sos arsenic

The arsenic for phosphorus swap is accidental, rather than a facultative one, and the question whether arsenic is nonessential or toxic is quantitative, not a qualitative one.

2011-09-28T09:14:00.001+02:00

Sci Total Environ. 409 (2011) 4889–4890.
Dani SU.
Department of Medicine I and Clinical Chemistry, University of Heidelberg, Germany.
Abstract - Arsenic shares many physicochemical properties with phosphorus, so that arsenic can be taken up inadvertently by cells through the pathways for phosphorus. As a phosphate analog, arsenate competes with phosphate and enters cells via phosphate transporters. In the cell, arsenate can be recognized as a substrate by enzymes that usually use phosphate as a substrate. The phosphate for arsenate swap results in wasteful 'futile cycles' in metabolic pathways, uncoupled oxidative phosphorylation and extreme DNA instability. The disrupting metabolic effects of arsenic have an evolutionary meaning, so that all living organisms-from chemoautotrophic organisms that grow by reducing or oxidizing arsenic to metazoan-carry highly conserved arsenic resistance genes. Arsenic resistance can result from different strategies including selective transport to maximize phosphate uptake and minimize entry of arsenate, active transport to export arsenate, arsenic storage in specialized compartments, enzyme selectivity toward phosphate, and increased efficiency of DNA repair systems. None of these strategies is infallible, though, and susceptibility to arsenic toxicity varies between taxa in many orders of magnitude. Even arsenic-hypertolerant organisms will stop to grow and will eventually die when exposed to arsenic over species-specific resistance limits. The arsenic for phosphorus swap is an accidental one, it does not warrant a conclusion in favor of the essentiality of arsenic to life as we know it.

Ohio Leads List of Top 20 US States With Toxic Air.

2011-07-26T22:29:00.000+02:00

From Reuters Health Information.

WASHINGTON (Reuters) Jul 21 - People living in Ohio, Pennsylvania and Florida are most at risk in the United States from toxic emissions spewing from coal and oil-fired power plants, two leading American environmental groups said in a report on Wednesday.

Electricity generation and chemical processing were the top culprits for dangerous emissions, which can lead to or worsen ailments such as asthma and cancer, according to the report by the Natural Resources Defense Council and Physicians for Social Responsibility.

While Ohio topped the list of 20 states most affected by toxic air pollution, Kentucky and Maryland were ranked fourth and fifth. Next were Indiana, Michigan, West Virginia, Georgia and North Carolina.

"Power plants are the biggest industrial toxic air polluters in our country, putting children and families at risk by dumping deadly and dangerous poisons into the air we breathe," said Dr. Dan Lashof, director of the climate center at the Natural Resources Defense Council.

The study, an analysis of toxic emissions data from 2009 released last month by the U.S. Environmental Protection Agency, found that coal and oil-fired plants were responsible for nearly half of all toxic air pollution in America.

The report was prepared by comparing data from the electric utilities sector to those from other industry sectors and ranked on the basis of total emissions by sector.

In 2009, electricity generation in America was responsible for 49% of all industrial toxic air pollution and accounted for about 75% of all mercury air pollution, the study said.

The findings underline the need for strong action by the Environmental Protection Agency to spur industry to clean up the emissions, Lashof said.

Amendments designed to block the U.S. environmental regulator's air pollution standards are expected to be brought before the U.S. House of Representatives this week, the groups said.

In February, the Republican-led House, in a bid to cut government spending and avoid a U.S. default on financial commitments, voted to thwart the EPA from making rules to limit mercury and other toxic emissions from cement plants.

SOURCE: http://bit.ly/qWu308
Natural Resources Defense Council, online July 20, 2011.

2000 visitors from 85 countries.

2011-07-26T22:19:00.000+02:00

Sosarsenic has completed one year with 2000 visitors from 85 countries. We appreciate your interest in our blog!

Chicken feed effects questioned, according to a 2004 report by John Vandiver.

2011-06-20T20:29:00.002+02:00

John Vandiver / Daily Times (Maryland) 4 jan 04

ALISBURY -- Since the 1940s, the poultry industry has used certain arsenic-based ingredients as chicken feed additives, but some researchers have started to scrutinize the long-standing practice because of possible health and environmental risks.

A common arsenic used by chicken companies is roxarsone, which is mixed with feed to control intestinal parasites and promote growth, according to research chemists.

After consuming roxarsone, the arsenic additive approved for use by the Food and Drug Administration, chickens then excrete the compound in a chemical form that is virtually unchanged.

On the Delmarva Peninsula, poultry growers raise more than 500 million birds annually, producing vast amounts of chicken litter that is spread on farmland as manure.

Questions about potential risks associated with the use of roxarsone center on the practice of spreading manure, not the consumption of poultry. Very low levels of roxarsone are retained in chicken. The FDA limits the amount to 0.5 parts per million in muscle tissue.

Dr. Ellen Silbergeld, a researcher from the Johns Hopkins School of Public Health, said the poultry industry's practice of using arsenic compounds in its feed is something that has not been studied.

"It's an issue everybody is trying to pretend doesn't exist," she said.

Silbergeld, who is leading a study on the effects of antibiotic resistant illnesses among Lower Shore poultry workers, said she intends to initiate a research project examining what risks are associated with exposure to arsenic on industry workers.

"The arsenicals are there. Are they significant amounts? That's the issue," she said.

In Maryland, 338,679 tons of litter is produced annually, 258,081 of which comes from the four Lower Shore counties, according to the Maryland Department of Agriculture.

For years, medical experts have warned that chronic human exposure to arsenic could lead to certain forms of cancer.

The National Academies, which advises the federal government on a range of health and science issues, reported to Congress in 2001 "that the data indicate arsenic causes cancer in humans at doses that are close to the drinking water concentrations that occur in the United States."

Scientists and environmentalists have debated the impact of arsenic on water quality and pollution in coal burning states for several years. The meat industry's use of arsenic has received less attention, some researchers suggest.

Executives from Perdue Farms Inc. could not be reached for comment on the composition of their feed, though a company spokesman said roxarsone is used "industry-wide."

Claims of cancer link

In a small Arkansas town surrounded by farmland, a group of residents have filed a lawsuit against Alpharma Inc. -- the manufacturer of the feed additive 3-Nitro -- and several poultry companies that use the product, including Tyson Foods Inc. Roxarsone is an active ingredient in 3-Nitro, according to Alpharma's Web site.

John Baker, an Arkansas attorney, said he is representing 100 clients from the community of Prairie Grove who are sick or have had family members die from alleged exposure to roxarsone.

The first of several lawsuits was filed Dec. 16, 2004, a case that includes cancer survivors and the parents of four children who died from leukemia and brain cancer.

According to Baker, several residents in the town of 2,500 have been diagnosed with rare cancers that usually occur at a rate of one in a million.

"We've tested homes of clients and found this stuff there. This arsenic is airborne and is inhaled," he said.

The Arkansas Department of Health, however, came to a different conclusion. Health officials one year ago investigated and ruled that there is no evidence Prairie Grove residents suffer cancer rates at levels disproportionate to other parts of the state.

Unsatisfied with the department's findings, the plaintiffs hired their own investigators.

"We don't think their data is accurate," Baker said.

Poultry industry representatives defend the use of roxarsone, arguing that no research supports the claim that the feed additive is linked to cancer.

Richard Lobb, a spokesman for the National Chicken Council, an industry trade group, questioned the motives of the attorneys and their clients.

"This is totally without merit. They're hoping to get a big payoff. (Roxarsone) is FDA approved and I don't think there are any real scientific concerns," he said.

Poultry, regulations and courts

The Arkansas lawsuit is the latest in a flurry of recent legal activity directed against the poultry industry.

On Nov. 10, 2003, a federal judge in Kentucky during a pretrial motion made a ruling that some industry observers suggest could have far-reaching consequences.

U.S. District Judge Joseph McKinley ruled that Tyson Chicken Inc. -- a subsidiary of Tyson Foods -- shares responsibility with growers for reporting air pollution violations, rejecting arguments by officials for the poultry company that its contract chicken growers are solely responsible for the environmental problems that stem from their farm operations.

The lawsuit filed by the Sierra Club against Tyson resembles the debate in Maryland over whether integrators should be held responsible for nutrient management practices on their growers' farms.

Theresa Pierno, vice president of environmental protection at the Chesapeake Bay Foundation, has said the Kentucky case could serve as the legal precedent to file similar claims against Maryland corporations.

William Satterfield, executive director of the regional trade group Delmarva Poultry Industry Inc., said his group keeps corporations here informed of legal action in other parts of the country.

"Certainly these things are a concern. If suits can be filed in one state they can be filed in another," he said.

In recent years, opposition against the industry has grown, Satterfield said.

"More and more people are challenging our industry and the way we feed the world ... We used to do more work on growing issues, now we're dealing with more of these external issues," he said.

Water, soil and cancer rates

Cancer rates on the Lower Shore are among the highest in Maryland and also exceed national averages, according to the American Cancer Society and regional medical experts.

Somerset County is a national leader, with a cancer death rate of 267 cases for every 100,000 people.

Nationwide, cancer deaths claimed 206 people out of every 100,000 from 1994 to 1999. Rates in Wicomico and Worcester counties also surpassed national and state averages with a statistical measurement of 233 deaths and 229 deaths per 100,000 people.

Health care experts on the Lower Shore have long debated why the rates here are so high, providing more questions than answers.

Explanations have ranged from poor eating habits on the Lower Shore to high numbers of people without health insurance and environmental factors.

In 2001, the National Academy determined that enough evidence existed to draw the conclusion that arsenic rates commonly found in the country's water supply were enough to lead to some forms of cancer. The findings came at a time when President Bush was working to repeal a Clinton administration proposal to reduce the allowable amount of arsenic in drinking water from 50 micrograms per liter to 10 micrograms per liter, which is the health standard used by the European Union and World Health Organization.

In March 2001, the Environmental Protection Agency withdrew the pending rule change, restoring the 50 micrograms standard.

During the political debate over arsenic limits, the Maryland Department of Environment commissioned a study of arsenic levels in all major aquifers on the Maryland Coastal Plain.

The results of the study, performed by the Maryland Geological Survey, were expected to be published in the summer of 2004, project leader David Bolton said.

The data collected from wells and aquifers from the Upper Shore to the Lower Shore indicate that arsenic levels are normal.

"There is nothing to suggest arsenic levels are a problem in drinking water," Bolton said.

Tests on Eastern Shore wells in most cases showed arsenic levels of 2 micrograms per liter -- well below the legal limit of 50 micrograms and below the 10 micrograms levels recommended by the EPA under the Clinton administration, he said.

In some aquifers found deep underground in Dorchester, Queen Anne's and Talbot counties, arsenic registers at a higher level than other parts of the coastal plain.

Bolton said levels as high as 42 micrograms per liter were found in Dorchester, still below the legal limit.

However, there is no evidence to show the practice of spreading arsenic-laced chicken litter on farmland is not responsible for Dorchester's higher arsenic levels, according to Bolton.

In addition to being an industrial byproduct, arsenic exists naturally in the environment. High concentrations are usually found in mining, copper smelting and coal burning states.

But natural causes explain the higher arsenic concentrations found in some parts of the shore, including Dorchester County, Bolton said.

Less information is available on how arsenic in litter affects soil and surface water.

According to the researchers with the U.S. Geological Survey, one chicken excretes about 150 milligrams of roxarsone in a 42-day growth period. Litter collected during that period contains between 30 to 50 milligrams per kilogram of total arsenic, according to the report.

On the Delmarva Peninsula, it means between 20 and 50 metric tons of arsenic are introduced to the environment annually by chicken farmers.

The U.S. Geological Survey is attempting to find out what impact the poultry industry's use of arsenic has on soil and water environments on Delmarva.

Silbergeld said she expects a better understanding of the health effects of roxarsone to emerge once scientists begin exploring the issue.

"We who've been doing research (on the poultry industry) really haven't looked at this," she said.

In the meantime, Gov. Robert Ehrlich has recommended that Maryland should explore alternative uses for poultry manure to help the industry and the environment.

Chicken litter could potentially serve as an alternative energy source, something Silbergeld says could be dangerous.

"If the levels of arsenic in waste are significant, burning it would be the worst thing to do," she said.

Source of this article:

http://www.mindfully.org/Farm/2004/Arsenic-Chicken-Roxarsone4jan04.htm

Better late than never: Arsenic compound may be banned in USA after decades of licit use.

2011-06-20T20:07:00.002+02:00

By Sergio U. Dani, Heidelberg, Germany.

People are sick, the environment is contaminated, companies face lawsuits. After almost 7 decades of licit use of 3-Nitro (Roxarsone) in animal feed all over the world, the FDA-Food and Drug Administration has finally found a reason to ban it in the United States of America. Roxarsone is an arsenic compound, and a number of arsenic compounds are known potent causes of cancer and a number of other human diseases. Alpharma, a subsidiary of Pfizer Inc. which has been law-suited in alleged cases of cancer provoqued by Roxarsone will suspend U.S. sales of the animal drug. Read the FDA PRESS RELEASE here…

For Immediate Release: June 8, 2011
Media Inquiries: Stephanie Yao
stephanie.yao@fda.hhs.gov

FDA: Pfizer will voluntarily suspend sale of animal drug 3-Nitro

Company takes action in response to FDA data

The U.S. Food and Drug Administration today announced that Alpharma, a subsidiary of Pfizer Inc., will voluntarily suspend U.S. sales of the animal drug 3-Nitro (Roxarsone), a product used by poultry producers since the 1940s.

The move follows a recent FDA study of 100 broiler chickens that detected inorganic arsenic, a known carcinogen, at higher levels in the livers of chickens treated with 3-Nitro compared with untreated chickens. FDA officials stress that the levels of inorganic arsenic detected were very low and that continuing to eat chicken as 3-Nitro is suspended from the market does not pose a health risk.

“FDA detected increased levels of inorganic arsenic in the livers of chickens treated with 3-Nitro, raising concerns of a very low but completely avoidable exposure to a carcinogen,” said Michael R. Taylor, FDA deputy commissioner for foods. “We are pleased to announce that the company is cooperating with us to protect the public health.”

Arsenic is in the environment as a naturally occurring substance or as a contaminant and is found in water, air, soil, and food. Published scientific reports have indicated that organic arsenic, a less toxic form of arsenic and the form present in 3-Nitro could transform into inorganic arsenic. In response, scientists from the FDA’s Center for Veterinary Medicine and the Center for Food Safety and Applied Nutrition developed an analytical method capable of detecting very low levels of inorganic arsenic in edible tissue.

Using the new method, FDA scientists recently found that the levels of inorganic arsenic in the livers of chickens treated with 3-Nitro were increased relative to levels in the livers of the untreated control chickens.

Alpharma decided to voluntarily suspend sale of 3-Nitro and to facilitate an orderly process for suspending use of the product in the United States. Alpharma’s plan provides for continued sales of 3-Nitro for 30 days from today. The company stated that allowing sales for this period will provide time for animal producers to transition to other treatment strategies and will help ensure that animal health and welfare needs are met.

In addition, the company is working with the FDA to examine all relevant scientific data regarding the use of 3-Nitro in animals.

In 1944, 3-Nitro became the first arsenic-containing new animal drug product approved by the FDA. It is used primarily in broiler chickens. Combined with other animal drugs, 3-Nitro has been used by some in the poultry industry to help control coccidiosis, a parasitic disease that affects the intestinal tracts of animals. It has also been used for weight gain, feed efficiency and improved pigmentation.

FDA has consulted with the U.S. Department of Agriculture and is working with Alpharma to minimize the impact on the animal agriculture industry as 3-Nitro is suspended from the market.

For more information:

• FDA Study on 3-Nitro (Roxarsone) and Chicken
http://www.fda.gov/AnimalVeterinary/SafetyHealth/ProductSafetyInformation/ucm257540.htm

• Questions and Answers Regarding 3-Nitro (Roxarsone)2
http://www.fda.gov/AnimalVeterinary/SafetyHealth/ProductSafetyInformation/ucm258313.htm

The FDA, an agency within the U.S. Department of Health and Human Services, protects the public health by assuring the safety, effectiveness, and security of human and veterinary drugs, vaccines and other biological products for human use, and medical devices. The agency also is responsible for the safety and security of our nation’s food supply, cosmetics, dietary supplements, products that give off electronic radiation, and for regulating tobacco products.

Arsenic in the aetiology of cancer.

2011-05-16T23:52:00.000+02:00

Mutat Res. 2006 Jun;612(3):215-46. Epub 2006 Mar 29.
Tapio S, Grosche B.
Federal Office for Radiation Protection, Department of Radiation Protection and Health, Ingolstaedter Landstrasse 1, 85764 Neuherberg, Germany. stapio@bfs.de
Abstract: Arsenic, one of the most significant hazards in the environment affecting millions of people around the world, is associated with several diseases including cancers of skin, lung, urinary bladder, kidney and liver. Groundwater contamination by arsenic is the main route of exposure. Inhalation of airborne arsenic or arsenic-contaminated dust is a common health problem in many ore mines. This review deals with the questions raised in the epidemiological studies such as the dose-response relationship, putative confounders and synergistic effects, and methods evaluating arsenic exposure. Furthermore, it describes the metabolic pathways of arsenic, and its biological modes of action. The role of arsenic in the development of cancer is elucidated in the context of combined epidemiological and biological studies. However, further analyses by means of molecular epidemiology are needed to improve the understanding of cancer aetiology induced by arsenic.

Assessing the genotoxic potentials of arsenic in tilapia (Oreochromis mossambicus) using alkaline comet assay and micronucleus test.

2011-05-16T23:16:00.000+02:00

Chemosphere. 2011 Mar 5. [Epub ahead of print]
Ahmed MK, Habibullah-Al-Mamun M, Hossain MA, Arif M, Parvin E, Akter MS, Khan MS, Islam MM.
Department of Fisheries, University of Dhaka, Dhaka-1000, Bangladesh.
Abstract: This experiment was conducted to study the genotoxic potentials of sodium arsenite (NaAsO(2)) in freshwater fish Oreochromis mossambicus by using alkaline comet assay and micronucleus (MN) test. Fish were exposed to three different concentrations (3ppm, 28ppm and 56ppm) of arsenic and gill, liver and blood tissue samples were collected after 48h, 96h and 192h of exposure. Arsenic exposure induced DNA damage in all tissues examined in a concentration dependent manner. A significant (p<0.05) increase in the comet tail DNA (%) of the exposed fish liver, gill, and blood was observed after 48h and 96h of exposure, but a decline in DNA damage was recorded in all the tissues at all the three concentrations studied after 192h of exposure. Liver tissue exhibited significantly (p<0.05) higher DNA damage at all the concentrations examined, followed by gill and blood. Higher liver tail DNA (51.38±0.21%) refers that it is more prone to injury to arsenic toxicity than the gill and blood. In blood samples arsenic induced micronucleus formation in a concentration dependent manner and highest (5.8±0.46%) value was recorded in 56ppm after 96h of exposure, whereas, it was decreased after 192h of exposure at all the three concentrations of NaAsO(2) examined which refers to the DNA repairing ability of fish to arsenic toxicity. The results of this study depict the genotoxic potentials of arsenic to fish which in turns provide insight on advanced study in aquatic toxicology.

Inhalable Metal-rich Air Particles and Histone H3K4 Dimethylation and H3K9 Acetylation in a Cross-sectional Study of Steel Workers.

2011-05-16T23:15:00.000+02:00

Environ Health Perspect. 2011 Mar 8. [Epub ahead of print]
Cantone L, Nordio F, Hou L, Apostoli P, Bonzini M, Tarantini L, Angelici L, Bollati V, Zanobetti A, Schwartz J, Bertazzi PA, Baccarelli A.
Università degli Studi di Milano e Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena.
Abstract: BACKGROUND: Epidemiology investigations have linked exposure to ambient and occupational air particles with increased risk of lung cancer. Air particles contain carcinogenic and toxic metals, including arsenic and nickel, which have been shown in in-vitro studies to induce histone modifications that activate gene expression by inducing open-chromatin states. Whether inhalation of metal components of air particles induces histone modifications in human subjects is undetermined. OBJECTIVES: We investigated whether the metal components of air particles determined activating histone modifications in 63 steel workers with well-characterized exposure to metal-rich particles. METHODS: We determined histone H3K4 dimethylation (H3K4me2) and H3K9 acetylation (H3K9ac) on histones from blood leukocytes. Exposure to inhalable metal components (aluminum, manganese, nickel, zinc, arsenic, lead, iron), and to total particulate matter (PM), was estimated for each study subject. RESULTS: Both H3K4me2 and H3K9ac increased in association with years of employment in the plant (p-trend=0.04 and 0.006, respectively). H3K4me2 increased in association with air levels of nickel (β=0.16; %95 CI 0.03 to 0.3), arsenic (β=0.16; %95 CI 0.02 to 0.3), and iron (β=0.14; %95 CI 0.01 to 0.26). H3K9ac showed non-significant positive associations with air levels of nickel (β=0.24; %95 CI -0.02 to 0.51), arsenic (β=0.21; %95 CI -0.06 to 0.48) and iron (β=0.22; %95 CI -0.03 to 0.47). Cumulative exposures to nickel and arsenic, defined as the product of years of employment by metal air levels, were positively correlated with both H3K4me2 (β=0.16; %95 CI 0.01 to 0.3 for nickel; β=0.16; %95 CI 0.03 to 0.29 for arsenic) and H3K9ac (β=0.27; %95 CI 0.01 to 0.54 for nickel; β=0.28; %95 CI 0.04 to 0.51 for arsenic). CONCLUSIONS: Our results indicate histone modifications as a novel epigenetic mechanism induced in human subjects by long-term exposure to inhalable nickel and arsenic.

Multiple metals exposure in a small-scale artisanal gold mining community.

2011-05-16T23:14:00.000+02:00

Environ Res. 2011 Apr;111(3):463-7.
Basu N, Nam DH, Kwansaa-Ansah E, Renne EP, Nriagu JO.
Department of Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor, MI 48109, USA.
Abstract: Urinary metals were characterized in 57 male residents of a small-scale gold mining community in Ghana. Chromium and arsenic exceeded health guideline values for 52% and 34%, respectively, of all participants. About 10-40% of the participants had urinary levels of aluminum, copper, manganese, nickel, selenium, and zinc that fell outside the U.S. reference range. Exposures appear ubiquitous across the community as none of the elements were associated with occupation, age, and diet.

Multielemental Analysis of Migori (Southwest, Kenya) Artisanal Gold Mine Ores and Sediments by EDX-ray Fluorescence Technique: Implications of Occupational Exposure and Environmental Impact.

2011-05-16T23:12:00.002+02:00

Bull Environ Contam Toxicol. 2011 May;86(5):484-9. Epub 2011 Mar 20.
Odumo OB, Mustapha AO, Patel JP, Angeyo HK.
Department of Physics, University of Nairobi, P.O. Box 30197-00100, Nairobi, Kenya, benodumoo@uonbi.ac.ke.
Abstract: The results of heavy element profiling of the gold ores and sediments associated with the artisanal gold mining activities of the Migori gold belt of Southwestern Nyanza, Kenya, were reported in this paper. The analysis was made to assess the occupational exposure of the miners as well as to investigate the environmental impact of toxic heavy metals. Gold ores and sediments from the artisanal gold processing were sampled in four artisanal gold mining areas: Osiri A, Osiri B, Mikei and Macalder (Makalda) and analyzed for heavy elemental content using (109)Cd radioisotope excited EDXRF spectrometry technique. Analysis consisted of direct irradiating of sample pellets. The concentrations of major elements detected were: titanium (711.41-10,766.67 mg/kg); cobalt (82.65-1,010.00 mg/kg); zinc (29.90-63,210 mg/kg); arsenic (29.30-8,246.59 mg/kg); gold (14.07-73.48 mg/kg); lead (16.31-14,999.40 mg/kg) and mercury (16.10-149.93 mg/kg). The average concentration of the heavy toxic metals i.e. arsenic, lead, titanium and zinc were found to be above 50 mg/Kg as recommended by World Health Organization.

Cancer excess after arsenic exposure from contaminated milk powder.

2011-05-16T23:10:00.000+02:00

Environ Health Prev Med. 2011 May;16(3):164-70. Epub 2010 Sep 29.
Yorifuji T, Tsuda T, Doi H, Grandjean P.
Department of Environmental Health, Harvard School of Public Health, 401 Park Drive, 3-112-12 East, Boston, MA, 02215, USA, tyorifuj@hsph.harvard.edu.
Abstract: OBJECTIVES: Long-term exposure to inorganic arsenic is related to increased risk of cancer in the lung, skin, bladder, and, possibly, other sites. However, little is known about the consequences of developmental exposures in regard to cancer risk. During early summer in 1955, mass arsenic poisoning of infants occurred in the western part of Japan because of contaminated milk powder. Okayama Prefecture was most severely affected. We examined whether the affected birth cohorts in this prefecture experienced increased cancer mortality. METHODS: We targeted subjects who were born from September 1950 to August 1960 and died in Okayama Prefecture between January 1969 and March 2008 due to malignant neoplasm (N = 3,141). We then compared cancer mortality (total, liver, pancreatic, lung, bladder/kidney, and hematopoietic cancers) between cohorts born before the milk poisoning (exposed group) and cohorts born after the poisoning (nonexposed group). We estimated mortality ratios and 95% confidence intervals. RESULTS: Total and liver cancers were elevated in the cohort up to 1 year of age at time of the poisoning. In addition, pancreatic and hematopoietic cancers were elevated in the cohorts up to 5 years of age, and mortality ratios were approximately twice those of the nonexposed group. Increased risk of lung and bladder/kidney cancers was not apparent. CONCLUSIONS: Although dilution is present in these cohort-based data, our study highlights the notion that developmental arsenic exposure may lead to a different pattern of cancer, including increases in pancreatic and hematopoietic cancer, as compared with adult or lifetime exposures to inorganic arsenic.

Arsenic affects expression and processing of amyloid precursor protein (APP) in primary neuronal cells overexpressing the Swedish mutation of human APP.

