|The unknown Equation
||A Potentially Explosive Cocktail
|Fact Sheet # 22 (December, 2003)||Fact Sheet # 21 (September 2003)|
|Fact Sheet # 20 (June, 2003)||Fact Sheet # 8 (March& June 2001)|
|Fact Sheet # 7 (December, 2000)||Fact Sheet # 6 (September 2000)|
|Fact Sheet # 5 ( June, 2000)||Fact Sheet # 4 (March, 2000)|
|Fact Sheet # 3 (Decemeber, 1999)|
'THE UNKNOWN EQUATION
Attempts to find a solution to the arsenic problem - solutions that would not only be effective but also cost-effective has turned people's attention to the use of aluminium sulphate as coagulant. The amount of aluminium sulphate in water is recommended as 300 mg/L as coagulant (reducing agent). The ideal pH range is 7-8. Initial 30-sec rapid mixing, 10-min slow mixing for flocs, and 1-hour retention time prior to filtration (a cotton cloth may be used for filtering). The use of a similar amount of bleaching powder (premixed) works as an oxidising agent to complete the other half of the electrochemical reaction. The reported result is an 80% removal of arsenic and 97% removal of iron. The presence of iron (III) helps the process, thus the process is named as iron-cum-arsenic removal using a
Long believed to be harmless, and as the people of Bangladesh have been using it for water clarification for years, particularly in those areas where the iron content is high, aluminium sulphate was thought to be culturally acceptable for reducing arsenic in groundwater. With evidence fast accruing that its use for water clarification could be dangerous, we now have to ask ourselves just how harmless it really is?
However, aluminium is the third most common element in the Earth's crust and this fact alone has made it acceptable and is used to forward the claim that aluminium salts cannot pose an environmental hazard. The fact is different for, even under normal environmental conditions, the toxic effects of aluminium are responsible for enormous ecological damage and economic losses throughout the world. It is also implicated in a number of devastating human morbid conditions as well as being a recognised complicating factors in renal dialysis. Of specific concern are the natural consequences of acid rain, the effects of development activities in areas with naturally-occurring acid-sulphate soils and the impacts resulting from the use of aluminium salts in industrial processes such as water treatment.
When mixed with water, aluminium sulphate has a strongly acidic reaction: Al2(SO4)3 . 14H2O + 6H2O = 2Al(OH)3 + 6H+ + 3SO42- + 14H2O
The hydrogen ions released combine with alkalinity anions (HCO3-, CO32-, and OH-) to produce carbon dioxide and water and lower the pH (Boyd, 1979). Provided that the pH can be controlled by adding sufficient cations (in the form of lime slurry in water treatment practice), the hydroxide remains as a colloidal solid, and acts as a filter for particulate matter in the raw water supply. However, if the pH drops to around 5 or less, the hydroxide redissolves, producing a clear extremely acidic solution.
This is of primary importance to us so before we dismiss it "out of hand" we should also be aware of some of the other applications in common use that involve aluminium. For example, aluminium hydroxide is a component of many anti-perspirant formulations. Although exposure to aluminium salts on the skin of mammals has long been considered to present little or no risk of absorption or of surface damage, hence the widespread use of aluminium hydroxide in anti-perspirants, transdermal transfer of aluminium from aluminium chloride solution across the skin and into the hippocampus in the brain of mice has been recently demonstrated. (Anane et al., 1995).
Aluminium also forms an important constituent of "ant-acid" remedies for the relief of stomach acidity. In its latter use, the possibility that it might be taken with drinks containing chelating agents such as citrate and sugar might cause some surprise, since the ability of the chelated aluminium to pass into the blood stream is undoubtedly an important mechanism which permits the element to by-pass the supposed cellular barrier to absorption (Kruck and McLauchlan, 1988). The fact that aluminium in public water supplies and various medicines can pose a threat to public health has been known for more than 60 years (Betts, 1926).
Over the past decade, interest in the possibility of a link between aluminium and a number of encephalopathies has grown, fuelled particularly by attempts to discover the cause of the increasing frequencies of Alzheimer's disease, commonly called senile dementia, in western populations. Empirical evidence to support a link between average
levels of aluminium in drinking water and the incidence of Alzheimer's disease in Norway was provided by Flaten (1986), and more convincingly in England and Wales by Martyn et al (1989). The latter reported that the frequency of Alzheimer's Disease is increased by 50% when the average level of aluminium in the public water supply reaches 0.11 mg/l.
Higher average aluminium concentrations were not however, found to result in a further increase in the frequency of the disease. To place this in context, the Maximum Admissible
Concentration (MAC) which is accepted in the European Community for aluminium in public drinking water is 0.2 mg/l.
But as the accumulation of aluminium in areas in the brain in which neurofibrillary tangles develop was demonstrated by Perl and Brody (1980), and in senile plaque by Candy et al (1980), both features are diagnostic of Alzheimer's Disease, and as aluminium also appears to be implicated in similar neuritic tangles in Down' syndrome, and to be one of the factors in the amyotrophic lateral sclerosis complex of Guam and the Kii Peninsula of Japan, it could be we are risking people's health by advocating the use of aluminium
sulphate in arsenic reduction.
Although there is some evidence that some of the factors involved in these encephalopathies and in aluminium toxicology may be genetic, nevertheless the wide use of
aluminium sulphate in the treatment of arsenic-contaminated groundwater is of concern as exposure to aluminium from water sources is far more common than has been acknowledged. The gene which produces the protein has been identified and is located on chromosome 21. However as the main source of aluminium which can enter the blood is from drinking water we cannot also pass this off as simply a genetic problem.
When aluminium sulphate is dissolved in water, it forms remarkably complex semi-solid hydroxides, releasing sulphuric acid as it dissolves. If enough aluminium sulphate
is added to water, the acidity of the water may increase to such a level that these compounds are redissolved. The process of flocculation using aluminium sulphate is not entirely stable as changes in the water quality can disturb the formation and management of the hydroxide sludge blanket. This may disintegrate suddenly, releasing large quantities of
semi-solid aluminium hydroxide into the water supply. If this water is drunk, then hydrochloric acid released from specialised cells in the stomach immediately dissolves the
hydroxide, forming an ionic solution of the chloride.
