Laure Terrier(*). Journée d’étude du CLERSÉ: Du « white collar crime » à la « délinquance écologique ». Recherches actuelles sur les illégalismes et infractions des classes dominantes. Lille, France, 11 février 2011.
(*) Ecole Doctorale de Sciences Juridiques et Politiques , Université Paris-Ouest Nanterre La Défense.
Paracatu est une ville d’environ 90000 habitants située dans l’Etat du Minas Gerais, au Brésil. Longtemps exploité artisanalement, le Morro do Ouro est désormais entre les mains de la compagnie minière canadienne RPM/Kinross Gold Corporation. Cette dernière détient le monopole de l’exploitation aurifère du Morro do Ouro, mine d’or à ciel ouvert à grande échelle, située à moins de 0,1 km de la ville de Paracatu. En 2008-2009, l’entreprise a lancé sa troisième phase d’expansion malgré la faible teneur en or (0,4 gramme d’or par tonne de minerai extrait). Au regard de l’ampleur du projet et des objectifs fixés (prolonger l’activité de la mine jusqu’en 2040, extraire 17 tonnes d’or par an), on peut s’interroger sur l’impact opéré sur la qualité de l’environnement, le bien-être et l’état de santé de ses environnés. L’implantation de l’entreprise RPM/Kinross Gold a exacerbé plusieurs problèmes socio-juridiques :
- accroissement de la superficie minière, proximité avec la ville
- intimidation, gardes armés, climat de terreur
- explosions quotidiennes de la roche : nuisances sonores, poussière d’arsenic
- barrage de rejets (drainage minier acide) : populations et habitations situées derrière le barrage : solutions de cyanure de sodium, métaux lourds (arsenic, plombs, cadmium, ….)
- invasion des terres agricoles
- détournement ou assèchement des sources d’eau potable
- expulsions de populations indigènes (Quilombolas) et atteinte au droit de propriété ;
- accroissement des problèmes sanitaires : maux de tête, d’estomac, démangeaisons et irruptions cutanées et cas fréquents de cancers dans la municipalité…
Si l’on s’en tient aux affirmations avancées par la compagnie minière RPM/Kinross Gold et telles qu’énoncées dans sa politique socio-environnementale, l’entreprise respecte l’ensemble des normes en vigueur (travail, santé, droits humains, environnement) et s’affiche comme une entreprise modèle. Si l’on se penche du côté des allégations formulées par les populations à l’encontre de la société minière canadienne, on se heurte à des éléments discordants. La RPM/Kinross Gold ne se rend-t-elle pas coupable – et en toute impunité – de violations en cascade des droits fondamentaux de ces populations appartenant souvent à des minorités, qui de ce fait, sont des victimes un peu plus vulnérables ? Quels instruments législatifs, conventionnels, juridiques sont à disposition des victimes de cette entreprise minière qu’on pourrait qualifier de « délinquante » voire de « criminelle » ? Quelles sanctions seraient applicables à toutes ces atteintes graves à l’environnement, aux Hommes et à leurs droits fondamentaux ?
Sunday, February 20, 2011
Thursday, February 17, 2011
Field Fluxes and Speciation of Arsines Emanating from Soils.
Environ Sci Technol. 2011 Feb 1, 45: 1798-804.
Mestrot A, Feldmann J, Krupp EM, Hossain MS, Roman-Ross G, Meharg AA.
Institute of Biological and Environmental Sciences, University of Aberdeen , Cruickshank Building, St. Machar Drive, Aberdeen, AB24 3UU, United Kingdom.
Abstract: The biogeochemical cycle of arsenic (As) has been extensively studied over the past decades because As is an environmentally ubiquitous, nonthreshold carcinogen, which is often elevated in drinking water and food. It has been known for over a century that micro-organisms can volatilize inorganic As salts to arsines (arsine AsH(3), mono-, di-, and trimethylarsines, MeAsH(2), Me(2)AsH, and TMAs, respectively), but this part of the As cycle, with the exception of geothermal environs, has been almost entirely neglected because of a lack of suited field measurement approaches. Here, a validated, robust, and low-level field-deployable method employing arsine chemotrapping was used to quantify and qualify arsines emanating from soil surfaces in the field. Up to 240 mg/ha/y arsines was released from low-level polluted paddy soils (11.3 ± 0.9 mg/kg As), primarily as TMAs, whereas arsine flux below method detection limit was measured from a highly contaminated mine spoil (1359 ± 212 mg/kg As), indicating that soil chemistry is vital in understanding this phenomenon. In microcosm studies, we could show that under reducing conditions, induced by organic matter (OM) amendment, a range of soils varied in their properties, from natural upland peats to highly impacted mine-spoils, could all volatilize arsines. Volatilization rates from 0.5 to 70 μg/kg/y were measured, and AsH(3), MeAsH(2), Me(2)AsH, and TMAs were all identified. Addition of methylated oxidated pentavalent As, namely monomethylarsonic acid (MMAA) and dimethylarsinic acid (DMAA), to soil resulted in elevated yearly rates of volatilization with up to 3.5% of the total As volatilized, suggesting that the initial conversion of inorganic As to MMAA limits the rate of arsine and methylarsines production by soils. The nature of OM amendment altered volatilization quantitatively and qualitatively, and total arsines release from soil showed correlation between the quantity of As and the concentration of dissolved organic carbon (DOC) in the soil porewater. The global flux of arsines emanating from soils was estimated and placed in the context of As atmospheric inputs, with arsines contributing from 0.9 to 2.6% of the global budget.
Mestrot A, Feldmann J, Krupp EM, Hossain MS, Roman-Ross G, Meharg AA.
Institute of Biological and Environmental Sciences, University of Aberdeen , Cruickshank Building, St. Machar Drive, Aberdeen, AB24 3UU, United Kingdom.
Abstract: The biogeochemical cycle of arsenic (As) has been extensively studied over the past decades because As is an environmentally ubiquitous, nonthreshold carcinogen, which is often elevated in drinking water and food. It has been known for over a century that micro-organisms can volatilize inorganic As salts to arsines (arsine AsH(3), mono-, di-, and trimethylarsines, MeAsH(2), Me(2)AsH, and TMAs, respectively), but this part of the As cycle, with the exception of geothermal environs, has been almost entirely neglected because of a lack of suited field measurement approaches. Here, a validated, robust, and low-level field-deployable method employing arsine chemotrapping was used to quantify and qualify arsines emanating from soil surfaces in the field. Up to 240 mg/ha/y arsines was released from low-level polluted paddy soils (11.3 ± 0.9 mg/kg As), primarily as TMAs, whereas arsine flux below method detection limit was measured from a highly contaminated mine spoil (1359 ± 212 mg/kg As), indicating that soil chemistry is vital in understanding this phenomenon. In microcosm studies, we could show that under reducing conditions, induced by organic matter (OM) amendment, a range of soils varied in their properties, from natural upland peats to highly impacted mine-spoils, could all volatilize arsines. Volatilization rates from 0.5 to 70 μg/kg/y were measured, and AsH(3), MeAsH(2), Me(2)AsH, and TMAs were all identified. Addition of methylated oxidated pentavalent As, namely monomethylarsonic acid (MMAA) and dimethylarsinic acid (DMAA), to soil resulted in elevated yearly rates of volatilization with up to 3.5% of the total As volatilized, suggesting that the initial conversion of inorganic As to MMAA limits the rate of arsine and methylarsines production by soils. The nature of OM amendment altered volatilization quantitatively and qualitatively, and total arsines release from soil showed correlation between the quantity of As and the concentration of dissolved organic carbon (DOC) in the soil porewater. The global flux of arsines emanating from soils was estimated and placed in the context of As atmospheric inputs, with arsines contributing from 0.9 to 2.6% of the global budget.