2011-05-16T23:09:00.002+02:00

Int J Dev Neurosci. 2011 Mar 31. [Epub ahead of print]
Zarazúa S, Bürger S, Delgado JM, Jiménez-Capdeville ME, Schliebs R.
Department of Biochemistry, Faculty of Medicine, University of San Luis Potosí, Av. V. Carranza 2405, Col. Los Filtros, 78210 San Luis Potosí, S.L.P., Mexico.
Abstract: Arsenic poisoning due to contaminated water and soil, mining waste, glass manufacture, select agrochemicals, as well as sea food, affects millions of people world wide. Recently, an involvement of arsenic in Alzheimer's disease (AD) has been hypothesized (Gong and O'Bryant, 2010). The present study stresses the hypothesis whether sodium arsenite, and its main metabolite, dimethylarsinic acid (DMA), may affect expression and processing of the amyloid precursor protein (APP), using the cholinergic cell line SN56.B5.G4 and primary neuronal cells overexpressing the Swedish mutation of APP, as experimental approaches. Exposure of cholinergic SN56.B5.G4 cells with either sodium arsenite or DMA decreased cell viability in a concentration- and exposure-time dependent manner, and affected the activities of the cholinergic enzymes acetylcholinesterase and choline acetyltransferase. Both sodium arsenite and DMA exposure of SN56.B5.G4 cells resulted in enhanced level of APP, and sAPP in the membrane and cytosolic fractions, respectively. To reveal any effect of arsenic on APP processing, the amounts of APP cleavage products, sAPPβ, and β-amyloid (Aβ) peptides, released into the culture medium of primary neuronal cells derived from transgenic Tg2576 mice, were assessed by ELISA. Following exposure of neuronal cells by sodium arsenite for 12h, the membrane-bound APP level was enhanced, the amount of sAPPβ released into the culture medium was slightly higher, while the levels of Aβ peptides in the culture medium were considerably lower as compared to that assayed in the absence of any drug. The sodium arsenite-induced reduction of Aβ formation suggests an inhibition of the APP γ-cleavage step by arsenite. In contrast, DMA exposure of neuronal cells considerably increased formation of Aβ and sAPPβ, accompanied by enhanced membrane APP level. The DMA-induced changes in APP processing may be the result of the enhanced APP expression. Alternatively, increased Aβ production may also be due to stimulation of caspase activity by arsenic compounds, or failure in Aβ degradation. In summary, the present report clearly demonstrates that sodium arsenite and DMA affect processing of APP in vitro.

Atmospheric arsenic (As) study at five characteristic sampling sites in Taiwan.

2011-05-16T23:08:00.002+02:00

Environ Monit Assess. 2011 Mar 30. [Epub ahead of print]
Fang GC, Huang YL, Huang JH.
Department of Safety, Health and Environmental Engineering, HungKuang University, Sha-Lu, Taichung, 433, Taiwan, gcfang@sunrise.hk.edu.tw.
Abstract: The main purpose for this study is to observe the seasonal and monthly variations for arsenic (As) in total suspended particulates (TSP) concentration and dry deposition at five characteristic sampling sites during the years 2009 and 2010 in central Taiwan. The results show that the highest and lowest monthly average As concentrations in TSP occurred in January and May at Bei-shi (suburban/coastal) and Quan-xing (industrial) sampling sites. In addition, the results show that the highest and lowest monthly average As dry deposition occurred in October and May at Chang-hua (downtown) and Gao-mei (wetland) sampling sites. This study reflected that the mean highest As concentrations in TSP and mean highest As dry deposition occurred at Quan-xing (industrial). However, the mean lowest As concentrations in TSP and mean lowest As dry deposition also occurred at Gao-mei (wetland). Regarding seasonal variation, the results show that the As average seasonal concentration order in TSP was winter > spring > fall > summer, respectively, at Chang-hua (downtown) and He-mei (residential) sampling sites. Finally, the order of As average seasonal dry deposition was fall > winter > spring > summer, respectively, at Chang-hua (downtown), He-mei (residential), and Gao-mei (wetland) sampling sites.

Probability of intellectual disability is associated with soil concentrations of arsenic and lead.

2011-05-16T23:07:00.002+02:00

Chemosphere. 2011 Mar 28. [Epub ahead of print]
McDermott S, Wu J, Cai B, Lawson A, Marjorie Aelion C.
University of South Carolina, School of Medicine, Department of Family and Preventive Medicine, 3209 Colonial Drive, Columbia, SC 29203, United States.
Abstract: BACKGROUND: The association between metals in water and soil and adverse child neurologic outcomes has focused on the singular effect of lead (Pb), mercury (Hg), and arsenic (As). This study describes the complex association between soil concentrations of As combined with Pb and the probability of intellectual disability (ID) in children. METHODS: We used a retrospective cohort design with 3988 mother child pairs who were insured by Medicaid and lived during pregnancy and early childhood in South Carolina between 1/1/97 and 12/31/02. The children were followed until 6/1/08, using computerized service files, to identify the diagnosis of ID in medical records and verified by either school placement or disability service records. The soil was sampled using a uniform grid and analyzed for eight metals. The metal concentrations were interpolated using Bayesian Kriging to estimate concentration at individual residences. RESULTS: The probability of ID increased for increasing concentrations of As and Pb in the soil. The Odds Ratio for ID, for one unit change in As was 1.130 (95% confidence interval 1.048-1.218) for Pb was 1.002 (95% confidence interval 1.000-1.004). We identified effect modification for the infants based on their birth weight for gestational age status and only infants who were normal size for their gestational age had increased probability of ID based on the As and Pb soil concentrations (OR for As at normal weight for gestational age=1.151 (95% CI: 1.061-1.249) and OR for Pb at normal for gestational age=1.002 (95% CI: 1.002-1.004)). For normal weight for gestational age children when As=22mgkg(-1) and Pb=200mgkg(-1) the risk for ID was 11% and when As=22mgkg(-1)and Pb=400mgkg(-1) the probability of ID was 65%. CONCLUSION: The probability of ID is significantly associated with the interaction between Pb and As for normal weight for gestational age infants.

Arsenic and manganese exposure and children's intellectual function.

2011-05-16T23:06:00.002+02:00

Wasserman GA, Liu X, Parvez F, Factor-Litvak P, Ahsan H, Levy D, Kline J, van Geen A, Mey J, Slavkovich V, Siddique AB, Islam T, Graziano JH.
Department of Psychiatry, College of Physicians and Surgeons, Columbia University, New York City, NY 10032, United States; NY State Psychiatric Institute, 1051 Riverside Drive, New York City, NY 10032, United States.
Abstract: Recently, epidemiologic studies of developmental neurotoxicology have been challenged to increase focus on co-exposure to multiple toxicants. Earlier reports, including our own work in Bangladesh, have demonstrated independent associations between neurobehavioral function and exposure to both arsenic (As) and manganese (Mn) in school-aged children. Our earlier studies, however, were not designed to examine possible interactive effects of exposure to both As and Mn. To allow investigation of possible synergistic impact of simultaneous exposures, we recruited a new sample of 299 8-11 year old children, stratified by design on As (above and below 10μg/L) and Mn (above and below 500μg/L) concentrations of household wells. When adjusted only for each other, both As and Mn in whole blood (BAs; BMn) were significantly negatively related to most WISC-IV subscale scores. With further adjustment for socio-demographic features and ferritin, BMn remained significantly associated with reduced Perceptual Reasoning and Working Memory scores; associations for BAs, and for other subscales, were expectably negative, significantly for Verbal Comprehension. Urinary As (per gram creatinine) was significantly negatively associated with Verbal Comprehension scores, even with adjustment for BMn and other contributors. Mn by As interactions were not significant in adjusted or unadjusted models (all p's>0.25). Findings are consistent with other reports documenting adverse impact of both As and Mn exposure on child developmental outcomes, although associations appear muted at these relatively low exposure levels.

Comparative genomic analyses identify common molecular pathways modulated upon exposure to low doses of arsenic and cadmium.

2011-05-16T23:05:00.002+02:00

BMC Genomics. 2011 Apr 1;12:173.
Benton MA, Rager JE, Smeester L, Fry RC.
Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA. rfry@unc.edu.
Abstract: BACKGROUND: Exposure to the toxic metals arsenic and cadmium is associated with detrimental health effects including cancers of various organs. While arsenic and cadmium are well known to cause adverse health effects at high doses, the molecular impact resulting from exposure to environmentally relevant doses of these metals remains largely unexplored. RESULTS: In this study, we examined the effects of in vitro exposure to either arsenic or cadmium in human TK6 lymphoblastoid cells using genomics and systems level pathway mapping approaches. A total of 167 genes with differential expression were identified following exposure to either metal with surprisingly no overlap between the two. Real-time PCR was used to confirm target gene expression changes. The gene sets were overlaid onto protein-protein interaction maps to identify metal-induced transcriptional networks. Interestingly, both metal-induced networks were significantly enriched for proteins involved in common biological processes such as tumorigenesis, inflammation, and cell signaling. These findings were further supported by gene set enrichment analysis. CONCLUSIONS: This study is the first to compare the transcriptional responses induced by low dose exposure to cadmium and arsenic in human lymphoblastoid cells. These results highlight that even at low levels of exposure both metals can dramatically influence the expression of important cellular pathways.

Atmospheric stability of arsine and methylarsines.

2011-05-16T23:01:00.000+02:00

Environ Sci Technol. 2011 May 1;45(9):4010-5. Epub 2011 Apr 6.
Mestrot A, Merle JK, Broglia A, Feldmann J, Krupp EM.
TESLA (Trace Element Speciation Laboratory), Chemistry Department, University of Aberdeen , Aberdeen, AB24 3UE, United Kingdom.
Abstract: Arsenic (As) occurs in a variety of different chemical forms, among them volatile (gaseous) species, usually referred to as arsine and methylarsines. Here we demonstrate that arsine and methylarsines are stable in air in concentrations at the μg/L gas level. We determined half-lives of approximately 8 h under daytime conditions (UV light) for all methylated arsines, while the same species were found to be considerably more stable in night-time (dark) conditions. Arsine (AsH(3)) showed under both day and night-time conditions, considerably higher stabilities than methylated arsines. We show here that volatile As species seem stable enough to travel considerable distances in the atmosphere from a point source before converting into nonvolatile, oxidized compounds. Also, the degradation pathway leading to the conversion to nonvolatile compounds was investigated using computational chemistry. Arsine and methylarsines' reactions with the hydroxyl radical (•OH) as well as As-C and As-H bonds strengths in the species studied were modeled. Results showed that conversion could not be explained by H abstraction, nor by OH addition. Moreover, it was found that As-C and As-H bonds strengths are not the determining factor responsible for the decrease in stability with ascending methylation of the different volatile arsine species, as previously suggested.

Human risk assessment of heavy metals: principles and applications.

2011-05-16T22:59:00.000+02:00

Met Ions Life Sci. 2011;8:27-60.
Dorne JL, Kass GE, Bordajandi LR, Amzal B, Bertelsen U, Castoldi AF, Heppner C, Eskola M, Fabiansson S, Ferrari P, Scaravelli E, Dogliotti E, Fuerst P, Boobis AR, Verger P.
European Food Safety Authority, Largo N. Palli 5, I-43100 Parma, Italy. jean-lou.dorne@efsa.europa.eu
Abstract: Humans are exposed to a number of "heavy metals" such as cadmium, mercury and its organic form methylmercury, uranium, lead, and other metals as wel as metalloids, such as arsenic, in the environment, workplace, food, and water supply. Exposure to these metals may result in adverse health effects, and national and international health agencies have methodologies to set health-based guidance values with the aim to protect the human population. This chapter introduces the general principles of chemical risk assessment, the common four steps of chemical risk assessment: hazard identification, hazard characterization, exposure assessment, risk characterization, and toxicokinetic and toxicity aspects. Finally, the risk assessments performed by international health agencies such as the World Health Organisation, the Environmental Protection Agency of the United States, and the European Food Safety Authority are reviewed for cadmium, lead, mercury, uranium, and arsenic.

Arsenic transformations in terrestrial small mammal food chains from contaminated sites in Canada.

2011-05-16T22:58:00.000+02:00

J Environ Monit. 2011 Apr 19. [Epub ahead of print]
Saunders JR, Hough C, Knopper LD, Koch I, Reimer KJ.
Stantec, Ottawa, Ontario K1B 1A7, Canada.
Abstract: Arsenic in terrestrial contaminated sites has the potential to cause harm to residential wildlife. The aim of this study was to determine the arsenic species in wild rodents living in arsenic contaminated habitats, specifically deer mice from Yellowknife, NT and meadow voles from Seal Harbour, NS, along with co-located plants. Methanol : water (1 : 1) extractions were used to optimize the extraction of methylated arsenic(v) species. Total arsenic concentrations were substantially higher in the Yellowknife deer mice (1.7-3.2 µg kg(-1) wet weight in livers) and Seal Harbour meadow voles (0.67-0.97 µg kg(-1) wet weight in livers) living on the contaminated sites with respect to the surrounding background locations (0.12-0.34 µg kg(-1) wet weight in livers). Around 50% of arsenic could be identified in Yellowknife deer mouse tissues, but only <10% was identified in Seal Harbour vole tissues; inorganic arsenic (iii and v) and dimethylarsinic acid were all found. Monomethylarsonic acid was only detected in both the mice and voles living in the contaminated sites. In the Yellowknife food chain, methyl arsenic (v) proportions increased from plants to mouse inner organs, but the trend was not for clear as the Seal Harbour food chain. Seal Harbour voles may be sequestering arsenic in a less mobile form, rather than transforming it.

Exposure to Moderate Arsenic Concentrations Increases Atherosclerosis in ApoE-/- Mouse Model.

2011-05-16T22:57:00.000+02:00

Toxicol Sci. 2011 Apr 21. [Epub ahead of print]
Lemaire M, Lemarié CA, Molina MF, Schiffrin EL, Lehoux S, Mann KK.
Lady Davis Institute for Medical Research, Dept. Oncology, McGill University, Montreal, H3T 1E2, Canada.
Abstract: Arsenic is a widespread environmental contaminant to which millions of people are exposed worldwide. Exposure to arsenic is epidemiologically linked to increased cardiovascular disease, such as atherosclerosis. However, the effects of moderate concentrations of arsenic on atherosclerosis formation are unknown. Therefore, we utilized an in vivo ApoE(-/-) mouse model to assess the effects of chronic moderate exposure to arsenic on plaque formation and composition in order to facilitate mechanistic investigations. Mice exposed to 200 ppb arsenic developed atherosclerotic lesions, a lower exposure than previously reported. In addition, arsenic modified the plaque content, rendering them potentially less stable and consequently, potentially more dangerous. Moreover, we observed that the lower exposure concentration was more atherogenic than the higher concentration. Arsenic-enhanced lesions correlated with several pro-atherogenic molecular changes, including decreased LXR target gene expression and increased pro-inflammatory cytokines. Significantly, our observations suggest that chronic moderate arsenic exposure may be a greater cardiovascular health risk than previously anticipated.

Arsenic trioxide induces procoagulant activity through phosphatidylserine exposure and microparticle generation in endothelial cells.

2011-05-16T22:56:00.000+02:00

Thromb Res. 2011 May;127(5):466-72. Epub 2011 Jan 26.
Zhou J, Li H, Fu Y, Shi J, Hou J, Zhang Y, Liu X, Song P.
Department of Hematology, the First Affiliated Hospital, Harbin Medical University, Harbin 150001, China.
Abstract: BACKGROUND: Coagulopathy is a major cause of early death when arsenic trioxide (As(2)O(3)) therapy fails. In addition to the procoagulant properties of blast cells, the cytotoxic therapy may contribute to the coagulation disorders. The aim of the present study was to evaluate the possible impact of As(2)O(3) on membrane alterations, including phosphatidylserine (PS) exposure and microparticle generation, and the consequent procoagulant properties of endothelial cells. METHODS: Procoagulant activity (PCA) of human umbilical vein endothelial cells (HUVECs) was assessed by measuring clotting time and through purified coagulation complex assays. PS exposure on HUVEC membrane was observed by confocal microscopy and quantified with flow cytometry. In addition, counts and PCA of endothelial microparticles were determined by flow cytometry and plasma coagulation assay. RESULTS: As(2)O(3) increased the ability of HUVECs to accelerate coagulation process and promote formation of coagulation complexes. Procoagulant activity corresponded to PS exposed on HUVECs. In coincidence with the PS externalization, As(2)O(3) increased the production of PS-bearing microparticles, which then accelerated fibrin strand formation significantly. By blocking PS, lactadherin was able to inhibit over 90% of the intrinsic tenase/prothrombinase activity of As(2)O(3)-treated HUVECs, and restored coagulation times of As(2)O(3)-treated cells and microparticles to control levels. CONCLUSIONS: As(2)O(3) increases PCA of HUVECs through PS exposure and PS-bearing microparticle generation, which might cause thrombosis and act as a contributing factor in As(2)O(3) therapy-related coagulopathy.

Epigenetic changes in individuals with arsenicosis.

2011-05-16T22:42:00.002+02:00

Chem Res Toxicol. 2011 Feb 18;24(2):165-7. Epub 2011 Feb 4.
Smeester L, Rager JE, Bailey KA, Guan X, Smith N, García-Vargas G, Del Razo LM, Drobná Z, Kelkar H, Stíyblo M, Fry RC.
Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, UNC-Chapel Hill, Chapel Hill, North Carolina 27599, United States.
Abstract: Inorganic arsenic (iAs) is an environmental toxicant currently poisoning millions of people worldwide, and chronically exposed individuals are susceptible to arsenicosis or arsenic poisoning. Using a state-of-the-art technique to map the methylomes of our study subjects, we identified a large interactome of hypermethylated genes that are enriched for their involvement in arsenic-associated diseases, such as cancer, heart disease, and diabetes. Notably, we have uncovered an arsenic-induced tumor suppressorome, a complex of 17 tumor suppressors known to be silenced in human cancers. This finding represents a pivotal clue in unraveling a possible epigenetic mode of arsenic-induced disease.

Arsenic: toxicity, oxidative stress and human disease.

2011-05-16T22:42:00.000+02:00

J Appl Toxicol. 2011 Mar;31(2):95-107. doi: 10.1002/jat.1649. Epub 2011 Feb 14.
Jomova K, Jenisova Z, Feszterova M, Baros S, Liska J, Hudecova D, Rhodes CJ, Valko M.
Department of Chemistry, Faculty of Natural Sciences, Constantine The Philosopher University, Nitra, Slovakia.
Abstract: Arsenic (As) is a toxic metalloid element that is present in air, water and soil. Inorganic arsenic tends to be more toxic than organic arsenic. Examples of methylated organic arsenicals include monomethylarsonic acid [MMA(V)] and dimethylarsinic acid [DMA(V)]. Reactive oxygen species (ROS)-mediated oxidative damage is a common denominator in arsenic pathogenesis. In addition, arsenic induces morphological changes in the integrity of mitochondria. Cascade mechanisms of free radical formation derived from the superoxide radical, combined with glutathione-depleting agents, increase the sensitivity of cells to arsenic toxicity. When both humans and animals are exposed to arsenic, they experience an increased formation of ROS/RNS, including peroxyl radicals (ROO•), the superoxide radical, singlet oxygen, hydroxyl radical (OH•) via the Fenton reaction, hydrogen peroxide, the dimethylarsenic radical, the dimethylarsenic peroxyl radical and/or oxidant-induced DNA damage. Arsenic induces the formation of oxidized lipids which in turn generate several bioactive molecules (ROS, peroxides and isoprostanes), of which aldehydes [malondialdehyde (MDA) and 4-hydroxy-nonenal (HNE)] are the major end products. This review discusses aspects of chronic and acute exposures of arsenic in the etiology of cancer, cardiovascular disease (hypertension and atherosclerosis), neurological disorders, gastrointestinal disturbances, liver disease and renal disease, reproductive health effects, dermal changes and other health disorders. The role of antioxidant defence systems against arsenic toxicity is also discussed. Consideration is given to the role of vitamin C (ascorbic acid), vitamin E (α-tocopherol), curcumin, glutathione and antioxidant enzymes such as superoxide dismutase, catalase and glutathione peroxidase in their protective roles against arsenic-induced oxidative stress.

Arsenic concentrations in soils impacted by dam failure of coal-ash pond in zemianske kostolany, slovakia.

2011-05-16T22:40:00.001+02:00

Bull Environ Contam Toxicol. 2011 Apr;86(4):433-7. Epub 2011 Feb 18.
Jurkovič L, Hiller E, Veselská V, Pet'ková K.
Faculty of Natural Sciences, Department of Geochemistry, Comenius University in Bratislava, Mlynska dolina, 842 15, Bratislava 4, Slovak Republic.
Abstract: In this study, the concentrations of arsenic were determined in the soils around old coal-ash pond. The soils in the study area were severely contaminated with arsenic after dam failure of the coal-ash pond. The mean concentrations of arsenic in soils collected from three sampling depths of 0-20, 20-40 and >40 cm were 173, 155 and 426 μg/g, respectively, exceeding greatly the Dutch intervention threshold for this element. Arsenic concentrations were positively correlated with total iron and aluminium contents in the soils (r = 0.73, p < 0.001 and r = 0.72, p < 0.001, respectively), indicating that oxyhydroxides of iron and aluminium may control the distribution of arsenic in these soils. Ammonium nitrate extractant was used to mimic availability of arsenic for plant uptake from the soils. Between 0.05 and 6.21% of the total soil arsenic were extracted using a single extraction test and a significant positive correlation between soil leachate pH and arsenic extractability (r = 0.70, p < 0.01) was observed. This suggested that soil pH might play a role in the bioavailability of arsenic.

The Fluctuation of Arsenic Levels in Lake Taihu.

2011-05-16T22:39:00.001+02:00

Biol Trace Elem Res. 2011 Feb 22. [Epub ahead of print]
Wei C, Zhang N, Yang L.
Institute of Geographic Sciences & Natural Resources Research, Chinese Academy of Sciences, 11A Datun Road, Chaoyang District, Beijing, 100101, China, weicy@igsnrr.ac.cn.
Abstract: This study was conducted to investigate the arsenic levels in the waters of lake Taihu, a huge, shallow, and very important lake which has been suffered with serious eutrophication in China. Unexpected great difference was detected for arsenic levels between the collected water samples of three successive surveys in Taihu in May 2009, Fall 2009, and May 2010, with arsenic levels in May 2009 being more than tenfold of those in Fall 2009 and May 2010. Such difference in arsenic levels do not routinely happen like seasonal changes as reported in many other lakes of the world. Considering arsenic contents as well as some basic aquatic monitoring data of the lake, such great arsenic fluctuations were probably due to the effects of strong hydraulic turbulence in Taihu for its very shallow depth. The spatial distribution of arsenic in Taihu were similar, despite great difference of arsenic levels in the three successive surveys, indicating such differences did not come from arsenic external input around the lake. The sudden increase of arsenic levels in Taihu highlights the importance of stabilization or removing of arsenic in lake sediments so as to keep arsenic lower than the national hygiene standard of China.

Association between arsenic exposure from drinking water and proteinuria: results from the Health Effects of Arsenic Longitudinal Study.

2011-05-16T22:38:00.000+02:00

Int J Epidemiol. 2011 Feb 22. [Epub ahead of print]
Chen Y, Parvez F, Liu M, Pesola GR, Gamble MV, Slavkovich V, Islam T, Ahmed A, Hasan R, Graziano JH, Ahsan H.
Department of Environmental Medicine, New York University School of Medicine, New York, NY, USA, Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York City, NY, USA, Department of Epidemiology, Mailman School of Public Health, Columbia University, New York City, NY, USA, Section of Pulmonary Disease, Department of Medicine, Harlem Hospital, New York, NY, USA, Columbia University Arsenic Research Project, Dhaka, Bangladesh and Department of Health Studies, Medicine and Human Genetics and Cancer Research Center, The University of Chicago, Chicago, IL, USA.
Abstract: BACKGROUND: Proteinuria has been recognized as a marker for an increased risk of chronic renal disease. It is unclear whether arsenic (As) exposure from drinking water is associated with proteinuria. METHODS: We evaluated the association between As exposure from drinking water and proteinuria in 11 122 participants in the Health Effects of Arsenic Longitudinal Study (HEALS). Proteinuria was detected by urinary dipstick tests at baseline and at 2-year intervals. As exposure variables included baseline well As and changes in urinary As during follow-up modelled as time-dependent variables in the analyses. RESULTS: At baseline, well As was positively related to prevalence of proteinuria; prevalence odds ratios (PORs) for proteinuria in increasing quintiles of well As (≤7, 8-39, 40-91, 92-179 and 180-864 µg/l) were 1.00 (ref), POR 0.99 [95% confidence interval (CI) 0.77-1.27], POR 1.23 (95% CI 0.97-1.57), POR 1.50 (95% CI 1.18-1.89) and POR 1.59 (95% CI 1.26-2.00) (P for trend <0.01). Hazard ratios for incidence of proteinuria were POR 0.83 (95% CI 0.67-1.03) and POR 0.91 (95% CI 0.74-1.12) for participants with a decreasing level of >70 and 17-70 µg/l in urinary As over time, respectively, and were POR 1.17 (95% CI 0.97-1.42) and POR 1.42 (95% CI 1.16-1.73) for participants with an increasing level of 16-68 and >68 µg/l in urinary As over time, respectively, compared with the group with relatively little changes in urinary As as the reference group (urinary As -16 to 15 µg/l). CONCLUSION: The findings suggest that there are adverse effects of As exposure on the risk of proteinuria and the effects are modifiable by recent changes in As exposure.

Molecular changes during arsenic-induced cell transformation.

2011-05-16T22:37:00.000+02:00

J Cell Physiol. 2011 Feb 22. doi: 10.1002/jcp.22683. [Epub ahead of print]
Li G, Lee LS, Li M, Tsao SW, Chiu JF.
Department of Biochemistry/Open Laboratory for Tumor Molecular Biology, Shantou University Medical College, Shantou 515041, China.
Abstract: Arsenic and its derivatives are naturally occurring metalloid compounds widely distributed in the environment. Arsenics are known to cause cancers of the skin, liver, lung, kidney, and bladder. Although numerous carcinogenic pathways have been proposed, the exact molecular mechanisms remain to be delineated. To further characterize the role of oxidative stress in arsenite- induced cell transformation via the reactive oxygen species (ROS)-mediated Ras/Erk pathway, here we demonstrated arsenite-induced rat lung epithelial cell (LEC) transformation, epithelial-mesenchymal transition, stimulation of the extracellular signal-regulated kinase signaling pathway, and enhancement of cell proliferation. However, there was no evidence of activation of the phosphoinositide 3-kinase/protein kinase B pathway in arsenite-induced transformed LECs. Since ROS is involved in arsenite-induced LEC cell transformation, Redox-status regulatory proteins (Cu/Zn SOD and thioredoxin) and arsenite-induced LEC cell transformation were significantly inhibited by concurrent treatment with the antioxidants. Our experimental results clearly demonstrated that induction of p-ERK and cell proliferation by arsenite is mediated via oxidative stress, since antioxidants can inhibit arsenite-induced cell transformation.

Bioaccessibility and health risk of arsenic, mercury and other metals in urban street dusts from a mega-city, Nanjing, China.

2011-05-16T22:34:00.001+02:00

Environ Pollut. 2011 May;159(5):1215-21. Epub 2011 Feb 22.
Hu X, Zhang Y, Luo J, Wang T, Lian H, Ding Z.
Key Lab of Analytical Chemistry for Life Science (Ministry of Education), Center of Material Analysis, Nanjing University, Nanjing 210093, Jiangsu Province, PR China.
Abstract: The oral bioaccessibility and the human health risks of As, Hg and other metals (Cu, Pb, Zn, Ni, Co, Cd, Cr, Mn, V and Fe) in urban street dusts from different land use districts in Nanjing (a mega-city), China were investigated. Both the total contents and the oral bioaccessibility estimated by the Simple Bioaccessibility Extraction Test (SBET) of the studied elements varied with street dusts from different land use districts. Cd, Zn, Mn, Pb, Hg and As showed high bioaccessibility. SBET-extractable contents of elements were significantly correlated with their total contents and the dust properties (pH, organic matter contents). The carcinogenic risk probability for As and Cr to children and adults were under the acceptable level (<1 × 10(-4)). Hazard Quotient values for single elements and Hazard Index values for all studied elements suggested potential non-carcinogenic health risk to children, but not to adults.