Discovery of the dangers of using aluminium sulphate for water treatment processes came as a result of the contamination in 1988 of the public water supply to the town of Camelford in Cornwall, England when the solution used in the purification of drinking water was accidentally discharged into the treated water tank at the Lowermoor Water
Treatment Works. This water treatment works supplied more than 7,000 properties and at least 20,000 local consumers and tourists in North Cornwall but despite the repeated
reassurances that aluminium in the drinking water posed no health hazards, many people in Camelford did in fact suffer from persistent medical problems, some of which are still so
severe that the victims are no longer able to lead a normal life, or operate their businesses.
An argument frequently put forward to deny that orally administered aluminium can be harmful is that the widespread use of antacids, (which may contain up to 50 times the normal daily intake of aluminium in a single dose), causes no observable harm. In fact the gut wall is by no means such an effective barrier as this optimistic view would suggest;
children with renal failure who are on oral treatment with aluminium hydroxide certainly can develop hyperaluminaemia, and dialysis encephalopathy may develop despite the fact that they may not be undergoing dialysis (Griswold et al, 1983).
Aluminium is mainly present in unprocessed foods as a relatively insoluble aluminosilicate, or else associated with chemicals such as tannin which form complexes which are very resistant to digestion. Such foods do not provide a significant quantity of aluminium which can be absorbed into the bloodstream. However a wide range of processed foods often contain relatively simple ionisable aluminium salts. For example sodium aluminium phosphate and sulphate added to baking powders may account for as much as 15mg of aluminium per cake, equivalent to two to three times the normal adult
The health risks of using aluminium sulphate in the purification of public water supplies is a potential health hazard and as it is also linked to the water fluoridation controversy, because the formation of the fluoro-aluminium complex appears to present yet more risks to brain chemistry, in those areas where we have flouride, this is of added concern. Obviously the risks from aluminium poisoning cannot be easily brushed aside for, although the Cornwall and Isles of Scilly Health Authority claims only traces of aluminium could be absorbed from the gut, regardless of the quantity swallowed, and even this would be rapidly removed from the body, this is simply not true, as an investigation immediately after the incident by Dr Richard Newman, a local GP and Doug Cross demonstrated.
These two eminent researchers found marked short-term increases in mouth ulcers, upper gastric tract complaints, diarrhoea, severe lethargy, nausea and vomiting. Mild arthritics reported substantial increases in the pain of their condition, and there was also an increase in reports of more persistent non-arthritic bone pain and of skin rashes (Cross and Newman, 1988). About four months after the incident, Newman noted that a number of his patients reported memory problems and impaired concentration and judgement (Newman 1990). After substantial lobbying by CSAP, arrangements were made for specialists to examine a small number of victims who appeared to be particularly seriously affected. Bone biopsies of two residents showed a discrete band of aluminium deposition consistent with a single, short-lived exposure (Freemont, 1990). Taylor (1990) found that 21 of 31 post-incident referrals showed significantly increased blood aluminium levels up to one year later; these included those patients who also had evidence of aluminium deposition in their bone.
Cognitive impairment in a group of 11 Camelford referral patients complaining of impaired memory was found to be consistent with minor brain injury (McMillan - 1990), and this was not attributable to emotional factors. Three-quarters of 32 referral patients had significant memory deficits, which had severely impaired their ability to run their businesses or had adversely affected their styles of living (Wilson - 1990). Newman considers that there are at least fifty additional cases which have not been examined by the clinical psychologists.
There is now convincing evidence of a direct link between aluminium in drinking water and the incidence of Alzheimer's disease, even at levels that are less than half the recommended EC maximum level, therefore using aluminium sulphate for reducing arsenic in groundwater and using aluminium pans for cooking, especially for cooking acidic foods, is liable to result in excessive contamination by the metal. As aluminium in drinking water is either dissolved or readily brought into solution, its bio-availability may therefore be much higher than aluminium from other sources. Although no studies have been undertaken on the effect of adding aluminium sulphate to arsenic-contaminated groundwater, the evidence demands we proceed with caution.
The literature on aluminium-related toxicity hazards now clearly indicates a probable causal link between environmental aluminium and a number of serious, irreversible neurological conditions - and as we are already ingesting arsenic from groundwater, we should proceed with great caution for the weight of scientific opinion today is that aluminium in drinking water is far more 'bio-available' than that in food, and that some people are genetically less competent in dealing with it when it does enter the blood. There is also evidence from Camelford that aluminium overload, even from relatively short periods of acute exposure, can lead to persistent neurological damage which can dramatically reduce the ability of individuals to cope with the problems of domestic and commercial life.
The various biochemical pathways responsible for absorption of aluminium from the gut, transfer through the body, and accumulation in bone and nerve tissues have been
documented in a recent review of the mechanisms of aluminium neurotoxicity. (Kruck and McLaughlan, 1988). Autopsies of victims of Alzheimer's disease have revealed excessive amounts of aluminum and silicon in the brain, this suggests that excessive amounts of aluminum in the diet, combined with a lack of several essential minerals, directly or indirectly predispose one to Alzheimer's disease. The threshold level for increased Alzheimers in relation to aluminium in drinking water is only half of the EC Maximum Admissible Concentration (MAC) - 0.2 mg/l.
The problem is that aluminium hydroxide - the floc that separates out when the sulphate is mixed with water - is amphoteric - i.e., it dissolves in both alkaline and acidic solutions. When aluminium sulphate mixes with water it releases both aluminium hydroxide solid AND sulphuric acid. If too much aluminium sulphate is added, the acidity due to the sulphuric acid becomes so high that the hydroxide re-dissolves. This gives a clear - and apparently pure-looking - solution which people think is safe to drink. It is not!
Since so many people are already vulnerable to arsenic poisoning, as well as iodine deficiency, it is totally unacceptable to discount exposure to a known neurotoxin - and one with such devastating results - on people already under severe environmental challenge. Experts say quite emphatically that exposure to environmental aluminium is one of the great disasters of our time, and one which will eventually become much more widely accepted as the evidence continues to accumulate. Faced with one disaster already, we do not want to be faced with another. The presence of fluoride in water contaminated with aluminium can be even worse for it can lead to a very dangerous condition - exposure to the alumino-fluoride complex. This is extremely worrying because it links to the very severe damage that can be caused by free radicals. The question that now needs answering is - will the use of aluminium sulphate for reducing arsenic in water have an adverse effect on the people who are already suffering from arsenicosis, especially those who have reached the point of no return?
1) Doug Cross - Environmental Analyst and Consultant.
2) Sabir Majumder Ph.D.