Interactions between arsenic-induced toxicity and nutrition in early life.
J Nutr. 2007 Dec;137(12):2798-804.
Vahter ME.
Institute of Environmental Medicine, Karolinska Institutet, 171 77 Stockholm, Sweden. marie.vahter@ki.se
Abstract
Exposure to arsenic through drinking water is a major public health problem affecting most countries, although the situation is particularly severe in low-income nations. The health consequences of chronic arsenic exposure include increased risk for various forms of cancer and numerous noncancer effects, including diabetes, skin diseases, chronic cough, and toxic effects on liver, kidney, cardiovascular system, and peripheral and central nervous systems. In recent years increasing reports of effects on fetal and child development have appeared. There seems to be a wide variation in susceptibility to arsenic toxicity, which is likely to be related to factors such as variation in arsenic metabolism, nutrition, host-related defense mechanisms, and genetic predisposition. The main mechanisms of arsenic-nutrition interactions include arsenic-induced oxidative stress, which requires nutrient-dependent defense systems, and arsenic metabolism (methylation) via 1-carbon metabolism, which requires methyl groups, folic acid, vitamin B-12, and betaine for the remethylation of homocysteine to methionine. An efficient first methylation step in combination with a slow second methylation step seems to be most critical from a toxicological point of view. A third mode of arsenic-nutrition interaction involves epigenetic effects and fetal programming via DNA methylation.
Vahter ME.
Institute of Environmental Medicine, Karolinska Institutet, 171 77 Stockholm, Sweden. marie.vahter@ki.se
Abstract
Exposure to arsenic through drinking water is a major public health problem affecting most countries, although the situation is particularly severe in low-income nations. The health consequences of chronic arsenic exposure include increased risk for various forms of cancer and numerous noncancer effects, including diabetes, skin diseases, chronic cough, and toxic effects on liver, kidney, cardiovascular system, and peripheral and central nervous systems. In recent years increasing reports of effects on fetal and child development have appeared. There seems to be a wide variation in susceptibility to arsenic toxicity, which is likely to be related to factors such as variation in arsenic metabolism, nutrition, host-related defense mechanisms, and genetic predisposition. The main mechanisms of arsenic-nutrition interactions include arsenic-induced oxidative stress, which requires nutrient-dependent defense systems, and arsenic metabolism (methylation) via 1-carbon metabolism, which requires methyl groups, folic acid, vitamin B-12, and betaine for the remethylation of homocysteine to methionine. An efficient first methylation step in combination with a slow second methylation step seems to be most critical from a toxicological point of view. A third mode of arsenic-nutrition interaction involves epigenetic effects and fetal programming via DNA methylation.
Arsenic exposure and type 2 diabetes: a systematic review of the experimental and epidemiological evidence.
Environ Health Perspect. 2006 May;114(5):641-8.
Navas-Acien A, Silbergeld EK, Streeter RA, Clark JM, Burke TA, Guallar E.
Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland 21205-2223, USA.
Abstract - Chronic arsenic exposure has been suggested to contribute to diabetes development. We performed a systematic review of the experimental and epidemiologic evidence on the association of arsenic and type 2 diabetes. We identified 19 in vitro studies of arsenic and glucose metabolism. Five studies reported that arsenic interfered with transcription factors involved in insulin-related gene expression: upstream factor 1 in pancreatic beta-cells and peroxisome proliferative-activated receptor gamma in preadipocytes. Other in vitro studies assessed the effect of arsenic on glucose uptake, typically using very high concentrations of arsenite or arsenate. These studies provide limited insight on potential mechanisms. We identified 10 in vivo studies in animals. These studies showed inconsistent effects of arsenic on glucose metabolism. Finally, we identified 19 epidemiologic studies (6 in high-arsenic areas in Taiwan and Bangladesh, 9 in occupational populations, and 4 in other populations). In studies from Taiwan and Bangladesh, the pooled relative risk estimate for diabetes comparing extreme arsenic exposure categories was 2.52 (95% confidence interval, 1.69-3.75), although methodologic problems limit the interpretation of the association. The evidence from occupational studies and from general populations other than Taiwan or Bangladesh was inconsistent. In summary, the current available evidence is inadequate to establish a causal role of arsenic in diabetes. Because arsenic exposure is widespread and diabetes prevalence is reaching epidemic proportions, experimental studies using arsenic concentrations relevant to human exposure and prospective epidemiologic studies measuring arsenic biomarkers and appropriately assessing diabetes should be a research priority.
Navas-Acien A, Silbergeld EK, Streeter RA, Clark JM, Burke TA, Guallar E.
Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland 21205-2223, USA.
Abstract - Chronic arsenic exposure has been suggested to contribute to diabetes development. We performed a systematic review of the experimental and epidemiologic evidence on the association of arsenic and type 2 diabetes. We identified 19 in vitro studies of arsenic and glucose metabolism. Five studies reported that arsenic interfered with transcription factors involved in insulin-related gene expression: upstream factor 1 in pancreatic beta-cells and peroxisome proliferative-activated receptor gamma in preadipocytes. Other in vitro studies assessed the effect of arsenic on glucose uptake, typically using very high concentrations of arsenite or arsenate. These studies provide limited insight on potential mechanisms. We identified 10 in vivo studies in animals. These studies showed inconsistent effects of arsenic on glucose metabolism. Finally, we identified 19 epidemiologic studies (6 in high-arsenic areas in Taiwan and Bangladesh, 9 in occupational populations, and 4 in other populations). In studies from Taiwan and Bangladesh, the pooled relative risk estimate for diabetes comparing extreme arsenic exposure categories was 2.52 (95% confidence interval, 1.69-3.75), although methodologic problems limit the interpretation of the association. The evidence from occupational studies and from general populations other than Taiwan or Bangladesh was inconsistent. In summary, the current available evidence is inadequate to establish a causal role of arsenic in diabetes. Because arsenic exposure is widespread and diabetes prevalence is reaching epidemic proportions, experimental studies using arsenic concentrations relevant to human exposure and prospective epidemiologic studies measuring arsenic biomarkers and appropriately assessing diabetes should be a research priority.
Arsenic poisoning: acute or chronic? Suicide or murder?
Am J Forensic Med Pathol. 1990 Sep;11(3):226-32.
Poklis A, Saady JJ.
Department of Pathology, Medical College of Virginia, Richmond 23298-0597.
Abstract
The case of the death by arsenic poisoning of a 62-year-old white man is presented. One year prior to death, he developed intermittent bouts of severe gastroenteritis with vomiting and diarrhea, hyperpigmentation and keratosis of the skin, neutropenia, and Guillain-Barré-like neuropathy for which he was hospitalized several times. Urine test results 6 months prior to death indicating 36 mg/L arsenic were believed to be in error. At the patient's last admission, he appeared in the emergency room with severe gastroenteritis, hypotension, and dehydration. He died 3 days later. Antemortem as well as autopsy specimens revealed elevated arsenic concentrations. Arsenic micrograms/g analysis by neutron activation of hair pulled from the man's head revealed by centimeter segmental analysis proximal to distal: 226, 104, 28, 56, 41, 40, and 74. The wife of the decedent was charged with murder by arsenic poisoning of this, her fifth, husband. The defense alleged that the decedent had committed suicide. The judge awarded a directed verdict of "not guilty." Particulars of the medical, toxicological, and investigative findings are presented.