[Soil arsenic content and its health risk assessment for agricultural products in the region surrounding Shimen arsenic sulphide mine]. [Article in Chinese]

2011-05-16T22:33:00.001+02:00

Ying Yong Sheng Tai Xue Bao. 2010 Nov;21(11):2946-51.
Li LF, Zeng XB, Bai LY, Li SH.
Ministry of Agriculture Key Laboratory of Agro-Environment & Climate Change, Institute of Environment and Sustainable Development in Agriculture, Chinese Academy of Agricultural Sciences, Beijing 100081, China. lilianfang@ieda.org.cn
Abstract: A systematic investigation was carried out on the arsenic content in the soils and plants surrounding Shimen arsenic sulphide mine. The arsenic content in top soils (0-20 cm) was averagely 99.51 mg x kg(-1), being 5.34 times higher than that of the background value in Hunan Province and 8.70 times higher than that of local farmland soil. The topsoil arsenic content in paddy field and dry land was 43.51 and 115.1 mg x kg(-1), respectively, being 0.45 and 1.87 times higher than that of the grade II level (paddy field 30 mg x kg(-1); dry land 40 mg x kg(-1)) commended by the National Soil Quality (GB 15618-1995), and the corresponding arsenic exceeding rate was 62.5% and 50.0%, respectively. The arsenic content in edible parts of foodstuff, vegetables, and fruits was 0.16, 0.06, and 0.01 mg x kg(-1), respectively, and the arsenic exceeding rate of crop samples compared to food security standard ranked in the order of foodstuff > vegetables > fruits. Rice and sweet potato were relatively seriously contaminated by arsenic. The highest arsenic content of rice was up to 0.84 mg x kg(-1), which was 4.6 times higher than that of the National Standard, with the exceeding rate of 62.5%. Statistical analysis demonstrated that there was a positive correlation between the arsenic contents of soil and plant. The average daily intake of arsenic by local people through the consumption of the crops was 6.416 microg x kg(-1) x d(-1), which was much higher than the standard commended by WHO, and the related health risk index was 21.39, which was 14.39 times higher than that in the control region.

[Comunicable diseases, mental health and exposure to environmental pollutants in population living near Las Bambas mining project before exploitation phase, Peru 2006]. [Article in Spanish]

2011-05-16T22:32:00.000+02:00

Rev Peru Med Exp Salud Publica. 2010 Oct-Dec;27(4):512-9.
Astete J, Gastañaga Mdel C, Fiestas V, Oblitas T, Sabastizagal I, Lucero M, Abadíe Jdel M, Muñoz ME, Valverde A, Suarez M.
Centro Nacional de Salud Ocupacional y Protección del Ambiente para la Salud, Instituto Nacional de Salud, Lima, Perú. astetemed@gmail.com
Abstract: OBJECTIVE: To determine the prevalence of communicable diseases, mental health and environmental pollutants exposure in population living near Las Bambas mining project before exploitation phase. MATERIAL AND METHODS: Cross sectional study performed in 453 subjects (children and adults) living in three Apurimac region districts: Haquira, Chalhuahuacho and Progreso. Psychomotor development, intelligence quotient, anxiety and depression levels and the presence of communicable diseases (viral hepatitis B, C and delta, syphilis and HIV) were evaluated, as well as heavy metals (lead in blood, and cadmium, arsenic and mercury in urine samples) and serum cholinesterase levels. RESULTS: Mean age was 29 ± 17.25 years, 59.2% were female and a range of 6 to 15 years of living in the area was found. No cases of HIV, hepatitis C and delta were found, 1.4% were positive for syphilis and in relation to hepatitis B, we found 1,7% of subjects positive to total anti HBc and 0.5% positive for HBsAg. Heavy metal testing identified people with exceeding limits of mercury in 1.8% arsenic in 4.6%, lead in 24.3% and cadmium in 43.9%. Besides, 29.1% of the population had cholinesterase levels below normal range. Among children, 12.5% were at psychomotor development levels of risk; 2.1% and 3.1% suffered from mild and borderline intellectual disability (mental retardation), respectively. 34.3% of subjects older than 12 had anxiety and 17.5% depression. CONCLUSIONS: Evidence of heavy metal environmental pollution and presence of communicable diseases in this population were already found. Future careless mining activity could worsen the current health situation.

Control of subterranean termites (Isoptera: Rhinotermitidae) infesting power poles.

2011-05-16T22:29:00.001+02:00

J Econ Entomol. 2010 Dec;103(6):2140-6.
Horwood MA, Westlake T, Kathuria A.
Forest Science Centre, Industry and Investment New South Wales, P.O. Box 100 Beecroft, NSW 2119, Australia. martinh@sf.nsw.gov.au
Abstract: A trial was conducted to determine the efficacy of termiticidal dusts (arsenic trioxide, triflumuron, and Metarhizium anisopliae), a timber fumigant (dazomet) and liquid termiticides (bifenthrin, chlorfenapyr, chlorpyrifos, fipronil, and imidacloprid) for controlling subterranean termites (Isoptera: Rhinotermitidae) infesting in-service power poles in New South Wales, Australia. Dusts were applied to parts of the pole where termites were present. Fumigant was inserted into holes drilled into the base of the pole. Liquid termiticides were mixed with soil around the base of the pole and injected into internal voids if present. Poles were inspected for up to 5 yr, and the time taken for reinfestation to occur was recorded. Before the start of the trial, the major Australian pole owners were surveyed to obtain an estimate of the annual national cost of termite infestation to the power supply industry. The annual costs of termite treatment and replacing damaged poles were estimated at AU$2 million and AU$13 million, respectively. Infestation rates were lower for all treatments compared with controls within the first 12 mo of the study. Dazomet, arsenic trioxide, fipronil, and chlorpyrifos were the most efficacious treatments. Efficacy was positively related to the amount of termiticide applied and negatively related to the infestation severity but was unaffected by geographical location. Survival curves were calculated of the time elapsed before the recurrence of termite infestations (survival absence of reinfestation). Survival was highest for poles treated with liquid termiticides.

Les pratiques de la transnationale canadienne RPM/Kinross Gold Corporation à Paracatu, Brésil : entre délinquance et criminalité

2011-02-20T10:09:00.000+01:00

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 ?

Field Fluxes and Speciation of Arsines Emanating from Soils.

2011-02-17T21:27:00.000+01:00

Environ Sci Technol. 2011 Feb 1. [Epub ahead of print]
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.

2011-02-17T21:26:00.001+01:00

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.

Arsenic exposure and type 2 diabetes: a systematic review of the experimental and epidemiological evidence.

2011-02-17T21:25:00.001+01:00

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. anavas@jhsph.edu
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?

2011-02-17T21:24:00.001+01:00

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.

In utero arsenic exposure induces early onset of atherosclerosis in ApoE-/- mice.

2011-02-17T21:23:00.001+01:00

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.

Analysis of the relationship between leukemia mortality and soil trace elements using chemometrics.

2011-02-17T21:22:00.000+01:00

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.

Leachability of arsenic and heavy metals from mine tailings of abandoned metal mines.

2011-02-17T21:21:00.000+01:00

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].

Association of genotoxic effects of arsenic with haematological malignancy in West Bengal.

2011-02-17T21:19:00.000+01:00

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.

The positive response of Ty1 retrotransposition test to carcinogens is due to increased levels of reactive oxygen species generated by the genotoxins.

2011-02-17T21:18:00.000+01:00

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.

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.

2011-02-17T21:17:00.000+01:00

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.

Genetic variants associated with arsenic metabolism within human arsenic (+3 oxidation state) methyltransferase show wide variation across multiple populations.

2011-02-17T21:16:00.000+01:00

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.

Spatial-temporal and cancer risk assessment of selected hazardous air pollutants in Seattle.

2011-02-17T21:15:00.001+01:00

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.

Carcinogenic effects of "whole-life" exposure to inorganic arsenic in CD1 mice.

2011-02-17T21:11:00.001+01:00

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.

Arsenic-associated oxidative stress, inflammation, and immune disruption in human placenta and cord blood.

2011-02-17T21:10:00.001+01:00

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.

Solidification of arsenic and heavy metal containing tailings using cement and blast furnace slag.

2011-02-17T21:09:00.001+01:00

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.

The immobilisation and retention of soluble arsenic, cadmium and zinc by biochar.

2011-02-17T21:08:00.001+01:00

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.

Influence of natural organic matter on As transport and retention.

2011-02-17T21:07:00.000+01:00

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.

Evidence from chile that arsenic in drinking water may increase mortality from pulmonary tuberculosis.

2011-02-17T20:55:00.000+01:00

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.

Arsenic sinks to new depths

2011-01-19T17:03:00.001+01:00

http://www.nature.com/news/2011/110117/full/news.2011.20.html?WT.ec_id=NEWS-20110118

Groundwater overuse can push poisonous element deeper — a serious risk for countries in Southern Asia.

Gayathri Vaidyanathan

More than a century of groundwater over-exploitation in Vietnam has drawn the water table down and, with it, arsenic. It may only be a matter of time before the toxic element also permeates deep aquifers in other Asian countries that follow the same practice, such as those around the Bengal Basin.

These conclusions, published today in the Proceedings of the National Academy of Sciences[1], point to high future costs in terms of both health and water-purification processes. Some 100 million people throughout Asia are currently at risk from unsafe levels of arsenic in their water supplies. The element can trigger conditions ranging from anaemia to skin cancer. With deeper aquifers so far thought to be arsenic-free, some municipal authorities in Bangladesh, and many in Vietnam, are drilling into lower sediments.

In Vietnam, a nation that began overusing its deep aquifers under French occupation more than 110 years ago, the effect is already pronounced. In the region surrounding the densely populated city of Hanoi — with nearly 2,000 people per square kilometre — it is difficult to escape arsenic-contaminated water, no matter how deeply you drill.

The researchers analysed 512 private tubewells reaching to depths ranging from 10 metres to more than 50 metres throughout the country's Red River Delta. Their findings revealed that 27% of the wells contained levels of arsenic in excess of the World Health Organization's standard of 10 micrograms per litre, says Michael Berg, a senior scientist at the Swiss Federal Institute of Aquatic Science and Technology in Dübendorf and a co-author on the study1. This puts some 3 million people at risk.

The survey, carried out in cooperation with the Hanoi University of Science and Technology, also found harmful levels of other elements — about 7 million people in the Red River Delta are exposed to unsafe levels of at least one element. After arsenic, the most important of these is manganese, which exceeded World Health Organization guidelines in 44% of the wells. Elevated levels of this element can affect neurological development in children.

Mapping the depths

From the survey data, Berg's team created the first three-dimensional groundwater map, using statistical modelling to show levels that are relatively arsenic-free. "It is now clear where water is safe and where it is unsafe. That is one of the most important findings for the public," says Berg.

The map makes it difficult for officials to ignore the arsenic problem, says Dieke Postma, a senior researcher at the Geological Survey of Denmark and Greenland, who has been working in the region since 2004 and is unconnected with the new study. "It's important for the Vietnamese authorities because they haven't had an overview of how big the problem is," he says.

Postma says he hopes that an international scientific conference on the issue, to be held in Hanoi in November, will draw further official attention to arsenic contamination in the region.

The implications of the finding could be serious for countries around the Bengal Basin in South Asia. In Bangladesh, where some 70 million people[2] are exposed, the use of deep aquifers is a more recent phenomenon. Decades ago, aid agencies introduced tube wells as a reliable and clean water source, only to find that the top-most sediment layers, formed in the 12,000 years since the start of the current Holocene epoch, contain naturally occurring arsenic that leaches into the groundwater.

To avoid contamination, wells in the Bengal Basin can be drilled into deep layers that were oxidized during the last ice age, in which the water is free of arsenic, Berg says. These aquifers were created during the Pleistocene epoch, between 12,000 and 2.5 million years ago, and lack the organic carbon that is needed for arsenic to leach into water.

Leaching lower

But if people in the Bengal Basin continue to exploit their water supplies at the current rates, arsenic-laden water from the upper layers may find its way into Pleistocene aquifers, the study suggests.

Berg's team is in contact with scientists in Dhaka to evaluate arsenic migration into deeper sediments.

The group is the first to give real-life evidence that arsenic in deeper layers can get into groundwater. Other lab-based studies[2,3] have suggested that sediments in deeper aquifers tend to keep arsenic out of the water, says William Burgess, a hydrogeologist at the Department of Earth Sciences at University College London. On the basis of the new study, he thinks that such sequestration may not always happen and probably depends on the composition of sediments and the complexity of water flow underground.

"Pumping from the Pleistocene aquifer has certainly had an adverse effect in terms of drawing down arsenic at significantly high concentrations over about 100 years," says Burgess. "These deep wells weren't being monitored 10, 20, 30 years ago, so we don't know how quickly arsenic got down there, but it got there sometime in the past 100 years."

References

[1] Winkel, L. H. E. et al. Proc. Natl Acad. Sci. USA doi:10.1073/pnas.1011915108 (2011).
[2] Burgess, W.G. et al. Nature Geosci. 3, 83-87 (2010).
[3] Stollenwerk, K. G. et al. Sci. Tot. Environ. 379, 133-150 (2007).

High post mining arsenic mobilization after more than 200 years in the oldest Brazilian Gold mining province

2010-12-18T18:14:00.000+01:00

Arsenic and trace metals in river water and sediments from the southeast portion of the Iron Quadrangle, Brazil.

Environ Monit Assess. 2011 Jan;172(1-4):631-42. Epub 2010 Mar 18.
Varejão EV, Bellato CR, Fontes MP, Mello JW.
Departamento de Química, Universidade Federal de Viçosa, Av. P.H. Rolfs, s/n, 36571-000, Viçosa, Minas Gerais, Brazil.
Abstract
The Iron Quadrangle has been one of the most important gold production regions in Brazil since the end of the seventeenth century. There, arsenic occurs in close association with sulfide-rich auriferous rocks. The most abundant sulfide minerals are pyrite and arsenopyrite, yet trace metal sulfides occur in subordinate phases as well. Historical mining activities have been responsible for the release of As and trace metals to both aquatic and terrestrial environments close to mining sites in the region. Therefore, this study was aimed to evaluate the distribution and mobility of As, Cd, Co, Cr, Cu, Ni, Pb, and Zn in streams in the southeast portion of the Iron Quadrangle between the municipalities of Ouro Preto and Mariana, the oldest Brazilian Au mining province. Total concentrations of some trace metals and arsenic in water were determined. The four-stage sequential extraction procedure proposed by the commission of the European Communities Bureau of Reference (BCR) was used to investigate the distribution of these elements in stream sediments. Arsenic concentration in water was > 10 μg L⁻¹ (maximum limit permitted by Brazilian environmental regulations for water destined for human consumption) at all sampling sites, varying between 36.7 and 68.3 μg L⁻¹. Sequential extraction in sediments showed high concentrations of As and trace metals associated with easily mobilized fractions.

Asbestos scandal

2010-12-15T21:53:00.000+01:00

Irresponsible policies could cause an epidemic of malignant lung disease.

"Governments must ban the extraction, processing and use of materials that can cause serious disease".

Nature Editorial

Nature 468: 868 (16 December 2010) doi:10.1038/468868a
Published online 15 December 2010

http://www.nature.com/nature/journal/v468/n7326/full/468868a.html

Viewed through an electron microscope, asbestos fibres look like thin glass straws, some no more than a fraction of a micrometre wide. If inhaled, they penetrate the soft alveoli of the lungs and the membranes that line the chest cavity. And there they stay. Over time, damaged cells can cause a malignant disease called mesothelioma, which often kills people, horribly, less than a year after diagnosis.

Before the widespread industrial use of asbestos began in the late nineteenth century, malignant mesothelioma was unheard of, yet it is now responsible for tens of thousands of deaths around the world every year. After the link between asbestos exposure and the disease was convincingly made in 1960, responsible nations eventually took strong measures to remove the mineral from commercial products and to halt mining and export. Less responsible nations did not; this is a scandal that deserves wider attention.

The United States has still not banned asbestos, despite the millions of dollars spent to clear it from homes and from communities near mines. And Canada has been criticized for plans to expand asbestos mining operations, which export the material to India, Indonesia and the Philippines. Although Canada enforces strict guidelines on asbestos use at home to protect its own people, those in countries to which it sends the mineral have little or no protection. Asbestos exported from Canada and other countries including Russia, Brazil and Kazakhstan is routinely mixed into building materials and consumer products, prized for the same durability that makes it troublesome for living tissue. Owing to the long time between exposure and the onset of disease, 30 years or more, the asbestos trade in North America and elsewhere is creating an epidemic that may take decades to peak and subside.

The minerals industry has long tried to convince regulators that white asbestos — or chrysotile — is safe when handled properly. It argues that only the already controlled forms — blue and brown asbestos, known collectively as amphibole — are of concern.

To support this, industry advocates point to scientific data and studies. Yet although the relevant literature is a mire of conflicting results, this should not be seen as an endorsement of their position. Rather, it reflects a string of industry-sponsored studies designed only to cast doubt on the clear links between chrysotile and lung disease. These are familiar tactics and several countries, including Britain, have seen through them and made the correct decision to ban all forms of asbestos, all of which have been proven to be carcinogenic in humans.

Meanwhile, researchers are finding new causes for concern with other natural fibrous minerals such as erionite (see page 884). Complacency is the problem. Much of the developed world has seen asbestos removed from public spaces, leaving in many minds a false sense of security. The public should once again be made aware of the risks associated with exposure to mineral fibres, as well as some man-made fibres. And governments must ban the extraction, processing and use of materials that can cause serious disease.

Increased lung cancer risks are similar whether arsenic is ingested or inhaled

2010-11-29T14:28:00.000+01:00

Increased lung cancer risks are similar whether arsenic is ingested or inhaled

Allan H. Smith, Ayse Ercumen, Yan Yuan and Craig M. Steinmaus

(From the Arsenic Health Effects Research Program,School of Public Health, University of California, Berkeley, California, USA, and the Office of Environmental Health Hazard Assessment, California Environmental Protection Agency, Oakland, California, USA).

Journal of Exposure Science and Environmental Epidemiology (2009) 19, 343–348

In 1980, the International Agency for Research on Cancer (IARC) determined there was sufficient evidence to support that inorganic arsenic was a human lung carcinogen based on studies involving exposure through inhalation. In 2004, IARC listed arsenic in drinking water as a cause of lung cancer, making arsenic the first substance established to cause human cancer through two unrelated pathways of exposure. It may initially seem counterintuitive that arsenic in drinking water would cause human lung cancer, and even if it did, one might expect risks to be orders of magnitude lower than those from direct inhalation into the lungs. In this paper, we consider lung cancer dose–response relationships for inhalation and ingestion of arsenic by focusing on two key studies, a cohort mortality study in the United States involving Tacoma smelter workers inhaling arsenic, and a lung cancer case–control study involving ingestion of arsenic in drinking water in northern Chile. When exposure was assessed based on the absorbed dose identified by concentrations of arsenic in urine, there was very little difference in the dose–response findings for lung cancer relative risks between inhalation and ingestion. The lung cancer mortality rate ratio estimate was 8.0 (95% CI 3.2–16.5, P<0.001) for an average urine concentration of 1179 mg/l after inhalation, and the odds ratio estimate of the lung cancer incidence rate ratio was 7.1 (95% CI 3.4–14.8, P<0.001) for an estimated average urine concentration of 825 mg/l following ingestion. The slopes of the linear dose-response relationships between excess relative risk (RR-1) for lung cancer and urinary arsenic concentration were similar for the two routes of exposure. We conclude that lung cancer risks probably depend on absorbed dose, and not on whether inorganic arsenic is ingested or inhaled.

Letter to Professor Alastair Summerlee

2010-11-21T21:45:00.000+01:00

Letter to Professor Alastair Summerlee, President and Vice-Chancellor of the University of Guelph, Ontario, Canada
November 21, 2010
To
Professor Alastair Summerlee
President and Vice-Chancellor of the University of Guelph
president@uoguelph.ca
Mr. President,
Having read the announcement that the University of Guelph accepted a $1-million gift from Kinross Gold Corporation [1], I feel obliged to inform you that this gift has been made possible thanks to questionable Kinross’ mining activities, especially at my home town Paracatu, state of Minas Gerais, Brazil.

Your declaration that ‘Kinross has an excellent reputation for leadership in resource management and for its commitment to social responsibility’ is appalling. There is simply no such thing as ‘Kinross’ commitment to social responsibility’, unless we are talking about ‘green washing’ and ‘social washing’.

To get its gold from Brazil’s largest opencast-, world’s lowest grade- (average 0.4 g of gold/ton of ore), largest arsenic grade- (average 2000 g of arsenic/g of gold) gold mine at Paracatu, Kinross Gold operates massive environmental damages, displacement of local people from their homes, chronic poisoning as well as murder.

Kinross claims that it operates under strict legal terms in Brazil. Truth is, Kinross has been sued in several Civil Actions proposed by the Brazilian State and Federal Public Ministries and the Acangau Foundation, among others. Kinross’ robbing and polluting drinking water, polluting soils and the atmosphere with millions of tons of arsenic, cyanide and sulphuric acid among other pollutants, expelling native people from their constitutionally and legally protected territories, hiding or manipulating information and killing people are simply against the Brazilian Constitution and against national and international law. It is also immoral, inhumane and bad for mankind.

The environmental and health liabilities left behind by Kinross Gold Corporation in Paracatu are estimated in the tens of billions, thus 5- to 10-fold the value of all the gold reserves exploited and to be exploited by Kinross in Paracatu. Whereas some of these liabilities are left for Brazilian taxpayers to pay, some are left for mankind to pay.

There is vast scientific evidence that arsenic released by hard rock mining is mobilized in many environmental compartments in the course of years, centuries and millennia. Chronic exposure to environmental arsenic has been implicated as a cause or predisposing factor for each of the top ten causes of death in the world, including vascular diseases, various forms of cancer, diabetes and immunological diseases (see www.sosarsenic.blogspot.com for reviews).

I have recently authored a study in the journal Medical Hypotheses in which I review the hazards of arsenic release from gold mines worldwide, including Kinross' Paracatu gold mine [2]. This study has won immediate coverage in the media [3,4]. In the study, I have estimated that thousands of gold mines worldwide have the potential to release 10-100 kg of arsenic per each human being presently living on planet Earth.

Whereas 100 milligrams of arsenic suffice to acutely kill an adult man, much lesser amounts – in the part per billion range – are enough to chronically kill or cause serious health and economical distresses to billions of people, eroding family and country economies worldwide. This means that less than 0.0001% of all arsenic released by gold mining is enough to cause extraordinary health and environmental damage to mankind. This also means that gold mining corporations like Kinross Gold had to operate at 99.9999% arsenic recovery and immobilization efficiency in order to prevent damage. This degree of efficiency is clearly unattainable, rendering hard rock gold mining a genocidal activity.

Particularly in the case of Paracatu, a study performed by Kinross in collaboration with CETEM indicates an efficiency of only 30% [5], and recent studies performed independently by renowned Brazilian and German institutions implicate Kinross’ mining activities in Paracatu as the cause of active and persistent pollution of air, soils, waters and sediments with arsenic reaching concentrations that are up to 750-fold increased in relation to nationally and internationally accepted safety levels.

Unfortunately, environmental remediation of arsenic is economically unfeasible for affected communities and countries, as has been recently shown by a Swedish team [6].

Therefore, Kinross mining operations in Paracatu and elsewhere are worse than crimes, they are errors that must be avoided because they are difficult if not impossible to remediate, and too bad for all of us.

We trust that you will prioritize the points that I made in this letter, in assessing Kinross’ gold mining activities in Paracatu.

Please do not hesitate to contact me in case of any doubt or in case I can be of any help.

Sincerely,

Sergio U. Dani, MD, DSc
The Medawar Institute for Medical and Environmental
Research/Acangau Foundation, Paracatu, Brazil

References and notes:

[1] Kinross Gold, U of G Announce Chair in Environmental Governance. November 17, 2010 - News Release. From http://www.uoguelph.ca/news/2010/11/kinross_gold_u.html [accessed November 18, 2010].

[2] Dani SU. Gold, coal and oil. Medical Hypotheses doi:10.1016/j.mehy.2009.09.047

[3] http://news.discovery.com/human/human-extinction-doomsday.html

[4] http://www.theglobeandmail.com/life/facts-and-arguments/arsenic-and-our-fate-appearances-count-and-middle-class-theft/article1361341/?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+TheGlobeAndMail-Front+(The+Globe+and+Mail+-+Latest+News

[5] Monte MBM, Lins FF, Dutra AJB, Albuquerque CRF, Tondo LA. The influence of the oxidation state of pyrite and arsenopyrite on the flotation of an auriferous sulphide ore. CT2002-195-00 Comunicação técnica elaborada para o periódico Minerals Engineering. CETEM-Centro de Tecnologia Mineral, MCT-Ministério da Ciência e Tecnologia, Coordenação de Inovação Técnológica - CTEC, Rio de Janeiro, Dezembro/2002.

[6] Forslund J, Samakovlis E, Johansson MV, Barregard L. Does remediation save lives? - on the cost of cleaning up arsenic-contaminated sites in Sweden. Sci Total Environ. 2010 Jul 15;408(16):3085-91.

MIMER notes November 19, 2010

2010-11-19T17:55:00.000+01:00

Urinary arsenic determined in a large US survey

Urinary concentrations of different forms of arsenic have been determined for the United States populations from the National Health and Nutritional Examination Survey (NHANES). The results have been published by the Centers for Disease Control (CDC) in the CDC Fourth National Report on Human Exposure to Environmental Chemicals ("the fourth report", published 2010). For the first time, the fourth report provides comprehensive information about arsenic presence. Urinary total arsenic varied from 5.66 mcg/l (equivalent to 6.58 mcg/g of creatinine) in children to 164 mcg/l (98.8 mcg/g of creatinine) in adults. Some children presented with total urinary arsenic concentration of 178 mcg/l (188 mcg/g creatinine). Arsenic has been associated with all top 10 causes of death worldwide, including cardiovascular disease, cerebrovascular diseases, diabetes, dementias and cancer. The ranges for arsenic are provided so the clinician can compare a patient's readings against national percentiles. The data will help the clinician identify current exposures and monitor the effectiveness of treatments.
Source:
http://www.cdc.gov/exposurereport/data_tables/URXUAS_DataTables.html [accessed 19 November 19, 2010]

Spontaneous pregnancy loss in humans and exposure to arsenic

2010-11-14T03:15:00.000+01:00

Int J Hyg Environ Health. 2010 Oct 1. [Epub ahead of print]
Spontaneous pregnancy loss in humans and exposure to arsenic in drinking water.
Bloom MS, Fitzgerald EF, Kim K, Neamtiu I, Gurzau ES.
Department of Environmental Health Sciences, School of Public Health, University at Albany, State University of New York, Rensselaer, NY, United States; Department of Epidemiology and Biostatistics, School of Public Health, University at Albany, State University of New York, Rensselaer, NY, United States.

