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PubMed2000

Arsenic methylation capacity and skin cancer.

Chronic ingestion of arsenic from drinking water is associated with the occurrence of skin cancer. To clarify the role of arsenic methylation capacity in the development of arsenic-associated skin lesions, an epidemiological case-control study was conducted in the southwestern region of Taiwan, in which 26 skin disorder patients were matched with control subjects. The objective of this study was to determine whether arsenic methylation capacity of patients with skin disorders differed from that of matched controls. Both cases and controls had been exposed to similar high concentrations of arsenic in drinking water. Results indicated that skin lesion cases had higher percents of inorganic arsenic (InAs, 13.1+/-3.7%), methylarsonic acid (MMA, 16.4+/-3.2%), lower percent of dimethylarsinic acid (DMA, 70.5+/-5.8%), and higher ratio of MMA to DMA (MMA/DMA, 0.24+/-0.06) than matched controls (InAs: 11.43+/-2.1%; MMA: 14.6+/-2.6%; DMA: 73.9+/-3.3%; MMA/ DMA: 0.20+/-0.04). Individuals with a higher percentage of MMA (>15.5%) had an odds ratio of developing skin disorder 5.5 times (95% confidence interval, 1.22-24.81) higher than those having a lower percentage of MMA. This association was not confounded by hepatitis B surface antigen, cigarette smoking, or alcohol and tea consumption. It is concluded that arsenic biotransformation including methylation capacity may have a role in the development of arsenic-induced skin disorders.

Aged↗
PubMedDate not supplied

[Arsenic levels in drinking water supplies from underground sources in the community of Madrid].

BACKGROUND: In 1998, arsenic concentrations of more than 50 micrograms/l were detected in some drinking water supplies from underground sources in the Autonomous Community of Madrid, which is the maximum permissible concentration for drinking water in Spain. These two facts have meant the getting under way of a specific plan for monitoring arsenic in the drinking water in the Autonomous Community of Madrid. METHODS: The results of the first two sampling processes conducted in the arsenic level monitoring plan set out are presented. In the initial phase, water samples from 353 water supplies comprised within the census of the Public Health Administration of the Autonomous Community of Madrid were analyzed. A water supply risk classification was made based on these initial results. In a second phase, six months later, the analyses were repeated on those 35 water supplies which were considered to possibly pose a risk to public health. RESULTS: Seventy-four percent (74%) of the water supplies studied in the initial phase were revealed to have an arsenic concentration of less than 10 micrograms/l, 22.6% containing levels of 10 micrograms/l-50 micrograms/l, and 3.7% over 50 micrograms/l. Most of the water supplies showing arsenic levels of more than 10 micrograms/l are located in the same geographical area. In the second sampling process (six months later), the 35 water supplies classified as posing a risk were included. Twenty-six (26) of these supplies were revealed to have the same arsenic level ((10-50 micrograms/l), and nine changed category, six of which had less than 10 micrograms/l and three more than 50 micrograms/l. CONCLUSIONS: In the Autonomous Community of Madrid, less than 2% of the population drinks water coming from supplies which are from underground sources. The regular water quality monitoring conducted by the Public Health Administration has led to detecting the presence of more than 50 micrograms/l of arsenic in sixteen drinking water supplies from underground sources, which is the maximum permissible level under the laws currently in force in Spain. Measures have been taken to prevent water from being used from these water supplies. Around 20% of the water supplies studies must take measures in the near future to lower the arsenic concentration to below 10 micrograms/l when the water directive which is currently in the process of being written into Spanish law enters into effect.

Arsenic↗
PubMed1975

[Chronic arsenic water pollution in the Republic of Argentina].

Arsenical pollution of water supplies is a chronic problem of great medical, social and sanitary importance in Argentina. The well-known cutaneous manifestations of chronic arsenical toxicity, palmar and plantar keratoses, melanoderma and multiple epitheliomas are described. The interest which this disease has evoked in the last few years is emphasized when new arsenical areas are discovered with clinical cases of chronic arsenical intoxication. Furthermore it is shown that the high content of arsenic in drinking water may be the determining factor in the incidence of visceral neoplasms. Contrary to classic beliefs, the chronic toxic effects from arsenic may be present in young children but the palmar and plantar keratoses may be absent. The histochemical localization of the arsenic in the skin and its relation to thyroid function and the production of leukoplakia and laryngeal cancer are noted. When one analyses all the recent reports it is evident that patients with chronic arsenical intoxication must now be thoroughly studied bearing in mind the multiple localization of this carcinogenic agent.

