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PubMed2001

The cellular metabolism and systemic toxicity of arsenic.

Although it has been known for decades that humans and many other species convert inorganic arsenic to mono- and dimethylated metabolites, relatively little attention has been given to the biological effects of these methylated products. It has been widely held that inorganic arsenicals were the species that accounted for the toxic and carcinogenic effects of this metalloid and that methylation was properly regarded as a mechanism for detoxification of arsenic. Elucidation of the metabolic pathway for arsenic has changed our understanding of the significance of methylation. Both methylated and dimethylated arsenicals that contain arsenic in the trivalent oxidation state have been identified as intermediates in the metabolic pathway. These compounds have been detected in human cells cultured in the presence of inorganic arsenic and in urine of individuals who were chronically exposed to inorganic arsenic. Methylated and dimethylated arsenicals that contain arsenic in the trivalent oxidation state are more cytotoxic, more genotoxic, and more potent inhibitors of the activities of some enzymes than are inorganic arsenicals that contain arsenic in the trivalent oxidation state. Hence, it is reasonable to describe the methylation of arsenic as a pathway for its activation, not as a mode of detoxification. This review summarizes the current knowledge of the processes that control the formation and fate of the methylated metabolites of arsenic and of the biological effects of these compounds. Given the considerable interest in the dose-response relationships for arsenic as a toxin and a carcinogen, understanding the metabolism of arsenic may be critical to assessing the risk associated with chronic exposure to this element.

Animals↗
PubMed1997

Issues in setting health-based cleanup levels for arsenic in soil.

Health risk assessments often do not take into account the unique aspects of evaluating exposures to arsenic in soil. For example, risks from ingestion of arsenic in soil are often based on toxicity factors derived from studies of arsenic (soluble arsenate or arsenite) in drinking water. However, the toxicity of arsenic in drinking water cannot be directly extrapolated to toxicity of soil arsenic because of differences in chemical form, bioavailability, and excretion kinetics. Because of the differences between soil arsenic and water arsenic, we conclude that risks from arsenic in soil are lower than what would be calculated using default toxicity values for arsenic in drinking water. Site-specific risk assessments for arsenic in soil can be improved by characterizing the form of arsenic in soil, by conducting animal feeding or in vitro bioavailability studies using site soils, and by conducting studies to evaluate the relationship between urinary arsenic and soil arsenic levels. Such data could be used to more accurately measure the contribution that soil arsenic makes to total intake of arsenic. Available data suggest that arsenic usually makes a small contribution to this total.

Adult↗
PubMed2005

Arsenic transport and transformation associated with MSMA application on a golf course green.

The impact of extensively used arsenic-containing herbicides on groundwater beneath golf courses has become a topic of interest. Although currently used organoarsenicals are less toxic, their application into the environment may produce the more toxic inorganic arsenicals. The objective of this work was to understand the behavior of arsenic species in percolate water from monosodium methanearsonate (MSMA) applied golf course greens, as well as to determine the influences of root-zone media for United State Golf Association (USGA) putting green construction on arsenic retention and species conversion. The field test was established at the Fort Lauderdale Research and Education Center (FLREC), University of Florida. Percolate water was collected after MSMA application for speciation and total arsenic analyses. The results showed that the substrate composition significantly influenced arsenic mobility and arsenic species transformation in the percolate water. In comparison to uncoated sands (S) and uncoated sands and peat (S + P), naturally coated sands and peat (NS + P) showed a higher capacity of preventing arsenic from leaching into percolate water, implying that the coatings of sands with clay reduce arsenic leaching. Arsenic species transformation occurred in soil, resulting in co-occurrence of four arsenic species, arsenite (As(III)), arsenate (As(V)), monomethylarsonic acid (MMA), and dimethylarsinic acid (DMA) in percolate water. The results indicated that substrate composition can significantly affect both arsenic retention in soil and arsenic speciation in percolate water. The clay coatings on the soil particles and the addition of peat in the soil changed the arsenic bioavailability, which in turn controlled the microorganism-mediated arsenic transformation. To better explain and understand arsenic transformation and transport after applying MSMA in golf green, a conceptual model was proposed.