Abstract
Maternal exposure to high concentrations of inorganic arsenic (iAs) in naturally contaminated drinking groundwater sources has been associated with an increased risk for the spontaneous loss of clinically recognized pregnancies in several epidemiologic studies. Whereas a large worldwide population depends on drinking groundwater sources with high levels of iAs contamination, in quantities exceeding 10 parts per billion (ppb), an even larger population is likely to be exposed to mild-moderate drinking groundwater iAs contamination, in quantities <10ppb. Only a single epidemiologic study to date has considered spontaneous pregnancy loss in association with consumption of drinking water with mild-moderate iAs contamination; the vast majority of published studies of spontaneous loss addressed populations with substantial exposure. The aim of this review is to evaluate the published literature to assess the plausibility for a causal association between exposure to iAs-contaminated drinking water and the spontaneous loss of clinically recognized pregnancy. In spite of numerous methodologic limitations resulting from circumstance or design, a consistent pattern of increased risk for loss is suggested by the epidemiologic literature. Moreover, these study results are corroborated by a large number of experimental studies, albeit usually conducted at concentrations exceeding that to which humans are exposed via contaminated drinking water. In this review, we discuss sources of human iAs exposure, highlight several experimental studies pertinent to a possible causal link between iAs and spontaneous pregnancy loss in humans, and provide a critical review of published epidemiologic studies of pregnancy loss and drinking water iAs exposures, and their limitations. Based on a review of the published literature, we recommend the future conduct of a two-stage comprehensive prospective study of low-moderate iAs drinking water exposure and spontaneous pregnancy loss.

Behaviour of arsenic in forested catchments

2010-11-14T03:13:00.000+01:00

Environ Pollut. 2010 Oct 5. [Epub ahead of print]
Behaviour of arsenic in forested catchments following a high-pollution period.
Novak M, Erbanova L, Fottova D, Cudlin P, Kubena A.
Department of Geochemistry, Czech Geological Survey, Geologicka 6, 152 00 Prague 5, Czech Republic.

Abstract
Due to high availability of adsorption sites, forested catchments could be net sinks for pollutant arsenic both during the period of increasing and decreasing pollution. We tested this hypothesis along a north-south pollution gradient in spruce die-back affected areas of Central Europe. For two water years (2007-2008), we monitored As fluxes via spruce-canopy throughfall, open-area precipitation, and runoff in four headwater catchments (Czech Republic). Since 1980, atmospheric As inputs decreased 26 times in the north, and 13 times in the south. Arsenic export by runoff was similar to atmospheric inputs at three sites, resulting in a near-zero As mass balance. One site exhibited a net export of As (2.2 g ha(-1) yr(-1)). In contrast, the preceding period (1995-2006) showed much higher As fluxes, and higher As export. Czech catchments do not serve as net sinks of atmospheric As. A considerable proportion of old industrial arsenic is flushed out of the soil.

Chronic arsenicosis in cattle in West Bengal, India

2010-11-14T03:11:00.000+01:00

Sci Total Environ. 2010 Nov 6. [Epub ahead of print]
Chronic arsenicosis in cattle with special reference to its metabolism in arsenic endemic village of Nadia district West Bengal India.
Datta BK, Mishra A, Singh A, Sar TK, Sarkar S, Bhatacharya A, Chakraborty AK, Mandal TK.
Department of Veterinary Pharmacology and Toxicology, West Bengal University of Animal and Fishery Sciences, 37, K.B. Sarani, Kolkata 700037, West Bengal, India.

Abstract
Thirty Milch cattle were selected randomly from a village of Nadia district of West Bengal, India containing high arsenic in water and soil samples. Milk, feces and hair samples were collected to analyze arsenic status in animals. Water and straw samples were also estimated for arsenic. Milk products prepared from milk of cattle rearing in arsenic prone village were also collected to quantify total arsenic and speciation of arsenic in milk and feces samples were also carried out. It was observed that high amount of arsenic was present in milk, feces, hair of cattle and water and straw samples in arsenic prone village. Milk product also contained significant amount of arsenic than that of milk product of control village. Speciation study revealed arsenite fraction was mainly eliminated through milk, whereas organoarsenic species were mainly excreted through feces.

Migration of arsenic in groundwater from West Bengal

2010-11-14T03:08:00.000+01:00

Water Res. 2010 Jul;44(14):4171-85. Epub 2010 May 21.
Migration of As, and (3)H/(3)He ages, in groundwater from West Bengal: Implications for monitoring.
McArthur JM, Banerjee DM, Sengupta S, Ravenscroft P, Klump S, Sarkar A, Disch B, Kipfer R.
Department of Earth Sciences, University College London, Gower Street, London WC1E 6BT, UK. j.mcarthur@ucl.ac.uk

Abstract
From 2002 to 2010 inclusive we monitored concentrations of arsenic (As) and major ions (Ca, Mg, Sr, Na, K, Fe, Mn, Cl, and SO(4)) in groundwater from 14 domestic wells and three piezometer nests in a shallow aquifer (<60 m depth), and 3 wells in a deep aquifer (>70 m depth), in southern West Bengal, India. In the deep aquifer, concentrations of As did not change over time despite increases in the concentration of Fe in two wells. The shallow aquifer occurs in two sedimentological settings: palaeo-channel and palaeo-interfluve. At the top of the shallow aquifer of the palaeo-channel, decreases in all constituent concentrations with time, and an (3)H/(3)He age of 1.4 years, proves that the aquifer is beginning to be flushed of pollutants. In As-polluted groundwater (>50 microg/L As) tapped from deeper grey sands of the shallow, palaeo-channel, aquifer, concentrations of As were mostly stable over time, but both increases and decreases occurred with time in response to downward migration of the chemically-stratified water column. In groundwater tapped from Pleistocene brown sands, the concentration of As remained either low and stable (<2 microg/L As), or increased at rates up to 34 microg/L per year. The increases were caused by the flow of As-rich groundwater either downward into brown sand at the base of palaeo-channels, or laterally into a confined, unpolluted, palaeo-interfluvial, aquifer of brown sand that lies regionally beneath a palaeosol. Under the present pumping regime, the prognosis for As-pollution in the shallow aquifer is complex. Wells in brown sand may become polluted over timescales of as little as 2 years, whilst some wells tapping As-polluted groundwater from grey sand will become fit for potable use (<50 microg/L) within a few decades. The evidence of flushing, and of declining As in some of the groundwater from palaeo-channels, which are conduits for recharge of the confined, As-free, palaeo-interfluve aquifer, and probably also the deeper aquifer, offers hopes that the spread of As-pollution will be limited.

Arsenic round the world: a review.

2010-11-14T03:04:00.000+01:00

Arsenic round the world: a review.
Talanta. 2002 Aug 16;58(1):201-35.
Mandal BK, Suzuki KT.
Graduate School of Pharmaceutical Sciences, Chiba University, Chiba 263-8522, Japan.

Abstract
This review deals with environmental origin, occurrence, episodes, and impact on human health of arsenic. Arsenic, a metalloid occurs naturally, being the 20th most abundant element in the earth's crust, and is a component of more than 245 minerals. These are mostly ores containing sulfide, along with copper, nickel, lead, cobalt, or other metals. Arsenic and its compounds are mobile in the environment. Weathering of rocks converts arsenic sulfides to arsenic trioxide, which enters the arsenic cycle as dust or by dissolution in rain, rivers, or groundwater. So, groundwater contamination by arsenic is a serious threat to mankind all over the world. It can also enter food chain causing wide spread distribution throughout the plant and animal kingdoms. However, fish, fruits, and vegetables primarily contain organic arsenic, less than 10% of the arsenic in these foods exists in the inorganic form, although the arsenic content of many foods (i.e. milk and dairy products, beef and pork, poultry, and cereals) is mainly inorganic, typically 65-75%. A few recent studies report 85-95% inorganic arsenic in rice and vegetables, which suggest more studies for standardisation. Humans are exposed to this toxic arsenic primarily from air, food, and water. Thousands and thousands of people are suffering from the toxic effects of arsenicals in many countries all over the world due to natural groundwater contamination as well as industrial effluent and drainage problems. Arsenic, being a normal component of human body is transported by the blood to different organs in the body, mainly in the form of MMA after ingestion. It causes a variety of adverse health effects to humans after acute and chronic exposures such as dermal changes (pigmentation, hyperkeratoses, and ulceration), respiratory, pulmonary, cardiovascular, gastrointestinal, hematological, hepatic, renal, neurological, developmental, reproductive, immunologic, genotoxic, mutagenetic, and carcinogenic effects. Key research studies are needed for improving arsenic risk assessment at low exposure levels urgently among all the arsenic research groups.

Does remediation save lives?

2010-09-08T20:16:00.000+02:00

Does remediation save lives? - on the cost of cleaning up arsenic-contaminated sites in Sweden.

Forslund J, Samakovlis E, Johansson MV, Barregard L.

Environmental Economics, National Institute of Economic Research, Stockholm, Sweden.

Sci Total Environ. 2010 Jul 15;408(16):3085-91. Epub 2010 May 1.

Abstract

Sweden has only just begun remediation of its many contaminated sites, a process that will cost an estimated SEK 60,000 million (USD 9100 million). Although the risk assessment method, carried out by the Swedish EPA, is driven by health effects, it does not consider actual exposure. Instead, the sites are assessed based on divergence from guideline values. This paper uses an environmental medicine approach that takes exposure into account to analyse how cancer risks on and near arsenic-contaminated sites are implicitly valued in the remediation process. The results show that the level of ambition is high. At 23 contaminated sites, the cost per life saved varies from SEK 287 million to SEK 1,835,000 million, despite conservative calculations that in fact probably underestimate the costs. It is concluded that if environmental health risks are to be reduced, there are probably other areas where economic resources can be used more cost-effectively.

Gold mining largest source of anthropogenic arsenic

2010-08-24T19:42:00.000+02:00

Gold mining is by far the largest single source of anthropogenic arsenic

By S. U. Dani, August 24, 2010

Table 1 shows that gold mining is by far the largest single source of world anthropogenic arsenic. If all estimated gold reserves are exploited, then gold mining will release estimated 104 million tonnes of arsenic in the environment. This is more than 20 times as much arsenic as has been released from all anthropogenic sources in the industrial age so far.

Subchronic arsenic toxicity in rats

2010-08-23T20:19:00.000+02:00

Environ Toxicol. 2010 Aug 19. [Epub ahead of print]

Pathological, immunological and biochemical markers of subchronic arsenic toxicity in rats

Nain S, Smits JE.

Ecosystem & Public Health, Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada T2N 4Z6.

Abstract

Subchronic exposure to arsenic in rats was investigated to identify sensitive indicators of subclinical toxicity in rats. Immunological, pathological, and biochemical bioindicators were examined in rats exposed to arsenic in their drinking water. Juvenile male Wistar rats were allocated to four treatment groups receiving 0, 0.4, 4, and 40 ppm of arsenite in drinking water for 18 wks. Besides daily monitoring for clinical signs of adverse health effects, clinical biochemistry, B-cell-mediated and innate immune responses, plus gross, and histopathology were examined. In vitro tests of oxidative damage to basic cellular constituents, lipids, proteins, and nucleic acids, were measured using thiobarbituric acid reacting substances (TBARS) assays, protein carbonyl formation, and 8-hydroxydeoxyguanosine (8-OHdG), respectively. Clinical changes in the rats were limited to decreased feed and water intake in the high- (40 ppm) dose group (P < 0.05), however, growth rate was not affected. Serum biochemical changes occurred in blood urea nitrogen, K(+), Cl(-), and alanine aminotransferase (ALT) from arsenic exposure. Immunotoxicity was evident through a dose-dependent suppression of the secondary antibody-mediated response to a T-cell-dependent antigen, keyhole limpet hemocyanin (KLH). Histopathology of the liver revealed marked fatty infiltration and vacuolization particularly evident in periacinar hepatocytes. This pattern of toxicopathology in the high-exposure group may be related to the significantly higher (P < 0.05) oxidative stress, demonstrated through lipid peroxidation (TBARS assay) in the rats exposed to 40 ppm arsenite. The present study revealed that young, growing rats exposed to arsenic for 18 wks tolerated exposures up to 4 ppm. At higher doses, there was evidence of hepatotoxicity, humoral immunity was compromised, and an adverse effect on hepatic organelle and cell membranes was evident through a dose dependent increased in oxidative stress. (c) 2010 Wiley Periodicals, Inc. Environ Toxicol, 2010.

Oil spills raise arsenic levels in the ocean

2010-08-16T20:39:00.000+02:00

Imperial College London News Release
For Immediate Release:
Friday 2 July 2010

Oil spills raise arsenic levels in the ocean, says new research

Oil spills can increase levels of toxic arsenic in the ocean, creating an additional long-term threat to the marine ecosystem - News Release

Oil spills can increase levels of toxic arsenic in the ocean, creating an additional long-term threat to the marine ecosystem, according to research published today in the journal Water Research.

Arsenic is a poisonous chemical element found in minerals and it is present in oil. High levels of arsenic in seawater can enable the toxin to enter the food chain. It can disrupt the photosynthesis process in marine plants and increase the chances of genetic alterations that can cause birth defects and behavioural changes in aquatic life. It can also kill animals such as birds that feed on sea creatures affected by arsenic.

In today’s study, a team from Imperial College London has discovered that oil spills can partially block the ocean’s natural filtration system and prevent this from cleaning arsenic out of the seawater. The researchers say their study sheds light on a new toxic threat from the Gulf of Mexico oil leak.

Arsenic occurs naturally in the ocean, but sediments on the sea floor filter it out of seawater, which keeps the levels of naturally occurring arsenic low. However, arsenic is also flushed into the ocean in wastewater from oil rigs and from accidental oil spills and leakages from underground oil reservoirs.

Oil spills can partially block sediments on the seafloor from filtering arsenic out of seawater

In the study, the researchers discovered that oil spills and leakages clog up sediments on the ocean floor with oil, which prevents the sediments from bonding with arsenic and burying it safely underground with subsequent layers of sediment. The scientists say this shutdown of the natural filtration system causes arsenic levels in seawater to rise, which means that it can enter the marine ecosystem, where it becomes more concentrated and poisonous the further it moves up the food chain.

The scientists say their work demonstrates how the chemistry of sediments in the Gulf of Mexico may be affected by the current oil leak.

Professor Mark Sephton, from the Department of Earth Science and Engineering at Imperial College London, says:

“We can’t accurately measure how much arsenic is in the Gulf at the moment because the spill is ongoing. However, the real danger lies in arsenic’s ability to accumulate, which means that each subsequent spill raises the levels of this pollutant in seawater. Our study is a timely reminder that oil spills could create a toxic ticking time bomb, which could threaten the fabric of the marine ecosystem in the future.”

Wimolporn Wainipee, postgraduate and lead author of the study from the Department of Earth Science and Engineering at Imperial College London, adds:

“We carried out our study before the leak in the Gulf of Mexico occurred, but it gives us a big insight into a potential new environmental danger in the region. Thousands of gallons of oil are leaked into the world’s oceans every year from big spills, offshore drilling and routine maintenance of rigs, which means many places may be at risk from rising arsenic levels, which could in the long run affect aquatic life, plants and the people who rely on the oceans for their livelihoods.”

For their research, the team analysed a mineral called goethite, one of the most abundant ocean sediments in the world, which is an iron bearing oxide.

The team carried out experiments in the laboratory that mimicked conditions in the ocean, to see how the goethite binds to arsenic under natural conditions. They discovered that seawater alters the chemistry of goethite, where low pH levels in the water create a positive change on the surface of goethite sediments, making them attractive to the negatively charged arsenic.

However, the scientists discovered that when they added oil, this created a physical barrier, covering the goethite sediments, which prevented the arsenic in the oil from binding to them. The team also found that the oil changed the chemistry of the sediments, which weakened the attraction between the goethite and arsenic.

In the future, the researchers plan to analyse other minerals such as clays and carbonates that are sediments on the ocean floor. Sediment content varies from ocean to ocean and the researchers will analyse how oil affects their ability to bind to arsenic after a spill.

----
For further information please contact:

Colin Smith
Press Officer
Imperial College London
Email: cd.smith@imperial.ac.uk
Tel: +44 (0)207 594 6712
Out of hours duty press officer: +44 (0)7803 886 248
Website: www.imperial.ac.uk

Notes to editors:

1.“The effect of crude oil on arsenate adsorption on goethite” Water Research journal, Friday 2 July 2010 (published in hardcopy)

The full listing of authors and their affiliations for this paper is as follows:
(1) Wimolporn Wainipee, (1) Dominik J. Weiss, (1) Mark A. Sephton, (1) Barry J. Coles , (1) Richard Court, (2) Catherine Unsworth,
(1) Department of Earth Science and Engineering, Imperial College London, London SW7 2AZ, UK
(2) Natural History Museum, Department of Mineralogy, London, SW7 5BD, UK

2. About Imperial College London

Consistently rated amongst the world's best universities, Imperial College London is a science-based institution with a reputation for excellence in teaching and research that attracts 14,000 students and 6,000 staff of the highest international quality. Innovative research at the College explores the interface between science, medicine, engineering and business, delivering practical solutions that improve quality of life and the environment - underpinned by a dynamic enterprise culture.

Since its foundation in 1907, Imperial's contributions to society have included the discovery of penicillin, the development of holography and the foundations of fibre optics. This commitment to the application of research for the benefit of all continues today, with current focuses including interdisciplinary collaborations to improve global health, tackle climate change, develop sustainable sources of energy and address security challenges.

In 2007, Imperial College London and Imperial College Healthcare NHS Trust formed the UK’s first Academic Health Science Centre. This unique partnership aims to improve the quality of life of patients and populations by taking new discoveries and translating them into new therapies as quickly as possible.

Website: www.imperial.ac.uk

Opencast coal mines in England

2010-08-15T11:43:00.001+02:00

BBC News
15 August 2010 Last updated at 06:30 GMT
http://www.bbc.co.uk/news/uk-10977640

More opencast mine bids 'likely on greenfield sites'

Applications for opencast mining on greenfield sites are likely to increase to meet the UK's demand for energy, the British Geological Survey has said.

The research council says the stock of brownfield sites suitable for opencast mining is now running out.

Mining corporation UK Coal says this supply of fossil fuel is vital to meet energy demands.

But opponents say opencast - or surface - mining is dirty and creates eyesores which destroy areas of countryside.

Most of opencast mining in the UK currently takes place on brownfield sites, but that stock is running out and the British Geological Survey says more applications are expected in the future to mine in the open countryside.

Environmental groups say opencast mining ruins the natural habitat, but UK Coal says there are safeguards in place to protect the countryside and mining companies are legally obliged to restore the land when the mine finally closes.

Opencast mines in the UK are expected to produce 10m tonnes of coal this year.

Mountain mining damages streams

2010-08-15T09:31:00.000+02:00

Published online 9 August 2010 | Nature 466, 806 (2010) | doi:10.1038/466806a

Mountain mining damages streams

Study shows that stripping mountains for coal has a much greater impact than urban growth.

Natasha Gilbert
Pittsburgh, Pennsylvania

West Virginia’s mountains contain valuable low-sulphur coal. Photograph: P. Souza/Chicago Tribune/MCT/Newscom

The controversial practice of stripping off the tops of mountains to mine coal, long suspected of polluting streams, is guilty as charged, scientists say.

On 3 August, researchers at the Ecological Society of America conference in Pittsburgh, Pennsylvania, presented what they say is the first conclusive evidence of a direct link between this type of mining and environmental damage. Their research has teased apart the effects of mountain-top mining and urbanization on local water quality in West Virginia, and found that even relatively small mining operations can cause serious harm to ecosystems.

"Even at very low levels of mining we found a dramatic impact on water quality and stream composition," Emily Bernhardt, a biologist at Duke University in Durham, North Carolina, and one of the study's lead researchers, told Nature. The scientists have called on the US Environmental Protection Agency (EPA) to tighten the water pollution limits faced by mining companies.

Mountain-top mining is widespread in eastern Kentucky, West Virginia and southwestern Virginia. To expose seams of coal, mining companies strip away forests and break up rock with explosives. The rubble is dumped in the valleys, often burying streams. The loss of vegetation and topsoil can cause flooding, and the water emerging from the debris contains toxic solutes including selenium, metals and sulphates, says Bernhardt.

The EPA recommends that mining activity should not increase the electrical conductivity of stream water (a measure of its ionic concentration) beyond 500 microsiemens per centimetre (µS cm−1). Yet a previous study1 demonstrated significant changes in the size and composition of macro-invertebrate communities — such as mayflies and caddis flies — at lower conductivity levels. A second study2 found that increases in the concentration of metals in stream water, and decreases in stream invertebrate biodiversity, were correlated with increased sulphate concentrations, an indicator of mining. But neither study established a direct link between mining and the environmental changes.

Bernhardt and her colleagues overlaid images taken by satellites and aircraft of mining activity in West Virginia's Appalachian Mountains onto topographic maps of the area, allowing them to estimate the amount of mining taking place in mountain watersheds between 1996 and 2009. The research team also had access to data on water quality and invertebrate biodiversity for 478 sites in the area, collected over the same period by the West Virginia Department of Environmental Protection.
“Even at very low levels of mining we found a dramatic impact on water quality and stream composition.”

Mining had occurred at 208 of those sites, where the average water conductivity was 650 µS cm−1. In the most intensively mined areas, where 92% of the watershed had been mined at some point, conductivity levels rose to 1,100 µS cm−1. Bernhardt says that even in areas where just 2.5% of the watershed had been mined, some 30% of streams still had conductivity levels greater than the EPA's recommendation. The team also noted "sharp declines" in some stream invertebrates in areas where as little as 1% of the watershed had been mined.

William Schlesinger, a biogeochemist at the Cary Institute of Ecosystem Studies in Millbrook, New York, says the results are "significant" as "they directly link changes in the stream water chemistry to the area of the watersheds that has been disturbed by mining activities".

The study also addresses the mining industry's contention that water-quality standards should not be tightened because stream conductivity changes often reflect urbanization and other changes in land use. Earlier this year, the National Mining Association (NMA), based in Washington DC, said in a statement: "No evidence has been presented that uniquely correlates higher conductivity levels with coal mining or valley fills."

In 202 of the sites Bernhardt and her colleagues studied, however, there was no mining activity, but some urban development. Water at these sites had an average conductivity of 228 µS cm−1 — much lower than the average at mined sites. In 30 other sites, no mining or urban development had taken place, and these control sites had an average conductivity of 105 µS cm−1.

Bernhardt says she was "shocked" by the differences. But she declined to say at what level she thinks the EPA should set the threshold, saying only that "it appears you get effects at much lower levels of conductivity than previously thought". Luke Popovich, the NMA's vice-president for external communications, declined to comment on the study without seeing its data, but notes that the conductivity limit set by the EPA is "difficult or impossible for mining operations to meet. In our view, this begs the larger question of whether conductivity as employed here can tell us much at all about the impacts of mining on biodiversity."

"Conductivity should not be used as an exclusive tool for isolating impacts from mining activity from the many other sources or factors that may impact water quality," he adds.

In a statement to Nature, the EPA says it believes that the study's results are "generally consistent" with its own research, which is "currently being reviewed" by its science advisory board. "EPA will continue to rely on the best available science as it reviews proposals for new surface coal mining projects under the Clean Water Act," it adds.

References

1. Pond, G. J. et al. J. N. Am. Benthol. Soc. 27, 717-737 (2008).
2. Palmer, M. A. et al. Science 372, 148-149 (2010).

General ban on the use of cyanide in Europe: resolution 2010-0145

2010-07-18T15:10:00.000+02:00

European Parliament resolution of 5 May 2010 on a general ban on the use of cyanide mining technologies in the European Union

The European Parliament ,

– having regard to Article 191 of the Treaty on the Functioning of the European Union,

– having regard to the precautionary principle, as set out in the Rio Declaration on Environment and Development and in the Convention on Biological Diversity adopted in Rio de Janeiro in June 1992,

– having regard to the environmental objectives of Directive 2000/60/EC of the European Parliament and of the Council of 23 October 2000 establishing a framework for Community action in the field of water policy ('Water Framework Directive'),

– having regard to Directive 2006/21/EC of the European Parliament and of the Council of 15 March 2006 on the management of waste from extractive industries, which provides for the use of cyanide in mining, at the same time laying down maximum permissible cyanide levels,

– having regard to Directive 2003/105/EC of the European Parliament and of the Council of 16 December 2003 amending Council Directive 96/82/EC (Seveso II) on the control of major-accident hazards involving dangerous substances, which states that '[…] certain storage and processing activities in mining [...] have potential to produce very serious consequences',

– having regard to Directive 2004/35/EC of the European Parliament and of the Council of 21 April 2004 on environmental liability, under which Member States may allow operators not to bear the costs of environmental damage if certain conditions can be shown to have been met,

– having regard to the 18-month programme of the Spanish, Belgian and Hungarian Presidencies and its priorities on water policy and biodiversity,

– having regard to the measures taken by the Czech Republic concerning a general ban on cyanide technologies, through the amendment of Mining Act No 44/1988 in 2000, to the amendment of Hungarian Mining Act No 48/1993 in 2009, introducing a ban on cyanide-based mining technologies on the territory of Hungary, and to the German decree passed in 2002 prohibiting cyanide-leach mining,

– having regard to Rule 115(5) of its Rules of Procedure,

A. whereas the United Nations has declared 2010 the International Year of Biodiversity, inviting the world to take action to safeguard the diversity of life on earth,

B. whereas cyanide is a highly toxic chemical used in the gold-mining industry, one which qualifies as a main pollutant under Annex VIII to the Water Framework Directive and which can have a catastrophic and irreversible impact on human health and the environment, and thus on biodiversity,

C. whereas in their Joint Position on sustainable mining issued at their 14th Meeting on 25 May 2007 in Prague (Czech Republic) the Environment Ministers of the Visegrad Group of Countries (Czech Republic, Hungary, Poland and Slovakia) expressed their concerns about the hazardous technologies used and planned for mining activities at various sites in the region, entailing considerable environmental hazards with potential transboundary consequences,

D. whereas, in the framework of the Sofia Convention on Cooperation for the Protection and Sustainable Use of the Danube River, the Parties agreed that, besides its status as a priority hazardous substance under the Water Framework Directive, cyanide qualifies as a relevant hazardous substance,

E. whereas over the past 25 years more than 30 major accidents involving cyanide spills have occurred worldwide, the worst taking place 10 years ago, when more than 100 000 cubic meters of cyanide-contaminated water were released from a gold-mine reservoir into the Tisza-Danube River system and caused the largest ecological disaster in the history of central Europe at that time, and whereas there is no real guarantee that such accidents will not occur again, especially taking into account the increasing incidence of extreme weather conditions, inter alia heavy and frequent precipitation events, as projected by the Fourth Assessment Report of the Intergovernmental Panel on Climate Change,

F. whereas several EU Member States are still considering new projects for large-scale open-cast gold mines using cyanide technologies in densely inhabited areas, projects which pose further potential threats to human health and the environment,

G. whereas under the Water Framework Directive Member States are obliged to achieve and preserve the 'good status' of water resources and to prevent their pollution with hazardous substances; whereas, however, that good status could also depend on water quality in a river basin located in neighbouring countries which use cyanide mining technologies,

H. whereas the cross-border effects of accidents involving cyanide, particularly with regard to contamination of large river basins and groundwater supplies, emphasises the need for an EU approach to the serious environmental threat posed by cyanide mining,

I. whereas prudential rules and proper financial guarantees are still lacking, and whereas the implementation of the existing legislation on cyanide mining also depends on the skills of the executive powers of each Member State, so that it is only a matter of time until human negligence leads to an accident,

J. whereas the Mining Waste Directive has not been fully implemented in some Member States,

K. whereas cyanide mining provides few jobs, and only for a period of eight-16 years, whilst it runs the risk of causing enormous cross-border ecological damage the cost of which is usually not met by the responsible operating companies, which generally disappear or go bankrupt, but by the state, i.e. by taxpayers,

L. whereas operating companies do not have long-term insurance that would cover the costs incurred in the event of a future accident or malfunction,

M. whereas one tonne of low-grade ore must be extracted in order to produce two grams of gold, leaving enormous amounts of mining waste on the sites, whilst 25-50% of the gold ultimately remains in the waste stockpile; whereas, in addition, large-scale cyanide mining projects use several million kilograms of sodium cyanide per year, the transportation and storage of which itself offers the potential for catastrophic consequences in the event of a failure,

N. whereas alternatives to cyanide mining which could replace cyanide-based technologies do exist,

O. whereas strong public protests are being organised against ongoing cyanide mining projects across Europe, involving not only individual citizens, local communities and NGOs, but also state organisations, governments and politicians,

1. Considers that compliance with the EU's objectives under the Water Framework Directive, namely to achieve good chemical status for water resources and to protect water resources and biological diversity, can be achieved only by banning cyanide mining technology;

2. Calls on the Commission to propose a complete ban on the use of cyanide mining technologies in the European Union before the end of 2011, since this is the only safe way to protect our water resources and ecosystems against cyanide pollution from mining activities, and to carry out an ordinary impact assessment at the same time;

3. Takes note of the relevant initiatives within the EU and the UN systems and strongly encourages the development and application of safer – in particular cyanide-free – mining alternatives;

4. Calls on the Commission and the Member States not to support, either directly or indirectly, any mining projects in the EU that involve cyanide technology until the general ban is applicable, nor to support any such projects in third countries;

5. Calls on the Commission to encourage industrial reconversion of the areas where cyanide mining was banned, through appropriate financial support for alternative green industries, renewable energy and tourism;

5. Calls on the Commission to propose an amendment to existing legislation on the management of waste from the extractive industries requiring that every operating company should take out insurance to cover compensation for damage and all remedial costs incurred in restoring a site to its original ecological and chemical status in the event of an accident or malfunction;

6. Instructs its President to forward this resolution to the Council, the Commission and the parliaments and governments of the Member States.