No. of words: 2409
A POTENTIALLY EXPLOSIVE COCKTAIL
by SYLVIA MORTOZA
Amid the growing perception that nobody is really interested in resolving the problem of arsenic-contamination, another worry has been added as a concentration on "chemical treatment at household level" for arsenic mitigation has resulted in an increase in the use of aluminium sulphate. This could result in aluminium poisoning. and anyone with arsenicosis is likely to have a greater manifestation of aluminium poisoning. (1)
When a Lecturer of the University College London, Dr. MacArthur, openly accuses the British Geological Survey (BGS) of denying him -- and others to access to the full data set from a major field programme in 1998 and asks "could wrangles over science delay a solution?" we should be concerned. for more than likely they will. (2)
If treatment to remove arsenic from the water is done at home, the risk of aluminium intoxication is vastly increased. The problem is that aluminium hydroxide - the floc that separates out when the sulphate is mixed with water - is amphoteric - i.e., it dissolves in both alkaline and acidic solutions. When aluminium sulphate mixes with water it releases both aluminium hydroxide solid AND sulphuric acid. If too much aluminium sulphate is added, the acidity due to the sulphuric acid becomes so high that the hydroxide re-dissolves. Although this gives a clear and apparently pure-looking solution, people think it is safe to drink. IT IS NOT! Since so many people are already vulnerable to arsenic poisoning, as well as iodine deficiency, it is totally unacceptable to discount exposure to a known neurotoxin - and one with such devastating results - on a people already under such severe environmental challenge. Exposure to environmental aluminium is one of the great disasters of our time, and one which will eventually become more widely accepted as evidence continues to accumulate. And since lemons are used so extensively in Bangladesh in cooking, you get a primary attack on the aluminium pots by the acidity of the lemon, then the formation of an aluminium-citric acid chelate, These chelates are one of the most dangerous routes of infiltration into the body for aluminium, and wherever special circumstances, such as this arise, it is highly dangerous to use aluminium for cooking utensils. (3)
A recent study shows that bisphenol-A (BPA) in plastic tableware and other utensils leached into hot liquid. Worn or scratched products leached even greater amounts of the chemical. Even low doses of bisphenol-A (BPA) have been found to cause reproductive malformations in male rat off-spring, including deformed genitals and enlarged prostates which should be of concern for new research has indicated that plastic feeding bottles and utensils in common use could have serious consequences for human life. In this case the use of plastic buckets for treating arsenic-contaminated water is of concern for BPA can leach out of plastic even at temperatures as low as 60 degrees Celsius. This means the continued use of plastic buckets for treating arsenic-contaminated groundwater and the use of plastic bottles for solar water disinfection technology (SWD) of surface water could be dangerous. (4)
The threshold level for increased Alzheimers in relation to aluminium in drinking water is only HALF of the EC Maximum Admissible Concentration (MAC) - 0.2 mg/l. Experts say if water treatment plants are operated properly, then even if there are excessive naturally-occurring levels of aluminium in the supply water, using aluminium sulphate can reduce the level in the treated water to less than 0.03 mg/l - a level widely accepted even by the anti-aluminium lobby as safe. But -- if the treatment is NOT properly done -- or done at home to reduce arsenic in water, the risk of aluminium intoxication may be vastly increased. Normally in a treatment works lime is added to prevent the formation of acidic solutions which re-dissolve the hydroxide. But for home use, this is too 'hit or miss'. Since so many people are already vulnerable to arsenic poisoning, as well as iodine deficiency, it is totally unacceptable to discount exposure to a known neurotoxin - and one with such devastating results - on people already under severe environmental challenge. I say quite emphatically that exposure to environmental aluminium is one of the great disasters of our time, and one which will eventually become much more widely accepted as the evidence continues to accumulate. And since lemons are used so extensively in Bangladesh in cooking, you get primary attack on the aluminium pots by the acidity of the lemon, then the formation of an aluminium-citric acid chelate, which is a chemical that passes directly through the gut wall (the so-called gut-blood barrier) into the blood, and then through the blood-brain barrier. These chelates are one of the most dangerous routes of infiltration into the body for aluminium, and wherever special circumstances, such as this arise, it is highly dangerous to use aluminium for cooking utensils. (5)
Scientists should therefore focus more on these problems instead of splitting hairs over whether or not the arsenic originated higher up the Ganges catchment from the out-crop of hard rock that eroded and was re-deposited here, or is the result of a man-made disaster. Those of them who can understand the plight of the sick should focus more on how to limit the exposure to arsenic so as to be sure people can avoid the acute toxic effects of consuming arsenic-contaminated water on a daily basis. Some among them will surely know the level of 0.05 mg/litre is far too high and if this is maintained as the standard, more people are sure to die as the chronic effects of prolonged low level exposure to arsenic are already showing up in Bangladesh in the form of skin pigmentation, keratoses and lung, bladder and other cancers -- such as were found in Taiwan by Dr. Chien-Jen Chen in 1986 and by Dr. Allen Smith in Chile in 1993 -- are emerging. These discoveries have already convinced WHO it should recommend a lowering the standard from 0.05 mg/litre to 0.01 mg/litre. But the United States is contemplating at least one proposal of an actual standard of 0.002 mg/litre to reduce calculated risks to 1 in 10,000 per lifetime of exposure -- and a recent report in the USA recommended a reduction to about 0.001 mg/litre.
The 1996 Safe Drinking Water Act Amendments require the U.S. Environmental Protection Agency (USEPA) to establish a new standard based upon updated science and cost-benefit analysis by January 1, 2001. In March, the National Research Council (NRC) released its "Report on Arsenic in Drinking Water" which linked arsenic to increased rates of skin, lung and bladder cancer. As a result of this the report recommended the existing standard be lowered from 0.05 mg/l but did not specify a level it deemed acceptable.
Bangladesh is geologically a part of the Bengal Basin that was formed by the alluvium of the Ganges. The arsenic that is now threatening the survival of the people may have originated higher up the Ganges catchment from the out-crop of hard rock that eroded and re-deposited here.
The limit on arsenic exposure was set primarily to be sure to avoid the acute toxic effects of consuming arsenic on a regular basis. The limit set by Bangladesh, the United Kingdom, and the United States is currently 0.05 mg/litre (50 ppb). Until recently this was also the standard recommended by World Health Organization (WHO).