Argentina↗
PubMed2003

[Arsenic adsorption by magnetic adsorbent CuFe2O4].

By the fact that Cu(II) and Fe(III) have strong affinity toward inorganic arsenic, the present paper reported the preparation of the magnetic adsorbent CuFe2O4 for the removal of arsenic. This adsorbent was composed with Cu(II) and Fe(III) oxides and can be recovered by magnetic separation technique. The characterization and the arsenic adsorption properties of the magnetic adsorbent were also studied. The sorption capacity was related to the pH of arsenic containing solution and the adsorption was more efficient for removing arsenic from acid and neutral solutions. As(V) was found to be more strongly adsorbed than As(III) on the adsorbent, and its adsorption capacity was 10 mg/g at equilibrium concentration of 10 micrograms/L (pH 3.5-6.5). Arsenic adsorption was not influenced by the presence of chloride and phosphate, but slightly influenced by sulfate at 10-20 times concentration of arsenic. As(V) desorption was performed more efficiently than As(III) desorption using 0.1 mol/L NaOH, which was the result of the different adsorption mechanism for the two arsenic species on adsorbent.

Adsorption↗
PubMed2003

[Renal dysfunction in workers exposed to arsenic and cadmium].

OBJECTIVE: To examine the nephrotoxicity induced caused by combined effect of arsenic and cadmium in exposed workers. METHODS: Urinary cadmium and arsenic were used as the exposure biomarkers of cadmium and arsenic. Urinary beta2-microglobulin (Ubeta2-MG), albumin (UALB) and N-acetyl-beta-D-glucosaminidase (UNAG) were measured as the effective biomarkers of tubular and glomerular dysfunction induced by cadmium and arsenic. RESULTS: The combination of cadmium and arsenic induced more severe renal injury than that caused by either of the chemicals given alone. There were positive correlations and significant dose-effect among the concentrations of urinary cadmium, arsenic and levels of Ubeta2-MG, UALB, UNAG (P<0.05, P<0.01). CONCLUSION: Cadmium combined with arsenic may have additive effect on renal dysfunction in workers exposed to arsenic and cadmium.

Adult↗
PubMed2006

Corynebacterium glutamicum as a model bacterium for the bioremediation of arsenic.

Arsenic is an extremely toxic metalloid that, when present in high concentrations, severely threatens the biota and human health. Arsenic contamination of soil, water, and air is a global growing environmental problem due to leaching from geological formations, the burning of fossil fuels, wastes generated by the gold mining industry present in uncontrolled landfills, and improper agriculture or medical uses. Unlike organic contaminants, which are degraded into harmless chemical species, metals and metalloids cannot be destroyed, but they can be immobilized or transformed into less toxic forms. The ubiquity of arsenic in the environment has led to the evolution in microbes of arsenic defense mechanisms. The most common of these mechanisms is based on the presence of the arsenic resistance operon (ars), which codes for: (i) a regulatory protein, ArsR; (ii) an arsenite permease, ArsB; and (iii) an enzyme involved in arsenate reduction, ArsC. Corynebacterium glutamicum, which is used for the industrial production of amino acids and nucleotides, is one of the most arsenic-resistant microorganisms described to date (up to 12 mM arsenite and >400 mM arseniate). Analysis of the C. glutamicum genome revealed the presence of two complete ars operons (ars1 and ars2) comprising the typical three-gene structure arsRBC, with an extra arsC1 located downstream from arsC1 (ars1 operon), and two orphan genes (arsB3 and arsC4). The involvement of both ars operons in arsenic resistance in C. glutamicum was confirmed by disruption and amplification of those genes. The strains obtained were resistant to up to 60 mM arsenite, one of the highest levels of bacterial resistance to arsenite so far described. Using tools for the genetic manipulation of C. glutamicum that were developed in our laboratory, we are attempting to obtain C. glutamicum mutant strains able to remove arsenic from contaminated water.