Arsenic in contaminated milk

2010-07-18T01:24:00.000+02:00

Long-term consequences of arsenic poisoning during infancy due to contaminated milk powder

Dakeishi M, Murata K, Grandjean P. 2006. Long-term consequences of arsenic poisoning during infancy due to contaminated milk powder. Environ. Health 5:31

Email Dr. Dakeishi at dake@med.akita-u.ac.jp

Arsenic toxicity is a global health problem affecting many millions of people. The main source of exposure is drinking water contaminated by natural geological sources. Current risk assessment is based on the recognized carcinogenicity of arsenic, but neurotoxic risks have been overlooked. In 1955, an outbreak of arsenic poisoning occurred among Japanese infants, with more than 100 deaths. The source was contaminated milk powder produced by the Morinaga company. Detailed accounts of the Morinaga dried milk poisoning were published in Japanese only, and an overview of this poisoning incident and its long-term consequences is therefore presented. From analyses available, the arsenic concentration in milk made from the Morinaga milk powder is calculated to be about 4-7 mg/L, corresponding to daily doses slightly above 500 microg/kg body weight. Lower exposures would result from using diluted milk. Clinical poisoning cases occurred after a few weeks of exposure, with a total dose of about 60 mg. This experience provides clear-cut evidence for hazard assessment of the developmental neurotoxicity. At the present time, more than 600 surviving victims, now in their 50s, have been reported to suffer from severe sequelae, such as mental retardation, neurological diseases, and other disabilities. Along with more recent epidemiological studies of children with environmental arsenic exposures, the data amply demonstrate the need to consider neurotoxicity as a key concern in risk assessment of inorganic arsenic exposure.

Difficult to clean up

2010-07-17T12:34:00.000+02:00

Several Sierra trails are toxic, group says

June 23, 2010|By Kelly Zito, Chronicle Staff Writer

A mountain biker cruises from the Sierra Buttes to Downieville, a hub for bikers. Although the Sierra Fund points to problems in Downieville, the Mountain Bike and Big Boulder trails were fine. Credit: Al Seib / Los Angeles Times 2007.

The thousands of mine shafts that pockmark the Sierra Nevada and testify to California's Gold Rush riches have also left a legacy of toxic contamination in some of the state's popular recreation areas, according to a new study.

Soil tests on a handful of trails near mine mouths in the foothills have revealed extremely high levels of lead, arsenic and asbestos, said researchers at the Sierra Fund, a small environmental advocacy group.

The naturally occurring minerals were pounded to dust generations ago and carted to the surface, where they are now stirred up and inhaled by hikers, off-roaders, bikers and horseback riders.

The Gold Rush "not only brought wealth and hundreds of thousands of people to California, it also brought mining machines that ripped down sides of mountains and tunneled thousands of feet into rock, leaving behind arsenic and lead," said Elizabeth Martin, chief executive of the nonprofit group. "This is the longest neglected environmental problem in California."

While their analysis was limited to 80 samples from 11 trails and recreation spots in the Foresthill, Downieville and Nevada City areas, the group says California's 47,000 abandoned mines pose significant threats to public safety, particularly in the dry summer months when families flock to the foothills.

"A lot of people are aware that their kids can fall into a hole at an old mine. But they don't know that asbestos fibers can lodge into their lungs or lead can be absorbed into their skin," Martin said in an interview Tuesday.

For that reason, the group said additional testing must be done in select areas where historic mine waste intersects with well-trafficked trails. The fund is also pushing for warning signs and, in some cases, restricting access to public trails with high levels of hazardous minerals.

Federal attention

So many mines are scattered across different landscapes and under various ownership that it is unclear who would coordinate such an effort and how - not just in California but across the country.

With development and recreational activity encroaching on remote areas, the problem has gained the attention of federal authorities.

A federal audit in 2008 charged the Bureau of Land Management, which controls a number of abandoned mining sites in California, Nevada, Arizona and other states, with endangering public health by failing to clean up arsenic, lead and mercury near the shafts or to erect barriers around them. In the Rand Mining District outside Los Angeles, the inspector general of the Interior Department found piles of toxic mine waste in residential areas as well as biking trails awash in arsenic particles.

That same year, the agency closed about half of the Clear Creek Management Area, a 31,000-acre off-road vehicle paradise in the hills outside of Hollister, after a U.S. Environmental Protection Agency report said waste from the defunct asbestos mining in the area posed a serious risk to those who work, camp, hunt and ride on the property.

Above safe levels

In the Sierra Fund's study, researchers reported levels of arsenic, asbestos and lead well above levels deemed safe for human exposure. At the Foresthill Off-Highway Vehicle area near the Marall Chrome Mine pit, science director Carrie Monohan said lead levels were nearly 18 times the state and federal standards, and 40 percent of the soil samples showed asbestos contamination.

Asbestos, a mineral that shows up in nature as bundles of tiny, twisty fibers, is of significant concern because it can embed in throat and lung tissue, causing cancer and other respiratory diseases.

Difficult to clean up

Because of the diffuse nature of the hazardous minerals in surface soils, they are almost impossible to clean up, according to David Christy, spokesman with the Bureau of Land Management's Central California division.

"The technology is a challenge," he said. "The approach to cleaning up mines is steam cleaning them and cementing over them, and that costs a lot of money."

Under President Obama's federal stimulus plan, California received about $20 million of the $73 million set aside for cleaning and maintaining abandoned mines nationwide. Some estimates peg the number of abandoned mines in the United States at 500,000 and the amount needed to detoxify them in the billions.

E-mail Kelly Zito at kzito@sfchronicle.com.
(C) San Francisco Chronicle 2010

The Worldwide Campaign

2010-07-15T22:00:00.001+02:00

Stop an invisible mass killing

The worldwide campaign

Millions of people worldwide are becoming ill or dying every day, without it being known that the cause of this mass killing is chronic arsenic poisoning.

Arsenic occurs naturally all over the world, but some human activities such as hard rock mining for gold, as well as burning coal and oil and using contaminated groundwater for drinking and irrigation have largely surpassed the natural sources of arsenic, with modern gold mining being by far the most important man-made source of arsenic [1].

In addition, arsenic is still used as an ingredient in various industries, in the production of feed additives, drugs, pesticides, wood preservatives and glass, among others.

Why is arsenic so poisonous?

Arsenic is one of the most potent environmental toxins. Because it targets widely dispersed enzyme reactions, arsenic affects nearly all organ systems. All 10 leading causes of death as ranked by the World Health Organization (WHO) can be caused by arsenic: cardiovascular diseases, cancer, diabetes, diseases of the nervous system, among others. Even infectious diseases can be aggravated by arsenic, because it disrupts the normal functioning of the immune system.

It requires less than 1 g of arsenic to kill 5 adult people within hours. Chronic poisoning by arsenic requires much lesser amounts within much longer exposure times.

Just 1 part of arsenic per billion parts of drinking water (1 ppb) over a long exposure time already poses a real health and environmental hazard [2-5]. However, many countries still adopt 10 parts per billion (10 ppb, or 10 microgram/liter) as maximum permitted concentration.

Less than 10 parts of arsenic per million parts of soil (<10 ppm, or <10 milligram/kg) are associated with prevalence and mortality from Alzheimer disease and other dementias [6]. However, many countries still adopt maximum permitted concentrations varying from 10-100 ppm.
Figure 1 – Arsenic concentration in European soils (2007). Source: FOREGS-Projekt. http://www.gtk.fi/publ/foregsatlas/maps/Floodplain/f_xrf_as_edit.pdf
How does arsenic get into our bodies?

Our bodies absorb arsenic primarily via ingestion and inhalation. We do not realize this, because arsenic is odourless, tasteless and colourless. The exposure dose is the cumulative exposure from all routes. As an effect of chronic exposure to even low-level arsenic, a number of cells become ill or die within our bodies every day - a truly invisible mass-killing.

Arsenic-associated diseases typically have a long latency, so that many patients exposed to arsenic remain symptom-free for years or even decades. The chronic illnesses caused by arsenic provoke enormous suffering, pose huge economical burdens to our families and countries, and to humanity.

Figure 2 – Arsenic in the groundwater worldwide. Source: Amini M, Abbaspour KC, Berg M, Winkel L, Hug SJ, Hoehn E, Yang H, Johnson CA. 2008. Preliminary statistical modeling of global geogenic arsenic contamination in groundwater. Environmental Science & Technology 42:3669-3675.

Why is gold mining so dangerous?

Modern, large scale hard rock gold mining is the most dangerous source of the pollution, because it releases millions of tonnes of arsenic from the rocks each year in various regions of our planet. These incredible amounts of released arsenic are a persistent cause of mass killing all over the world.

Modern gold mining also employs cyanide compounds as base metal solubilizing agents. The European Parliament has decided to prohibit cyanide in metal mining, beginning in 2011. This is an important move that we must support because cyanide is a potent acute killer of a wide range of plant and animal species including humans. However, arsenic is even more dangerous than cyanide, and large scale gold mining activities release millions of tonnes of arsenic each year, causing persistent mass killings all over the world.

Gold is naturally found inside the rocks that contain the highest amounts of arsenic. Hard rock mining activities that involve crushing and milling arsenic-bearing rocks, such as arsenopyrite result in the dispersal of incredible amounts of toxic arsenic that would otherwise remain trapped in these rocks.

The released arsenic can travel long distances with wind and water, affecting plant, animal and human health on a global scale, even decades or centuries after mining operations have stopped. Typically, the losses and damages impinging upon our health only become manifested long after the mining operations have finished.

Some estimates peg the number of abandoned small gold mines worldwide at the hundreds of thousands and the amount needed to detoxify them in the billions. However, modern gold mining has turned into a large-scale business, and liabilities have grown accordingly in the trillions.

One of the world’s largest gold mines is located on the outskirts of the city of Paracatu, Brazil, with 84 thousand inhabitants. The Paracatu gold mine is Brazil’s largest open cut gold mine. It is operated by the Canadian Kinross Gold Corporation. This mining operation is leading to one of the most serious, persistent man-made increases in the environmental concentration of arsenic ever seen on the history of gold mining [7]. With over one million tonnes of arsenic to be released from the rocks in the next 30 years of mining activities, the Paracatu mine is one of the world’s worst examples of environmental pollution caused by man-made arsenic release from hard rocks.

Figure 3 – The Paracatu gold mine is Brazil’s largest open cut gold mine. It is operated by the Canadian Kinross Gold Corporation on the outskirts of a town with 84 thousand inhabitants. This mining operation is leading to one of the most serious, persistent man-made increases in the concentration of arsenic in the natural environment. Photograph by Beto Magalhães (2008).

There are hundreds of large mines in the prospecting or developing phases worldwide. Both active and abandoned gold mines persistently release arsenic to the environment during decades, centuries and millennia. It would require trillions to counteract the effects of environmental pollution caused by gold mining. If mining corporations did pay for these liabilities, then hard rock gold mining would be economically unfeasible.

However, mining corporations do not pay for the destruction and the invisible, persistent pollution that they impinge on the environment, or the global damage they cause to human health. Therefore liabilities are left for peoples and governments to pay: peoples pay with their health and their lives, and governments pay with taxpayer’s money.

Blood stained gold

The world is witnessing a new gold rush. This is due, in part, to the sharp rise in gold price that jumped for the first time on the stock exchanges in March 2008 to about 1,000 U.S. dollars per troy ounce.

Within six years, the price of gold nearly quadrupled. In 2003, the world market demanded around 2600 tonnes of gold, about one hundred times more than in the 19th Century.

According to the World Gold Council, in that same year 78 % of the gold was used in jewellery production. The electronics industry and dentistry absorbed only about 15 % of production.

Modern gold mining worldwide destroys the environment, expels people from their land and releases incredible amounts of arsenic. This gold rush is financing an invisible mass killing worldwide.

Figure 4 – Gold deposits and gold districts of the world. From: Gosselin P, Dubé B (2005). Geological Survey of Canada, Open File 4893. http://apps1.gdr.nrcan.gc.ca/mirage/show_image_e.php

This irresponsible, invisible killing must stop. Each one of us can help by supporting this worldwide campaign to attain the following goals:

• Impose an immediate worldwide ban on the mining of arsenic-bearing hard rocks, such as arsenopyrite in gold mines. Critics say: basically, no more gold should be mined today. In the cellars of the state banks alone, there are thousands of tonnes of hoarded gold. If one were to reintroduce these reserves to the market, then gold mining could drastically be reduced, if not suspended for years. The top hoarders of gold stocks in 2007 were the U.S. with 8133 tonnes and Germany with 3417 tonnes. Before the International Monetary Fund (IMF), Germany still held some 3217 tonnes.

• Impose an immediate ban on arsenic in plant, animal and human food, feed additives and fertilizers;

• Lower the provisional drinking water limit for arsenic from 10 ppb to <1 ppb (<1 microgram/litre). Since there is no safe dose for a cancer-causing substance like arsenic, the ideal arsenic concentration in drinking water should be 0 ppb. The <1 ppb limit is fixed solely on the basis of the workable detection limit of analytical laboratories; • Prohibit any man-made increase of arsenic concentrations both in natural and man-made environments. The natural concentration of arsenic in surface water worldwide averages 1 part per billion (ppb) [8]. Groundwater arsenic concentrations may largely exceed this limit in many regions of the world [9], therefore, the use of arsenic-contaminated groundwater must be subject to legal restrictions. Worldwide natural concentrations of arsenic in soils and sediments average 1 ppm (1 milligram/kg) [range <0.10 to 100 ppm] [10]. Any man-made increase in natural arsenic concentrations in soil poses increased ingestion and inhalation risks and, therefore, must be prohibited and dealt with accordingly. • List arsenic as a worldwide hazardous air, soil and water pollutant, defined as a substance that may cause increased morbidity and mortality in humans due to chronic exposure to even only low-level concentrations [11]. • Make gold mining corporations truly pay for liabilities. Gold mining corporations are fond of greenwashing, which means apparent paying for just the visible, minute part of the liabilities. Bad governments and bad politicians tend to accept these ‘facilitation payments’ in order to obtain votes, favours or simply money. Independent scientists must be involved in calculating the real liabilities, and lawsuits must be brought to courts to make corporations pay their debts. What can each one of us do personally to help?

• We can avoid purchasing mass-industrialized gold jewelry. Those who buy gold should be aware of the actual price of the necklace or the bracelet: millions of tonnes of arsenic, devastated landscapes, billions of litres of polluted water in rivers and poisoned people living in misery and disease, or expelled from their land. How heavy the expensive glossy objects are, is shown by the amount of mostly toxic waste, soil and rock which is necessary for modern gold mining to win the gold for just one wedding ring: 20 tonnes, of which approximately 20 kilograms are toxic arsenic!

• We can have old jewelry and other products reworked or recycled.

• We can talk to the jewelers about the environmental problems involved in the mining of gold and send reports of these conversations to organizations for human rights and protection of nature [12]. We can draw attention to the use of "certified gold" which is gold obtained through processes of highest social and environmental standards, as opposed to "dirty gold."

• We can convert the pure image of gold to the ugly reality, for example, through letters and other articles in newspapers and magazines, videoclips, music, films, etc.

• We can avoid "golden gifts" on Christmas trees or other special occasions.

• We can place this report in the waiting room of our physician, hairdresser or other locations.

• We can support the call by non-governmental organizations [12] to governments and financial institutions such as the World Bank to discourage future loans for gold mines.

• We can talk to members of parliament in our constituency about the problem and ask them to be active in this sense.

• We can support lawsuits to make Gold Mining Corporations pay for the environmental and health liabilities they cause, and not simply leave liabilities for tax-payers to pay with their lives.

• We can reflect on these questions: What use is gold? Can we live without it? Why must we die for it?

References and notes:

1. Dani SU. Gold, coal and oil. Medical Hypotheses 2010 Mar; 74 (3):534-41.

2. Arsenic in drinking water: 2001 Update, National Academy of Sciences of the USA.

3. United Nations Synthesis Report on Arsenic in Drinking-Water. WHO, 2001. http://www.who.int/water_sanitation_health/dwq/arsenic3/en/

4. Eisler R. A review of arsenic hazards to plants and animals with emphasis on fishery and wildlife resources. In: J. O. Nriagu, ed. Arsenic in the Environment, Part II: Human Health and Ecosystem Effects. John Willey and Sons, New York, NY, USA, 1994: pp. 185-259.

5. Smith AH, Steinmaus C, Yuan Y, Liaw J, Hira-Smith MM. High concentrations of arsenic in drinking water result in the highest known increases in mortality attributable to any environmental exposure. Proceedings of a Symposium: Arsenic – The Geography of a Global Problem. Royal Geographical Society: Arsenic Conference, 29th August 2007. www.geog.cam.ac.uk/research/projects/arsenic/symposium.

6. Dani SU. Arsenic for the fool: an exponential relation. Science of the Total Environment 2010 Mar 15; 408 (8):1842-6.

7. www.sosarsenic.blogspot.com, www.alertaparacatu.blogspot.com

8. Agency for Toxic Substances and Disease Registry. 2007. Toxicological profile for arsenic. Draft for Public Comment. Atlanta GA [updated 2007 August]. http://www.atsdr.cdc.gov/toxprofiles/tp2.html.

9. Ravenscroft P, Brammer H, Richards K. 2009. Arsenic Pollution: A Global Synthesis. Wiley-Blackwell. ISBN-978-1-4051-8601-8

10. Shacklette HT, Boerngen JG. 1984. Element concentrations in soils and other surficial materials of the conterminous United States: Reston VA: U.S. Geological Survey. Professional Paper 1270. p. 6.

11. U.S. Environmental Protection Agency. Arsenic compounds hazard summary. Technology transfer network air toxics website. Washington DC [updated 2007 November 6]. http://www.epa.gov/ttn/atw/hlthef/arsenic.html.

12. A non-exclusive list of organizations that can take part in the campaign includes: AVAAZ, Bill and Melinda Gates Foundation, Care International, Caritas International, Concern Worldwide, Consciencia Solidaria, Doctors Without Borders (Médecins Sans Frontières), FIAN, Friends of the Earth, Friends of Peoples Close to Nature (Freunde der Naturvölker e.V.), Acangau Foundation (Fundação Acangaú), Gesellschaft Deutscher Naturforscher und Ärzte e. V. (GDNÄ), Greenpeace, Halifax Initiative, International Society for Threatened People (GfbV-Gesellschaft für bedrohte Völker), IUCN, Mines and Communities, Mining Watch Canada, Misereor, Rettet den Regenwald, Survival International, Urwald, WHO-World Health Organization, World Wide Fund for Nature (WWF), among others.

E-mail Dr. Sergio U. Dani at srgdani@gmail.com

Widespread biovolatilization of arsenic

2010-07-10T22:55:00.000+02:00

Atmospheric stability of arsines and the determination of their oxidative products in atmospheric aerosols (PM10): evidence of the widespread phenomena of biovolatilization of arsenic.

Jakob R, Roth A, Hass K, Krupp EM, Raab A, Smichowski P, Gómez D, Feldmann J. 2010. J Environ Monit 12 (2):409-16 .

Trace Element Speciation Laboratory Aberdeen, Department of Chemistry, University of Aberdeen, Meston Building, Meston Walk, Aberdeen, Scotland, UK.

Abstract

Biovolatilisation of arsenic as their arsines in the form of AsH(3), and mono-, di and trimethylarsine has often been determined under laboratory conditions. Although environmental point sources such as landfill sites or hot springs have been characterised, only limited knowledge is available on how widespread the formation of volatile methylated arsenic compounds are in the environment. Here we studied the atmospheric stability of the different arsines and quantified their oxidation products in atmospheric particulate matter (PM(10)) in two locations in Argentina. The atmospheric half-life of the arsines range from 19 weeks for AsH(3) to 2 d for trimethylarsine (TMAs) at 20 degrees C in the dark, while during simulated daytime conditions the stability is reduced for all arsines and in particular for the methylated arsines by three orders of magnitude which suggests that TMAs can only be dispersed at night. At both locations the arsenic concentration was in all samples below 1 ng As m(-3), which is considered as rural background for arsenic. The oxidation products, i.e. methylarsonate (MA), dimethylarsinate (DMA) and trimethylarsine oxide (TMAO) were identified by using HPLC-ICP-MS/ES-MS in more than 90% of the 49 PM(10) samples taken from 8 sampling points at the two geographically different locations. TMAO was the predominate organoarsenicals in both locations (66 and 69%, respectively) while DMA was determined to be between 13 and 19% of all organoarsenicals at the two locations. The concentration of the organoarsenicals ranged from 4 to 60 pg As as TMAO m(-3), while the maximum concentration for DMA and MA were 16 and 6 pg As m(-3), respectively. No difference in terms of the concentration or distribution of the organoarsenicals in the PM(10) samples was identified as significant. Since the two locations were different in climate and industrial impact and sampled in different seasons, these data suggest that methylated arsenicals do occur as background chemicals in the environment. Due to the low atmospheric stability of the methylated arsines, it is suggested that biovolatilization of arsenic as methylated arsines is a widespread phenomenon. More studies however are necessary to identify the major sources and determine the flux of the volatilization process in order to determine whether or not the process has environmental significance.

One in five deaths linked to arsenic in water

2010-07-04T10:00:00.000+02:00

New study links 1 in 5 deaths in Bangladesh to arsenic in the drinking water

Increased mortality is linked to chronic diseases with a 70 percent increased mortality risk among those with the highest level of exposure

Source: EurekAlert (*)

June 23, 2010 – Between 33 and 77 million people in Bangladesh have been exposed to arsenic in the drinking water—a catastrophe that the World Health Organization has called "the largest mass poisoning in history." A new study published in the current issue of the medical journal The Lancet provides the most complete and detailed picture to date of the high mortality rates associated with this exposure, which began with the widespread installation of tube wells throughout the country 30 years ago—a measure intended to control water-bourne diseases.

Among the surprising findings of the study, conducted by a team of researchers at Columbia University's Mailman School of Public Health, Lamont-Doherty Earth Observatory, and the University of Chicago, and led by Dr. Joseph Graziano are these:

One in five deaths in Bangladesh (population: 125 million) is associated with exposure to water from wells with arsenic concentrations greater than 10 micrograms per liter.
Arsenic exposure was associated with increased mortality due to heart disease and other chronic diseases in addition to the more familiar medical consequences of arsenic exposure: skin lesions, cancers of the skin, bladder and lung.
An increase of nearly 70 percent in all-cause mortality was found among those exposed to the highest concentration of arsenic in water (150 to 864 micrograms/liter). But researchers found a dose-related effect that included increased mortaility even at relatively low levels of exposure, including the Bangladesh safety standard (50 micrograms/liter) and the WHO recommended standard (10 micrograms/liter).

The study draws its results from a carefully designed, prospective, longitudinal study involving 12,000 people in Bangladesh who were tracked for over a decade. To gather data for the Health Efects of Arsenic Longtudinal Study (HEALS), researchers traversed the tropical landscape over wooden bridges to interview each of the 12,000 participants and take urine samples every two years. Lifestyle and health data were tracked, allowing researchers to control for factors such as smoking, blood pressure and body-mass index. In addition, nearly 6,000 wells were tested to establish the arsenic concentration of the water source for each participant.

In an accompanying commentary in the same issue of The Lancet, Margaret P. Karagas of Dartmouth Medical School, describes the study design as "a substantial advance over previous ecological studies."

The mass poisoning in Bangladesh was a result of well-intentioned efforts on the part of aid and development agencies in the 1970s, which built 10 million tube wells in an attempt to reduce water-bourne diseases such as cholera and dysentery, according to Dr. Graziano, professor of Environmental Health Sciences at the Mailman School. While the new wells reduced exposure to the microbes causing such diseases, they yielded water contamined with arsenic, which occurs naturally in the region. Arsenic can be avoided, however, by digging deeper wells—an approach that is already yielding safer drinking water for roughly 100,000 people. The Columbia Mailman School team has been at the forefront of this effort.

"The need for a global response is apparent because the situation goes far beyond the Bangladesh borders," says Dr. Graziano. "Arsenic in ground water is affecting 140 million people across many countries and especially in South Asia. "There needs to be a concerted effort to bring safe to millions of people. Investment has not been commensurate with the magnitude of the problem."