That this was safe seemed to be reinforced by animal studies that seemed to show that arsenic is beneficial (to animals) at low doses. Others have written about the possible beneficial effects at very low levels. This is no longer believed to be true and in October 1999, the American Waterworks Association (AWWA) wrote to James Taft, USEPA's Targeting and Analysis Branch Chief, recommending that the standard for arsenic be set at no less than 0.01 mg/l. AWWA based its recommendation on the following: Aside from bladder cancer, the NRC did not quantify what health risks could be associated with exposure to low levels of arsenic, and would not be able to prior to a new arsenic standard being finalised. The NRC was unable to fully assess the risk of lung cancer posed by arsenic and would not be able to prior to a new arsenic rule being finalised. USEPA has however conceded that the health risks associated with arsenic are not well established in U.S. populations, and that further evaluation of arsenic's health impacts on Americans were needed before a final decision could be made on arsenic's threat to American public health.
The chronic effects of prolongued low level exposure that are showing up with increasing regularity in Bangladesh, like skin pigmentation, keratoses and lung, bladder and other cancers such as were found in Taiwan by Dr. Chien-Jen Chen in 1986 and by Dr. Allen Smith in Chile in 1993 demand an immediate review of the acceptable arsenic level in water. These discoveries have already convinced WHO it should recommend a lowering the standard from 0.05 mg/litre to 0.01 mg/litre for arsenic in water but has not yet forced the Dept.of Health to lower the standard for Bangladesh to 0.01 mg/litre from the current 0.05 mg/litre. Why is this? Surely the current situation demands an immediate lowering of the present standard?
The European Union (EU) plans to enforce a standard of 0.01 mg/litre by 2003, and the United States is contemplating stronger action including one proposal of an actual standard of 0.002 mg/litre to reduce calculated risks to 1 in 10,000 per lifetime of exposure -- and a recent report in the USA recommended a reduction to about 0.001 mg/litre. The 1996 Safe Drinking Water Act Amendments require the U.S. Environmental Protection Agency (USEPA) to establish a new standard based upon updated science and cost-benefit analysis by January 1, 2001. In March, the National Research Council (NRC) released its "Report on Arsenic in Drinking Water" which linked arsenic to increased rates of skin, lung and bladder cancer.
As a result, the report recommended the existing standard be lowered from 0.05 mg/l but did not specify a level it deemed acceptable. The AWWA publicly endorsed the report's findings and called for the arsenic standard to be reduced so as to ensure public health.
HOW DID ARSENIC GET INTO THE GROUNDWATER?
This is a question that is increasingly being asked by scientists who are today still not in agreement about causes. But while the scientists continue to debate the issues - why this tragedy has befallen the people of Bangladesh is of little concern to the dead and dying.
We must briefly review the theories being put forward for some may even stand up to scientific scrutiny -- but long-drawn out arguments and squabbling will do more harm than good. However the main hypothesis seems to hinge on two diametrically opposite views however -- the oxidation of the arsenic found in the arsenopyrite rocks and the depletion of oxygen in the aquifers due to the withdrawal of groundwater and the subsequent breakdown of iron oxyhydroxides.
The First Theory: The stone layer under the ground contains a compound called pyrite (Fcs2*) which holds the arsenic. Previously this was not harmful but now the pyrite is getting oxidised, and the acid so formed by oxidation has released the arsenic which is now infiltrating the water table causing widespread arsenic contamination and eventual poisoning.
Heavy withdrawal of ground water and the fluctuating water table plus the thousands of boreholes caused by the sinking of tube-wells, has caused the underground aquifers to become aerated, thus transforming an essential anaerobic environment into an aerobic one.
This newly introduced oxygen oxidised the arsenopyrites and released the arsenic into the water. When it comes into contact with water and air, the arsenopyrites form hydrated arsenate which is highly soluble in water and very soft. The light pressure from the tubewell water helps to break down the hydrated arsenic into fine particles and it gets dissolved. If water is pumped incessantly over a long period of time, the quantity of arsenic will gradually increase. (6)
The process is irreversible.
The Second Theory: The extraction of groundwater has nothing to do with creation of reducing conditions or release of arsenic to groundwater. Reducing conditions (a lack of oxygen) exist in Bangladesh because of the decay of the large amounts of organic carbon (up to 6 per cent in our sediment samples) which are found in the late-Pleistocene to Recent Bangladeshi sediments. In order to decay and form carbon dioxide, the organic carbon reacts with oxygen from several sources, one of which is iron oxyhydroxide. In this way the iron oxyhydroxide is broken down and arsenic is released.
According to the Mott MacDonald - BGS report, the groundwater arsenic problem in Bangladesh arises because of an unfortunate combination of three factors: a source of arsenic (arsenic is present in the aquifer sediments), mobilisation (arsenic is released from the sediments to the groundwater) and transport (arsenic is flushed away in the natural groundwater circulation).
This process in itself is not responsible for the timing of the arsenic problem as it started thousands of years ago, probably shortly after the sediments were laid down, and may have been occurring ever since. The reason why the arsenic crisis has only surfaced recently in Bangladesh is two-fold. Firstly tubewells tapping the aquifer layers containing arsenic have only started to proliferate in Bangladesh since the seventies. Thus most people have had up to a maximum of about 30 years of exposure. Coupled with this we know that visible symptoms of arsenicosis start to appear following 5-10 years of exposure. Thus, people will ask why were there no cases of arsenicosis in the late seventies-early eighties? The most probable answer is that there were. However, as no doctor was aware of arsenic poisoning as a potential diagnosis at that time these ailments were probably diagnosed as something else: eczema or other skin conditions. Indeed, if you question arsenicosis patients in the field as to when their problems started, many will say 10 years, 15 years, even 20 years ago.(7)
The lack of oxygen in Bangladesh groundwater is one reason why the theory of oxidation of arsenopyrites' cannot account for the release of arsenic to groundwater. There are other reasons too for reaching this conclusion. Very small amounts of sulphur (a constituent of arsenopyrite) are found in Bangladesh sediments. The amount of sulphur does not correlate with the amount of iron (the other constituent of arsenopyrite). The amount of arsenic does correlate with amount of iron (suggesting that it may be another iron mineral which is responsible.) Sulphate is not found in large quantities in Bangladesh groundwater (one of the products of oxidation of arsenopyrite). Iron and bi-carbonate are found in large quantities in Bangladesh groundwater (products of the reduction of iron oxyhydroxide). (8)
Despite the contamination, there are many water engineers who still want to sink more tube wells, this time tapping the deeper alluvium which is currently arsenic free. But Dr. Dipankar Chakraborty of SOES, Javedpur, Calcutta fears this will simply draw the arsenic down to the new wells. For example the arsenic content of water from one deep well in Samta village in the district of Jessore increased five-fold in just six months!