Arsenates↗
PubMed2006

Total and inorganic arsenic in Mid-Atlantic marine fish and shellfish and implications for fish advisories.

Sampling was conducted in 2002 to determine the total concentration and chemical speciation of arsenic in several marine fish and shellfish species collected from the Delaware Inland Bays and the Delaware Estuary, both of which are important estuarine waterbodies in the US Mid-Atlantic region that support recreational and commercial fishing. Edible meats from summer flounder (Paralicthys dentatus), striped bass (Marone saxatilis), Atlantic croaker (Micropogonias undulates), and hard clam (Mercenaria mercenaria) were tested. Total arsenic was highest in summer flounder, followed by hard clam, then striped bass, and finally, Atlantic croaker. Total arsenic was higher in summer flounder collected during the spring, as these fish migrated into the Inland Bays from the continental shelf, compared with levels in summer flounder collected during the fall, after these fish had spent the summer in the Inland Bays. Similarly, striped bass collected in the early spring close to the ocean had higher total arsenic levels compared with levels detected in striped bass collected later during the year in waters with lower salinity. Speciation of arsenic revealed low concentrations (0.00048-0.02 microg/g wet wt) of toxic inorganic arsenic. Dimethylarsinic acid was more than an order of magnitude greater in hard clam meats than in the other species tested, a finding that was attributed to arsenic uptake by phytoplankton and subsequent dietary uptake by the clam. Risk assessment using the inorganic arsenic concentrations was used to conclude that a fish consumption advisory is not warranted.

Animals↗
PubMed1991

[Assessment of the health risk of a residential area contaminated with arsenic and lead. Biological monitoring in Mundelstrup].

Industrial use of toxic substances has resulted in contamination of the outer environment so that polluted area now constitutes a considerable environmental problem. This article describes biological monitoring employed as part of the basis for assessment of the health risk due to contaminated housing soil. As an example was chosen the environmental contamination with lead and arsenic in Mundelstrup Station Town, where a manure factory previously was situated. This area, which was found to be contaminated to a considerable extend with lead and arsenic, was subdivided for living area in 1921. The present material includes 99 residents from a housing area with 30 family houses with gardens in Mundelstrup. At the commencement of the investigation in 1988/1989, blood lead levels and arsenic levels in the urine were measured and the latter were repeated in 1989/1990. For both adults and children, the blood lead levels were the same as in the reference populations. Children below 12 years had in the average higher arsenic contents in the urine compared with women and men: 16.3 mu/l 8.6 mu/l and 11.5 mu/l, respectively. For both children and adults, the arsenic values were similar to those in a limited Danish reference population. In Ruston, an area in USA heavily polluted with arsenic, contamination of the surface was found to correspond to a factor ten times higher than in Mundelstrup where arsenic is measured at a deeper level. Correspondingly, arsenic values in the urine revealed higher average values in children, 30 micrograms/l for females and 65 micrograms/l for males. The average values for the reference group were found to be 11.3-13.0 micrograms/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1980

The effect of a milk diet on the retention of 74As labelled arsenic in mice.

The effect of 3 diets with different proportion of milk proteins on retention of arsenic was studied in mice. Arsenic was administered via drinking water in concentration 50 mg As [III] per litre labelled with 74As in amount 2.96 MBq per 100 ml. After 2, 4, 8, 16 and 32 days of exposure the mice in groups of 6 each from all 3 experimental cohorts were decapitated and the content of 74As was determined in whole body, blood, liver, kidneys, spleen, lungs and heart by measuring of the activity in Gamma Scintillation Counter Tesla. From the intake of drinking water and amount of arsenic found in the experimental animals was calculated retention of arsenic in mice at different exposure intervals in all three diets. The values of arsenic found at the exposure intervals in examined materials of all three experimental cohorts were compared. The results obtained indicate that a milk diet has no adverse effect at exposure to arsenic in the sense of enhancing of its retention in mice at given experimental conditions. The found data seemed to suggest that the milk protein rich diet caused retardation of the increase of arsenic concentrations in blood, liver and kidneys that might lead at a lower exposure rate to a decrease in arsenic content in tissues of exposed animals.