Poklis A, Saady JJ.
Department of Pathology, Medical College of Virginia, Richmond 23298-0597.
Abstract
The case of the death by arsenic poisoning of a 62-year-old white man is presented. One year prior to death, he developed intermittent bouts of severe gastroenteritis with vomiting and diarrhea, hyperpigmentation and keratosis of the skin, neutropenia, and Guillain-Barré-like neuropathy for which he was hospitalized several times. Urine test results 6 months prior to death indicating 36 mg/L arsenic were believed to be in error. At the patient's last admission, he appeared in the emergency room with severe gastroenteritis, hypotension, and dehydration. He died 3 days later. Antemortem as well as autopsy specimens revealed elevated arsenic concentrations. Arsenic micrograms/g analysis by neutron activation of hair pulled from the man's head revealed by centimeter segmental analysis proximal to distal: 226, 104, 28, 56, 41, 40, and 74. The wife of the decedent was charged with murder by arsenic poisoning of this, her fifth, husband. The defense alleged that the decedent had committed suicide. The judge awarded a directed verdict of "not guilty." Particulars of the medical, toxicological, and investigative findings are presented.
In utero arsenic exposure induces early onset of atherosclerosis in ApoE-/- mice.
Reprod Toxicol. 2007 Apr-May;23(3):449-56. Epub 2007 Jan 25.
Srivastava S, D'Souza SE, Sen U, States JC.
Department of Medicine, University of Louisville, Louisville, KY
40202, United States.
Abstract - Consumption of arsenic contaminated drinking water has been linked to higher rates of coronary disease, stroke, and peripheral arterial disease. Recent evidence suggests that early life exposures may play a significant role in the onset of chronic adult diseases. To investigate the potential for in utero arsenic exposure to accelerate the onset of cardiovascular disease we exposed pregnant ApoE-knockout (ApoE(-/-)) mice to arsenic in their drinking water and examined the aortic trees of their male offspring for evidence of early disease 10 and 16 weeks after birth. Mice were maintained on normal chow after weaning. ApoE(-/-) mice are a commonly used model for atherogenesis and spontaneously develop atherosclerotic disease. Mice exposed to arsenic in utero showed a >2-fold increase in lesion formation in the aortic roots as well as the aortic arch compared to control mice at both 10 and 16 weeks of age. The mice exposed to arsenic also had a 20-40% decrease in total triglycerides, but no change in total cholesterol, phospholipids and total abundance of VLDL or HDL particles. Subfractionation of VLDL particles showed a decrease in large VLDL particles. In addition, the arsenic-exposed mice showed a vasorelaxation defect in response to acetylcholine suggesting disturbance of endothelial cell signalling. These results indicate that in utero arsenic exposure induces an early onset of atherosclerosis in ApoE(-/-) mice without a hyperlipidemic diet and support the hypothesis that in utero arsenic exposure may be atherogenic in humans.
Srivastava S, D'Souza SE, Sen U, States JC.
Department of Medicine, University of Louisville, Louisville, KY
40202, United States.
Abstract - Consumption of arsenic contaminated drinking water has been linked to higher rates of coronary disease, stroke, and peripheral arterial disease. Recent evidence suggests that early life exposures may play a significant role in the onset of chronic adult diseases. To investigate the potential for in utero arsenic exposure to accelerate the onset of cardiovascular disease we exposed pregnant ApoE-knockout (ApoE(-/-)) mice to arsenic in their drinking water and examined the aortic trees of their male offspring for evidence of early disease 10 and 16 weeks after birth. Mice were maintained on normal chow after weaning. ApoE(-/-) mice are a commonly used model for atherogenesis and spontaneously develop atherosclerotic disease. Mice exposed to arsenic in utero showed a >2-fold increase in lesion formation in the aortic roots as well as the aortic arch compared to control mice at both 10 and 16 weeks of age. The mice exposed to arsenic also had a 20-40% decrease in total triglycerides, but no change in total cholesterol, phospholipids and total abundance of VLDL or HDL particles. Subfractionation of VLDL particles showed a decrease in large VLDL particles. In addition, the arsenic-exposed mice showed a vasorelaxation defect in response to acetylcholine suggesting disturbance of endothelial cell signalling. These results indicate that in utero arsenic exposure induces an early onset of atherosclerosis in ApoE(-/-) mice without a hyperlipidemic diet and support the hypothesis that in utero arsenic exposure may be atherogenic in humans.
Analysis of the relationship between leukemia mortality and soil trace elements using chemometrics.
Biol Trace Elem Res. 2010 Dec;137(3):289-300. Epub 2009 Dec 24.
Tan C, Chen H, Xia C.
Department of Chemistry and Chemical Engineering, Yibin University, People's Republic of China. chaotan1112@163.com
Abstract
The relationship between the mortality of leukemia and the contents of trace elements in the soils of 29 regions of China was investigated. A total of 27 elements were determined for each region. Considering that an efficient variable selection can be highly beneficial both to improve the predictive ability of the model and to greatly reduce its complexity, genetic algorithm-partial least squares was used to screen out 13 qualified elements. As a result, only 13 elements, i.e., As, Hg, Mn, Sr, Ba, Cu, Ti, Co, K, Ca, Rb, Zn, and Mg, were picked out and, a partial least squares model with three latent variables was obtained, whose prediction exhibited a correlative coefficient of 0.874 with actual mortality. Especially, it showed a high negative correlation between the content of soil As and the mortality of leukemia. Such a fact can be explained by the apoptotic effect of cancerous cells by trace-amount arsenic trioxide. Furthermore, according to whether the mortality was larger than two out of 100,000 (2 × 10⁻⁵), all the 29 regions were divided into 21 high-mortality regions and eight low-mortality regions and were assigned the label -1 or 1, respectively. Using the same 13 elements, a Fisher's discriminant analysis model was developed, which can successfully discriminate low- and high-mortality groups.
Tan C, Chen H, Xia C.
Department of Chemistry and Chemical Engineering, Yibin University, People's Republic of China. chaotan1112@163.com
Abstract
The relationship between the mortality of leukemia and the contents of trace elements in the soils of 29 regions of China was investigated. A total of 27 elements were determined for each region. Considering that an efficient variable selection can be highly beneficial both to improve the predictive ability of the model and to greatly reduce its complexity, genetic algorithm-partial least squares was used to screen out 13 qualified elements. As a result, only 13 elements, i.e., As, Hg, Mn, Sr, Ba, Cu, Ti, Co, K, Ca, Rb, Zn, and Mg, were picked out and, a partial least squares model with three latent variables was obtained, whose prediction exhibited a correlative coefficient of 0.874 with actual mortality. Especially, it showed a high negative correlation between the content of soil As and the mortality of leukemia. Such a fact can be explained by the apoptotic effect of cancerous cells by trace-amount arsenic trioxide. Furthermore, according to whether the mortality was larger than two out of 100,000 (2 × 10⁻⁵), all the 29 regions were divided into 21 high-mortality regions and eight low-mortality regions and were assigned the label -1 or 1, respectively. Using the same 13 elements, a Fisher's discriminant analysis model was developed, which can successfully discriminate low- and high-mortality groups.
Leachability of arsenic and heavy metals from mine tailings of abandoned metal mines.
Int J Environ Res Public Health. 2009 Nov;6(11):2865-79. Epub 2009 Nov 17.
Lim M, Han GC, Ahn JW, You KS, Kim HS.