###

The research is supported by the National Institutes of Health. In addition to senior author Dr. Joseph Graziano, Dr. Habibul Ahsan, of the University of Chicago and professor of Epidemiology at the Mailman School, was first author.

About the Mailman School of Public Health

The only accredited school of public health in New York City and among the first in the nation, Columbia University's Mailman School of Public Health pursues an agenda of research, education, and service to address the critical and complex public health issues affecting millions of people locally and globally. The Mailman School is the recipient of some of the largest government and private grants in Columbia University's history. Its more than 1000 graduate students pursue master's and doctoral degrees, and the School's 300 multi-disciplinary faculty members work in more than 100 countries around the world, addressing such issues as infectious and chronic diseases, health promotion and disease prevention, environmental health, maternal and child health, health over the life course, health policy, and public health preparedness. www.mailman.columbia.edu

(*) Source:

http://www.eurekalert.org/pub_releases/2010-06/cums-nsl062310.php

Contact: Stephanie Berger
sb2247@columbia.edu

Arsenic and Alzheimer disease

2010-06-19T12:32:00.000+02:00

The arsenic exposure hypothesis for Alzheimer disease

By G. Gong and S. E. O'Bryant (*)

Published in Alzheimer Disease and Associated Disorders, 2010 May 13 [Epub ahead of print].

Abstract: Prior research has shown that arsenic exposure induces changes that coincide with most of the developmental, biochemical, pathologic, and clinical features of Alzheimer disease (AD) and associated disorders. On the basis of this literature, we propose the Arsenic Exposure Hypothesis for AD that is inclusive of and cooperative with the existing hypotheses. Arsenic toxicity induces hyperphosphorylation of protein tau and overtranscription of the amyloid precursor protein, which are involved in the formation of neurofibrillary tangles and brain amyloid plaques, consistent with the amyloid hypothesis of AD. Arsenic exposure has been associated with cardiovascular diseases and associated risk factors, which is in agreement with the vascular hypothesis of AD. Arsenic exposure invokes brain inflammatory responses, which resonates with the inflammatory hypotheses of AD. Arsenic exposure has been linked to reduced memory and intellectual abilities in children and adolescents, which provides a biologic basis for the developmental origin of health and disease hypothesis for AD. Arsenic and its metabolites generate free radicals causing oxidative stress and neuronal death, which fits the existing oxidative stress hypothesis. Taken together, the arsenic exposure hypothesis for AD provides a parsimonious testable hypothesis for the development and progression of this devastating disease at least for some subsets of individuals.

(*) F. Marie Hall Institute for Rural and Community Health Department of Neurology, Texas Tech University Health Sciences Center, Lubbock, TX.

Thrifty gene

2010-06-08T23:24:00.000+02:00

Thrifty gene provides for survival

Source: Excegen Genetica SA, June 2010

Under dietary restriction, bovines carrying a wild type of the growth hormone gene (GH) are able to sustain body growth, whereas bovines carrying the domestic form of the gene stop growing, according to a study published in the journal Genetics and Molecular Research (GMR).

In the study, a Brazilian team compared the weight gain of cattle of the Nelore breed (Bos indicus) that carry either the common or domestic form of the GH, known as the G2 allele, or the wild type form, known as the G1 allele.

Under ad libitum conditions, G2 animals gained more weight than G1 animals. However, when food became scarce, the situation was inverted: G2 animals lost weight, whereas G1 animals maintained weight gain.

GH controls metabolism, growth, development and aging in a wide range of animals, from insects to human beings. Genetic mutations that reduce GH signaling usually increase life span and longevity in a way similar to that seen in dietary restriction models. However, the mechanisms by which dietary restriction works are poorly understood.

'Our results show that the ideal dietary regimen is just as much the consequence of genetic selection as its cause. Dietary regimens work as any selection force, in the sense of adapting the genes to given nutritional conditions', explains Sergio Dani, the scientist who led the Brazilian research team.

The G2 allele has been dubbed the 'demanding allele', because it is optimally fitted to ad libitum nutrient intake. The G1 allele has been dubbed 'the thrifty allele', because it is optimally fitted to dietary restriction.

As the thrifty allele is rare in domestic cattle, almost all animals that carry a copy of this allele also carry a copy of the demanding allele. This condition is termed heterozygosis.

'Given its recessive trend, the thrifty allele is conserved within herds even under ad libitum conditions", explains Hani Yehia, co-author of the study. 'Under ad libitum conditions, the selection against heterozygous animals is somewhat relaxed, resulting in the thrifty allele being conserved. Such heterozygous animals eventually give birth to thrifty, homozygous G1G1 animals. Under exacting conditions, these homozygous animals are fundamental for the survival of the species", concludes Yehia.

The study shows that dietary regimens per se must not increase or reduce life span or longevity: “It is all a question of adaptation to the environment. As long as there is abundant food, the demanding organisms have advantage over the thrifty ones. As soon as food becomes a prize, the demanding vanish and the thrifty thrive', explains Sergio Dani. 'When it comes to shrinking resources, it's survival of the thriftiest', he concludes.

Learn more:

. Dani S. U., Dani M. A. C., Freire, I. L., Gouvea S. P., Knackfuss F. B., Lima F. P., Mercadante M. E. Z., Monteiro E., Paggiaro S. M. G., Razook A. G., and Yehia H. C. Survival of the thriftiest: restricted nurture reveals the thrifty nature of a growth gene in Bos indicus. Genetics and Molecular Research 9 (2): 1032-1044 (2010). To obtain a free copy of the article access: http://www.funpecrp.com.br/gmr/year2010/vol9-2//pdf/gmr844.pdf

. Scientists of the following institutions colaborated in the study: Excegen Genética SA, Genon Genetica ltda., Coarana Biotecnologia ltda., Institute of Zootecnics of Sertaozinho/APTA and Federal University of Minas Gerais;

. The study was carried out at four locations in Brazil, during 7 years;

. 6864 bovines were genotyped;

. Two patents were filed with INPI/Brazil: PI 0403770-7 A (2006) e PI 0503427-2 (2007);

. The study was financed by: Excegen Genetica SA, Genon Genetica ltda., FAPEMIG, CNPq, FAPESP and SEBRAE.

. The study was supported by: Acangau Foundation, Beckhauser Troncos e Balanças, Bellman Nutrição Animal, Brascan Cattle SA, Quilombo Empreendimentos e Participações ltda., Vallée.

. More information with Sergio U. Dani: srgdani@gmail.com.

MIMER Notes, June 6, 2010: Global map of arsenic in groundwater

2010-06-06T02:31:00.000+02:00

Modeled global probability of geogenic arsenic contamination in groundwater for (a) reducing groundwater conditions, and (b) high-pH/oxidizing conditions where arsenic is soluble in its oxidized state. (FIGURE 2 from Amini et al., 2008). Copyright American Chemical Society. Material published under license agreement.

Ref.: Amini M., K.C. Abbaspour, M. Berg, L. Winkel, S. J. Hug, E. Hoehn, H. Yang, C.A Johnson (2008) Preliminary Statistical Modeling of Global Geogenic Arsenic Contamination in Groundwater. Environmental Science & Technology 42:3669-3675.

Arsenic toenails

2010-05-13T16:00:00.000+02:00

Arsenic Toenails

By Catalyst, ABC Television, Australia, March 11, 2010
Watch the video at: http://www.abc.net.au/catalyst/stories/2843289.htm

Is the glittering prosperity from Australia's gold mining being tarnished by the environmental impact of extraction techniques? Dr Paul Willis meets up with researchers from the University of Ballarat who are collecting children's toenails to find out how much arsenic they contain.

TRANSCRIPT
Arsenic Toenails

NARRATION
Meet Rose. She's your typical 9 year old girl.

Rose's Dad
She's a fairly quiet child, but she's certainly enjoys living in this town and she's got lots of friends right over the whole town.

NARRATION
In fact there didn't seem to be anything unusual about Rose until she participated in an unusual study conducted in western Victoria looking at arsenic in the environment and the children.

Johnathan Nettelbeck
It turned out that Rose had the highest levels of all the kids tested. And ah so, you know, I was naturally quite concerned.

Dora Pearce
We thought there might be a problem out there because of the arsenic and the soil oo we decided to take a closer look.

Dr Paul Willis
And that 'closer look' took a most unusual form. Dora Pearce from the University of Ballarat set about collecting toenails from children across western Victoria.

Dora Pearce
We use toenails because collecting them is non-invasive. They're easy to store. Doesn't hurt the children to provide them. And they provide us a timeline over several months of what the kids have been exposed to.

NARRATION
Perhaps the simplest part of the study was the collection of toenails. The parents cut their child's toenails, put them in a plastic bag, and gave them to Dora!

Rose
Well Mr Schausen, our science teacher told us about bringing toenails to school and all the other kids giggled because the thought it was gross. But it's not actually that gross because virtually everybody has them.

NARRATION
The link between arsenic and toenails is a subtle one. If arsenic enters the body it can be excreted by shunting it into the toe and fingernails and hair. But why would there be any extra arsenic in the environments across Western Victoria? Western Victoria was once the largest producer of gold in the world. During the great Gold Rush of the 1850s and 60s thousands of people from all over the world rushed to this area in search of their fortunes.

Dr Paul Willis
Most of the gold was found like this, small traces finely spread through other rocks. So the rock was crushed, releasing the gold — and the arsenic.

NARRATION
Crushing quarts became an industry on a scale that now seems unimaginable.

Dr Paul Willis
One hundred years later and western Victoria is dotted with mulluck heaps and tailings heaps like the one behind me. Some of them contain hundreds if not thousands of milligrams per kilogram of arsenic.

NARRATION
Dora teamed up with Kim Dowling from the University of Ballarat, an expert in arsenic and other toxins in the environment.

Kim Dowling
In the mining process arsenic which is locked in minerals deep in the earth is bought to the surface, and it's oxidised which means it can be made more mobile and so it moves around and again that's the thing that can have an impact it's completely natural and if it stays here for long enough it will age and not be as mobile. But at the moment it stays in the lansdscape and we've got piles of the stuff.

NARRATION
So Kim suspected that there would be hotspots of arsenic dotted across the old gold diggings. Dora wondered if these presented any threat to public health. And that's why she started collecting toenails. But figuring out how much arsenic was in the toenails required a lot of work. And there were limits to what conventional lab techniques could say about how much arsenic there was in a sample and where it came from.

Dora Pearce
When you generally take a measure of the arsenic in the toenail clippings what you're getting is an average reading. And so the arsenic concentration at one time point can be much higher than it is at a different time point. So what we really need to be able to measure is arsenic concentration at a given time point so we know we can relate that back to the actual exposure that caused that.

NARRATION
Dora needed the precision and resolution that could only be achieved by a synchrotron. By using high-energy sub atomic particles a synchrotron can determine exactly what kinds of atoms are present at specific locations down to a few thousandths of a millimetre. Trouble is, when Dora was doing her study, the Melbourne Synchrotron hadn't yet come on line. She had to go to Chicago. Dora teamed up with Andrea Gerson to help navigate her way through the high-tech world of synchrotrons.

Andrea Gerson
I think with Dora's study what the synchrotron offered was the ability to map on a micron scale the arsenic distribution within the toenails and then go back to the regions of interest and interrogate the particular speciation of the arsenic at the positions within the toenails.

NARRATION
Slowly a pattern built up, not only of how much arsenic was in the toenail clippings, but more importantly whereabouts inside the samples the arsenic was located. And these results were astounding.

Dora Pearce
We found that about 10 per cent of children in our study had levels of arsenic in their toenails higher than what might be considered a "normal" dose and also we found about half had levels greater than the highest value recorded in a non gold mining area — but we do need a larger study to confirm those findings.

Dr Paul Willis
These astounding figures raise two questions: How were the kids picking up so much arsenic and was it enough to damage their health?

Dora Pearce
The arsenic species that we detected in the children's toenail clippings suggested that the arsenic was possibly taken up in two different ways. One way is that the arsenic is absorbed systemically through the body when the kids are out there playing in the dirt or they can also inhale the arsenic from dust when they're playing out there especially on the mine waste.

Dr Paul Willis
Locals and residents have long known that there is arsenic in the environment and most of them have taken sensible precautions against exposure to contaminated areas. But Dora's study suggests that simply trying to avoid contamination isn't enough.

NARRATION
Rose was one of the participants in the study and one of the first to have her clippings analysed by a synchrotron. Her elevated levels of arsenic were, at first, something of a mystery.

Johnathan Nettelbeck
Many people in the gold fields area would be aware that arsenic's associated with the mine tailings. We certainly wouldn't buy a house directly next to, you know, right on top of something like that. Um and we'd certainly, we'd keep Rose away from those areas.

NARRATION
The second question: 'Was this exposure to arsenic dangerous?' would prove more difficult to answer.

Dora Pearce
We really don't know what a safe level of arsenic in toenails is, especially not in children because the baseline study's really haven't been able to provide us with that information. Far more work needs to be done in unexposed populations so that we can tell what a background level is.

NARRATION
Dora's toenail study has revealed some worrying facts about arsenic in western Victoria. But there are thousands of gold mine sites right across the country and we just don't know how contaminated they are or if the locals are exposed to this historic toxic time bomb.

Kim Dowling
In fact there's a raft of metals and other elements that we're interested in. For example mercury is also in this system, ah cadmium, there's a raft of metals that could have impacts on human health and indeed one of the reasons Dora's study is so exciting is we can use the exact same technique to work out where those metals are coming from and if they are affecting people's health.

Dora Pearce
There's still far more that needs to be done to further elucidate the type of arsenic that's present in these clippings so we can work out what the general levels should be, how the arsenic gets there and what we need to do to be able to reduce the exposures in these communities.

NARRATION
For children like Rose, the priority now is to prevent any more arsenic from getting in.

Johnathan Nettelbeck
As that awareness grows, you know, across the whole community if there were, there were sensible things to do we would certainly do that.

Dr Paul Willis
The gold rush was a significant event in our Australian history. It formed the foundations for our nationhood. But there is also a more toxic legacy left behind by the gold diggers, one that could affect generations of Australian's and one that we are only just starting to become aware of.

Topics: Health

Reporter: Dr Paul Willis
Producer: Dr Paul Willis
Researcher: Dr Paul Willis
Camera: Don Whitehurst and Mark Farnell
Sound: Chris Coltman and Graham Fettling
Editor: David Tucker
Story Contacts: Dora Pearce

Kinross Gold Corporation meets Ali Baba on the Hill of the Souls

2010-04-11T14:23:00.000+02:00

Kinross Gold Corporation meets Ali Baba on the Hill of the Souls

By Cylene Gama, from Paracatu-MG, Brazil, April 11, 2010

In the tale of ‘Ali Baba and the Forty Thieves’ the treasure is in a cave, the mouth of which is sealed by magic. It opens on the words ‘Open Sesame’, and seals itself on the words ‘Close Sesame’.

Canadian Kinross Gold Corporation is longing to put its craws on a treasure hidden in the Hill of the Souls at Paracatu, northwestern Minas Gerais State, Brazil. However, the Hill is sealed by a malediction long known by the Bacuen Indians, also known as the ‘Tapuias’. The Hill of the Souls was sacred for the Bacuen who believed that disturbing the hill would cause it to release evil souls.

But Kinross people do not want to believe in ancient maledictions. As in the Arabic tale, Kinross also found its own magic words to open the way to its overtly illegal Paracatu mining project down the public permitting pipeline in Brazil. The magic words ‘facilitation payments’ are written in Kinross’ ‘Code of Ethics in Business’.

As put by Transparency International ‘facilitation payments’ mean ‘corruption’ and Kinross makes it public in its ‘Code of Ethics in Business’, implying ‘facilitation payments’ are due to government authorities in order to facilitate businesses in foreign countries.

Bottlenecked twice by State and Federal lawsuits which prevented Kinross to build up the world’s largest toxic tailings impoundment on top of Paracatu’s oldest drinking water source, the mining company responded by hiring the shortly resigned Secretary of State of Minas Gerais, Wilson Brumer in May, 2009.

The relationships between Kinross and Brumer date back to the time when Kinross bought shares in the Paracatu mine from Rio Tinto and Brumer was serving as a State Secretary in Minas Gerais, Brazil.

Brumer´s appointment as a Kinross Director in May 2009 has been interpreted as Kinross desperate move to place its most important Brazilian operation in the hands of someone with ‘easy transit and flow’ within Brazilian government offices. At that time, Kinross’ Paracatu mine manager Jairo Leal claimed that the company could close its doors if it did not get the governmental permits.

At the end, Kinross did manage to get its illegal permits seemingly legalized in August 2009, in middle of a corruption plot which is currently under investigation by the Public Ministry of the State of Minas Gerais. It is hard to tell whether Kinross’ success in getting the permits is due to Brumer’s efforts. However, it is beyond doubt that Brumer’s track record in selling solid Brazilian public assets to foreign groups at bargain prices matches Kinross’ expectations and ethics in business.

In 2006, Kinross finished the acquisition of all Paracatu mining rights from Rio Tinto for just 280 million dollars - a bargain as described by Brazilian geologist Eupidio Reis, surprised by the low valuation of the largest Brazilian gold mine reserve estimated at some 16 million ounces, equivalent to more than 60% of Kinross’ legally declared gold mine reserves. Eupidio Reis simply could not understand how the Paracatu mine could have been sold so cheap when estimates pointed to 10 billion dollars.

What seemed to be a bargain to the Toronto white collars is turning out to be a real nightmare. Brazilian Medawar Institute scientist Sergio Dani explains that the Paracatu gold mining project has been poorly managed from its beginning, as early as in 1987.

However, Kinross invested a half billion dollars to upgrade this mining project after full acquisition from Rio Tinto in 2006. ‘Kinross has made more evident the succession of mistakes and corruption involved in this mining operation’, said Dani. ‘The hardrock turned out to be harder, the gold grades the world’s lowest, and the environmental and socio-economical damages and liabilities are visible to the naked eye’, he concludes (see http://alertaparacatu.blogspot.com/ and www.sosarsenic.blogspot.com).

In order to explore the world’s lowest grade gold ore (0.4 g/ton) the mining company competes with the local population for precious drinking and irrigation water. Kinross plans to dispose of one billion tons of toxic waste into a gigantic tailings dam on top of a water head meant to supply drinking water for 80 thousand people.

Frequent blasts at the mining site meant to crack the hardrock are also cracking buildings in the historical 18th century city. Technical difficulties have prevented the mining company meeting economical and financial goals. ‘Kinross financial discipline’ is mostly obtained by exploiting labour - increasing working hours and maintaining low salaries - and failing to account socio-environmental liabilities.

The Paracatu mine ore is arsenopirite which releases arsenic, sulphuric acid and other pollutants into the environment, when the ore is milled to obtain gold. Arsenic is the most potent environmental cancer causing agent known and sulphuric acid permeates and contaminates creeks and underground water.

Kinross’ liabilities in Paracatu outweigh the value of its gold reserves - indeed bad news for investors and stockholders. A lawsuit proposed by the Acangau Foundation in August 2009 estimates the damages caused by the mine expansion project at some 21 billion dollars over thirty years of open-cut hardrock mining in Paracatu. These estimates equal twice the value of the Paracatu mine gold reserves.

Liabilities estimates are based on EPA (Environmental Protection Agency of the USA) studies on socio-economical costs related to environmental contamination by arsenic, and on data from Kinross itself.

One questions whether a stockholder would jump into an adventure of such a known great risk? And how much does a Kinross stockholder know about the size of the risk he or she is buying?

Kinross goes to great pains to hide its own mistakes and tries to disqualify the scientific community - as happened in 2007 when Kinross disqualified an independent report on the Paracatu mine expansion project III, and simply ignored a strategic evacuation plan. During a public audience in 2007, irritated Public Prosecutor Serrano Neves pointed out to a Kinross director that the Brazilian people ‘won´t tolerate that a foreign company labels us as fools or idiots’.

‘Kinross Paracatu mine is stuck in stone age’, says Sergio Dani. ‘The gigantic liabilities increase the fly-by-night risk’, he adds. ‘It comes as no surprise that Wilson Brumer may have initially refused an invitation to join Kinross, as announced by the Belo Horizonte ‘O Tempo’ newspaper. He is reported to having said he would prefer to carry on with his own businesses. It could have being just part of the deal. When risks and challenges are too big, there is room to refuse dirtying hands for too cheap’, concludes Dani.

Brumer´s putative refusal to promptly accepting a seat on the Kinross Board opened space for speculations. Brumer had worked for Billiton, the first owner of the Paracatu mine. Brumer led his support to the Rio Tinto x Kinross mine expansion project when he was serving as Secretary of the Minas Gerais State in the period 2003-2007. He did not need to say ‘no thanks’ at the time.

Brumer ended up accepting the invitation to become a Kinross Board member in May 2009. It must have been irresistible. No new Kinross director makes less than US$100,000.00/year plus fringe benefits and most likely some perks. Kinross CEO Tye Burton received over 10 million US dollars in 2008 in salary and bonuses. It is hard to imagine if Brumer would get close to it carrying out his own businesses in Brazil. It is left to the imagination what would Brumer really have dealt with Kinross.

Will Brumer work for the expansion of the Kinross Paracatu mine, or will he help Kinross sell this controversial mine, as Billiton and Rio Tinto did at a time when the mine did not appeared so controversial?

Billiton and Rio Tinto won with Brumer in the past, but the situation appears to have changed for worse with Kinross. In February 2010, Kinross announced ‘ramp up problems’ in the Paracatu mine expansion, in an attempt to justify lower than expected results.

Soon afterwards it is heard that an unforeseen mill has to be bought and installed to cope with the Paracatu hardrock.

What might Kinross have done wrong in the Hill of the Souls? Have Bacuen’s evil souls been released? Maybe it is time for Kinross to learn from Ali Baba, say: ‘Close Sesame’.

Drinking-water-for-poison swap

2010-04-04T11:24:00.000+02:00

Nothing in the drinking-water-for-poison swap in Paracatu makes sense except down the corruption pipeline

By Sergio U. Dani, from Göttingen, April 4, 2010

The Santa Isabel river is drying up. It has lost 3 billion liters of water in the last 18 years. Since 1996 this river has been the main source of drinking water for the 84 thousand inhabitants of Paracatu, a city located in the northwestern part of the Minas Gerais State, Brazil.

Until 1996, water supply to this 300 year old city relied upon the Rico Creek and water springs and wells located within the city and in the neighbour Santa Rita river basin. Beginning in 1987, an open pit gold mine has destroyed the waterheads of Rico Creek, and has contributed to the depletion or contamination the city’s wells.

Now the Santa Rita waterheads, which are considered the earliest and most valuable source of drinking water out of the urban environment of Paracatu – the water used to be delivered to the city by gravity through the famous “Master of Field Trench” – are at risk of being transformed into a deposit of over one billion tons of toxic mine tailings.

The tailings will contain one million tons of arsenic which is enough poison to kill billions of people. Besides directly destroying the sources of drinking water, mining activities are contaminating groundwater with poison and acid drainage.

The waterheads of the Santa Rita and Santa Isabel rivers make up a connected hydrogeological system known as "Serra da Anta System". Damage to any of the constituents of this system will severely impact water supply to Paracatu.

The huge social and environmental damage caused by gold mining operations in Paracatu exceeds the gross value of gold reserves, according to estimates based on studies by the EPA-Environmental Protection Agency of the U.S. and by Kinross Gold Corporation itself put together in a lawsuit by the Acangau Foundation.

In 2009, mining activities contributed only 4% of the total tax income and 6% of the jobs in Paracatu. In an Internet poll run in 2009, 93% of over 1000 people voted against the expansion project of the mining which is bound to destroy valuable sources of drinking water.

Only corruption accounts for the governmental issuing of permits to the expansion of the gold mine in August 2009. Kinross Gold Corporation admits the practice of "facilitating payments" in its code of ethics in business.

Public managers are jointly responsible for damage, as is the case of the Municipality which has already been brought officially to run an epidemiological survey of chronic poisoning by arsenic in Paracatu and nothing published about the results. The State administrator aggravates his guilt when he tries to justify his failure by claiming instrumental helplessness or ignorance.

In March 2010, Paracatu was included in the official map of conflicts involving environmental injustice and health in Brazil. This map has been prepared by the Oswaldo Cruz Foundation-Fiocruz and by the Socio-educational Foundation-FASE, with the support of the Brazilian Ministry of Health.

Paracatu has been included in this map in recognition of the serious consequences of the open pit gold mining activities within the city which include: severe and persistent environmental pollution, chronic exposure to arsenic and other toxic substances, destruction of drinking water sources and expelling of traditional communities, among other injustices.

Contamination of soil, air and water pollution and corruption caused by Kinross Gold Corporation in Paracatu threaten the sustainability of the city's economic development and directly affect society.

Something in the water

2010-03-07T16:38:00.000+01:00

Interview: Something in the water
From Metallomics, 24 February 2010

Bibudhendra Sarkar talks to May Copsey about metalloenzymes, helping sick children and hunting for toxic metals in the environment Bibudhendra Sarkar is an Emeritus Professor at The University of Toronto and the Hospital for Sick Children, Toronto, Canada. His major research interests are in the area of metal-related genetic diseases with a special emphasis on Wilson and Menkes diseases and studying the effects of toxic metals in the environment and their impact on human health. He is also a member of the Metallomics editorial board.

How did your career in science start?
While I was an undergraduate in India, a scientist called Babul Dhar encouraged me to study abroad so I went to the University of Southern California, Los Angeles, US, to do a PhD.

That was the time when Dorothy Hodgkin had just discovered the structure of vitamin B12, which has cobalt in it. Her work inspired me to study the metalloenzyme structure. It was the late 1950s, and the term inorganic biochemistry was not yet recognised. There was no link between inorganic chemists and nutritionists.

Even in my graduate days I still remember that many biochemists did not realise that enzymes contained metal centres which were an integral part of the protein, and many believed that it was metal-contamination.

How did your move to The Hospital for Sick Children, in Toronto come about?
I had been asked to give a seminar at the hospital which is affiliated with the University of Toronto, where they were setting up a major research institute and wanted to develop the area of metal-related diseases. Then I was offered the position of an assistant professor.

When I first arrived, I didn't think it would last six months. I had come from southern California where it hardly rains to a place with lots of snow!

What was your first area of research?
We focussed on genetic metabolic disorders with a particular interest in Wilson and Menkes diseases. I was surrounded by many sick children and I thought that whatever I do, it must lead from bench to bedside so I can see the results.

What do you consider as your greatest discovery?
The Menkes disease treatment discovery is one of the greatest satisfactions that I have had in my lifetime; that a child who would have died at the age of three years lived to be 22. Copper-histidine was prepared in my lab, and now it is used all over the world to treat the disease. It is not a cure, Menkes is a genetic disease, but you can improve it.

What is currently hot in the field of metal-proteins?
The discovery of even more metal-binding proteins is a rather recent development in my work. The old paradigm of one protein to one gene is not true anymore and in eukaryotic cells, the situation is more like six to eight proteins per gene. So there are an enormous number of proteins to find, once splice site variation and post-translational modifications are considered. The challenge is to separate, enrich and then analyse them.