Arsenic↗
PubMed2005

Forced uptake of trivalent and pentavalent methylated and inorganic arsenic and its cyto-/genotoxicity in fibroblasts and hepatoma cells.

Mammals are able to convert inorganic arsenic to mono-, di-, and trimethylated metabolites. In previous studies we have shown that the trivalent organoarsenic compounds are more toxic than their inorganic counterparts and that the toxicity is associated with the cellular uptake of the arsenicals. In the present study, we investigated cyto-/genotoxic effects of the arsenic compounds arsenate [As(i)(V)], arsenite [As(i)(III)], monomethylarsonic acid [MMA(V)], monomethylarsonous acid [MMA(III)], dimethylarsinic acid [DMA(V)], dimethylarsinous acid [DMA(III)], and trimethylarsine oxide [TMAO(V)] after an extended exposure time (24 h) and compared the uptake capabilities of fibroblasts (CHO-9 cells: Chinese hamster ovary) used for genotoxicity studies, with those of hepatic cells (Hep G2: hepatoma cell-line). To find out whether the arsenic compounds are bound to membranes or if they are present in the cytosol, the amount of arsenic was measured in whole-cell extracts and in membrane-removed cell extracts by inductively coupled plasma-mass spectrometry (ICP-MS). In addition, we forced the cellular uptake of the arsenic compounds into CHO-9 cells by electroporation and measured the intracellular arsenic concentrations before and after this procedure. Our results show that organic and inorganic arsenicals are taken up to a higher degree by fibroblasts compared to hepatoma cells. The arsenic metabolite DMA(III) was the most membrane permeable species in both cell lines and induced strong genotoxic effects in CHO-9 cells after an exposure time of 24 h. The uptake of all other arsenic species was relatively low (<1% by Hep G2 and <4% by CHO cells), but was dose-dependent. Electroporation increased the intracellular arsenic levels as well as the number of induced MN in CHO-9 cells. With the exception of As(i)(III) and DMA(III) in CHO-9 cells, the tested arsenic compounds were not bound to cell membranes, but were present in the cytosol. This may indicate the existence of DMA(III)-specific exporter proteins as are known for As(i)(III). Our results indicate that the uptake capabilities of arsenic compounds are highly dependent upon the cell type. It may be hypothesized that the arsenic-induced genotoxic effects observed in fibroblasts are due to the high uptake of arsenicals into this cell type. This may explain the high susceptibility of skin fibroblasts to arsenic exposure.

Animals↗
PubMed2001

Pharmacokinetics, metabolism, and carcinogenicity of arsenic.