Animals↗
PubMed1996

Concentration of arsenic, selenium, zinc, iron and copper in the urine of blackfoot disease patients at different clinical stages.

Atomic absorption spectrophotometric methods were developed for the determination of arsenic, selenium, iron, zinc, and copper in the urine samples. Data collected from blackfoot disease patients at five clinical stages were compared with those from healthy controls. Spectrophotometry was also used to compare the concentrations and detection levels of these elements in blood and hair samples. The copper concentration in urine changed slightly for all clinical stages, whereas the concentrations in blood and hair showed less correlation with the stages of blackfoot disease. The zinc concentration in urine increased with the clinical stage, the fourth stage having the highest concentration. The zinc concentrations in urine were not correlated with those of blood and hair samples. Zinc appears to be associated with the occurrence of scaling and cracking of the skin of the fingers or feet, and is even closely correlated with the degree of ulceration and gangrene of blackfoot disease patients. The more advanced degrees of blackfoot disease patients were associated with a greater zinc concentration in the urine. Arsenic, which is claimed to be a major causative agent of blackfoot disease, increased from the zero stage and showed a particularly high concentration in the second stage. The arsenic concentration in urine showed a positive correlation with that in the blood and the hair. Arsenic is indicated as major causative agent of blackfoot disease. The selenium concentration decreased from the zero stage, showing its lowest value during the second stage, then increased in the later stages. Changes in the selenium concentration in the urine were the inverse of those observed for the arsenic concentration in blood and hair. The decrease of selenium is attributed to the antagonistic effect of arsenic; selenium is retained during the initial stages. Iron increased from the zero stage to the second stage and showed the highest concentration of all the measured elements. It then decreased in the advanced stages of the disease. Iron may have an interactive effect with arsenic in the initial stages, resulting in loss of haemoglobin during the advanced stages. The antagonistic effect of selenium and the interactive effect of iron on arsenic warrant further study.

Arsenic↗
PubMed1996

[An experimental study on effects of arsenic on dental fluorosis in rats].

In order to study the effects of arsenic on fluorosis and interaction between arsenic and fluoride, nuclear proton microprobe technique and quantitative histological method were used to observe the distribution of arsenic and fluoride in teeth and their effects in rats fed with water containing arsenic (30 mg/L) and fluoride (100 mg/L). Results revealed (1) fluoride could cause dental fluorosis in rats, similar to that seen in human beings, and characteristics of fluorosis was evaluated by a grading system; (2) no detectable amount of arsenic was deposited in dentine, and no damage to teeth could be seen; (3) no obviously combined effects of arsenic and fluoride on dental tissues were seen, and the toxic effect of fluoride was not influenced by arsenic; and (4) a synergistically inhibitory effect of both arsenic and fluoride on body weight was found.

Animals↗
PubMed1999

Comparative effects of single intraperitoneal or oral doses of sodium arsenate or arsenic trioxide during in utero development.

Numerous studies have suggested that single-day intraperitoneal (IP) injection of inorganic arsenic results in failure of neural tube closure and other malformations in rats, hamsters, and mice. Most of these studies involved treatment of limited numbers of animals with maternally toxic doses of arsenic (generally As(V)), without defining a dose-response relationship. In the present Good Laboratory Practice-compliant study, sodium arsenate (As(V)) was administered IP and arsenic trioxide (As(III)) was administered either IP or orally (by gavage) on gestational day 9 to groups of 25 mated Crl:CD(R)(SD)BR rats. Only at dose levels that caused severe maternal toxicity, including lethality, did IP injection of arsenic trioxide produce neural tube and ocular defects; oral administration of higher doses of arsenic trioxide caused some maternal deaths but no treatment-related fetal malformations. In contrast, IP injection of similar amounts of sodium arsenate (based on the molar amount of arsenic) caused mild maternal toxicity but a large increase in malformations, including neural tube, eye, and jaw defects. In summary, neural tube and craniofacial defects were observed after IP injection of both As(V) and As(III); however, no increase in malformations was seen following oral administration of As(III), even at maternally lethal doses. These results demonstrate that the frequently cited association between prenatal exposure to inorganic arsenic and malformations in laboratory animals is dependent on a route of administration that is not appropriate for human risk assessment.