Korea Institute of Geoscience and Mineral Resources, Gwahang-no, Yuseong-gu, Daejeon, Korea. limmh@paran.com
Abstract
Mine tailings from an abandoned metal mine in Korea contained high concentrations of arsenic (As) and heavy metals [e.g., As: 67,336, Fe: 137,180, Cu: 764, Pb: 3,572, and Zn: 12,420 (mg/kg)]. US EPA method 6010 was an effective method for analyzing total arsenic and heavy metals concentrations. Arsenic in the mine tailings showed a high residual fraction of 89% by a sequential extraction. In Toxicity Characteristic Leaching Procedure (TCLP) and Korean Standard Leaching Test (KSLT), leaching concentrations of arsenic and heavy metals were very low [e.g., As (mg/L): 0.4 for TCLP and 0.2 for KSLT; cf. As criteria (mg/L): 5.0 for TCLP and 1.5 for KSLT].
Lim M, Han GC, Ahn JW, You KS, Kim HS.
Korea Institute of Geoscience and Mineral Resources, Gwahang-no, Yuseong-gu, Daejeon, Korea. limmh@paran.com
Abstract
Mine tailings from an abandoned metal mine in Korea contained high concentrations of arsenic (As) and heavy metals [e.g., As: 67,336, Fe: 137,180, Cu: 764, Pb: 3,572, and Zn: 12,420 (mg/kg)]. US EPA method 6010 was an effective method for analyzing total arsenic and heavy metals concentrations. Arsenic in the mine tailings showed a high residual fraction of 89% by a sequential extraction. In Toxicity Characteristic Leaching Procedure (TCLP) and Korean Standard Leaching Test (KSLT), leaching concentrations of arsenic and heavy metals were very low [e.g., As (mg/L): 0.4 for TCLP and 0.2 for KSLT; cf. As criteria (mg/L): 5.0 for TCLP and 1.5 for KSLT].
Association of genotoxic effects of arsenic with haematological malignancy in West Bengal.
Hum Exp Toxicol. 2011 Feb;30(2):165-70. Epub 2010 Apr 12.
Paul S, Chakraborty T, Halder A, Bandopadhyay D, Chaudhuri U, De M.
Department of Genetics, Vivekananda Institute of Medical Sciences, Ramakrishna Mission Seva Pratisthan, Kolkata 700026, India. sonalismail@rediffmail.com.
Abstract
Arsenic is a naturally occurring metalloid that has been associated with increased incidence of human cancers in certain highly exposed populations. This present work aimed to study whether arsenic plays any role in the increased incidence of blood cancer among residents of West Bengal, India, which is one of the worst arsenic-affected areas of the world. Our study group included both blood cancer patients and age-, sex-matched healthy controls. We studied the arsenic concentration in the hair and nail samples of our study group. We found significantly higher arsenic concentration in the biological tissues of patients, which also correlated with their greater incidence of chromosomal aberrations. Thus, arsenic may act as a predisposing factor for blood cancer.
Paul S, Chakraborty T, Halder A, Bandopadhyay D, Chaudhuri U, De M.
Department of Genetics, Vivekananda Institute of Medical Sciences, Ramakrishna Mission Seva Pratisthan, Kolkata 700026, India. sonalismail@rediffmail.com.
Abstract
Arsenic is a naturally occurring metalloid that has been associated with increased incidence of human cancers in certain highly exposed populations. This present work aimed to study whether arsenic plays any role in the increased incidence of blood cancer among residents of West Bengal, India, which is one of the worst arsenic-affected areas of the world. Our study group included both blood cancer patients and age-, sex-matched healthy controls. We studied the arsenic concentration in the hair and nail samples of our study group. We found significantly higher arsenic concentration in the biological tissues of patients, which also correlated with their greater incidence of chromosomal aberrations. Thus, arsenic may act as a predisposing factor for blood cancer.
The positive response of Ty1 retrotransposition test to carcinogens is due to increased levels of reactive oxygen species generated by the genotoxins.
Arch Toxicol. 2011 Jan;85(1):67-74. Epub 2010 Apr 17.
Dimitrov M, Venkov P, Pesheva M.
Sofia University, Bulgaria.
Abstract
In previous laboratory and environmental studies, the Ty1 short-term test showed positive responses (i.e. induced mobility of the Ty1 retrotransposon) to carcinogenic genotoxins. Here, we provide evidence for a causal relationship between increased level of reactive oxygen species and induction the mobility of the Ty1 retrotransposon. Results obtained in concentration and time-dependent experiments after treatment, the tester cells with carcinogenic genotoxins [benzo(a)pyrene, benzo(a)anthracene, ethylmethanesulfonate, formamide], free bile acids (chenodeoxycholic, lithocholic acids) and metals (arsenic, hexavelant chromium, lead) showed a simultaneous increase in both cellular level of the superoxide anions and Ty1 retrotransposition rates. Treatment with the noncarcinogenic genotoxins [benzo(e)pyrene, benzo(b)anthracen, anthracene], conjugated bile acids (taurodeoxycholic, glycodeoxycholic acids) and metals (zinc, trivalent chromium) did not change significantly superoxide anions level and Ty1 retrotransposition rate. The induction by carcinogens of the Ty1 mobility seems to depend on the accumulation of superoxide anions, since the addition of the scavenger N-acetylcysteine resulted in loss of both increased amount of superoxide anions and induced Ty1 retrotransposition. Increased hydrogen peroxide levels are also involved in the induction of Ty1 retrotransposition rates in response to treatment with carcinogenic genotoxins, as evidenced by disruption of YAP1 gene in the tester cells. It is concluded that the carcinogen-induced high level of reactive oxygen species play a primary and key role in determination the selective response of Ty1 test to carcinogenic genotoxins.
Dimitrov M, Venkov P, Pesheva M.
Sofia University, Bulgaria.
Abstract
In previous laboratory and environmental studies, the Ty1 short-term test showed positive responses (i.e. induced mobility of the Ty1 retrotransposon) to carcinogenic genotoxins. Here, we provide evidence for a causal relationship between increased level of reactive oxygen species and induction the mobility of the Ty1 retrotransposon. Results obtained in concentration and time-dependent experiments after treatment, the tester cells with carcinogenic genotoxins [benzo(a)pyrene, benzo(a)anthracene, ethylmethanesulfonate, formamide], free bile acids (chenodeoxycholic, lithocholic acids) and metals (arsenic, hexavelant chromium, lead) showed a simultaneous increase in both cellular level of the superoxide anions and Ty1 retrotransposition rates. Treatment with the noncarcinogenic genotoxins [benzo(e)pyrene, benzo(b)anthracen, anthracene], conjugated bile acids (taurodeoxycholic, glycodeoxycholic acids) and metals (zinc, trivalent chromium) did not change significantly superoxide anions level and Ty1 retrotransposition rate. The induction by carcinogens of the Ty1 mobility seems to depend on the accumulation of superoxide anions, since the addition of the scavenger N-acetylcysteine resulted in loss of both increased amount of superoxide anions and induced Ty1 retrotransposition. Increased hydrogen peroxide levels are also involved in the induction of Ty1 retrotransposition rates in response to treatment with carcinogenic genotoxins, as evidenced by disruption of YAP1 gene in the tester cells. It is concluded that the carcinogen-induced high level of reactive oxygen species play a primary and key role in determination the selective response of Ty1 test to carcinogenic genotoxins.
A simple method based on ICP-MS for estimation of background levels of arsenic, cadmium, copper, manganese, nickel, lead, and selenium in blood of the Brazilian population.
J Toxicol Environ Health A. 2010;73(13-14):878-87.
Nunes JA, Batista BL, Rodrigues JL, Caldas NM, Neto JA, Barbosa F Jr.