The carcinogenicity of arsenic in humans has been unambiguously demonstrated in a variety of epidemiological studies encompassing geographically diverse study populations and multiple exposure scenarios. Despite the abundance of human data, our knowledge of the mechanism(s) responsible for the carcinogenic effects of arsenic remains incomplete. A deeper understanding of these mechanisms is highly dependent on the development of appropriate experimental models, both in vitro and in vivo, for future mechanistic investigations. Suitable in vitro models would facilitate further investigation of the critical chemical species (arsenate/arsenite/MMA/DMA) involved in the carcinogenic process, as well as the evaluation of the generation and role of ROS. Mechanisms underlying the clastogenic effects of arsenic, its role in modulating DNA methylation, and the phenomenon of inducible tolerance could all be more completely investigated using in vitro models. The mechanisms involved in arsenic's inhibition of ubiquitin-mediated proteolysis demand further attention, particularly with respect to its effects on cell proliferation and DNA repair. Exploration of the mechanisms responsible for the protective or anticarcinogenic effects of arsenic could also enhance our understanding of the cellular and molecular interactions that influence its carcinogenicity. In addition, appropriate in vivo models must be developed that consider the action of arsenic as a promoter and/or progressor. In vivo models that allow further investigation of the comutagenic effects of arsenic are also especially necessary. Such models may employ initiation-promotion-progression bioassays or transgenic animals. Both in vitro and in vivo models have the potential to greatly enhance our current understanding of the cellular and molecular interactions of arsenic and its metabolites in target tissues. However, refinement of our knowledge of the mechanistic aspects of arsenic carcinogenicity is not alone sufficient; an understanding of the pharmacokinetics and target tissue doses of the critical chemical species is essential. Additionally, a more thorough characterization of species differences in the tissue kinetics of arsenic and its methylated metabolites would facilitate the development of more accurate and relevant PBPK models. Improved models could be used to further investigate the existence of a methylation threshold for arsenic and its relevance to arsenic carcinogenicity in humans. The significance of alterations in relative tissue concentrations of SAM and SAH deserves further attention, particularly with respect to their role in modulating methyltransferases involved in arsenic metabolism and DNA methylation. The importance of genetic polymorphisms and nutrition in influencing methyltransferase activities must not be overlooked. In vivo models are necessary to evaluate these factors; transgenic or knockout models would be particularly useful in the investigation of methylation polymorphisms. Further evaluation of methylation polymorphisms in human populations is also warranted. Other in vivo models incorporating dietary manipulation could provide valuable insight into the role of nutrition in the carcinogenicity of arsenic. With more complete knowledge of the pharmacokinetics of arsenic metabolism and the mechanisms associated with its carcinogenic effects, development of more reliable risk assessment strategies are possible. Integration of data, both pharmacokinetic and mechanistic in nature, will lead to more accurate descriptions of the interactions that occur between the active chemical species and cellular constituents which lead to the development of cancer. This knowledge, in turn, will facilitate the development of more accurate and reliable risk assessment strategies for arsenic.

Animals↗
PubMed2006

Sequential soil washing techniques using hydrochloric acid and sodium hydroxide for remediating arsenic-contaminated soils in abandoned iron-ore mines.

Sequential washing techniques using single or dual agents [sodium hydroxide (NaOH) and hydrochloric acid (HCl) solutions] were applied to arsenic-contaminated soils in an abandoned iron-ore mine area. We investigated the best remediation strategies to maximize arsenic removal efficiency for both soils and arsenic-containing washing solution through conducting a series of batch experiments. Based on the results of a sequential extraction procedure, most arsenic prevails in Fe-As precipitates or coprecipitates, and iron exists mostly in the crystalline forms of iron oxide. Soil washing by use of a single agent was not effective in remediating arsenic-contaminated soils because arsenic extractions determined by the Korean standard test (KST) methods for washed soils were not lower than 6mg kg(-1) in all experimental conditions. The results of X-ray diffraction (XRD) indicated that iron-ore fines produced mobile colloids through coagulation and flocculation in water contacting the soils, containing dissolved arsenic and fine particles of ferric arsenate-coprecipitated silicate. The first washing step using 0.2M HCl was mostly effective in increasing the cationic hydrolysis of amorphous ferrihydrite, inducing high removal of arsenic. Thus, the removal step of arsenic-containing flocs can lower arsenic extractions (KST methods) of washed soils. Among several washing trials, alternative sequential washing using 0.2M HCl followed by 1M HCl (second step) and 1M NaOH solution (third step) showed reliable and lower values of arsenic extractions (KST methods) of washed soils. This washing method can satisfy the arsenic regulation of washed soil for reuse or safe disposal application. The kinetic data of washing tests revealed that dissolved arsenic was easily readsorbed into remaining soils at a low pH. This result might have occurred due to dominant species of positively charged crystalline iron oxides characterized through the sequential extraction procedure. However, alkaline extraction using NaOH was effective in removing arsenic readsorbed onto the surface of crystalline minerals. This is because of the ligand displacement reaction of hydroxyl ions with arsenic species and high pH conditions that can prevent readsorption of arsenic.

Arsenic↗
PubMed2005

Arsenic exposure in Hungary, Romania and Slovakia.