Abnormalities, Drug-Induced↗
PubMed1986

Comparative pulmonary toxicity of gallium arsenide, gallium(III) oxide, or arsenic(III) oxide intratracheally instilled into rats.

The relative toxicity of gallium arsenide (GaAs) and its metal oxides was assessed by intratracheally instilling particulate suspensions of GaAs (100 mg/kg), equimolar gallium as Ga2O3 (65 mg/kg), or a maximally tolerated nonlethal dose of arsenic as As2O3 (17 mg/kg). Two weeks after dosing, five rats from each group were randomly selected for the biochemical determination of lung lipid, protein, DNA, and collagen (4-hydroxyproline; 4-HP) content. The pulmonary retention of gallium and/or arsenic and the concentration of these metals in blood were also determined. Lungs from the remaining rats (n = 3) were examined histopathologically. Pulmonary exposure to Ga2O3 particulates significantly (p less than 0.05) increased the total lipid content of lungs relative to that observed in the vehicle-treated control animals. This response appeared to be associated with the pulmonary retention of gallium particulates (means = 36% of the gallium dose). In contrast, As2O3 particulates were not retained in the lung. Blood arsenic concentrations were 36 ppm which represented 20% of the total arsenic administered. Treatment with As2O3 significantly elevated lung dry weight as well as protein, DNA, and 4-HP content. These data suggest that As2O3 induced an acute fibrogenic response. The intratracheal instillation of GaAs particulates produced effects similar to those observed with the individual oxides. The total lung content of lipids, protein, and DNA was significantly elevated. These biochemical changes were accompanied by significant increases in lung dry weight and lung wet weight. Lungs from rats receiving GaAs particulates retained 44% of the dose as gallium and 28% of the dose as arsenic at the end of the 14-day study. Blood arsenic concentrations were 44 ppm (7% of the arsenic dose) while gallium was not detected in blood at this time. The primary histopathological observations 14 days after the intratracheal instillation of all metal particulates were an inflammatory response and pneumonocyte hyperplasia. The biological severity of these lesions, in descending order, was GaAs greater than As2O3 much greater than Ga2O3. It must be noted, however, that As2O3 was dosed at 0.25 X moles of GaAs.

Analysis of Variance↗
PubMed1993

Urinary excretion of porphyrins by smelter workers chronically exposed to arsenic dust.

Urinary arsenic (inorganic arsenic and methylated metabolites), uroporphyrin and coproporphyrin I and III isomers were determined in 84 smelter workers exposed to arsenic trioxide and in 22 non-exposed controls. Both 'high' and 'low' exposure groups were defined, based on individual's work area (arsenic recovery plant and maintenance) and mean urinary excretion of arsenic was compared to the control group (257 and 129 micrograms/g creatinine against 9.9 micrograms/g creatinine). Total coproporphyrin (I+III) increased in each exposure group as compared to control (63.3 and 59 micrograms/g creatinine against 27.2 micrograms/g creatinine), as a consequence of a 2-fold increase in each coproporphyrin isomer. The mean concentration of uroporphyrin in each exposure group was very similar to that of the non-exposed controls (9.5 and 8.8 micrograms/g creatinine against 10.7 micrograms/g creatinine). These results suggest that long-term occupational exposure of humans to arsenic is associated with coproporphyrinuria and raise the question of the use of this parameter in addition to urinary arsenic for biological monitoring.

Adult↗
PubMed1998

Suppression of arsenic-induced chromosome mutagenicity by antimony.

Arsenic and antimony are two semimetals sharing some chemical as well as toxicological properties. Both elements are clastogenic but not point mutagenic in their trivalent state of valency. Environmental exposure to arsenic was proven to be associated with increased rates of various types of cancers. Antimony is suspected to be carcinogenic to humans. Arsenic and antimony can be found as environmental co-contaminants resulting in co-exposure to man. However, in most regions where arsenic was found in elevated environmental amounts, it was not investigated whether an additional exposure to antimony was predominating. In this study, the chromosome mutagenicity induced by arsenic(III) was significantly suppressed by antimony(III) in the micronucleus test with V79 cells. The results demonstrate the necessity to identify putative environmental co-contaminations of antimony in the regions contaminated with arsenic and to determine the impact of antimony co-exposure on arsenic genotoxicity and carcinogenicity in man in vivo.