Laboratorio de Toxicologia e Essencialidade de Metais, Depto. de Analises Clinicas, Toxicologicas e Bromatologicas, Faculdade de Ciencias Farmaceuticas de Ribeirao Preto-USP, Ribeirao Preto-SP, Brazil.
Abstract
Throughout the world, biomonitoring has become the standard for assessing exposure of individuals to toxic elements as well as for responding to serious environmental public health problems. However, extensive biomonitoring surveys require rapid and simple analytical methods. Thus, a simple and high-throughput method is proposed for the determination of arsenic (As), cadmium (Cd), copper (Cu), manganese (Mn), nickel (Ni), lead (Pb), and selenium (Se) in blood samples by using inductively coupled plasma-mass spectrometry (ICP-MS). Prior to analysis, 200 microl of blood samples was mixed with 500 microl of 10% v/v tetramethylammonium hydroxide (TMAH) solution, incubated for 10 min, and subsequently diluted to 10 ml with a solution containing 0.05% w/v ethylenediamine tetraacetic acid (EDTA) + 0.005% v/v Triton X-100. After that, samples were directly analyzed by ICP-MS (ELAN DRC II). Rhodium was selected as an internal standard with matrix-matching calibration. Method detection limits were 0.08, 0.04, 0.5, 0.09, 0.12, 0.04, and 0.1 microg//L for As, Cd, Cu, Mn, Ni, Pb, and Se, respectively. Validation data are provided based on the analysis of blood samples from the trace elements inter-\comparison program operated by the Institut National de Sante Publique du Quebec, Canada. Additional validation was provided by the analysis of human blood samples by the proposed method and by using electrothermal atomic absorption spectrometry (ETAAS). The method was subsequently applied for the estimation of background metal blood values in the Brazilian population. In general, the mean concentrations of As, Cd, Cu, Mn, Ni, Pb, and Se in blood were 1.1, 0.4, 890, 9.6, 2.1, 65.4, and 89.3 microg/L, respectively, and are in agreement with other global populations. Influences of age, gender, smoking habits, alcohol consumption, and geographical variation on the values were also considered. Smoking habits influenced the levels of Cd in blood. The levels of Cu, Mn, and Pb were significantly correlated with gender, whereas Cu and Pb were significantly correlated with age. There were also interesting differences in Mn and Se levels in the population living in the north of Brazil compared to the south.
Nunes JA, Batista BL, Rodrigues JL, Caldas NM, Neto JA, Barbosa F Jr.
Laboratorio de Toxicologia e Essencialidade de Metais, Depto. de Analises Clinicas, Toxicologicas e Bromatologicas, Faculdade de Ciencias Farmaceuticas de Ribeirao Preto-USP, Ribeirao Preto-SP, Brazil.
Abstract
Throughout the world, biomonitoring has become the standard for assessing exposure of individuals to toxic elements as well as for responding to serious environmental public health problems. However, extensive biomonitoring surveys require rapid and simple analytical methods. Thus, a simple and high-throughput method is proposed for the determination of arsenic (As), cadmium (Cd), copper (Cu), manganese (Mn), nickel (Ni), lead (Pb), and selenium (Se) in blood samples by using inductively coupled plasma-mass spectrometry (ICP-MS). Prior to analysis, 200 microl of blood samples was mixed with 500 microl of 10% v/v tetramethylammonium hydroxide (TMAH) solution, incubated for 10 min, and subsequently diluted to 10 ml with a solution containing 0.05% w/v ethylenediamine tetraacetic acid (EDTA) + 0.005% v/v Triton X-100. After that, samples were directly analyzed by ICP-MS (ELAN DRC II). Rhodium was selected as an internal standard with matrix-matching calibration. Method detection limits were 0.08, 0.04, 0.5, 0.09, 0.12, 0.04, and 0.1 microg//L for As, Cd, Cu, Mn, Ni, Pb, and Se, respectively. Validation data are provided based on the analysis of blood samples from the trace elements inter-\comparison program operated by the Institut National de Sante Publique du Quebec, Canada. Additional validation was provided by the analysis of human blood samples by the proposed method and by using electrothermal atomic absorption spectrometry (ETAAS). The method was subsequently applied for the estimation of background metal blood values in the Brazilian population. In general, the mean concentrations of As, Cd, Cu, Mn, Ni, Pb, and Se in blood were 1.1, 0.4, 890, 9.6, 2.1, 65.4, and 89.3 microg/L, respectively, and are in agreement with other global populations. Influences of age, gender, smoking habits, alcohol consumption, and geographical variation on the values were also considered. Smoking habits influenced the levels of Cd in blood. The levels of Cu, Mn, and Pb were significantly correlated with gender, whereas Cu and Pb were significantly correlated with age. There were also interesting differences in Mn and Se levels in the population living in the north of Brazil compared to the south.
Genetic variants associated with arsenic metabolism within human arsenic (+3 oxidation state) methyltransferase show wide variation across multiple populations.
Arch Toxicol. 2011 Feb;85(2):119-25. Epub 2010 Jun 23.
Fujihara J, Yasuda T, Kato H, Yuasa I, Panduro A, Kunito T, Takeshita H.
Department of Legal Medicine, Faculty of Medicine, Shimane University, 89-1 Enya, Izumo, 693-8501, Shimane, Japan.
Abstract
Human arsenic (+3 oxidation state) methyltransferase (AS3MT) is known to catalyze the methylation of arsenite. The objective of this study was to investigate the diversity of the AS3MT gene in Mexican and German populations. The distribution of 18 single nucleotide polymorphisms (SNPs) in AS3MT was assessed on healthy individuals: 38 Mestizo, 69 Nahuas, 50 Huicholes, and 32 Germans. All 18 SNPs were polymorphic in the German and Mexican populations. Of the three Mexican populations, a minor allele frequency was the highest in the Mestizo, followed by the Nahuas and Huicholes. In the German and three Mexican groups, haplotype #1(TATAGAAGTCTTCATGAC) was the most predominant. Seven haplotypes were newly found in the German and three Mexican populations. The D' values between SNP pairs were high in the German and Nahua populations; they had a similar pattern. The pattern of the Mestizo was more similar to the African than to the other Mexican populations. Huicholes had a moderate pattern of the African and German/Nahua populations. The network had three clusters. One originated in the African population and another may have originated in an Asian (Chinese and/or Japanese) population. The third one may have originated among Caucasians. This study is the first to demonstrate the existence of genetic heterogeneity in the distribution of 18 SNPs in AS3MT of German and Mexican populations.
Fujihara J, Yasuda T, Kato H, Yuasa I, Panduro A, Kunito T, Takeshita H.
Department of Legal Medicine, Faculty of Medicine, Shimane University, 89-1 Enya, Izumo, 693-8501, Shimane, Japan.
Abstract
Human arsenic (+3 oxidation state) methyltransferase (AS3MT) is known to catalyze the methylation of arsenite. The objective of this study was to investigate the diversity of the AS3MT gene in Mexican and German populations. The distribution of 18 single nucleotide polymorphisms (SNPs) in AS3MT was assessed on healthy individuals: 38 Mestizo, 69 Nahuas, 50 Huicholes, and 32 Germans. All 18 SNPs were polymorphic in the German and Mexican populations. Of the three Mexican populations, a minor allele frequency was the highest in the Mestizo, followed by the Nahuas and Huicholes. In the German and three Mexican groups, haplotype #1(TATAGAAGTCTTCATGAC) was the most predominant. Seven haplotypes were newly found in the German and three Mexican populations. The D' values between SNP pairs were high in the German and Nahua populations; they had a similar pattern. The pattern of the Mestizo was more similar to the African than to the other Mexican populations. Huicholes had a moderate pattern of the African and German/Nahua populations. The network had three clusters. One originated in the African population and another may have originated in an Asian (Chinese and/or Japanese) population. The third one may have originated among Caucasians. This study is the first to demonstrate the existence of genetic heterogeneity in the distribution of 18 SNPs in AS3MT of German and Mexican populations.