Inorganic arsenic is a potent human carcinogen and toxicant which people are exposed to mainly via drinking water and food. The objective of the present study was to assess current exposure to arsenic via drinking water in three European countries. For this purpose, 520 individuals from four Hungarian, two Slovakian and two Romanian countries were investigated by measuring inorganic arsenic and methylated arsenic metabolites in urine by high performance liquid chromatography with hydride generation and inductively coupled plasma mass spectrometry. Arsenic in drinking water was determined by atomic absorption spectrometry. Significantly higher concentrations of arsenic were found in both the water and the urine samples from the Hungarian counties (median: 11 and 15 microg dm(-3), respectively; p < 0.001) than from the Slovakian (median: 0.94 and 4.5 microg dm(-3), respectively) and Romanian (median: 0.70 and 2.1 microg dm(-3), respectively) counties. A significant correlation was seen between arsenic in water and arsenic in urine (R(2)= 0.46). At low water arsenic concentrations, the relative amount of dimethylarsinic acid (DMA) in urine was increased, indicating exposure via food. Also, high body mass index was associated with higher concentrations of arsenic in urine (p= 0.03), mostly in the form of DMA. Smokers had significantly higher urinary arsenic concentrations than non-smokers (p= 0.03). In conclusion, elevated arsenic exposure via drinking water was prevalent in some of the counties. Exposure to arsenic from food, mainly as DMA, and cigarette smoke, mainly as inorganic arsenic, are major determinants of arsenic exposure at very low concentrations of arsenic in drinking water.

Adult↗
PubMed2006

Biomonitoring for chromium and arsenic in timber treatment plant workers exposed to CCA wood Preservatives.

This study reports a survey of occupational exposure to copper chrome arsenic (CCA) based wood preservatives during vacuum pressure timber impregnation. The survey involved biological monitoring based on analysis of chromium and arsenic in urine samples collected from UK workers. The aim of the study was to determine the extent of occupational exposure to arsenic and chromium in the UK timber treatment industry. The objectives were to collect and analyse urine samples from as many workers as possible, where CCA wood preservatives might be used, at 6 monthly intervals for 2 years. In addition, to investigate day-to-day variations in urinary excretion of chrome and arsenic by collecting and analysing three samples a week for 3 weeks in subsets of workers and controls (people not occupationally exposed). All urine samples were analysed for chromium and inorganic arsenic. To investigate any residual interference every sample was accompanied by a short questionnaire about recent consumption of seafood and smoking. The analytical methods for arsenic used a hydride generation technique to reduce interference from dietary sources of arsenic and also a technique that would measure total arsenic concentration in urine. The main findings show that workers exposed to CCA wood preservatives have concentrations of inorganic arsenic and chromium in urine that are significantly higher than those from non-occupationally exposed people but below biological monitoring guidance values that would indicate inhalation exposure at UK occupational exposure limits for chromium and arsenic. The effects of consumption of seafood on urinary arsenic were not significant using the hydride generation method for inorganic arsenic but were significant if 'total' arsenic was measured. The 'total' arsenic method could not distinguish CCA workers from controls and is clearly unsuitable for assessment of occupational exposure to arsenic. There was a significant increase in the urinary concentration of chromium in workers over the four sample collection rounds indicating increasing exposure to chromium during the 2 years of the study. This unexpected finding may be worth further investigation. Overall, the study demonstrated the utility of biological monitoring for assessment of occupational exposure to chromium and arsenic.

Arsenic↗
PubMed1999

The enigma of arsenic carcinogenesis: role of metabolism.

Inorganic arsenic is considered a high-priority hazard, particularly because of its potential to be a human carcinogen. In exposed human populations, arsenic is associated with tumors of the lung, skin, bladder, and liver. While it is known to be a human carcinogen, carcinogenesis in laboratory animals by this metalloid has never been convincingly demonstrated. Therefore, no animal models exist for studying molecular mechanisms of arsenic carcinogenesis. The apparent human sensitivity, combined with our incomplete understanding about mechanisms of carcinogenic action, create important public health concerns and challenges in risk assessment, which could be met by understanding the role of metabolism in arsenic toxicity and carcinogenesis. This symposium summary covers three critical major areas involving arsenic metabolism: its biodiversity, the role of arsenic metabolism in molecular mechanisms of carcinogenesis, and the impact of arsenic metabolism on human risk assessment. In mammals, arsenic is metabolized to mono- and dimethylated species by methyltransferase enzymes in reactions that require S-adenosyl-methionine (SAM) as the methyl donating cofactor. A remarkable species diversity in arsenic methyltransferase activity may account for the wide variability in sensitivity of humans and animals to arsenic toxicity. Arsenic interferes with DNA methyltransferases, resulting in inactivation of tumor suppressor genes through DNA hypermethylation. Other studies suggest that arsenic-induced malignant transformation is linked to DNA hypomethylation subsequent to depletion of SAM, which results in aberrant gene activation, including oncogenes. Urinary profiles of arsenic metabolites may be a valuable tool for assessing human susceptibility to arsenic carcinogenesis. While controversial, the idea that unique arsenic metabolic properties may explain the apparent non-linear threshold response for arsenic carcinogenesis in humans. In order to address these outstanding issues, further efforts are required to identify an appropriate animal model to elucidate carcinogenic mechanisms of action, and to define dose-response relationships.