THE CURRENT SITUATION
As Dr. MacArthur, Lecturer at University College London has accused the British Geological Survey (BGS) of denying him -- and others -- access to the analytical results from Phase I of the joint Mott BGS-Mott MacDonald study, "Groundwater Studies For Arsenic Contamination In Bangladesh -- January 1999" we must ask them to resolve this issue.
Fred Pearce in his latest article on the arsenic problem, "Danger in every drop" published in the New Scientist, 12 Feb 2000 writes: "Five years ago New Scientist reported how arsenic had poisoned water supplies for millions in the Ganges delta. The danger hasn't receded. Could
wrangles over science delay a solution?" He also refers to "an extraordinary row between British geologists" over BGS’s refusal so far to allow other scientists access to the full data set from a major field programme in 1998.
THE BAD NEWS
The bad news is that arsenic-contamination is increasing both in intensity and assessment, and even if it does turn out that tube-well water was contaminated with arsenic long before it was recognised as a problem -- how does this help us? Now we have an approximate four and a half million tube-wells throughout the country and how many are contaminated -- or are likely to be contaminated in the future -- we do not know. Would it not be better if the scientists concentrated on aspects such as these? After all the objective of the scientists should be to reduce exposure to arsenic contaminated water to a level as close to zero as possible, considering the health effects and cost of treatment technology.
We know that the toxicity of arsenic is dependent on its oxidation state, chemical form and solubility in the biological media and that the scale of toxicity decreases in the order: arsine > inorganic As(III) > organic As(III) > inorganic As(V) > organic As(V) > arsonium compounds and elemental arsenic. We also know that the toxicity of As(III) is about ten times that of AS(V) - and Bangladesh is getting both -- so if we only consider the health effects from consuming arsenic and the cost of installing treatment technologies, the magnitude of the problem is large enough without going into endless debate. Don’t we know enough by now to know arsenic-contamination and arsenic-poisoning is a problem that is real and demands action?
When someone like Dr. Allen Smith of the University of California at Berkley and a WHO adviser says that arsenic is the major cause of cancer deaths and "In some places it kills more people than cigarettes" and adds that this may soon be true of Bangladesh, isn’t it time to do less talk and more action? And as Bangladesh is geologically a part of the Bengal Basin that was formed by the alluvium of the Ganges, we cannot continue to isolate the problem from the one in West Bengal. Even the World Bank is willing to concede that the high levels of arsenic in numerous shallow and deep wells in various parts of Bangladesh has raised serious health concerns. It adds that recent investigations, though incomplete, confirm that the occurrence of arsenic in groundwater is more widespread than assumed at first and that it already affects a large number of people.
The World Health Organisation (WHO) has also acknowledged that the arsenic in the drinking water in Bangladesh was a "Major Public Health Issue" which should be dealt with on an "Emergency Basis," and has launched an initiative with other concerned agencies like UNESCO, IAEA, UNICEF, UNIDO, FAO and the World Bank to test household arsenic removal techniques and the quality of alternative drinking water sources and although this year the programme has been expanded, results seem to be inadequate.
The highly contaminated areas in the catchments of the Ganges, Brahmaputra and Meghna rivers need urgent attention. As the only sure way to avoid arsenic toxicity is to avoid any intake of arsenic-contaminated food and drink it is time to think about installing permanent solutions instead of depending on doubtful substances like aluminium sulphate which is no longer recommended because of the neurological affect of aluminium poisoning. Even the use of plastic bottles and buckets is now suspect as they leach BPA so it could be we are only replacing one problem with another. So enough of wrong perceptions, enough of misconceptions and enough of ill-conceived solutions and let us get down to the task of saving the nation from eventual annihilation for what we have seen so far is only the tip of the iceberg.
Dr. Dipankar Chakraborty says, "We have information now of hundreds of tubewells which were safe earlier but are now contaminated now. Recently in one of our studies in Betai, Nadia district of West Bengal we have found 95% of the tubewells that we had coloured green and told people they were safe to drink just 2 years before are now predominantly contaminated.
WHEN WAS THE ARSENIC-CONTAMINATION DISCOVERED?
The answer to this question seems clouded in mystery but there is some indication it was known at least by the mid-eighties or by 1990 at the outside. Certainly the World Health organisation had an inkling of what was happening in this part of the world for it published an article in its Bulletin in 1988. This is corroborated by the fact that as early as 1988 a "Technology Mission" had been formed to find the source of arsenic contamination in Bangladesh. This mission discovered an underground layer at a depth of 20 to 80 metre which contained an arsenic compound, whereas there was virtually none below the 100 metre level. Further to this a scientists at NIPSOM is reported to have told the writer of the report Fred Pierce of The London Guardian, that the arsenic problem was known in government circles in 1990.
Why wasn’t any action taken? Mainly be cause the government was in a state of denial and because other agencies thought it was a localised problem. It could even be that tube-well water was contaminated with arsenic long before it was recognised as such, mainly because groundwater was by tradition, considered "safe." Moreover as tube-wells were confined to the relatively better off section of society, very few people would have been exposed so the few that had symptoms were likely to have escaped notice or were misdiagnosed -- perhaps as leprosy.
About fifteen years ago, with the assistance of many international organizations such as the World Bank, many shallow tube wells were dug which were to meet the daily water requirements of the local people. There are now an estimated 4.5 million tubewells throughout the country many of which are now dispensing arsenic.
As far as is known, people with arsenic-poisoning began to surface sometime during the eighties, several years after they began to drink tube-well water on a daily basis but Dr. Dipankar Chakraborty says, "From our interview with hundreds of aged villagers from some affected districts we are now hearing that they had observed such arsenical skin-lesions since the late seventies." Which raises the possibility that arsenic may have been present in the groundwater long before 1970.
Prof. Quazi Quamruzzaman of the Dhaka Community Hospital said the government knew by 1985 that Bangladeshis crossing the border to India for skin complaints were being diagnosed with arsenic poisoning. Why was action not taken? Probably because the health authorities did not believe it. A bigger question is why did they not investigate the reports for themselves? Ignoring it had a predictable result for with more than 90 per cent of the population of Bangladesh drinking groundwater on a daily basis, it was only a matter of time before people were turning up with arsenical skin lesions in the late stages of manifestation of arsenic toxicity.