Once we get this set of proteins, and find out what they all do in metal transport and in the metal disease field, it will ultimately help in the identification of biomarkers to improve clinical diagnosis and to develop new therapies.

One area of interest to you is environmental metallomics, can you explain more about this?
My interest started about 13 years ago when I was invited to talk about Menkes disease at the Indian Science Congress in Delhi. After the talk, I was asked, as a metals expert, whether I was aware of the catastrophe in the Bengal Delta, where it looked as though people had arsenic poisoning from the drinking water in wells. I went to several villages to see for myself and the experience was unbelievable. The awful cases of melanosis and advanced gangrene cases were terrible, and the sufferers were treated as social outcasts.

In 1998, I was the first person to report the effects of arsenic in an 8-year-old child. This was strange as arsenic poisoning normally takes time to develop, it is normally a slow poison. After seeing this child, I formed an international, multidisciplinary team of volunteer scientists, known as Scientists Without Borders. Our first major work was a national-scale mapping of not only arsenic but 29 other metals. Anyone can now go and look at the map that we produced to see the most contaminated areas. The next job was to develop a very inexpensive method by which you can routinely measure arsenic in water which goes below 10 micrograms per litre.

We found that it is not just arsenic but other toxic metals such as antimony coming from the underground water that can enhance arsenic toxicity. Recently we found uranium and manganese in the drinking water. Uranium can cause kidney and bone diseases and manganese can cause Parkinsonian disorders and neurological problems. All this work is one example of what environmental metallomics has to offer the scientific and global community.

Related Links:
Bibudhendra Sarkar's homepage
University of Toronto

MIMER Notes, February 14, 2010

2010-02-14T16:27:00.000+01:00

Arsenic on the rise. Scientific publications on arsenic are on the rise. A survey on publications indexed in PubMed in the period 1990-2009 shows that the number of annual publications on arsenic have increased at a higher rate relatively to publications on mercury, cadmium and lead, which are considered the most important metal pollutants (Figure).

Evidence that low level arsenic causes Alzheimer disease and other dementias

2010-02-06T17:40:00.001+01:00

MIMER notes, February 6th, 2010
Arsenic for the fool

Anthropogenic arsenic is insidiously building up together with natural arsenic to a level unprecedented in the history of mankind. Arsenopyrite (FeAsS) is the principal ore of arsenic and gold in hard rock mines; it is formed by a coupled substitution of sulphur by arsenic in the structure of pyrite (FeS(2)) - nicknamed "fool's gold". Other important sources of anthropogenic arsenic are fossil fuels such as coal and oil.

In a paper accepted for publication in the journal Science of the Total Environment, researcher Sergio Dani of Brazil's Medawar Institute for Medical and Environmental Research found that arsenic in topsoil is exponentially related to dementias in European countries.

Dani found an association of total arsenic concentrations in topsoils – as determined by ICP-MS (inductively coupled plasma mass spectrometry) data made available from the FOREGS Project led by Salminen and colleagues in 2005 – with the prevalence of Alzheimer's disease and other dementias in Europe as reported by the Delphi consensus study led by Ferri and colleagues in 2005, and mortality data as reported by WHO for the year 2009.

This is the first indication that the environmental concentration of total arsenic in topsoils - in the 7-18 ppm range - is exponentially related to the prevalence and mortality of Alzheimer's disease and other dementias. This evidence defies the imputed absence of verified cases of human morbidity or mortality resulting from exposure to low-level arsenic in topsoils.

Reference:

Dani SU. Arsenic for the fool: An exponential connection. Science of the Total Environment (2010), doi:10.1016/j.scitotenv.2010.01.027

Hopi and Navajo Residents Stop Peabody's Coal Mine Expansion on Black Mesa

2010-01-17T14:16:00.000+01:00

From: Center for Biological Diversity
Published January 11, 2010 10:54 AM
Hopi and Navajo Residents Stop Peabody's Coal Mine Expansion on Black Mesa

BLACK MESA, Arizona, USA- Peabody Western Coal Company's Black Mesa Coal Complex has suffered a major setback as an administrative law judge for the U.S. Department of the Interior vacated a permit for the massive coal-mining complex. The judge vacated the permit in response to one of several appeals filed by Navajo and Hopi residents as well as a diverse coalition of tribal and environmental groups. The permit, issued by Interior's Office of Surface Mining, Reclamation and Enforcement, allowed Peabody to operate and expand the Black Mesa and Kayenta mines under a single permit.

The Processes of Globalisation

2009-12-30T07:26:00.000+01:00

The Processes of Globalisation
Boaventura de Sousa Santos

What is the current state of globalisation, how are we to understand the processes involved and where will a globalised world system lead us? These are some of the questions Boaventura de Sousa Santos aims to elucidate in a thorough and wide ranging essay. Arguing that our current globalisation is indeed something unparalleled in history, Santos discusses the unequal economic and political realities between North and South which globalisation enforces. Globalisation is to be understood as a non-linear process marked by contradictory yet parallel discourses and varying levels of intensity and speed. Even states however have to adopt as the supremacy of the nation state is eroded, giving way to new transnational alliances and the convergence of the judicial systems as the supreme regulator of a globalised economy. Will all these processes usher into a new model of social development, or will this lead to the crisis of the world system as others fear? Read the article at: http://www.eurozine.com/articles/2002-08-22-santos-en.html

Kinross to greenwash cyanide

2009-12-24T12:23:00.000+01:00

Kinross to greenwash cyanide

By Sergio U. Dani, from Göttingen, Germany, December 24, 2009

Kinross Gold Corporation, a transnational Canadian company that pollutes the environment, robs drinking water and kills people in Paracatu-MG, Brazil, has announced its new greenswashing move this Tuesday [1]. Kinross announces “Cyanide Management Certification” in its gold mines in the Americas and Russia. Stephen Odoi-Larbi has written about this greenwashing modality in Africa in a recent article [2] attached hereto. It reproduces to perfection the pathetical and notious greenwashing move as has been observed in Paracatu and elsewhere: polluting companies’ self regulation; violation of human rights, despise of nations’ sovereignty; wrong voluntary code of conduct; greenwashing intended to better the interest of the mining companies operating in countries.
Sources:

[1] http://www.kinross.com/news-articles/2009/kupol-becomes-first-mine-in-russia-to-obtain-icmi-environmental-certification-.aspx, accessed December 24, 2009.

[2] http://allafrica.com/stories/200910210070.html, accessed December 24, 2009.

Read attachment [2] here:

Ghana: Mining coys, WACAM in fight over cyanide management

Stephen Odoi-Larbi

16 October 2009

Accra — In a bid to protect the environment within catchment areas of their operations, some mining companies in Ghana have signed the International Cyanide Management Code for the manufacture, transport, and use of cyanide in the production of gold.

This is a voluntary initiative spearheaded by the International Cyanide Management Institute (ICMI). Cyanide management has always been a headache to many mining firms in Ghana and other mining countries in the sub-region.

As a result of this, players in the industry gathered in Accra recently for a day's workshop on the auditing and management of the International Cyanide Management Code, a move they described as a step towards protecting the environment.
The training aims to build on the capacity of personnel in the mining industry to handle, and, or mitigate cyanide related emergencies.

"Environmental management is a key corporate priority, and members have integrated it into the continuum of operations from exploration, through design and construction to mining, processing, and rehabilitation and decommissioning. Our members continue to cooperate assiduously with the EPA and the Mines Inspectorate, in adhering to the Environmental Laws of this country," noted Ms. Joyce Aryee, Chief Executive Officer of the Ghana Chamber of Mines, in her opening remarks to participants attending the workshop.

So far, 21 mining companies, including four from Ghana, namely, Newmont Ahafo mine, Anglogold Ahanti Obuasi and Iduapriem mines, Golden Star Wassa and Bogoso mines, as well as Gold Fields Tarkwa and Damang, are signatories to the International Cyanide Management Code.

The aforementioned companies, according Ms. Joyce Aryee, have either been fully certified, or over 90% certified.

Two cyanide producing members of the Chamber, Cyplus and Orica, and three transporting companies, Barbex Technical Services, Allship Logistics and Vehrad Transport, are all subject to the code's requirements.

But, WACAM, a lead advocate non-governmental organisation on environmental issues, has described the move as "pure green-washing" intended to better the interest of the mining companies operating in the country.

Its Chief Executive Officer (CEO), Daniel Owusu Koranteng, told The Chronicle in a telephone interview, that the aforementioned companies, now signatories to the International Cyanide Management Code, were all guilty of cyanide spillage.

"These are the very companies that are guilty of cyanide spillage. They are trying to move to a voluntary code of conduct, which is wrong. This is pure green-washing," fumed Mr. Koranteng.

According to him, much as the companies are trying to protect the environment, they shouldn't be allowed to regulate themselves.

He accused the Environmental Protection Agency (EPA) of doing too little to save the environment and communities in the catchment areas of the mining companies.

"The companies are not supposed to regulate themselves. They are on a daily basis doing things to better their interests. We must have strong regulations, enforce them, so that they benefit the communities these mining companies operate," he noted.
Mr. Koranteng challenged the basis under which the environment and communities in the mining areas are protected.

Under the Minerals and Mining Act, 2006 (Act 703), there is no clause or section for addressing cyanide spillage in the country. This, according to Mr. Koranteng, does not augur well for the country.

"There is no clause in the Minerals and Mining Act, 2006 (Act 703) concerning spillage. There is nothing," he noted.

He quoted the Minerals and Mining Act, 2006, (Act 703) sections 17 and 108 to buttress his argument.

Section 17 of the Mineral and Mining Act, 2006, (Act 703) reads: "Subject to obtaining the requisite approvals or licenses under the Water Resources Commission Act 1996 (Act 552), a holder of a mineral right may, for purposes of or ancillary to the mineral operations, obtain, divert, impound, convey and use water from a river, underground reservoir or watercourse, within, and the subject of the mineral right."

Mr. Koranteng therefore advocated the polluter pay principle (PPP), where the polluter is made to pay for the harm inflicted on the environment.

He said elsewhere in the world, clean up cost of cyanide amounted to US$100 million, but in Ghana, it was the mining companies that decide on what to pay. Under Section 108 (1) of the Minerals and Mining Act, 2006 (Act 703) "A person found guilty of an offence under this Act, for which a penalty has not been provided, is on summary conviction liable, on first conviction, to a penalty of a fine not more than the cedi equivalent of US$5,000."

This, Mr. Koranteng noted, was a meager amount to the multi-national mining companies operating in the country.

"What is this US$5,000 to these multi-national mining companies, and where does our sovereignty as a country lie," he fumed.

Mr. Koranteng therefore called on the EPA to institute regulator policies that would be reinforced to benefit the communities in the catchment areas of mining companies in the country.

In March 2008, investigations conducted into the operations of mining companies in the country by the Commission on Human Rights and Administrative Justice (CHRAJ), Ghana, revealed that state institutions with regulatory and monitoring responsibilities for the mining sector, had not performed optimally, due to capacity constraints.

The CHRAJ sited the EPA as an example, for amply demonstrating lack of capacity in terms of human and financial resources to hold mining companies accountable for their environmental stewardship, as required by law.

This lack of capacity, according to CHRAJ, has been demonstrated in the increasing record numbers of reported cases of cyanide spillages from a number of mining companies, polluted community water sources, threat to communities' health by inappropriate siting of mine waste facilities, and uncovered mine pits and trenches.

The CHRAJ, in its concluding report, noted: "Communities have expressed little confidence in the ability of the agency (EPA), in particular, to protect their environment against the activities of miners."

What is at stake in Copenhagen

2009-12-18T10:38:00.000+01:00

A who-shall-die-last game? Or the ascent of a new kind of world leadership?

"Let us give good science, good systemic projects and good systemic leaders a chance to save our humanity by saving our planet."

Sergio U. Dani, from Göttingen, Germany, December 18, 2009

For those wondering why official politicians and negotiators are unable to set an agreement at Copenhagen, I offer a guess. Official politicians and negotiators are common sense thinkers backed by mainstream economy, industrial and financial institutions in their respective countries. They are created in a competitive system where money endows power, makes one strong to defeat weaker competitors. Since enough political money – and therefore enough political strength – is in possession of the rich, what most people aren’t, then conducting politics and negotiation has become an exclusive right of a fistful of rich and nouveau rich people.

A fistful of privileged rich people and institutions are intrinsically programmed to win competitions, not to lose them. They deal with global warming as if it was a competition as any other one. Their task, their default is to win this competition and keep growing. The reason why they are up to mischief is certainly this. There is no such thing as a growth competition when it comes to global warming and critically degrading resources. Global warming and environmental degradation have to be dealt with in their own rights. After all, global warming affects all of us, the rich and the poor, the intelligent and the fool, the beautiful and the ugly, the young and the elderly, the winners and the losers. Science of the environment has taught us that systemic changes do not abide by political rules or geographic frontiers.

This is the reason why these official people are fundamentally not entitled to deal with the problem. They are part of the problem, not the solution. They simply do not have the ability to find efficient solutions on such serious matters. Please note that I am not telling that governments are not entitled to decide and take action on such serious environmental matters. I am telling that present government people – of the kind of most of those we know, anyway – are incompetent to deal with systemic matters, simply because they have been reared in a competitive system.

Hear, for instance, what Dilma Rousseff, a high-rank member of the Brazilian government has uttered in Copenhagen: “It is beyond doubt that environment poses a hurdle to sustainable development. This is to say that environment threatens the future of our planet and our countries”. Rousseff champions a controversial growth acceleration program in Brazil, causing dramatic governmental-led environmental degradation in Brazil. Her violent style forced the resignation of Brazilian environment minister and world-renowned ecological leader Marina Silva last year. If Rousseff's and Lula's model of accelerated growth were to be adopted worldwide, we would certainly have an accelerated death. And yet, this fistful of ill-prepared Brazilian governmental authorities - including President Lula himself - believe they can teach the world ecological lessons.

Evaluate the solution offered by the American government to fight global warming, as uttered by Hillary Clinton in Copenhagen: “The US is prepared to work with other countries towards a goal of jointly mobilising $100 billion a year by 2020 to address the climate change needs of developing countries.” In other words, she believes US responsibility in fighting global change is as simple as telling developing countries to “go shopping”. She voiced no word about how the US are going to reduce its atmospheric emissions of global warming gases.

Watch the behavior of Canada’s government in Copenhagen, as reported by George Monbiot: “The Canadian government … is now behaving with all the sophistication of a chimpanzee's tea party. Unless we can stop it, the harm done by Canada in December 2009 will outweigh a century of good works,” explains Monbiot. “In Copenhagen (this) week, this country (is doing) everything in its power to wreck the talks. The rest of the world must do everything in its power to stop it. Canada now threatens the wellbeing of the world.”

A fruitful international agreement on governmental actions against global warming depends on grassroots work aimed at replacing unable governmental people with better prepared people. This is a gigantic effort and a challenge for the 21st century, as it encompasses fundamental changes in societal knowledge and societal values, including a profound restructuring of our democratic institutions.

We have to find democratic ways of replacing common sense leaders with systemic leaders. Systemic leaders will foster and spread good systemic ideas instead of lobbying for bad sectorial ideas; socio-environmentally responsible programes instead of bad growth acceleration programes; low-consume economies instead of high-consume economies; peace industries instead of war industries; real nature’s capital valuation instead of surreal speculative capital valuation; sustainability of the human, instead of the sustainable development mith. Let us give good science, good systemic projects and good systemic leaders a chance to save our humanity by saving our planet.

How do toxic chemicals move around the planet?

2009-12-03T10:58:00.000+01:00

How do toxic chemicals move around the planet?

Read Elizabeth Grossman's article in Scientific American for awesome explanations.

Swimmers, hoppers and fliers: How do toxic chemicals move around the planet?
By Elizabeth Grossman
Toxic chemicals created by human activity reach unusual concentrations in the Arctic, among other places

http://www.scientificamerican.com/article.cfm?id=how-do-toxic-chemicals-move-around-planet&SID=mail&sc=emailfriend

World's top 10 most polluted places

2009-12-03T10:52:00.000+01:00

Open cut gold mine at Paracatu-MG, Brazil: arsenic contamination and mass murder. Photo by Beto Magalhães, July 2008.

World's top 10 most polluted places
Where toxic pollution and human habitation collide with devastating effects

By David Biello
From the December 2007 special edition of Scientific American

1. Sumqayit, Azerbaijan—This area gained the dubious distinction of landing atop the Blacksmith Institute’s list of the world’s most polluted sites. Yet another heir to the toxic legacy of Soviet industry, this city of 275,000 bears heavy metal, oil and chemical contamination from its days as a center of chemical production. As a result, locals suffer cancer rates 22 to 51 percent higher than their countrymen, and their children suffer from a host of genetic defects, ranging from mental retardation to bone disease.

“As much as 120,000 tons of harmful emissions were released on an annual basis, including mercury,” says Richard Fuller, founder of Blacksmith, an environmental health organization based in New York City. “There are huge untreated dumps of industrial sludge.”

2. Chernobyl, Ukraine—The fallout from the world’s worst nuclear power accident continues to accumulate, affecting as many as 5.5 million people and leading to a sharp rise in thyroid cancer. The incident has also blighted the economic prospects of surrounding areas and nations.

3. DzerzHinsk, Russia—The 300,000 residents of this center of cold war chemical manufacturing have one of the lowest life expectancies in the world thanks to waste injected directly into the ground. “Average life expectancy is roughly 45 years,” says Stephan Robinson, a director at Green Cross Switzerland, an environmental group that collaborated on the report. “Fifteen to 20 years less than the Russian average and about half a Westerner’s.”

4. Kabwe, Zambia—The second largest city in this southern African country was home to one of the world’s largest lead smelters until 1994. As a result of that industry, the entire city is contaminated with the heavy metal, which can cause brain and nerve damage in children and fetuses.

5. La Oroya, Peru—Although this is one of the smallest communities on the list (population 35,000), it is also one of the most heavily polluted because of extensive lead, copper and zinc mining by the U.S.–based Doe Run mining company.

6. Linfen, China—A city in the heart of China’s coal region in Shanxi Province, Linfen is home to three million inhabitants, who choke on dust and air pollution and drink arsenic that leaches from the fossil fuel.

7. Norilsk, Russia—This city above the Arctic Circle contains the world’s largest metal-smelting complex and some of the planet’s worst smog. “There is no living piece of grass or shrub within 30 kilometers of the city,” Fuller says. “Contamination [with heavy metals] has been found as much as 60 kilometers away.”

8. Sukinda, India—Home to one of the world’s biggest chromite mines—chromite makes steel stainless, among other uses—and 2.6 million people. The waters of this valley contain carcinogenic hexavalent chromium compounds courtesy of 30 million tons of waste rock lining the Brahmani River.

9. Tianying, China—The center of Chinese lead production, this town of 160,000 has lead concentrations in its air and soil that are 8.5 to 10 times those of the national health standards. The concentrations of lead dusting the local crops are 24 times too high.

10. Vapi, India—This town at the end of India’s industrial belt in the state of Gujarat houses the dumped remnant waste of more than 1,000 manufacturers, including petrochemicals, pesticides, pharmaceuticals and other chemicals. “The companies treat wastewater and get most of the muck out,” says David Hanrahan, Blacksmith’s London-based director of global operations. “But there’s nowhere to put the muck, so it ends up getting dumped.”

Source:

http://www.scientificamerican.com/article.cfm?id=body-worlds-top-10-most-polluted-places&SID=mail&sc=emailfriend

Poisoned water haunts Bhopal 25 years after chemical accident

2009-12-03T10:24:00.000+01:00

Poisoned water haunts Bhopal 25 years after chemical accident

By Sara Goodman

A new report says water contamination is worsening as chemicals leach through soil into the aquifer

http://www.scientificamerican.com/article.cfm?id=groundwater-contamination-india-pesticide-factory&SID=mail&sc=emailfriend

A message for the people of Canada: Support “Bill C-300” and let us live our lives in health and peace!

2009-11-30T10:34:00.000+01:00

A message for the people of Canada: Support “Bill C-300” and let us live our lives in health and peace!

By Sergio U. Dani, from Göttingen, Germany, November 30, 2009

If you are a Canadian woman or man, you should know that 2 out of 3 extractive companies operating in the world are based in Canada. The reason for this astonishing concentration of mining, oil and gas companies in Canada can be hinted at in a recent report released by three Canadian gold mining companies [1]: “the international competitiveness of Canadian mining companies working in developing countries in a manner unique to Canada”.

Indeed, many Canadian companies receive taxpayer dollars of Canadian governmental investment. They also receive political and diplomatic support from the Canadian government to operate around the world, and they pretend to operate legally. Truth is, many of these companies operate massive environmental damages, displacement of local people from their homes as well as rapes and even murder. Did you know all that? Have you ever allowed your government and Canadian companies to operate like this, financed by the taxes you pay?

I must tell you that Canadian gold mining corporations manage to thrive and to operate illegally in developing countries by making "facilitation payments" that favor local governments while hurting human rights, people's health and the environment [2]. An illustrative example of such practices is provided by Kinross Gold Corporation, which facilitates corruption and sets the stage for a true genocide in Paracatu, Brazil, whereas pretending to be legal [3,4]. Kinross claims that it operates under strictly legal terms in Brazil. This is overtly not true, and Kinross has been sued in several civil actions proposed by the Brazilian State and Federal Public Ministries, the Acangau Foundation and private persons, too. Robbing and polluting drinking water, polluting soils and the atmosphere, expelling native people from their legally protected territories, hiding or manipulating information and killing people is simply against the Brazilian law. It is also immoral, inhumane and bad for mankind. Thus it is also bad for you, my Canadian brother or sister.

Whereas some of the liabilities for these crimes and errors are left for taxpayers to pay again, some are left for humankind to pay forever. An imperceptible though dangerous toxin called arsenic is being released to the biosphere by mining operations, particularly gold mining operations. Gold mines pose the highest concerns worldwide because arsenic is most abundant in gold ores.

I have recently authored a study in the journal Medical Hypotheses in which I review the hazards of arsenic release from gold mines worldwide, including Kinross' Paracatu gold mine [5]. This study has won immediate media coverage [6,7]. I have estimated that thousands of gold mines worldwide have the potential to release 10-100 kg of arsenic per each human being presently living on planet Earth. Whereas 100 milligrams of arsenic suffice to acutely kill an adult man, much lesser amounts – in the part per billion range – are enough to chronically kill or cause serious health and economical distresses to billions of people, eroding family and country economies worldwide.

There is vast scientific evidence that arsenic released by human activities is mobilized in many environmental compartments in the course of years, centuries and millennia. Chronic exposure to environmental arsenic has been implicated as a cause or predisposing factor for each of the top ten causes of death in the world, including vascular diseases, various forms of cancer, diabetes and immunological diseases. Unfortunately, environmental remediation of arsenic is economically unfeasible.

Therefore, some mining operations are worse than crimes, they are huge errors that must be avoided because they are bad for all of us. This is why you Canadian should support Bill C-300 and legislation of the same kind. Let us live our lives in health and peace!

References and notes:

[1] Barrick Gold Corporation, Kinross Gold Corporation and Goldcorp Inc. (2009) Submission to the Standing Committee on Foreign Affairs and International Development. Bill C-300. An Act respecting Corporate Accountability for the Activities of Mining, Oil or Gas in Developing Countries. Retrieved from http://www.barrick.com/Theme/Barrick/files/docs_csr/Bill-C-300-Submission-to-the-Standing-Committee.pdf, November 28, 2009.

[2] Dani SU. How can Canadian companies operate illegal mining worldwide? Accessible at: http://sosarsenic.blogspot.com/search?q=how+can

[3] Dani SU. Kinross Gold Corporation: a history of bad management, facilitated corruption and mass murder. Accessible at http://sosarsenic.blogspot.com/2009/11/kinross-gold-corporation-history-of-bad.html#more

[4] Dani SU. Canadian Kinross Gold Corporation operates corruption plots and a true genocide in Brazil Accessible at http://sosarsenic.blogspot.com/2009/11/canadian-kinross-gold-corporation.html

[5] Dani SU. Gold, coal and oil. Medical Hypotheses doi:10.1016/j.mehy.2009.09.047

[6] http://news.discovery.com/human/human-extinction-doomsday.html

[7] http://www.theglobeandmail.com/life/facts-and-arguments/arsenic-and-our-fate-appearances-count-and-middle-class-theft/article1361341/?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+TheGlobeAndMail-Front+(The+Globe+and+Mail+-+Latest+News)

Related material:

. A short documentary film on Canadian MP John McKay's Private Member's Bill C-300 and some of the MPs who support it. Accessible at: http://www.youtube.com/watch?v=Nf563OSDOws

. Full text of Bill C-300 available at: http://www2.parl.gc.ca/HousePublications/Publication.aspx?DocId=3658424&Language=e&Mode=1

. Lawsuit exposes Canada’s toxic tailings secret: Groups say feds flouting law, hiding mining pollution from public. Accessible at: http://www.miningwatch.ca/en/lawsuit-exposes-canada-s-toxic-tailings-secret-groups-say-feds-flouting-law-hiding-mining-pollution-

. Mining Day on the Hill - What you should know about mining and Canadian mining companies. Accessible at: http://www.miningwatch.ca/en/mining-day-hill-what-you-should-know-about-mining-and-canadian-mining-companies

Main ingredients in household dust come from outdoors

2009-11-19T12:16:00.000+01:00

Main ingredients in household dust
come from outdoors

Arsenic and other particles tracked indoors can be harmful, researchers warn

By Robert Preidt, HealthDay

WEDNESDAY, Nov. 11, 2009 (HealthDay News) -- Most of the dust that coats your furniture and floors comes from outdoors and can pose a health threat, a new study suggests.

The researchers developed a computer model that can track the distribution of outdoor soil and airborne particles into homes and found that more than 60 percent of household dust originates from tracked-in soil and airborne particles from the outdoors. The remainder is from dead skin shed by residents, fibers from carpets and upholstered furniture.

This outdoor-based dust can contain lead, arsenic and other potentially harmful substances, said the Arizona researchers. For example, they estimated that 60 percent of arsenic in floor dust may come from arsenic in the surrounding air, with the remainder coming from tracked-in soil.

The substances in household dust that originates outdoors may be a special concern for homes with children, who put dust-contaminated toys and other objects into their mouths, said David Layton and Paloma Beamer of the University of Arizona in Tucson, who added that their computer model may prove useful in evaluating ways to reduce contaminants in dust and associated human exposure.

The study was released online in advance of publication in the Nov. 1 print issue of the journal Environmental Science & Technology.

SOURCE: Environmental Science & Technology, news release, November 2009

Reference: David W. Layton and Paloma I. Beamer (2009) Migration of contaminated soil and airborne particulates to indoor dust. Environmental Science & Technology 43:8199–8205

Gold mining liabilities left for taxpayers to pay

2009-11-19T12:15:00.000+01:00

Gold mining liabilities left
for taxpayers to pay

The Giant Mine was a large gold mine located on the Ingraham Trail just outside of Yellowknife, Northwest Territories, Canada. Mining operations at Giant Mine over five decades (from 1948 to early 2004) created a massive environmental liability, a problem which the mine's previous owners left to the Canadian and Northwest Territories governments to sort out.

