Arsenic is a ruthless killer in Bangladesh’s drinking water is making millions of people sick and may be causing as many as 3,000 deaths each year. That killer–naturally occurring arsenic in the water drawn from family wells–appears to have been released through a process involving crop irrigation, at least in one part of the country. At a research site in the southern part of Bangladesh, scientists calculated that irrigation pumping, which began in the last several decades, has dramatically altered groundwater flow through the aquifer.
They show that the resulting changes to the chemistry of the groundwater have the potential to either increase or decrease arsenic levels, in a paper written by an MIT-led team of scientists in the Nov. 22 issue of Science. Arsenic poisoning, usually characterized by sores on the chest, or blackened knotty palms, and cases of skin, lung, liver, bladder and pancreas cancers have been linked to arsenic in the drinking water. In 1998 the World Bank agreed to provide Bangladesh a $32. 4 million credit to develop a method of controlling the arsenic.
But today, most Bangladeshis continue to drink arsenic-laced water. The World Bank describes the problem as one of the world’s primary environmental challenges. The World Health Organization refers to it as “the largest mass poisoning of a population in history” in a fact sheet published in March. The mass poisoning began, sadly enough, with a well-meaning attempt to provide clean drinking water for Bangladeshis, who suffered from cholera and other diseases caused by bacteria in water taken from surface reservoirs.
To remedy that problem, the Bangladesh government, with the help of international aid organizations, drilled between 6 and 10 million wells at depths ranging from 50 to 300 feet to provide clean, safe water for individual households. At about the same time, farmers in this largely rural country began irrigating land so that rice, the country’s main food staple, could be grown during all six of the dry months when monsoon flooding abates. Cholera deaths dropped.
But about 10 years into the use of the tube wells, villagers started displaying symptoms consistent with arsenic-related illnesses, and incidents of skin cancer and internal cancers became common.
We have some purposes of this report. These are given below:
- To find out the causes of arsenic problem of Bangladesh.
- To analyze how arsenic comes in food chain.
- To find out the arsenic affected areas.
- To find out the implications of arsenic poisoning.
- To find out the impact of the arsenic crisis on agriculture.
- To analyze the arsenic content of rice in Bangladesh and impacts on rice productivity.
- To analyze how we can mitigate of arsenic.
- To find out the role of private sector in arsenic mitigation.
- We faced some limitations to research our project, these are given below:
- Shortage of time.
- No financial support.
- It was very tough for our group members to fix a same time to group work.
Causes of Arsenic Problem of Bangladesh
Intermittent incidents of arsenic contamination in groundwater can arise both naturally and industrially. The natural occurrence of arsenic in groundwater is directly related to the arsenic complexes present in soils. Arsenic can liberate from these complexes under some circumstances.
Since arsenic in soils is highly mobile, once it is liberated, it results in possible groundwater contamination. The alluvial and deltaic sediments containing pyrite has favored the arsenic contamination of groundwater in Bangladesh. Most regions of Bangladesh are composed of a vast thickness of alluvial and deltaic sediments, which can be divided into two major parts – the recent floodplain and the terrace areas. The floodplain and the sediments beneath them are only a few thousand years old. The terrace areas are better known as Madhupur and Barind Tracts and the sediments underlying them are much older than the adjacent floodplain.
Most of the arsenic is occurring in the younger sediments derived from the Ganges Basin. The investigators found that there is a layer containing arsenic compound at a depth of 20 to 80 meters. This layer is rich in arseno-pyrite, pyrite, iron sulfate, and iron oxide as revealed by the geological investigation. The researchers also inferred that, although arsenic is occurring in the alluvial sediments, the ultimate origin of arsenic is perhaps in the outcrops of hard rocks higher up the Ganges catchments.
These outcrops were weather-beaten in the recent geological past and then the eroded soil was deposited in West Bengal and Bangladesh by the ancient courses of the Ganges. Arsenic in sediment or water can move in adsorbed phase with iron, which is available in plenty in the Himalayas. Here about 100 to 300 mg/kg arsenic combined with iron oxides can be found in the sediments under aerobic conditions. When these sediments were deposited in Bengal basin under tidal environment, it came under anaerobic condition. The sulfate available in Bengal basin was reduced to hydrogen sulfide in presence of sulfur reducing bacteria.