Animals↗
PubMed1976

Arsenic trioxide absorption and excretion in industry.

1. A study of 24 smelter workers routinely exposed to arsenic trioxide was conducted to evaluate some characteristics of its absorption and excretion. A statistically significant correlation was found between airborne arsenic trioxide concentrations below 300 mug/m3 and urinary arsenic values below 500 mug/liter. These men wore personal monitors for five consecutive work days and were determined to have been exposed to average airborne arsenic concentrations of 53 mug/m3 (70 mug/m3 of arsenic trioxide) which increased their urinary arsenic values from 152 mug/liter to 200 mug/liter (an average gain on 32%). 2. The background average urinary arsenic value for adult males not exposed to arsenic trioxide in industry was determined to be 52.6 mug/liter for 204 men during preemployment examinations. 3. After removal from industrial arsenic trioxide exposure, the rate of fall in urinary arsenic values varies with the magnitude of the urinary arsenic level. An initial decrease of 9.5% per day was measured for workers having urinary arsenic values below 200 mug/liter. The initial decrease is about 21% per day for workers with urinary arsenic values over 600 mug/liter. 4. It was determined that arsenic in seafood can alter, in a dramatic fashion, the urinary arsenic values determined for smelter workers within 24 hours following consumption. It is recommended, therefore, that the absorption of arsenic trioxide due to industrial exposure is best evaluated from urine samples collected at least two days after seafood has been eaten.

Adult↗
PubMed2006

In vivo assessment of arsenic bioavailability in rice and its significance for human health risk assessment.

BACKGROUND: Millions of people worldwide consume arsenic-contaminated rice; however, little is known about the uptake and bioavailability of arsenic species after arsenic-contaminated rice ingestion. OBJECTIVES: In this study, we assessed arsenic speciation in greenhouse-grown and supermarket-bought rice, and determined arsenic bioavailability in cooked rice using an in vivo swine model. RESULTS: In supermarket-bought rice, arsenic was present entirely in the inorganic form compared to greenhouse-grown rice (using irrigation water contaminated with sodium arsenate), where most (approximately 86%) arsenic was present as dimethylarsinic acid (organic arsenic). Because of the low absolute bioavailability of dimethylarsinic acid and the high proportion of dimethylarsinic acid in greenhouse-grown rice, only 33 +/- 3% (mean +/- SD) of the total rice-bound arsenic was bioavailable. Conversely, in supermarket-bought rice cooked in water contaminated with sodium arsenate, arsenic was present entirely in the inorganic form, and bioavailability was high (89 +/- 9%). CONCLUSIONS: These results indicate that arsenic bioavailability in rice is highly dependent on arsenic speciation, which in turn can vary depending on rice cultivar, arsenic in irrigation water, and the presence and nature of arsenic speciation in cooking water. Arsenic speciation and bioavailability are therefore critical parameters for reducing uncertainties when estimating exposure from the consumption of rice grown and cooked using arsenic-contaminated water.

Animals↗
PubMed2003

Arsenic speciation in the earthworms Lumbricus rubellus and Dendrodrilus rubidus.