Spatial-temporal and cancer risk assessment of selected hazardous air pollutants in Seattle.
Environ Int. 2011 Jan;37(1):11-7.
Wu CF, Liu LJ, Cullen A, Westberg H, Williamson J.
Department of Public Health, National Taiwan University, Taipei, Taiwan. changfu@ntu.edu.tw
Abstract
In the Seattle Air Toxics Monitoring Pilot Program, we measured 15 hazardous air pollutants (HAPs) at 6 sites for more than a year between 2000 and 2002. Spatial-temporal variations were evaluated with random-effects models and principal component analyses. The potential health risks were further estimated based on the monitored data, with the incorporation of the bootstrapping technique for the uncertainty analysis. It is found that the temporal variability was generally higher than the spatial variability for most air toxics. The highest temporal variability was observed for tetrachloroethylene (70% temporal vs. 34% spatial variability). Nevertheless, most air toxics still exhibited significant spatial variations, even after accounting for the temporal effects. These results suggest that it would require operating multiple air toxics monitoring sites over a significant period of time with proper monitoring frequency to better evaluate population exposure to HAPs. The median values of the estimated inhalation cancer risks ranged between 4.3 × 10⁻⁵ and 6.0 × 10⁻⁵, with the 5th and 95th percentile levels exceeding the 1 in a million level. VOCs as a whole contributed over 80% of the risk among the HAPs measured and arsenic contributed most substantially to the overall risk associated with metals.
Wu CF, Liu LJ, Cullen A, Westberg H, Williamson J.
Department of Public Health, National Taiwan University, Taipei, Taiwan. changfu@ntu.edu.tw
Abstract
In the Seattle Air Toxics Monitoring Pilot Program, we measured 15 hazardous air pollutants (HAPs) at 6 sites for more than a year between 2000 and 2002. Spatial-temporal variations were evaluated with random-effects models and principal component analyses. The potential health risks were further estimated based on the monitored data, with the incorporation of the bootstrapping technique for the uncertainty analysis. It is found that the temporal variability was generally higher than the spatial variability for most air toxics. The highest temporal variability was observed for tetrachloroethylene (70% temporal vs. 34% spatial variability). Nevertheless, most air toxics still exhibited significant spatial variations, even after accounting for the temporal effects. These results suggest that it would require operating multiple air toxics monitoring sites over a significant period of time with proper monitoring frequency to better evaluate population exposure to HAPs. The median values of the estimated inhalation cancer risks ranged between 4.3 × 10⁻⁵ and 6.0 × 10⁻⁵, with the 5th and 95th percentile levels exceeding the 1 in a million level. VOCs as a whole contributed over 80% of the risk among the HAPs measured and arsenic contributed most substantially to the overall risk associated with metals.
Carcinogenic effects of "whole-life" exposure to inorganic arsenic in CD1 mice.
Toxicol Sci. 2011 Jan;119(1):73-83. Epub 2010 Oct 11.
Tokar EJ, Diwan BA, Ward JM, Delker DA, Waalkes MP.
Laboratory of Comparative Carcinogenesis, National Cancer Institute, National Institute of Environmental Health Sciences, The National Institute of Environmental Health Sciences, Research Triangle Park, Raleigh, North Carolina 27709, USA.
Abstract
In a previously developed mouse model, arsenic exposure in utero induces tumors at multiple sites in the offspring as adults, often duplicating human targets. However, human environmental inorganic arsenic exposure occurs during the entire life span, not just part of gestation. Thus, "whole-life" inorganic arsenic carcinogenesis in mice was studied. CD1 mice were exposed to 0, 6, 12, or 24 ppm arsenic in the drinking water 2 weeks prior to breeding, during pregnancy, lactation, and after weaning through adulthood. Tumors were assessed in offspring until 2 years of age. Arsenic induced dose-related increases in lung adenocarcinoma (both sexes), hepatocellular carcinoma (both sexes), gallbladder tumors (males), and uterine carcinomas. Arsenic induced dose-related increases in ovarian tumors (including carcinomas) starting with the lowest dose. Adrenal tumors increased at all doses (both sexes). Arsenic-induced lung and liver cancers were highly enriched for cancer stem cells, consistent with prior work with skin cancers stimulated by prenatal arsenic. Reproductive tract tumors overexpressed cyclooxygenase-2 and estrogen receptor-α. Arsenic target sites were remarkably similar to prior transplacental studies, although tumors from whole-life exposure were generally more aggressive and frequent. This may indicate that arsenic-induced events in utero dictate target site in some tissues, whereas other exposure periods of arsenic enhance incidence or progression, though other factors could be at play, like cumulative dose. Whole-life arsenic exposure induced tumors at dramatically lower external doses than in utero arsenic only while more realistically duplicating human exposure.
Tokar EJ, Diwan BA, Ward JM, Delker DA, Waalkes MP.
Laboratory of Comparative Carcinogenesis, National Cancer Institute, National Institute of Environmental Health Sciences, The National Institute of Environmental Health Sciences, Research Triangle Park, Raleigh, North Carolina 27709, USA.
Abstract
In a previously developed mouse model, arsenic exposure in utero induces tumors at multiple sites in the offspring as adults, often duplicating human targets. However, human environmental inorganic arsenic exposure occurs during the entire life span, not just part of gestation. Thus, "whole-life" inorganic arsenic carcinogenesis in mice was studied. CD1 mice were exposed to 0, 6, 12, or 24 ppm arsenic in the drinking water 2 weeks prior to breeding, during pregnancy, lactation, and after weaning through adulthood. Tumors were assessed in offspring until 2 years of age. Arsenic induced dose-related increases in lung adenocarcinoma (both sexes), hepatocellular carcinoma (both sexes), gallbladder tumors (males), and uterine carcinomas. Arsenic induced dose-related increases in ovarian tumors (including carcinomas) starting with the lowest dose. Adrenal tumors increased at all doses (both sexes). Arsenic-induced lung and liver cancers were highly enriched for cancer stem cells, consistent with prior work with skin cancers stimulated by prenatal arsenic. Reproductive tract tumors overexpressed cyclooxygenase-2 and estrogen receptor-α. Arsenic target sites were remarkably similar to prior transplacental studies, although tumors from whole-life exposure were generally more aggressive and frequent. This may indicate that arsenic-induced events in utero dictate target site in some tissues, whereas other exposure periods of arsenic enhance incidence or progression, though other factors could be at play, like cumulative dose. Whole-life arsenic exposure induced tumors at dramatically lower external doses than in utero arsenic only while more realistically duplicating human exposure.
Arsenic-associated oxidative stress, inflammation, and immune disruption in human placenta and cord blood.
Environ Health Perspect. 2011 Feb;119(2):258-64. Epub 2010 Oct 12.
Ahmed S, Mahabbat-E Khoda S, Rekha RS, Gardner RM, Ameer SS, Moore S, Ekström EC, Vahter M, Raqib R.
International Centre for Diarrhoeal Disease Research, Bangladesh, Dhaka, Bangladesh.