Iron minerals and hydrogen sulfide rapidly tie together to form iron sulfide. Arsenic had been absorbed on the surface of iron sulfide and produced arsenopyrite. This mineral usually remains stable unless it is exposed to oxygen or nitrate. In aerobic environment, arseno-pyrite is oxidized in presence of oxygen and arsenic adsorbed with iron sulfide becomes mobilized. The groundwater in Bangladesh has declined progressively due to the excessive extraction of water for irrigation and domestic water supply, lack of water management and inadequate recharge of the aquifer.
The groundwater declined beyond 8 meters in 12% areas of Bangladesh in 1986. This extent rose to 20% areas in 1992 and 25% areas in 1994. The study on forecasting groundwater level fluctuation in Bangladesh indicated that 54% areas of Bangladesh are likely to be affected up to 20 meters in some areas particularly in northern part of the country. Excessive groundwater extraction may be the vital reason for creating a zone of aeration in clayey and peaty sediments containing arseno-pyrite. Under aerobic condition, arseno-pyrite decomposes and releases arsenic that mobilizes to the subsurface water. The mobilization of arsenic is further enhanced by the compaction of aquifers caused by groundwater withdrawal.
Sources of Arsenic in Groundwater
The Arsenic present in the aquatic environment may stem from natural or anthropogenic sources. But the problems of arsenic in groundwater of Bangladesh and West Bengal – India are expected to be form natural sources. The main source of arsenic is parent hard rock which deposits on sediment particles. Arsenic problem becomes acute when arsenic containing particles are disassociated and carried out with sediments during erosion.
These sediments may contain abundant amounts of total arsenic. For this reason, geochemical analyses of groundwater, pore water and aquifer sediments are necessary to understand the origin and release mechanisms of dissolved arsenic in the aquifer. Arsenic undergoes reactions of oxidation – reduction, precipitation-dissolution, absorption-deposition, and organic and biochemical methylation. The mentioned reaction governs the mobilization and accumulation of arsenic in the ecosystem. Still today, conclusive reactions for arsenic contamination in groundwater are not clear.
There are more questions, but less answers available. From direct and indirect studies, the following hypothesis have been put forward bye research scientists:
- Wooden electricity poles which are treated with arsenic based preservative compounds.
- Uses of pesticides and chemical fertilizers.
- Release of untreated effluent from facilities.
- Hydro geochemical investigations suggest that the groundwater of Bangladesh is aquifers exist under strongly reduced condition.
- The available geochemical report suggests the claim that reduction of oxy hydroxides is the source for arsenic in groundwater.
Among the hypothesis mentioned above, the first three are not directly responsible for arsenic in groundwater. The pyrite oxidation hypothesis has been also criticized. The reduction of oxy hydroxides theory has been accepted among the scientific community. It is also suggested that clay minerals or organic matter may be responsible for transporting. As through the river system based on the oxy hydroxide theory. It is also expected that organic matter plays an important role in regulation of arsenic in groundwater (BGS 1999).
However the actual cause of arsenic contamination in groundwater in Bangladesh is yet to be determined. Arsenic in Food Chain: Arsenic contamination of ground water in Bangladesh and the incidence of arsenicosis patients do not go hand in hand. People living in the same household and drinking from the same source of arsenic-affected water are not equally affected. Moreover, the manifestation of arsenicosis also varies from region to region in the country. This has raised the question about the sole contribution of arsenic-contaminated drinking water as to the cause of arsenicosis. Much effort has been directed towards ensuring supply of arsenic-free drinking water with varying successes.
Even if arsenic-safe drinking water is assured, the question of irrigating soils with arsenic-laden ground water will continue for years to come. The possibility of arsenic accumulation in soils through irrigation water and its subsequent entry into the food chain through various food materials cannot be overlooked. With this view in mind, more than 1000 water, soil and vegetables samples collected from arsenic affected area as well as from unaffected areas have been analyzed for arsenic in them. Other sources of foods have also been analyzed.
Comparison of the results form affected and unaffected areas reveals that many of the commonly grown vegetables, otherwise suitable as good sources of nourishment, accumulate substantially elevated amount of the element in the inorganic form toxic than the organic form.