Two species of earthworm, Lumbricus rubellus Hoffmeister and Dendrodrilus rubidus (Savigny) collected from an arsenic-contaminated mine spoil site and an uncontaminated site were investigated for total tissue arsenic concentrations and for arsenic compounds by liquid chromatography-mass spectrometry (LC-MS) and liquid chromatography-inductively coupled plasma-mass spectrometry (HPLC-ICP-MS). For L. rubellus, whole-body total tissue arsenic concentrations were 7.0 to 17.0 mg arsenic/ kg dry weight in uncontaminated soil and 162 to 566 mg arsenic/kg dry weight in contaminated soil. For D. rubidus, whole-body tissue concentrations were 2.0 to 5.0 mg arsenic/kg dry weight and 97 to 321 mg arsenic/kg dry weight, respectively. Arsenobetaine was the only organic arsenic species detected in both species of earthworms, with the remainder of the extractable arsenic being arsenate and arsenite. There was an increase in the proportion of arsenic present as arsenobetaine in the total arsenic burden. Lumbricus rubellus and D. rubidus have similar life styles, both being surface living and litter feeding. Arsenic speciation was found to be similar in both species for both uncontaminated and contaminated sites, with dose-dependent formation of arsenobetaine. When L. rubellus and D. rabidus from contaminated sites were incubated in arsenic-free soils, the total tissue burden of arsenic diminished. Initially, L. rubellus from the tolerant populations (from the contaminated site) eliminated arsenic in the first 7 d of exposure before accumulating arsenic in tissues, whereas nontolerant populations (from the uncontaminated site) accumulated arsenic linearly. The tolerant and nontolerant L. rubellus eliminated tissue arsenic linearly over 21 d when incubated in uncontaminated soil.

Animals↗
PubMed1985

Metabolism and excretion of orally administrated arsenic trioxide in the hamster.

It was shown that a single dose of arsenic trioxide administered to hamsters was chiefly methylated in vivo into methylarsonic acid (MAA) and dimethylarsinic acid (DMAA), and that inorganic arsenic accounted for the major portion of total arsenic that deposited in organs and tissues, followed by MAA and DMAA in decreasing sequence of significance. The single oral dose of arsenic trioxide was followed by a very small amount of trimethylarsenic compounds (TMA) occurring only in the liver but not in any other organs, tissues, blood or feces. The distribution pattern of arsenic in the blood following the single oral dose of arsenic trioxide was such that inorganic arsenic and MAA occurred chiefly in the blood cells; DMAA, chiefly in the plasma; and the arsenic compounds disappeared rapidly from blood. The single oral dose of arsenic trioxide was further followed by excretion of an amount of arsenic equivalent to about 60% of the administered dose: 49% in the urine and 11% in the feces. In other words, more arsenic tended to be excreted in the urine. DMAA accounted for the major portion of arsenic excreted in the urine and feces, and this finding re-confirmed that DMAA is the major metabolite of arsenic trioxide. Although it is believed that arsenic trioxide is not converted into TMA, the results of the present study suggest that a very small amount of arsenic trioxide is converted into TMA in the liver.

Animals↗
PubMed2003

Effect of arsenic on benzo[a]pyrene DNA adduct levels in mouse skin and lung.

Concomitant exposures to arsenic and polycyclic aromatic hydrocarbons (PAHs) such as benzo[a]pyrene (BaP) are widespread. While BaP acts by binding to and inducing mutations in critical sites on DNA, the mechanism(s) of arsenic carcinogenesis remains unknown. Data from epidemiological studies of arsenic copper smelter workers and arsenic ingestion in drinking water suggest a positive interaction for arsenic exposure and smoking and lung cancer. A previous in vitro study showed that arsenic potentiated the formation of DNA adducts at low doses of BaP and arsenic. The present study was conducted to test the effect of arsenic on BaP-DNA adduct formation in vivo. We hypothesized that arsenic co-treatment would significantly increase BaP adduct levels in C57BL/6 mouse target organs: skin and lung. Treatment groups were: five mice, -BaP/-arsenic; five mice, -BaP/+arsenic; 15 mice, +BaP/-arsenic; 15 mice, +BaP/+arsenic. Mice in the appropriate groups were provided sodium arsenite in drinking water (2.1 mg/l), ad libitum, for 13 days (starting 9 days before BaP treatment), and 200 nmol BaP/25 ml acetone (or acetone alone) was applied topically, once per day for 4 days. DNA was extracted from skin and lung and assayed by (32)P-postlabeling. Statistical comparisons were made using independent t-tests (unequal variances assumed). BaP-DNA adduct levels in the +BaP groups were significantly higher than -BaP controls. Arsenic co-treatment increased average BaP adduct levels in both lung and skin; the increase was statistically significant in the lung (P = 0.038). BaP adduct levels in the skin of individual animals were positively related to skin arsenic concentrations. These results corroborate our in vitro findings and provide a tentative explanation for arsenic and PAH interactions in lung carcinogenesis.