Abstract
Background: Arsenic (As) exposure during pregnancy induces oxidative stress and increases the risk of fetal loss and low birth weight.Objectives: In this study we aimed to elucidate the effects of As exposure on immune markers in the placenta and cord blood, and the involvement of oxidative stress.Methods: Pregnant women were enrolled around gestational week (GW) 8 in our longitudinal, population-based, mother-child cohort in Matlab, an area in rural Bangladesh with large variations in As concentrations in well water. Women (n = 130) delivering at local clinics were included in the present study. We collected maternal urine twice during pregnancy (GW8 and GW30) for measurements of As, and placenta and cord blood at delivery for assessment of immune and inflammatory markers. Placental markers were measured by immunohistochemistry, and cord blood cytokines by multiplex cytokine assay.Results: In multivariable adjusted models, maternal urinary As (U-As) exposure both at GW8 and at GW30 was significantly positively associated with placental markers of 8-oxoguanine (8-oxoG) and interleukin-1β (IL-1β); U-As at GW8, with tumor necrosis factor-α (TNFα) and interferon-γ (IFNγ); and U-As at GW30, with leptin; U-As at GW8 was inversely associated with CD3+ T cells in the placenta. Cord blood cytokines (IL-1β, IL-8, IFNγ, TNFα) showed a U-shaped association with U-As at GW30. Placental 8-oxoG was significantly positively associated with placental proinflammatory cytokines. Multivariable adjusted analyses suggested that enhanced placental cytokine expression (TNFα and IFNγ) was primarily influenced by oxidative stress, whereas leptin expression appeared to be mostly mediated by As, and IL-1β appeared to be influenced by both oxidative stress and As.Conclusion: As exposure during pregnancy appeared to enhance placental inflammatory responses (in part by increasing oxidative stress), reduce placental T cells, and alter cord blood cytokines. These findings suggest that effects of As on immune function may contribute to impaired fetal and infant health.
Ahmed S, Mahabbat-E Khoda S, Rekha RS, Gardner RM, Ameer SS, Moore S, Ekström EC, Vahter M, Raqib R.
International Centre for Diarrhoeal Disease Research, Bangladesh, Dhaka, Bangladesh.
Abstract
Background: Arsenic (As) exposure during pregnancy induces oxidative stress and increases the risk of fetal loss and low birth weight.Objectives: In this study we aimed to elucidate the effects of As exposure on immune markers in the placenta and cord blood, and the involvement of oxidative stress.Methods: Pregnant women were enrolled around gestational week (GW) 8 in our longitudinal, population-based, mother-child cohort in Matlab, an area in rural Bangladesh with large variations in As concentrations in well water. Women (n = 130) delivering at local clinics were included in the present study. We collected maternal urine twice during pregnancy (GW8 and GW30) for measurements of As, and placenta and cord blood at delivery for assessment of immune and inflammatory markers. Placental markers were measured by immunohistochemistry, and cord blood cytokines by multiplex cytokine assay.Results: In multivariable adjusted models, maternal urinary As (U-As) exposure both at GW8 and at GW30 was significantly positively associated with placental markers of 8-oxoguanine (8-oxoG) and interleukin-1β (IL-1β); U-As at GW8, with tumor necrosis factor-α (TNFα) and interferon-γ (IFNγ); and U-As at GW30, with leptin; U-As at GW8 was inversely associated with CD3+ T cells in the placenta. Cord blood cytokines (IL-1β, IL-8, IFNγ, TNFα) showed a U-shaped association with U-As at GW30. Placental 8-oxoG was significantly positively associated with placental proinflammatory cytokines. Multivariable adjusted analyses suggested that enhanced placental cytokine expression (TNFα and IFNγ) was primarily influenced by oxidative stress, whereas leptin expression appeared to be mostly mediated by As, and IL-1β appeared to be influenced by both oxidative stress and As.Conclusion: As exposure during pregnancy appeared to enhance placental inflammatory responses (in part by increasing oxidative stress), reduce placental T cells, and alter cord blood cytokines. These findings suggest that effects of As on immune function may contribute to impaired fetal and infant health.
Solidification of arsenic and heavy metal containing tailings using cement and blast furnace slag.
Environ Geochem Health. 2011 Jan;33 Suppl 1:151-8. Epub 2010 Nov 10.
Kim JW, Jung MC.
Department of Energy & Mineral Resources Engineering, Sejong University, Seoul, Korea.
Abstract
The objective of this study is to examine the solidification of toxic elements in tailings by the use of cement and blast furnace slag. Tailings samples were taken at an Au-Ag mine in Korea. To examine the best mixing ratio of tailings and the mixture of ordinary Portland cement (OPC) and blast furnace slag (SG) of 5:5, 6:6, 7:3, and 8:2, the 7:3 ratio of tailings and OPC+SG was adapted. In addition, the mixing ratios of water and OPC + SG were applied to 10, 20, and 30 wt%. After 7, 14, and 28 days' curing, the UCS test was undertaken. A relatively high strength of solidified material (137.2 kg cm⁻² in average of 3 samples) at 28 days' curing was found in 20 wt% of water content (WC). This study also examined the leachability of arsenic and heavy metals (Cd, Cu, Pb, and Zn) under the Korean Standard Leaching Test, and it showed that the reductions in leachabilities of As and heavy metals of solidified samples were ranged from 76 to 99%. Thus, all the solidified samples were within the guidelines for special and hazardous waste materials by the Waste Management Act in Korea. In addition, the result of freeze-thaw cycle test of the materials indicated that the durability of the materials was sufficient. In conclusion, solidification using a 7:3 mixing ratio of tailings and a 1:1 mixture of OPC + SG with 20% of WC is one of the best methods for the remediation of arsenic and heavy metals in tailings and other contaminated materials.
Kim JW, Jung MC.
Department of Energy & Mineral Resources Engineering, Sejong University, Seoul, Korea.
Abstract
The objective of this study is to examine the solidification of toxic elements in tailings by the use of cement and blast furnace slag. Tailings samples were taken at an Au-Ag mine in Korea. To examine the best mixing ratio of tailings and the mixture of ordinary Portland cement (OPC) and blast furnace slag (SG) of 5:5, 6:6, 7:3, and 8:2, the 7:3 ratio of tailings and OPC+SG was adapted. In addition, the mixing ratios of water and OPC + SG were applied to 10, 20, and 30 wt%. After 7, 14, and 28 days' curing, the UCS test was undertaken. A relatively high strength of solidified material (137.2 kg cm⁻² in average of 3 samples) at 28 days' curing was found in 20 wt% of water content (WC). This study also examined the leachability of arsenic and heavy metals (Cd, Cu, Pb, and Zn) under the Korean Standard Leaching Test, and it showed that the reductions in leachabilities of As and heavy metals of solidified samples were ranged from 76 to 99%. Thus, all the solidified samples were within the guidelines for special and hazardous waste materials by the Waste Management Act in Korea. In addition, the result of freeze-thaw cycle test of the materials indicated that the durability of the materials was sufficient. In conclusion, solidification using a 7:3 mixing ratio of tailings and a 1:1 mixture of OPC + SG with 20% of WC is one of the best methods for the remediation of arsenic and heavy metals in tailings and other contaminated materials.
The immobilisation and retention of soluble arsenic, cadmium and zinc by biochar.
Environ Pollut. 2011 Feb;159(2):474-80. Epub 2010 Nov 24.
Beesley L, Marmiroli M.
