteers at the beginning of the fasting and at the end of approximately 12 h of fasting period. Inductively coupled plasma mass spectrometry (ICP-MS) and high performance liquid chromatography (HPLC) coupled with ICP-MS was used to measure the total arsenic and arsenic speciation in the urine samples, respectively. The mean total levels of arsenic at the beginning of fasting (18.3 microg g(-1) creatinine) and at the end of approximately 12 h of fasting (17.7 microg g(-1) creatinine) did not differ significantly (p > 0.05). However, the percentages of urinary arsenic as the methylated arsenic species methylarsonate (MA) were found to be significantly different (p < 0.05) and this species was observed more frequently at the end of fasting, although its overall concentration was similar. There were no significant differences (p > 0.05) in both the concentrations and percentages of other urinary arsenic species detected, namely arsenobetaine (AB) and dimethylarsinate (DMA). Arsenite (As(III)) and arsenate (As(V)) were also analyzed, but were not detected. We conclude that fasting for a period of 12 h results in a significant increase in the percentage of urinary arsenic as MA, and its frequency of detection in the volunteers at the end of the fasting period is almost nine fold higher. This suggests that metabolism of arsenic is altered by fasting.

Adult↗
PubMed2005

Murshidabad--one of the nine groundwater arsenic-affected districts of West Bengal, India. Part I: magnitude of contamination and population at risk.

INTRODUCTION: To understand the severity of the arsenic crisis in West Bengal, India, a detailed, 3-year study was undertaken in Murshidabad, one of the nine arsenic-affected districts in West Bengal. The district covers an area of 5324 km2 with a population of 5.3 million. METHODS: Hand tubewell water samples and biologic samples were collected from Murshidabad and analyzed for arsenic by FI-HG-AAS method. Inter laboratory analysis and analyses of standards were undertaken for quality assurance. RESULTS: During our survey we analyzed 29,612 hand tubewell water samples for arsenic from both contaminated and non-contaminated areas, and 26% of the tubewells were found to have arsenic above 50 microg/L while 53.8% had arsenic above 10 microg/L. Of the 26 blocks in Murshidabad, 24 were found to have arsenic above 50 microg/L. Based on our generated data we estimated that approximately 0.2 million hand tubewells are installed in all 26 blocks of Murshidabad and 1.8 million in nine arsenic-affected districts of West Bengal. It was estimated on the basis of our data that about 2.5 million and 1.2 million people were drinking arsenic-contaminated water with concentrations above 10 and 50 microg/L levels respectively in this district. The analysis of total 3800 biologic (nail, urine, and hair) samples from arsenic-affected villages revealed that 95% of the nail and 94% of the urine samples contained arsenic above the normal levels and 75% of the hair samples were found to have arsenic above the toxic level. Thus, many villagers in the affected areas of Murshidabad might be subclinically affected. DISCUSSION AND CONCLUSION: Comparing our extrapolated data with international dose response results, we estimated how many people may suffer from arsenical skin lesions and cancer. Finally, if the exposed population is provided safe water, better nutrition, and proper awareness about the arsenic problem, lives can be saved and countless suffering of the affected population can be avoided.

Arsenic Poisoning↗