Due to this carcinogenicity of some arsenic compounds, the objective should now be to reduce exposure to arsenic contaminated water to a level as close to zero as possible, taking into consideration its health effects and toxicology, occurrence and human exposure, availability and cost of treatment technology, the practical quantitation limit of arsenic normally found in drinking water.
Toxicity of arsenic is dependent on its oxidation state, chemical form and solubility in the biological media. The scale of toxicity decreases in the order: arsine > inorganic As(III) > organic As(III) > inorganic As(V) > organic As(V) > arsonium compounds and elemental arsenic. The toxicity of As(III) is about ten times that of AS(V) - and Bangladesh is getting both -- so if we only consider the health effects from consuming arsenic and the cost of installing treatment technologies, the magnitude of the problem looms large.
The toxic effect of arsenic also depends on its chemical forms; route of entry; age; sex; dosage and duration of exposure. Organic forms are about 10-fold less poisonous than the inorganic one; that is arsenite is more poisonous than arsenate. The major portion of the absorbed arsenic is excreted through urine (about 50 per cent); a small portion through faeces; skin; hair; and nails; and is firmly bound to Keratin. Storage in metabolically dead tissues slowly eliminates it from the body. Surveys have revealed that the villagers are the worst affected because, due to their manual labour, they often consume about five litre water per day. Moreover they consume plenty of rice-water and all their food is prepared using arsenic-contaminated water. The same water
is used for bathing, washing and other domestic uses.
Dr. Allen Smith of the University of California at Berkley and a WHO adviser says that arsenic is the major cause of cancer deaths and "In some places it kills more people than cigarettes." This he says will soon be true of Bangladesh too.
The continuous absorption of arsenic in slow doses via the gastro-intestinal or respiratory tract (cumulative action) can result in three distinct types of chronic arsenic poisoning which often goes unrecognised. The first sign may be an irritation of the gastro-intestinal and upper respiratory tracts. The second an overgrowth of the Kasatin skin-structure with the development of numerous warts, ridges on the finger-nails and coarseness of the hair and the third - symptoms which indicate an inflammation of the peripheral nerves. If the condition is allowed to persist, palsies may set in and the patient becomes apathetic.
Long term exposure causes hyper-keratosis, conjunctivitis, hyperpigmentation, skin cancer and gangrene in the limbs. Cancer cases minus the tell-tale skin lesions, are also on the increase.
THE RELEVANT HISTORY OF ARSENIC-CONTAMINATION AND STRATEGIES BEING FOLLOWED.
As Bangladesh is geologically a part of the Bengal Basin that was formed by the alluvium of the Ganges, the arsenic problem cannot be addressed in isolation as it is of exactly the same genesis as Bangladesh. The only difference is they have been aware of the problem for far longer and have been diagnosing arsenicosis patients since the mid-eighties. The question then arises -- when the government of West Bengal and donor agencies in India knew about -- why didn’t the government of Bangladesh and donor agencies here also know?
When the problem did become known during the mid-nineties a "Rapid Action Programme" was organised by the Ministry of Health and Family Welfare of the government of Bangladesh with funding assistance from UNDP to survey 200 villages out of a total of 60,000 in the country.
Tubewell Survey and Patient Survey was contracted to the Dhaka Community Hospital. They measured both concentrations in the wells and diagnosed chronic arsenic poisoning. Most regions
in the country had villages which had wells above the Bangladeshi standard of 0.05 mg/litre By a rough extrapolation they estimate that half of all wells in the country exceed this limit. These measurements were made with a Merck field kit, which cannot measure arsenic levels below 0.05 mg/litre so it is not known how many people are drinking water with levels of arsenic above the new WHO recommendation of 0.01 mg/litre. (9)
These kits are also under suspicion as it is now known they emit "arsine" gas. (10)
A UNDP survey indicated that 40% of all wells are contaminated. The other unusual fact to take into consideration is that despite the enormous number of people at risk only a small percentage actually have visual symptoms of arsenicosis. In Jhikorgacha for example, where BRAC are working on this problem, out of a population at risk of about 1,13,000 (drinking water from contaminated tubewells) only 109 patients have been found. Is it possible they could have been overlooked previously? It would seem highly probable.
According to the World Bank, the first detection in 1993 -- and the subsequent confirmation after 1995 of high levels of arsenic in numerous shallow and deep wells in various parts of Bangladesh has raised serious health concerns. Recent investigations, though incomplete, confirm that the occurrence of arsenic in groundwater is more widespread than assumed at first and that it already affects a large number of people. Wells in 59 out of Bangladesh's 64 districts are
estimated to be contaminated with arsenic
In 1997 the World Health Organisation (WHO) acknowledged that the arsenic in the drinking water in Bangladesh was a "Major Public Health Issue" which should be dealt with on an "Emergency Basis," and launched an initiative with other concerned agencies like UNESCO, IAEA, UNICEF, UNIDO, FAO and the World Bank to test household arsenic removal techniques and the quality of alternative drinking water sources. This programme has been expanded this year.
Previously a number of anthropogenic explanations had been advanced for the occurrence of arsenic in groundwater. While it is possible that some may explain isolated cases of arsenic contamination, none of the anthropogenic explanations can account for the regional extent of groundwater contamination in Bangladesh and West Bengal. There is no doubt that the source of arsenic is geological. The arsenic content of alluvial sediments in Bangladesh is usually in the range 2-10 mg/kg; only slightly greater than typical sediments (2-6 mg/kg). However, it appears that an unusually large proportion of the arsenic is present in a potentially soluble form. The high groundwater arsenic concentrations are associated with the grey sands rather than the brown sands.
There is a good correlation between extractable iron and arsenic in the sediments and a relatively large proportion (often half or more) of the arsenic can be dissolved by acid ammonium oxalate, an extract that selectively dissolves hydrous ferric oxide and other poorly ordered oxides. It therefore appears likely that a high proportion of the arsenic in the sediments is present as adsorbed arsenic. This would not be true of arsenic present in primary minerals such as arsenic-rich pyrite.
The greatest arsenic concentrations are mainly found in the fine-grained sediments especially the grey clays. A large number of other elements are also enriched in the clays including iron, phosphorus and sulphur. In Nawabganj, the clays near the surface are not enriched with arsenic to any greater extent than the clays below 150 m - in other words, there is no evidence for the weathering and deposition of a discrete set of arsenic-rich sediments at some particular time in the past. It is not yet clear how important these relatively arsenic-rich sediments are for providing arsenic to the adjacent, more permeable sandy aquifer horizons. There is unlikely to be a simple relationship between the arsenic content of the sediment and that of the water passing through it.