Animals↗
PubMed1998

[Teratogenic effects of arsenic on rats].

OBJECTIVE: To further clarify the effects of arsenic on pregnant rats, fetuses, fetal cells and to verify the experimental results in vitro, and to study the developmental toxicity and its mechanisms of arsenic in depth. METHODS: Teratogenic methods in vivo combined with scanning electron microscopy and histochemical techniques were used in rats. RESULTS: No apparently toxic symptoms or deaths were observed in rats exposed to various doses of arsenic trioxide of 0, 1, 4 and 10 mg/kg. Fetal death rates in rats were 10.2%, 17.4%, 24.8% and 61.1%, proportions of skeletal deformity were 1.89%, 3.12%, 17.28% and 78.57%, and embryo deformity rates were 3.16%, 5.32%, 13.79% and 40.48% 48 hours after exposure, respectively for those exposed to various doses of arsenic. Damage in fetal epidermal cells and cavities of different size between cell surface and cell junction in multiple sites could be seen under scanning microscope. Dysrhaphia, body anomalies and small limb bud, etc. were main manifestation of embryo deformity. There was a close relationship between nitric oxide and anomalies in fetal development, with a dose-response pattern, showed by inducible nitric oxide synthetase (iNOS) histochemical examinations. In vivo staining showed that excessive apoptosis could be induced by arsenic. And, teratogenic mechanisms of arsenic was analyzed in various ways. CONCLUSION: Arsenic has certain teratogenic effects on rats in vivo.

Animals↗
PubMed1991

Arsenic poisoning in livestock.

Arsenic is an important heavy metal intoxicant to livestock. Arsenical pesticides present significant hazards to animal health. The toxicity of arsenic varies with several factors--its chemical form, oxidation states, solubility. The phenylarsonic compounds are the least toxic and are used as feed additives in swine and poultry rations. However, roxarsone has a higher absolute toxicity than arsanilic acid. The mechanism of action is related to its reaction with sulfhydryl groups values to enzyme function and to its ability to uncouple oxydative phosphorylation. Most animals excrete arsenic quite readily. Toxicoses caused by inorganic and aliphatic organic arsenicals result in a different clinical syndrome than that from the phenylarsonic compounds. Arsenic poisoning may be confused with other types of intoxication. The specific antidote for inorganic arsenical poisoning is dimercaprol (BAL).

Animals↗
PubMed2004

Arsenic exposure exacerbates atherosclerotic plaque formation and increases nitrotyrosine and leukotriene biosynthesis.

A correlation between arsenic and cardiovascular disease (CVD) has been established through epidemiological studies, although the mechanisms are unknown. Using a mouse model that develops atherosclerotic lesions on a normal chow diet, we have confirmed a connection between long-term arsenic intake and CVD. Our results reveal a significant increase in the degree of atherosclerotic plaque stenosis within the innominate artery of ApoE-/-/LDLr-/- mice treated with 10 ppm sodium arsenite (133 microM) in drinking water for 18 weeks compared to controls. Immunohistochemistry shows nitrotyrosine formation, a marker of reactive nitrogen species generation, is significantly higher within the atherosclerotic plaque of arsenic-treated mice. In addition, there is a significant increase in the 5-lipoxygenase (5-LO) product, leukotriene E4 (LTE4), in the serum of arsenic-treated mice. This is supported by induction of the 5-LO protein and subsequent increases in LTE4 synthesis in bovine aortic endothelial cells. This increase in LTE4 is partially inhibited by inhibitors of nitric oxide synthase, suggesting a link between reactive nitrogen species and arsenic-induced inflammation. Furthermore, there is a significant increase in prostacyclin (PGI2) in the serum of arsenic-treated mice. We conclude that changes in specific inflammatory mediators such as LTE4 and PGI2 are related to arsenic-induced atherosclerosis. In addition, amplified synthesis of reactive species such as peroxynitrite results in increased protein nitration in response to arsenic exposure. This finding is consistent with the pathology seen in human atherosclerotic plaques.

Animals↗