Implications of arsenic poisoning
Because it targets ubiquitous enzyme reactions, arsenic affects nearly all organ systems. Arsenic is strongly associated with lung and skin cancers and may cause other cancers. Two mechanisms of arsenic toxicity that impair tissue respiration have been described. Arsenic binds with sulfhydryl groups and disrupts sulfhydryl-containing enzymes; As(III) is particularly potent in this regard.
As a result of critical enzyme effects, there is inhibition of the pyruvate and succinate oxidation pathways and the tricarboxylic acid cycle, impaired gluconeogenesis, and reduced oxidative phosphorylation. Another mechanism involves substitution of As(V) for phosphorus in many biochemical reactions. Replacing the stable phosphorus anion in phosphate with the less stable As(V) anion leads to rapid hydrolysis of high-energy bonds in compounds such as ATP. That leads to loss of high-energy phosphate bonds and effectively “uncouples” oxydative phosphorylation. Unlike other arsenicals, arsine gas causes a hemolytic syndrome. Arsine gas poisoning results in a considerably different syndrome from that caused by other forms of arsenic. After inhalation, arsine rapidly fixes to red cells, producing irreversible cell-membrane damage. At low levels, arsine is a potent hemolysin, causing dose-dependent intravascular hemolysis. At high levels, arsine produces direct multisystem cytotoxicity.
Gastrointestinal, Hepatic, and Renal Effects: Gastrointestinal effects are seen primarily after arsenic ingestion, and less often after inhalation or dermal absorption. The gastrointestinal (GI) effects of arsenic generally result from exposure via ingestion; however, GI effects may also occur after heavy exposure by other routes. The fundamental GI lesion appears to be increased permeability of the small blood vessels, leading to fluid loss and hypotension. Extensive inflammation and necrosis of the mucosa and submucosa of the stomach and intestine may occur and progress to perforation of the gut wall. A hemorrhagic gastroenteritis may develop, with bloody diarrhea as a presenting symptom.
Acute arsenic toxicity may be associated with hepatic necrosis and elevated levels of liver enzymes. Arsenic intoxication may also result in hepatic toxicity, including toxic hepatitis and elevated liver enzyme levels. Autopsies of Japanese children poisoned with arsenic-contaminated milk revealed hepatic hemorrhagic necrosis and fatty degeneration of the liver. Chronic arsenic ingestion may lead to cirrhotic portal hypertension. Case reports have also linked chronic high-level arsenic exposure with hepatic angiosarcoma, a rare form of cancer. Arsenic is capable of causing acute renal failure, as well as chronic renal insufficiency.
The systemic toxicity occurring in severe acute arsenic poisoning may be accompanied by acute tubular necrosis, and acute renal failure; chronic renal insufficiency from cortical necrosis has also been reported. The actual cause of injury may be hypotensive shock, hemoglobinuric or myoglobinuric tubular injury, or direct effects of arsenic on tubule cells. Glomerular damage can result in proteinuria. The kidney is not a major target organ for chronic toxicity.
Cardiovascular Effects: Acute arsenic poisoning may cause both diffuse capillary leak and cardiomyopathy, resulting in shock. The extent of cardiovascular injury may vary with age, arsenic dose, and individual susceptibility. In acute arsenic poisoning-usually suicide attempts-the fundamental lesion, diffuse capillary leak, leads to generalized vasodilation, transudation of plasma, hypotension, and shock. Delayed cardiomyopathy may also develop. Myocardial damage can result in a variety of electrocardiographic findings, including broadening of the QRS complex, prolongation of the QT interval, ST depression, flattening of T waves, and atypical, multifocal ventricular tachycardia.
Long-term ingestion of arsenic in drinking water has resulted in pronounced peripheral vascular changes. Epidemiological evidence indicates that chronic arsenic exposure is associated with vasospasm and peripheral vascular insufficiency. Gangrene of the extremities, known as Blackfoot disease, has been associated with drinking arsenic-contaminated well water in Taiwan, where the prevalence of the disease increased with increasing age and well-water arsenic concentration (10 to 1,820 ppb). Persons with Blackfoot disease also had a higher incidence of arsenic-induced skin cancers.