Faculty of Science, Liverpool John Moores University, Liverpool L3 3AF, UK. l.beesley@macaulay.ac.uk
Abstract
Water-soluble inorganic pollutants may constitute an environmental toxicity problem if their movement through soils and potential transfer to plants or groundwater is not arrested. The capability of biochar to immobilise and retain arsenic (As), cadmium (Cd) and zinc (Zn) from a multi-element contaminated sediment-derived soil was explored by a column leaching experiment and scanning electron microanalysis (SEM/EDX). Sorption of Cd and Zn to biochar's surfaces assisted a 300 and 45-fold reduction in their leachate concentrations, respectively. Retention of both metals was not affected by considerable leaching of water-soluble carbon from biochar, and could not be reversed following subsequent leaching of the sorbant biochar with water at pH 5.5. Weakly water-soluble As was also retained on biochar's surface but leachate concentrations did not duly decline. It is concluded that biochar can rapidly reduce the mobility of selected contaminants in this polluted soil system, with especially encouraging results for Cd.
Beesley L, Marmiroli M.
Faculty of Science, Liverpool John Moores University, Liverpool L3 3AF, UK. l.beesley@macaulay.ac.uk
Abstract
Water-soluble inorganic pollutants may constitute an environmental toxicity problem if their movement through soils and potential transfer to plants or groundwater is not arrested. The capability of biochar to immobilise and retain arsenic (As), cadmium (Cd) and zinc (Zn) from a multi-element contaminated sediment-derived soil was explored by a column leaching experiment and scanning electron microanalysis (SEM/EDX). Sorption of Cd and Zn to biochar's surfaces assisted a 300 and 45-fold reduction in their leachate concentrations, respectively. Retention of both metals was not affected by considerable leaching of water-soluble carbon from biochar, and could not be reversed following subsequent leaching of the sorbant biochar with water at pH 5.5. Weakly water-soluble As was also retained on biochar's surface but leachate concentrations did not duly decline. It is concluded that biochar can rapidly reduce the mobility of selected contaminants in this polluted soil system, with especially encouraging results for Cd.
Influence of natural organic matter on As transport and retention.
Environ Sci Technol. 2011 Jan 15;45(2):546-53. Epub 2010 Dec 13.
Sharma P, Rolle M, Kocar B, Fendorf S, Kappler A.
Center for Applied Geosciences, University of Tübingen, Tübingen, Germany.
Abstract
Natural organic matter (NOM) can affect the behavior of arsenic within surface and subsurface environments. We used batch and column experiments to determine the effect of peat humic acids (PHA), groundwater fulvic acids (GFA), and a soil organic matter (SOM) extract on As sorption/transport in ferrihydrite-coated sand columns. A reactive transport model was used to quantitatively interpret the transport of As in flow-through column (breakthrough) experiments. We found that As(III) breakthrough was faster than As(V) by up to 18% (with OM) and 14% (without OM). The most rapid breakthrough occurred in systems containing SOM and GFA. Dialysis and ultrafiltration of samples from breakthrough experiments showed that in OM-containing systems, As was transported mostly as free (noncomplexed) dissolved As but also as ternary As-Fe-OM colloids and dissolved complexes. In OM-free systems, As was transported in colloidal form or as a free ion. During desorption, more As(III) desorbed (23-37%) than As(V) (10-16%), and SOM resulted in the highest and OM-free systems the lowest amount of desorption. Overall, our experiments reveal that (i) NOM can enhance transport/mobilization of As, (ii) different fractions of NOM are capable of As mobilization, and (iii) freshly extracted SOM (from a forest soil) had greater impact on As transport than purified GFA/PHA.
Sharma P, Rolle M, Kocar B, Fendorf S, Kappler A.
Center for Applied Geosciences, University of Tübingen, Tübingen, Germany.
Abstract
Natural organic matter (NOM) can affect the behavior of arsenic within surface and subsurface environments. We used batch and column experiments to determine the effect of peat humic acids (PHA), groundwater fulvic acids (GFA), and a soil organic matter (SOM) extract on As sorption/transport in ferrihydrite-coated sand columns. A reactive transport model was used to quantitatively interpret the transport of As in flow-through column (breakthrough) experiments. We found that As(III) breakthrough was faster than As(V) by up to 18% (with OM) and 14% (without OM). The most rapid breakthrough occurred in systems containing SOM and GFA. Dialysis and ultrafiltration of samples from breakthrough experiments showed that in OM-containing systems, As was transported mostly as free (noncomplexed) dissolved As but also as ternary As-Fe-OM colloids and dissolved complexes. In OM-free systems, As was transported in colloidal form or as a free ion. During desorption, more As(III) desorbed (23-37%) than As(V) (10-16%), and SOM resulted in the highest and OM-free systems the lowest amount of desorption. Overall, our experiments reveal that (i) NOM can enhance transport/mobilization of As, (ii) different fractions of NOM are capable of As mobilization, and (iii) freshly extracted SOM (from a forest soil) had greater impact on As transport than purified GFA/PHA.
Evidence from chile that arsenic in drinking water may increase mortality from pulmonary tuberculosis.
Am J Epidemiol. 2011 Feb 15;173(4):414-20. Epub 2010 Dec 29.
Smith AH, Marshall G, Yuan Y, Liaw J, Ferreccio C, Steinmaus C.
Abstract
Arsenic in drinking water causes increased mortality from several cancers, ischemic heart disease, bronchiectasis, and other diseases. This paper presents the first evidence relating arsenic exposure to pulmonary tuberculosis, by estimating mortality rate ratios for Region II of Chile compared with Region V for the years 1958-2000. The authors compared mortality rate ratios with time patterns of arsenic exposure, which increased abruptly in 1958 in Region II and then declined starting in 1971. Tuberculosis mortality rate ratios in men started increasing in 1968, 10 years after high arsenic exposure commenced. The peak male 5-year mortality rate ratio occurred during 1982-1986 (rate ratio = 2.1, 95% confidence interval: 1.7, 2.6; P < 0.001) and subsequently declined. Mortality rates in women were also elevated but with fewer excess pulmonary tuberculosis deaths (359 among men and 95 among women). The clear rise and fall of tuberculosis mortality rate ratios in men following high arsenic exposure are consistent with a causal relation. The findings are biologically plausible in view of evidence that arsenic is an immunosuppressant and also a cause of chronic lung disease. Finding weaker associations in women is unsurprising, because this is true of most arsenic-caused health effects. Confirmatory evidence is needed from other arsenic-exposed populations.
Smith AH, Marshall G, Yuan Y, Liaw J, Ferreccio C, Steinmaus C.
Abstract
Arsenic in drinking water causes increased mortality from several cancers, ischemic heart disease, bronchiectasis, and other diseases. This paper presents the first evidence relating arsenic exposure to pulmonary tuberculosis, by estimating mortality rate ratios for Region II of Chile compared with Region V for the years 1958-2000. The authors compared mortality rate ratios with time patterns of arsenic exposure, which increased abruptly in 1958 in Region II and then declined starting in 1971. Tuberculosis mortality rate ratios in men started increasing in 1968, 10 years after high arsenic exposure commenced. The peak male 5-year mortality rate ratio occurred during 1982-1986 (rate ratio = 2.1, 95% confidence interval: 1.7, 2.6; P < 0.001) and subsequently declined. Mortality rates in women were also elevated but with fewer excess pulmonary tuberculosis deaths (359 among men and 95 among women). The clear rise and fall of tuberculosis mortality rate ratios in men following high arsenic exposure are consistent with a causal relation. The findings are biologically plausible in view of evidence that arsenic is an immunosuppressant and also a cause of chronic lung disease. Finding weaker associations in women is unsurprising, because this is true of most arsenic-caused health effects. Confirmatory evidence is needed from other arsenic-exposed populations.
Subscribe to:
Posts (Atom)