Animals↗
PubMed2004

Two possible pathways for the release of arsenic during pyrolysis of chromated copper arsenate (CCA)-treated wood.

The behavior of arsenic during pyrolysis at temperatures between 135 and 500 degrees C has been widely studied. We examined the release of arsenic during the pyrolysis of chromated copper arsenate (CCA)-treated wood, and here we propose two models for the volatilization of arsenic: (a) a reacted arsenic compound, chromium arsenate, in CCA-treated wood was initially decomposed to arsenic pentoxide, which then appeared to be released at around 400-500 degrees C as a form of arsenic trioxide; and (b) an unreacted arsenic compound, arsenic pentoxide, in CCA-treated wood was released at much lower temperatures than reacted arsenic compound, as a form of arsenic trioxide. In order to restrain the release of arsenic during pyrolysis, it is possible to pyrolyze CCA-treated wood carefully at temperatures around 300-350 degrees C only if the wood contains little unreacted arsenic compound. Under these conditions, almost all toxic elements remain in the pyrolysis residue, and a weight reduction of the wood of approximately 50% can be obtained. On the other hand, the release of arsenic can be achieved easily using an unreacted arsenic compound under the same pyrolysis conditions. However, in the present study it was difficult to determine the accurate release point of arsenic in both cases due to the level of experimental uncertainty.

Arsenic↗
PubMedDate not supplied

Carcinogenic and systemic health effects associated with arsenic exposure--a critical review.

Arsenic and arsenic containing compounds are human carcinogens. Exposure to arsenic occurs occupationally in several industries, including mining, pesticide, pharmaceutical, glass and microelectronics, as well as environmentally from both industrial and natural sources. Inhalation is the principal route of arsenic exposure in occupational settings, while ingestion of contaminated drinking water is the predominant source of significant environmental exposure globally. Drinking water contamination by arsenic remains a major public health problem. Acute and chronic arsenic exposure via drinking water has been reported in many countries of the world, where a large proportion of drinking water is contaminated with high concentrations of arsenic. General health effects that are associated with arsenic exposure include cardiovascular and peripheral vascular disease, developmental anomalies, neurologic and neurobehavioural disorders, diabetes, hearing loss, portal fibrosis, hematologic disorders (anemia, leukopenia and eosinophilia) and multiple cancers: significantly higher standardized mortality rates and cumulative mortality rates for cancers of the skin, lung, liver, urinary bladder, kidney, and colon in many areas of arsenic pollution. Although several epidemiological studies have documented the sources of exposure and the global impact of arsenic contamination, the mechanisms by which arsenic induces health effects, including cancer, are not well characterized. Further research is needed to provide a better understanding of the pathobiology of arsenic-induced diseases and to better define the toxicologic pathology of arsenic in various organ systems. In this review, we provide and discuss the underlying pathology and nature of arsenic-induced lesions. Such information is critical for understanding the magnitude of health effects associated with arsenic exposure throughout the world.

Arsenic↗
PubMed1977

Occurrence and distribution of arsenic in soils and plants.