It is likely that the original sources of arsenic existed as both sulphide and oxide minerals. Oxidation of pyrite in the source areas and during sediment transport would have released soluble arsenic and sulphate. The sulphate would have been lost to the sea but the arsenic, as As(V), would subsequently have been sorbed by the secondary iron oxides formed. These oxides are present as colloidal-sized particles and tend to accumulate in the lower parts of the delta. Physical separation of the sediments during their transport and reworking in the delta region has resulted in a separation of the arsenic-rich minerals. The finer-grained sediments tend to be concentrated in the lower energy parts of the delta. This is likely to be responsible for the greater contamination in the south and east of Bangladesh.
The highly contaminated areas are found in the catchments of the Ganges, Brahmaputra and Meghna rivers strongly suggesting that there were multiple source areas for the arsenic. The types of sediment deposited in the delta region have been strongly influenced by global changes in sea level during the Pleistocene glaciations. For example, sea level was more than 100 m lower at the peak of the last lee Age around 18,000 years ago. At that time the major rivers cut deeply incised valleys into the soft sediments of the delta. All of the highly contaminated groundwaters occur in sediments deposited since that time, while those sediments predating the low sea level stand contain little or no arsenic-contaminated groundwater.
Burial of the sediments, rich in organic matter, has led to the strongly reducing groundwater conditions observed. The process has been aided by the high water table and fine-grained surface layers which impede entry of air to the aquifer. Microbial oxidation of the organic carbon has depleted the dissolved oxygen in the groundwater. This is reflected by the high bicarbonate concentrations found in groundwater in recent sediments. There is a relationship between the degree of reduction of the groundwaters and the arsenic concentration - the more reducing, the greater the arsenic concentration.
The highly reducing nature of the groundwaters has led to the reduction of some of the arsenic to As(III) and possible desorption of arsenic since As(III) is normally less strongly sorbed by the iron oxides than As(V) under the near neutral pH groundwater conditions observed. Further reduction will lead to the partial dissolution of the poorly crystallised ferric oxide with consequent release of iron and additional arsenic. Other strongly sorbed ions, especially phosphate, will also be released by iron oxide dissolution. The relatively high phosphate concentrations present in the groundwaters will compete with As(V) for sorption sites and is another factor that favours high groundwater arsenic concentrations. It may also make arsenic treatment more difficult. (11)
The only sure way to avoid arsenic toxicity is to avoid any intake of arsenic-contaminated food and drink. The alternative is to use either surface water such as river water, ponds, lakes, canals, haors, etc. which must be purified either by boiling or by the use of ferrous salts. Aluminium sulphate is no longer recommended because of the neurological affect of aluminium poisoning.
If water is purified by chemical method, it must remain undisturbed for at least 12 hours to allow for the dissolved arsenic to be converted into a no-soluble element which then settles on the bottom. Water may be decanted only down to the bottom one-third. Research has shown that arsenic removal was 81 - 96 per cent when the source was treated with 3-10 mg/l of ferric
Various treatment methods have been adopted around the world to remove arsenic from drinking water under both laboratory and field conditions. The major mode of sequestering arsenic from water is by physical-chemical treatment. These methods include:
- adsorption-coprecipitation using iron and aluminium
- adsorption on activated alumina/activated
- reverse osmosis;
- ion exchange; and
- oxidation followed by filtration
During the Second World War R. A. Peter and his associates discovered an antidote against arsenic poisoning popularly known as BAL (2, 3 dimercapto-propanol). Originally intended as a remedy for injuries caused by a gas used in warfare (leunsite) which contained arsenic. BAL may be used as a solution or as an ointment and is specially effective against the skin lesions resulting from arsenic poisoning.
As(III) removals by coagulation were found to be primarily controlled by coagulant dose and relatively unaffected by solution pH. The converse was true for As(V). Iron and aluminum coagulants were of demonstrably equal effectiveness in removing As(V) at pH less than 7.5. Iron-based coagulants were superior when soluble metal residuals were problematic, if pH was greater than 7.5, or if the raw water contained As (III).
DETOXIFYING ARSENIC SLUDGE
The sludge left behind after treatment could be equally dangerous therefore methods must be taken to render it safe. If not it could become mixed with soil from where it might enter the groundwater again. Tests have shown that mixing with cow-dung; leaves of the arum plant; water-hyacinth; cabbage; converts the arsenic into methyl acid which then evaporates off.
There are a few simple technologies for household removal of arsenic from water. but most need to be adapted to local needs - and then proven sustainable in every different setting - before they can be recommended for general use.
Technologies under review perform most effectively when treating arsenic in the form of As(V). As (III) may be converted through pre-oxidation to As(V). Data on oxidants indicate that ferric chloride is the most effective for oxidizing As(III) to As(V).
Coagulation/Filtration (C/F), is an effective treatment process for removal of As(V) according to laboratory and pilot-plant tests. The type of coagulant and dosage used affects the efficiency of the process. Within either high or low pH ranges, the efficiency of C/F is significantly reduced.
Lime Softening (LS) operated within the optimum pH range of greater than 10.5 is likely to provide a high percentage of As removal for influent concentrations of 0.05 mg/litre.
Ion Exchange (IE) can effectively remove arsenic. However, sulfate, TDS, selenium, fluoride, and nitrate compete with arsenic and can affect run length. Passage through a series of columns could improve removal and decrease regeneration frequency. Suspended solids and precipitated iron can
cause clogging of the IE bed. Systems containing high levels of these constituents may require pretreatment.
Reverse Osmosis (RO) provided removal efficiencies of greater than 95 percent when operating pressure is at ideal psi. If RO is used by small systems in the western U. S., 60% water recovery will lead to an increased need for raw water. The water recovery is the volume of water produced by the process divided by the influent stream (product water/influent stream). Discharge of reject water or brine may also be a concern. If small RO systems as available "off-the shelf" are used, water recovery will likely need to be optimised due to the scarcity of water resources. The increased water recovery can lead to increased costs for arsenic removal.
Electrodialysis Reversal (EDR) is expected to achieve removal efficiencies of 80 percent. One study demonstrated arsenic removal to 0.003 mg/L from an influent concentration of 0.021 mg/L.
Nanofiltration (NF) was capable of arsenic removals of over 90%. The recoveries ranged between 15 to 20%. A recent study showed that the removal efficiency dropped significantly during pilot-scale tests where the process was operated at more realistic recoveries. Like the off-the-shelf" RO systems, water recovery will likely need to be optimised due to the scarcity of water resources. The increased water recovery can lead to increased costs for arsenic removal.