The Giant Mine contains 237,000 t (233,000 LT; 261,000 ST) of arsenic trioxide dust produced during the gold roasting process. This dust is water soluble and contains approximately 60% arsenic. The site's 950 ha (2,300 acres) footprint includes 8 open pits, 4 tailing ponds, 325,000 m3 (11,500,000 cu ft) of contaminated soils, and approximately 100 buildings including a roaster/bag house complex that is highly contaminated with arsenic and fibrous asbestos.

A $200 million (probably more) taxpayer-funded remediation project is underway. A main aspect of the successful proposed solution, known as the "Frozen Block Alternative," is to permanently freeze the arsenic trioxide storage chambers to keep groundwater seepage out.

Sources:

[1] "Disaster brewing at Giant mine site". (July 10, 2006) news/north p.1
[2] "Giant Mine Remediation Project". http://nwt-tno.inac-ainc.gc.ca/giant/index_e.html. Retrieved 2006-07-15.
[3] http://en.wikipedia.org/wiki/Giant_Mine, retrieved 2009-11-19.

Giant Mine arsenic spill raises safety questions

2009-11-19T12:12:00.000+01:00

Giant Mine arsenic spill raises safety questions

CBC News, October 2009. A recent arsenic spill at the defunct Giant Mine near Yellowknife is raising concerns about safety and the reporting of spills at mine sites.

Drilling at the former gold mine has been stopped while the federal government awaits results from soil, water and air-quality tests done since the spill last week. According to a spill report, arsenic dust was released from a borehole at the mine site around 1 a.m. on Oct. 22, contaminating the area within five to 10 metres of the hole. A male worker in the area, who was wearing a waterproof suit and respirator, was washed down afterwards with a pressure washer. The man has not experienced health problems so far, according to the report.

The federal Indian and Northern Affairs Department, which is overseeing cleanup and remediation of the Giant site, did not find out about the spill until Oct. 24, two days after it happened. The company that was working at the site at the time, the Deton'Cho Nuna joint venture, declined to comment.

Since June, test drilling has been done at the Giant Mine site as part of the federal government's plan to freeze toxic arsenic trioxide dust, the byproduct of gold production, in large refrigerated chambers underground.

The federal department determined the work did not require a land-use permit. But the department's head of inspections and enforcement at the Giant site said Deton'Cho Nuna joint venture was operating under old regulations, using principles that have applied in the past.

"They're not operating willy-nilly out there," Darnell McCurdy said. "They are being guided by some principles that were issued in previous permits. And that goes back to when Giant was actually operating and that type of thing."

Source:
http://www.cbc.ca/canada/north/story/2009/10/29/giant-arsenic-spil.html?ref=rss
Last Updated: Thursday, October 29, 2009 | 3:27 PM CT

Dissolved arsenic in Bangladesh drinking water is from human alteration of landscape

2009-11-19T11:24:00.000+01:00

Dissolved arsenic in Bangladesh drinking water is from human alteration of landscape

ScienceDaily (Nov. 16, 2009) — Researchers in MIT's Department of Civil and Environmental Engineering believe they have pinpointed a pathway by which arsenic may be contaminating the drinking water in Bangladesh, a phenomenon that has puzzled scientists, world health agencies and the Bangladeshi government for nearly 30 years. The research suggests that human alteration to the landscape, the construction of villages with ponds, and the adoption of irrigated agriculture are responsible for the current pattern of arsenic concentration underground.

The pervasive incidence of arsenic poisoning in Bangladesh and its link to drinking water were first identified in the scientific literature in the early 1980s, not long after the population began switching from surface water sources like rivers and ponds to groundwater from newly installed tube wells. That national effort to decrease the incidence of bacterial illnesses caused by contaminated drinking water led almost immediately to severe and widespread arsenic poisoning, which manifests as sores on the skin and often leads to cancers of the skin, lung, liver, bladder and pancreas.

Since then, scientists have struggled to understand how the arsenic, which is naturally occurring in the underground sediment of the Ganges Delta, is being mobilized in the groundwater.

By 2002, a research team led by Charles Harvey, the Doherty Associate Professor of Civil and Environmental Engineering at MIT, had determined that microbial metabolism of organic carbon was mobilizing the arsenic off the soils and sediments, and that crop irrigation was almost certainly playing a role in the process. But the exact sources of the contaminated water have remained elusive, until now.

In a paper appearing online in Nature Geoscience Nov. 15, Harvey, former graduate students Rebecca Neumann and Khandakar Ashfaque and co-authors explain that ponds excavated for the purpose of providing soil to build up villages for flood protection are the source of the organic carbon that presently mobilizes the arsenic in their 6-square-mile test site. The carbon settles to the bottom of the ponds, then seeps underground where microbes metabolize it. This creates the chemical conditions that cause arsenic to dissolve off the sediments and soils and into the groundwater.

The researchers also found that in their test area, which is flooded by annual monsoons, the rice fields irrigated with arsenic-laden water actually serve to filter out much of the arsenic from the water system.

"Our research shows that water from the ponds carries degradable organic carbon into the shallow aquifer. Groundwater flow, drawn by irrigation pumping, transports that pond water to the depth where dissolved arsenic concentrations are greatest and where it is then pumped up into the irrigation and drinking wells," says Harvey. "The other interesting thing we found is that the rice fields are a sink of arsenic - more arsenic goes in with the irrigation water than comes out in the groundwater."

Scott Fendorf, a professor at Stanford University who studies arsenic content in soils and sediments along the Mekong River in Cambodia, says Harvey's previous research, published in 2002, "transformed the scientific community's outlook on the problem." The current work, he adds, has two big ramifications: "It shows that human modifications are impacting the arsenic content in the groundwater; and that while the rice cropping system appears to be buffering the arsenic, the ponds excavated to provide fill to build up the villages are having a negative impact on the release of arsenic."

Neumann, now a postdoctoral associate at Harvard University, took seven trips and spent nearly a year doing fieldwork in Bangladesh, studying the hydrologic behavior and chemical nature of rice fields and ponds, and performing tests on rice field and pond waters to determine if the organic carbon in these water bodies would stimulate arsenic mobilization. She and Ashfaque developed an understanding of the surface and underground water flow patterns over a seven-year period, using natural tracers and a 3-D model to track rice field and pond water as it traveled into and through the subsurface.

"When we compared the chemical signatures of the different water sources in our study area to the signatures of the aquifer water, we saw that water with high arsenic content originates from the human-built ponds, and water with lower arsenic content originates from the rice fields," says Neumann. "It's likely that these same processes are occurring at other sites, and it suggests that the problem could be alleviated by digging deeper drinking water wells below the influence of the ponds or by locating shallow drinking wells under rice fields." The researchers suggest that irrigation wells remain at the shallow level.

At 159 million people, Bangladesh is the seventh most populous country in the world, and it is growing quickly. That means that new tube wells and ponds are being dug every day to accommodate the growing population. Most of those wells are being drilled to less than 100 feet. At that depth, they draw water directly from the contaminated shallow aquifer.

Holly Michael, a professor at the University of Delaware and former PhD student in the Harvey Lab, also studies the physics of groundwater flow and transport of the dissolved arsenic in Bangladesh, but in the deeper aquifer.

"Charlie's team is looking at the impacts at and near the surface, and my team is looking at the potential impacts of human activities at depth," says Michael. "My team found that if only the drinking-water wells are put into the deep, low-arsenic parts of the aquifer -- at depths greater than 450 feet -- then it is likely that the supply of low-arsenic water will continue for a very long time over much of the arsenic-affected area. Because so much more water is pumped for irrigation, it is important that irrigation wells are not installed deeper, as this would likely cause high-arsenic groundwater to flow downward toward the wells."

Harvey estimates that the prevalence of arsenic poisoning in Bangladesh is approximately 2 million cases and that the incidence of death from arsenic-induced cancer will rise to approximately 3,000 cases per year if consumption of contaminated water continues. He and a team of environmental scientists and physicians are making plans for a multi-year study that would provide deep wells for two villages in Bangladesh whose inhabitants suffer from arsenic poisoning. There they would combine continual testing of the well water and hydrogeological modeling of the groundwater system with a study of how the clean water effects the villagers' health, placing special emphasis on the neurological development of children.

"There are all sorts of studies to show how arsenic hurts people. We're trying to turn it around and show how removal of the arsenic will help them," says Harvey.
Other co-authors on the paper are graduate student Julie Shoemaker, who helped with fieldwork, sample analysis and data synthesis, and Bangladeshis A.B.M. Badruzzaman and M. Ashraf Ali of the Bangladesh University of Engineering and Technology, who provided logistical support for the field site in the Munshiganj district of Bangladesh.

Source:

Massachusetts Institute of Technology, Department of Civil and Environmental Engineering (2009, November 16). Dissolved arsenic in Bangladesh drinking water is from human alteration of landscape. ScienceDaily. Retrieved November 19, 2009, from http://www.sciencedaily.com/releases/2009/11/091115134130.htm?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+sciencedaily+%28ScienceDaily%3A+Latest+Science+News%29

How can Canadian companies operate illegal mining worldwide?

2009-11-17T16:13:00.000+01:00

How can Canadian companies operate illegal mining worldwide?

Picture: Mexican people demonstrate against Canadian mining company in Cerro de San Pedro

Sergio Ulhoa Dani, from Göttingen, Germany, November 10, 2009

The people of San Luis Potosí, Mexico, have been fighting an open pit gold mine in Cerro de San Pedro. Last year it became part of a larger company, New Gold Inc. ("New Gold", TSX and NYSE AMEX: NGD), who has been pretending that all is well and legal while continuing to operate illegally, the people of San Luis Potosí say.

The configuration is very similar to that of Paracatu, Brazil, where Canadian Kinross Gold Corporation (NYSE: KGC; TSX: K) operates a true genocide through the release of arsenic from its open cut gold mine located in the outskirts of the city, with the invaluable support of a fistful of government people.

But San Luis Pososí and Paracatu are not isolate cases. Some Canadian companies have been operating corruption and murdering plots worldwide. The Congo affair gained notoriety through the intervention of the UNO Secretary General.

How and why can Canadian gold companies thrive so easily and illegally in foreign countries, despising local people and the environment?

“Over the last ten years a small group opposed to the mine has conducted an ongoing series of challenges, appeals and counter appeals related to the EIS (Environmental Impact Statement) approval process”, it reads in New Gold’s website. It reads in the same website that Mr. Santos Loredo Tenorio, President of the Cerro de San Pedro Municipality, appreciates New Gold’s supports to schools, health services and infrastructure improvement. Still according to information in New Gold’s website, Tenorio would have said that "the company's contribution to sustainable community development and our future is greatly appreciated."

What we have learned from Kinross Gold Corporation in Paracatu is that it makes “facilitation payments” to local government people in order to “facilitate” its business in Brazil. What we have learned from Stephen Harper, Canada’s Prime Minister, is that “Canada will rule”, which sounds much like “Canada will take over the world”. To make his point clear, he is caring for the militarization of Canada. In other words, the boss sets the tune and provides for backing.

“Quite simply, Stephen Harper is unfit to govern. Surely the only prime minister in Canadian history who has actually expressed contempt for his own country, Harper has demonstrated a disregard for the rule of law that should, in a rational world, disqualify him from leading any government,” wrote Murray Dobbin in a recent article.

Harvey Oberfeld discloses another aspect of Canadian Prime Minister’s personality when talking about Harper’s customary use of French – the minority language in Canada – instead of English: “He is really clearly placing 25 per cent of Canada’s population ahead of the other 75 per cent. And it’s about time, people started telling him to restore respect for the majority, as well as the minority.”

About New Gold’s mines

In addition to Cerro de San Pedro mine, New Gold Inc. has other operations: (i) Mesquite, a gold heap-leach, run of mine operation 70 km northwest of Yuma, Arizona, Imperial County California; (ii) Peak Mines, a gold-copper underground mining operation in the Cobar Gold Field, New South Wales, Australia; and (iii) Amapari Mine, a gold heap leach operation located in the State of Amapá in Brazil.

New Gold’s Amapari mine is located in central Amapa State, in the middle of the Amazon Forest, near Amapari river, Brazil. It is a open cut mine (see satellite images in this report). The method employed by New Gold Inc. to extract gold at the Amapari mine is heap leaching. The mined ore is crushed into small chunks and heaped on an impermeable plastic and/or clay lined leach pad where it is irrigated with a leach solution containing the extremely toxic sodium cyanide which is employed to dissolve gold. The solution containing gold and usually other metals (so called "pregnant solution") continues percolating through the crushed ore until it reaches the liner at the bottom of the heap where it drains into a storage (pregnant solution) pond. This can take several weeks.

The leach solution containing the dissolved metal is then collected. After separating the precious metals from the pregnant solution, the dilute cyanide solution (now called "barren solution") is normally re-used in the heap-leach-process or occasionally sent to an industrial water treatment facility where the residual cyanide is treated and residual metals are removed. The water is then discharged to the environment, posing water pollution. Same occurs with the residual ores, called tailings, which are contaminated with residual cyanide, sulphuric acid and mobilized heavy metals.

In addition to the environmental hazards presented with this extraction method, there is also the hazard presented by the cyanide itself. These hazards are present in virtually all gold mines. Some cases have gained public recognition, like the environmental disaster in Central-Eastern Europe in year 2000, when during the night of 30 January, a dam at a goldmine reprocessing facility in Romania released approximately 100,000 m³ of wastewater contaminated with heavy metal sludge and up to 120 tons of cyanide into the rivers of Tisza.

To learn more about Kinross mine in Paracatu, Brazil, access:

http://sosarsenic.blogspot.com/2009/10/kinross-gold-mine-at-paracatu-brasil.html
http://sosarsenic.blogspot.com/2009/11/kinross-gold-corporation-history-of-bad.html

Sources:

[1] Mining Watch Canada
[2] Google Earth
[3] Available at www.newgold.com, accessed November 10, 2009.
[4] Wikipedia
[5] Ali, Saleem H. Gold mining and the golden rule: a challenge for developed and developing countries. Journal of Cleaner Production, Vol 14:3 (2006)
[6] http://www.dominionpaper.ca/images/2228
[7] www.alertaparacatu.blogspot.com
[8] Murray Dobbin. Stephen Harper: unfit to govern. September 10, 2009. Available at: http://www.rabble.ca/news/2009/09/stephen-harper-unfit-govern, accessed November 10, 2009.
[9] http://harveyoberfeld.ca/blog/stephen-harper-insults-english-canada-again/

Anthropogenic influences on groundwater arsenic concentrations in Bangladesh

2009-11-17T13:07:00.000+01:00

A new article in Nature Geoscience points to the role of human-made ponds in releasing arsenic from Bangladesh's aquifers:

http://www.nature.com/ngeo/journal/vaop/ncurrent/abs/ngeo685.html

Nature Geoscience
Published online: 15 November 2009

Anthropogenic influences on groundwater arsenic concentrations in Bangladesh

Rebecca B. Neumann, Khandaker N. Ashfaque, A. B. M. Badruzzaman, M. Ashraf Ali, Julie K. Shoemaker & Charles F. Harvey

Abstract

The origin of dissolved arsenic in the Ganges Delta has puzzled researchers ever since the report of widespread arsenic poisoning two decades ago. Today, microbially mediated oxidation of organic carbon is thought to drive the geochemical transformations that release arsenic from sediments, but the source of the organic carbon that fuels these processes remains controversial. At a typical site in Bangladesh, where groundwater-irrigated rice fields and constructed ponds are the main sources of groundwater recharge, we combine hydrologic and biogeochemical analyses to trace the origin of contaminated groundwater. Incubation experiments indicate that recharge from ponds contains biologically degradable organic carbon, whereas recharge from rice fields contains mainly recalcitrant organic carbon. Chemical and isotopic indicators as well as groundwater simulations suggest that recharge from ponds carries this degradable organic carbon into the shallow aquifer, and that groundwater flow, drawn by irrigation pumping, transports pond water to the depth where dissolved arsenic concentrations are greatest. Results also indicate that arsenic concentrations are low in groundwater originating from rice fields. Furthermore, solute composition in arsenic-contaminated water is consistent with that predicted using geochemical models of pond-waterâ€“aquifer-sediment interactions. We therefore suggest that the construction of ponds has influenced aquifer biogeochemistry, and that patterns of arsenic contamination in the shallow aquifer result from variations in the source of water, and the complex three-dimensional patterns of groundwater flow.

Metallomics opening new frontiers for brain research in Germany

2009-11-13T06:24:00.000+01:00

Metallomics opening new frontiers for brain research in Germany

Sergio U. Dani, Germany, Tuesday 3, November, 2009.

BrainMet, a new lab dedicated to the bioimaging of metals in brain and metallomics is scheduled for opening on December 9 this year. The new lab has been set up at the Central Division for Chemical Analyses of the Research Centre Jülich, in Jülich, Germany.

BrainMet is led by Dr. J. Sabine Becker, a worldwide renowned pioneer and expert in the field of mass spectroscopy. Becker and her group are credited with creating and developing a novel elemental analytical LA-ICP-MS technique using the near field effect with spatial resolution at the nanometer scale.

“Since trace elements are involved in a number of metabolic and physiological processes in the human body, and their deficiency and excess may lead to different metabolic disorders, much attention is paid with respect to the spatial distribution and the local concentration of trace elements in tissues”, says Becker.

BrainMet will be opened with a colloquium. For more information and registration to the BrainMet Colloquium, contact Mrs. A. Wiebecke at:

Forschungszentrum Jülich GmbH
Zentralabteilung für Chemische Analysen (ZCH)
52425 Jülich
Tel.: [++49] (2461) 61-4263
Telefax: [++49] (2461) 61-2560
E-mail: a.wiebecke@fz-juelich.de

MIMER Notes, November 9, 2009

2009-11-12T10:16:00.000+01:00

Medawar Institute for Medical and Environmental Research (MIMER)

Acute and chronic toxicities of arsenic in selected mammals including man: some notes on doses and vulnerabilities

By Sergio Ulhoa Dani, November 9, 2009.

Acute mortality

Different mammal species have different susceptibilities to arsenic acute toxicity, as assessed by LD50 and LC50 [1-12]. The LD50 defines the oral lethal dose that will kill 50% of the tested animals that eat the substance; and the LC50 defines the inhaled lethal concentration that will kill 50% of the tested animals breathing the substance.

A sequence of increased arsenic vulnerability as assessed by LD50 (LC50 for cat) is as follows: mouse (Ca or Pb arsenate p.o., 145-794 mg/kg) < rat (Ca or Pb arsenate p.o., 20-763 mg/g) < cat (AsCl3 gas, 100-200 mg/m3) < rabbit (Ca or Pb arsenate p.o., 50-75 mg/kg) < dog (Ca or Pb arsenate p.o., 38 mg/kg) < human (arsenate p.o., 1 mg/kg).

The vulnerability sequence as derived LC50 values (30 min exposure time) would be as follows [13]: mouse (73-209 mg As/m3) < rat (5.3-534 mg As/m3) < rabbit (8.8-13 mg As/m3) < dog (10 mg As/m3) < cat (5.2-7.8 mg As/m3) < human (estimated 5 mg As/m3).

Chronic morbidity and mortality

Dose-response relationships have been well documented for arsenic in drinking water and several of the leading causes of morbidity and mortality, starting from low-to-moderate As levels [6,14-22].

There are national and international guidelines which can help you define levels of As in water, but safety standards tend to be kept at minimal levels possible, largely based on analytical capacity.

As a “rule of thumb” or a “digit rule” (not as a safety rule) one could arbitrarily stage As levels in water as follows: a low level would be a one-digit figure, e.g. 1 part of As per billion parts of water (1 ppb); moderate level would be a two-digit figure (e.g., 10 ppb); high level would be a three-digit figure (100 ppb and above). Caveats: (i) As levels may not correlate linearly with health effects; (ii) high levels of As in drinking water result in the highest known increases in mortality attributable to any environmental exposure [19,21,22] and (iii) there is no such thing as a “safe dose” of a carcinogenic substance like As.

Arsenic can also be absorbed by inhalation. NIOSH recommends as part of its occupational carcinogen policy that the "most protective" respirators be worn for inorganic arsenic compounds at concentrations above 0.002 mg As/m3 [10]. Note that this recommendation is given for acute occupational exposure and that chronic exposure may require much lower As concentrations to affect human health. References:

[1] Arena JM, Drew RH (eds.) Poisoning. 5th ed., 1986. Springfield: Charles C Thomas.
[2] Dart RC. Medical Toxicology. 2004. Philadelphia: Williams & Wilkins. pp. 1393–1401
[3] Davydova VE, Neizuestnva EM, et al. Toxicity of metallic arsenic. Gig Tr Prof Zabol 31:58 (1987)
[4] Flury F. Arsentrichlorid. In: Über Kampfgasvergiftungen. IX. Lokal reizende arsenverbindungen. Zeit Ges Exp Med 13:527-528 (1921)
[5] Gilani SH, Alibhai Y. Teratogenicity of metals to chick embryos. J Toxicol Environ Health. 30:23-31 (1990)
[6] IARC. IARC Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Humans – some metals and metallic compounds. Vol. 23, 1980. Lyon: International Agency for Research on Cancer, pp. 39-141 and Supplements 4 (1982, pp. 50-51), 6 (1987, pp. 71-76), 7 (1987, pp. 100-106). Available at: http://www.cie.iarc.fr/htdocs/monographs/suppl7/arsenic.html, accessed 2009.
[7] Lehman AJ. Chemicals in foods: a report to the Association of Food and Drug Officials on current developments. Part II. Pesticides. Q Bulletin Assoc Food Drug Off U.S. 15:122-125 (1951)
[8] MacEwen JD, Vernot EH. Toxic Hazards Research Unit annual technical report: 1972. Wright-Patterson Air Force Base, OH: Aerospace Medical Research Laboratory, Report AMRL-TR-72-62 (1972)
[9] Muehlberger CW. Toxicity studies of fluorine insecticides. J Pharmacol Exp Ther 39:246-248 (1930).
[10] NIOSH. CG17500. Arsenic chloride. In: Registry of toxic effects of chemical substances (RTECS) 1976 ed. Cincinnati, OH: U.S. Department of Health, Education, and Welfare, Public Health Service, Center for Disease Control, National Institute for Occupational Safety and Health, DHEW (NIOSH) Publication No. 76-191, p. 126. (1976)
[11] Perkow W. Wirksubstanzen der Pflanzenschütz and Schadlingsbekampfungsmittel. 1971/1976. Berlin, Germany: Verlag Paul Parey.
[12] Spector WS, ed. Handbook of toxicology. Vol. 1. Acute toxicities of solids, liquids and gases to laboratory animals. 1955. Philadelphia, PA: W.B. Saunders Co., pp. 324-325.
[13] http://www.cdc.gov/niosh/ipcsneng/neng0013.html, accessed September 2009.
[14] Chen Y, Parvez F, Gamble M, Islam T, Ahmed A, Argos M, Graziano JH, Ahsan H. Arsenic exposure at low-to-moderate levels and skin lesions, arsenic metabolism, neurological functions, and biomarkers for respiratory and cardiovascular diseases: review of recent findings from the Health Effects of Arsenic Longitudinal Study (HEALS) in Bangladesh. Toxicol Appl Pharmacol 239:184-92 (2009)
[15] Harrington JM, Middaugh JP, Morse DL, Housworth J. A survey of a population exposed to high concentrations of arsenic in well water in Fairbanks, Alaska. Am J Epidemol 108:377-385 (1978)
[16] Valentine JL, Reisbord LS, Kang HK, Schluchter MD. Arsenic Effects on Population Health Histories. In: Mills CF, Bremner I, Chester JK (eds.) Trace Elements in Man and Animals – TEMA5. Proceedings of the Fifth International Symposium on Trace Elements in Man and Animals. 1985. Slough, UK: Commonwealth Agricultural Bureau.
[17] Chiou H-Y, Huang W-I, Su C-L, Chang S-F, Hsu Y-H, Chen C-J. Dose-response relationship between prevalence of cerebrovascular disease and ingested inorganic arsenic. Stroke 28:1717-1723 (1997)
[18] Khan MMH, Aklimunnessa K, Kabir M, Mori M. Case-control study of arsenicosis in some arsenic contaminated villages of Bangladesh. Sapporo Med J 75:51-61 (2006)
[19] Marshall G, Ferreccio C, Yuan Y, Bates MN, Steinmaus C, Selvin S, Liaw J, Smith AH. Fifty-year study of lung and bladder cancer mortality in Chile related to arsenic in drinking water. J Natl Cancer Inst 99:920-8 (2007)
[20] Meliker JR, Wahl RL, Cameron LL, Nriagu JO. Arsenic in drinking water and cerebrovascular disease, diabetes mellitus, and kidney disease in Michigan: a standardized mortality ratio analysis. Environ Health 6:4 (2007)
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[22] Yuan Y, Marshall G, Ferreccio C, Steinmaus C, Selvin S, Liaw J, Bates MN, Smith AH. Acute myocardial infarction mortality in comparison with lung and bladder cancer mortality in arsenic-exposed region II of Chile from 1950 to 2000. Am J Epidemiol 166:1381-91 (2007)

Global hazards of gold, coal and oil

2009-11-09T09:00:00.000+01:00

Global hazards of gold, coal and oil

Present day anthropogenic arsenic emissions from gold, coal and oil
mining already surpass natural emissions from volcanic sources which
were linked to the extinction of dinosaurs in geological time. “This
is a change of paradigm of catastrophic proportions”, says Sergio
Dani, author of "Gold, coal and oil" on his article published in
Medical Hypotheses.

Arsenic ranks first in national and international lists of hazardous
substances. Colourless, odourless and tasteless arsenic has been
traditionally referred to and used as "the king of poisons". One tenth
of a gram is enough to kill an adult man within a few hours. Much
lesser quantities – something as the millionth part of a gram being
chronically inhaled or ingested over months or years – can cause
various types of cancer, vascular and renal diseases, neurological
diseases and diabetes among other diseases.

Source: Medawar Institute for Medical and Environmental
Research/Acangaú Foundation, October 2009.
Find out more about this story at:
www.alertaparacatu.blogspot.com
www.sosarsenic.blogspot.com

--
Sergio Ulhoa Dani, Dr.med., D.Sc. habil.
Göttingen, Germany
Tel. 00(XX)49 15-226-453-423
srgdani@gmail.com

Gold, Coal and Oil

2009-11-09T08:58:00.001+01:00

Gold, Coal and Oil

Neither the Three Wise Men's “Gold, Frankincense and Myrrh” nor Jared
Diamond´s “Guns, Germs and Steel”. "Gold, Coal and Oil" determine
mankind’s fate in a much more important and insidious way: the release
of arsenic, an invisible poison. This is the conclusion of an in-depth
study published in Europe by the journal Medical Hypotheses.

Source: Medawar Institute for Medical and Environmental
Research/Acangaú Foundation, October 2009.
Find out more about this story at:
www.alertaparacatu.blogspot.com
www.sosarsenic.blogspot.com

--
Sergio Ulhoa Dani, Dr.med., D.Sc. habil.
Göttingen, Germany
Tel. 00(XX)49 15-226-453-423
srgdani@gmail.com