Inorganic arsenicals have been used in agriculture as pesticides or defoliants for many years and, in localized areas, oxides of arsenic have contaminated soils as a result of fallout from ore-smelting operations and coal-fired power plants. Use of inorganic arsenicals is no longer permitted in most agricultural operations, and recent air pollution controls have markedly reduced contamination from smelters. Thus, this paper will concentrate on the effect of past applications on arsenic accumulation in soil, phytotoxicity to and uptake by plants as influenced by soil properties, and alleviation of the deleterious effects of arsenic. Once incorporated into the soil, inorganic arsenical pesticides and arsenic oxides revert to arsenates, except where the soil is under reducing conditions. The arsenate ion has properties similar to that of orthophosphate, and is readily sorbed by iron and aluminum components. This reaction greatly restricts the downward movement (leaching) of arsenic in soils and the availability of arsenic to plants. Several methods of estimating plant available arsenic in soils have been developed. They involve extraction of the soil with reagents used to estimate phosphorus availability. This extractable arsenic is reasonably well correlated with reduced plant growth by, and plant uptake of arsenic. For most plants, levels of arsenic in the edible portion of the plant are well below the critical concentration for animal or human consumption, even when severe phytotoxicity occurs. Alleviation of arsenic phytotoxicity has been attempted by increasing the soil pH, by use of iron or aluminum sulfate, by desorbing arsenate with phosphate and subsequent leaching, and by cultural practices such as deep plowing. Only limited benefits have accrued from these procedures the cost of which is often prohibitively high. Since attempts to reduce arsenic toxicity have not been very successful, its excessive accumulation in soils should be avoided.

Arsenic↗
PubMed2006

Arsenic carcinogenesis in the skin.

Chronic arsenic poisoning is a world public health issue. Long-term exposure to inorganic arsenic (As) from drinking water has been documented to induce cancers in lung, urinary bladder, kidney, liver and skin in a dose-response relationship. Oxidative stress, chromosomal abnormality and altered growth factors are possible modes of action in arsenic carcinogenesis. Arsenic tends to accumulate in the skin. Skin hyperpigmentation and hyperkeratosis have long been known to be the hallmark signs of chronic As exposure. There are significant associations between these dermatological lesions and risk of skin cancer. The most common arsenic-induced skin cancers are Bowen's disease (carcinoma in situ), basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). Arsenic-induced Bowen's disease (As-BD) is able to transform into invasive BCC and SCC. Individuals with As-BD are considered for more aggressive cancer screening in the lung and urinary bladder. As-BD provides an excellent model for studying the early stages of chemical carcinogenesis in human beings. Arsenic exposure is associated with G2/M cell cycle arrest and DNA aneuploidy in both cultured keratinocytes and As-BD lesions. These cellular abnormalities relate to the p53 dysfunction induced by arsenic. The characteristic clinical figures of arsenic-induced skin cancer are: (i) occurrence on sun-protected areas of the body; (ii) multiple and recrudescent lesions. Both As and UVB are able to induce skin cancer. Arsenic treatment enhances the cytotoxicity, mutagenicity and clastogenicity of UV in mammalian cells. Both As and UVB induce apoptosis in keratinocytes by caspase-9 and caspase-8 signaling, respectively. Combined UVB and As treatments resulted in the antiproliferative and proapoptotic effects by stimulating both caspase pathways in the keratinocytes. UVB irradiation inhibited mutant p53 and ki-67 expression, as well as increased in the number of apoptotic cells in As-BD lesions which resulted in an inhibitory effect on proliferation. As-UVB interaction provides a reasonable explanation for the rare occurrences of arsenical cancer in the sun-exposed skin. The multiple and recurrent skin lesions are associated with cellular immune dysfunction in chronic arsenism. A decrease in peripheral CD4+ cells was noticed in the inhabitants of arsenic exposure areas. There was a decrease in the number of Langerhans cells in As-BD lesion which results in an impaired immune function on the lesional sites. Since CD4+ cells are the target cell affected by As, the interaction between CD4+ cells and epidermal keratinocytes under As affection might be closely linked to the pathogenesis of multiple occurrence of arsenic-induced skin cancer. In this review, we provide and discuss the pathomechanisms of arsenic skin cancer and the relationship to its characteristic figures. Such information is critical for understanding the molecular mechanism for arsenic carcinogenesis in other internal organs.

Arsenic↗