OTHER PROSPECTIVE TECHNOLOGIES
Ion Exchange with Brine Recycle. Research by the University of Houston (Clifford) at McFarland, CA and Albuquerque, NM has shown that ion exchange treatment can reduce arsenic (V) levels to below 0.02 mg/L even with sulphate levels as high as 200 mg/L. Sulphate does impact run length, however; the higher the sulphate concentration, the shorter the run length to arsenic breakthrough. The research also showed the brine regeneration solution could be reused as many as 20 times with no impact on arsenic removal provided that some salt was added to the solution to provide adequate chloride levels for regeneration. Brine recycle reduces the amount of waste for disposal and the cost of operation.
Iron (Addition) Coagulation with Direct Filtration. The University of Houston (Clifford) recently completed pilot studies at Albuquerque, NM on iron addition (coagulation) followed by direct filtration (microfiltration system) resulting in arsenic (V) being consistently removed to below 0.02 mg/L. Critical operating parameters are iron dose, mixing energy, detention time,
Conventional Iron/Manganese (Fe/Mn) Removal Processes. Iron coagulation/filtration and iron addition with direct filtration methods are effective for arsenic (V) removal. Source waters containing naturally occurring iron and/or manganese and arsenic can be treated for arsenic removal by using conventional Fe/Mn removal processes. These processes can significantly reduce the arsenic by removing the iron and manganese from the source water based upon the same mechanisms that occur with the iron addition methods. The addition of iron may be required if the
concentration of naturally occurring iron/manganese is not sufficient to achieve the required arsenic removal level.
ORIGINAL ASSUMPTIONS THAT ARE NO LONGER VALID
The original assumption that aluminium sulphate could be used for arsenic reduction because the people are familiar with its use is no longer valid as aluminium is now recognised to be causing neurological problem.
Dr. Dipankar Chakraborty reports: "I do not like to use aluminium sulphate in those places where the dose is not maintained properly so if villagers need to use any chemical, I no longer tell them to use aluminium-sulphate as in our Filter-Tablet system we told the villagers to use one tablet for a bucket of water but often I find that 3 or 4 tablets have been used. The reason for doing this is that some villagers think the more tablets used, the better the water."
OUR VISION FOR THE FUTURE
Do we have a vision for the future or are we content with these small "make-shift" systems now being introduced in villages? One of the questions that comes to mind is will villagers continue to use these systems after the NGO supervisors have left? The likelihood of villagers tiring of the trouble involved in getting relatively pure drinking water is real and must be considered in the long run. If this happens arsenic will again become a problem.
REAFFIRMING THE GOALS
It is time now to re-affirm the goals for the future. What are the intentions and expectations? Obviously piped water from central systems is not a practical option for Bangladesh but small community systems or "water stations" such as have been installed in Mexico and Malaysia are and these should be investigated for long-term sustainability and cost, including the cost of production of the potable water.
KEY POINTS TO REMEMBER TO GIVE PEOPLE CONFIDENCE AND IMPROVE MORALE
People must be kept informed of all aspects of arsenic-contamination and poisoning. Public education must be undertaken on a large scale and all rural clinics must be able to deal with arsenic cases including diagnosis and follow-up treatment. Mothers with arsenicosis must be warned that their progeny could be born with arsenicosis.
People must be made aware that any continuous absorption of arsenic, even in slow doses via the
gastro-intestinal or respiratory tract (cumulative action) can lead to chronic arsenic-poisoning which often goes unrecognised until too late.
There are several stages of arsenic-poisoning:
1. Preclinical: the patient shows no symptoms, but arsenic can be detected in urine or body tissue samples.
2. Clinical: at this stage various effects can be seen on the skin. A general darkening of the skin (melanosis) is the most common symptom, often observed on the palms. Dark spots on the chest, back, limbs, or gums have also been reported. Oedema (swelling of hands and feet) is often seen. A more serious symptom is keratosis, or hardening of skin into nodules, often on palms and soles.
WHO estimates that this stage requires five to ten years of exposure to arsenic.
3. Complications: clinical symptoms become more pronounced, and internal organs are affected. Enlargement of liver, kidneys, and spleen have been reported. Some research indicates that conjunctivitis (pinkeye), bronchitis and diabetes may be linked to arsenic exposure at this stage.
4. Malignancy: tumours or cancers (carcinoma) affect skin or other organs. In this stage the affected person may develop gangrene or skin, lung, or bladder cancer.
(1) Mohammad Naqibuddin, Fellow - School of Medicine, John Hopkins Hospital.
(2) Fred Pearce - "Danger in every drop" published in the New Scientist 12 Feb 2000.
(3) & (5) Doug Cross - Environment Consultant
(4) Fred Pearce - "Danger in every drop" published in the New Scientist 12 Feb 2000.Koji Arizono et al - Prefectural University of Kumamoto & University of Nagasaki, Japan
(6) T. Roy Chowdhury, Gautam Kumar Basu, Badal Kumar Mandal, Bhajan Kumar Biswas, Gautam Samanta, Uttam Kumar Chowdhury, Chitta Ranjan Chanda, Dilip Lodh, Sagar Lal Roy, Khitish Chandra Saha, Sibtosh Roy, Saiful Kabir, Qazi Quamruzzaman, Dipankar Chakraborti. "Arsenic Poisoning In The Ganges Delta" - published in NATURE -VOL 401/7 October 1999, pg. 545-547.
(7) BRAC questionnaire of arsenicosis patients, Jhikorgacha thana, Jessore district.
(8) Nickson, R.T. et al -- "Mechanism of Arsenic Release to Groundwater, Bangladesh and West Bengal." - published in NATURE and APPLIED GEOCHEMISTRY 1999.
(9) Dr. Richard Wilson - Harvard Arsenic Project
(10) A. Hussam - Chemistry Department, George Mason University, Fairfax, Virginia 22030-4444; M. Alauddin - Chemistry Department, Wagner College, Staten Island, New York 10301;
A. H. Khan - Department of Chemistry, University of Dhaka-1000; S. B. Rasul and A. K. M. Munir
Sono Diagnostics Center Environment Initiative, Courtpara, Kushtia, Bangladesh - "Evaluation of Arsine Generation in Arsenic Field Kit."
(11) BGS-Mott MacDonald Report - "Groundwater Studies For Arsenic In Bangladesh."
(12) Various sources
No. of words: 7400