However, investigators believe other vasoactive substances found in the water may have been contributory. Raynaud’s phenomenon and acrocyanosis resulted from contamination of the city’s drinking water supply in Antofagasta, Chile, at arsenic concentrations ranging from 20 to 400 ppb. Autopsies of Antofagasta children who died of arsenic toxicity revealed fibrous thickening of small and medium arteries and myocardial hypertrophy. Similar vascular disorders, as well as abnormal electrocardiographs (ECGs), have been noted in vineyard workers exposed to arsenical pesticides.
Neurologic Effects: Arsenic-exposed patients develop destruction of axonal cylinders, leading to peripheral neuropathy. Peripheral neuropathy is a common complication of arsenic poisoning. The classic finding is a peripheral neuropathy involving sensory and motor nerves in a symmetrical, stocking-glove distribution. Sensory effects, particularly painful dysesthesia, occur earlier and may predominate in moderate poisoning, whereas ascending weakness and paralysis may predominate in more severe poisoning. Those cases may at first seem indistinguishable from Guillain-Barre syndrome (i. e. , acute inflammatory demyelinating polyneuropathy).
Cranial nerves are rarely affected, even in severe poisoning. Encephalopathy has been reported after both acute and chronic exposures. Onset may begin within 24 to 72 hours following acute poisoning, but it more often develops slowly as a result of chronic exposure. The neuropathy is primarily due to destruction of axonal cylinders (axonopathy). Nerve conduction and electromyography studies can document severity and progression. Subclinical neuropathy, defined by the presence of abnormal nerve conduction with no clinical complaints or symptoms, has been described in chronically exposed individuals.
Recovery from neuropathy induced by chronic exposure to arsenic compounds is generally slow, sometimes taking years, and complete recovery may not occur. Follow-up studies of Japanese children who chronically consumed arsenic-contaminated milk revealed an increased incidence of severe hearing loss, mental retardation, epilepsy, and other brain damage. Hearing loss as a sequela of acute or chronic arsenic intoxication has not been confirmed by other case reports or epidemiologic studies.
Dermal Effects: Pigment changes and palmoplantar hyperkeratosis are characteristic of chronic arsenic exposure. Benign arsenical keratoses may progress to malignancy. The types of skin lesions occurring most frequently in arsenic-exposed humans are hyperpigmentation, hyperkeratosis, and skin cancer. Patchy hyperpigmentation, a pathologic hallmark of chronic exposure, may be found anywhere on the body, but occurs particularly on the eyelids, temples, axillae, neck, nipples, and groin. The classic appearance of the dark brown patches with scattered pale spots is sometimes described as “raindrops on a dusty road. ” In severe cases, the pigmentation extends broadly over the chest, back, and abdomen.
Pigment changes have been observed in populations chronically consuming drinking water containing 400 ppb or more arsenic. Arsenical hyperkeratosis occurs most frequently on the palms and soles. Keratoses usually appear as small corn-like elevations, 0. 4 to 1 cm in diameter. In most cases, arsenical keratoses show little cellular atypia and may remain morphologically benign for decades. In other cases, cells develop marked atypia (precancerous) and appear indistinguishable from Bowen disease, which is an in situ squamous cell carcinoma discussed in Carcinogenic Effects.
Respiratory Effects: Inhalation of high concentrations of arsenic compounds produces irritation of the respiratory mucosa. Smelter workers experiencing prolonged exposures to high concentrations of airborne arsenic at levels rarely found today had inflammatory and erosive lesions of the respiratory mucosa, including nasal septum perforation. Lung cancer has been associated with chronic arsenic exposure in smelter workers and pesticide workers.
Hematopoietic Effects: Bone marrow depression may result from acute or chronic arsenic intoxication and may initially manifest as pancytopenia.
Both acute and chronic arsenic poisoning may affect the hematopoietic system. A reversible bone marrow depression with pancytopenia may occur. Anemia and leukopenia are common in chronic arsenic toxicity, and are often accompanied by thrombocytopenia and mild eosinophilia. The anemia may be normocytic or macrocytic, and basophilic stippling may be noted on peripheral blood smears.
Skin Cancer: Latency for skin cancer associated with ingestion of arsenic may be 3 to 4 decades, whereas the noncarcinogenic skin effects typically develop several years after exposure.An increased risk of skin cancer in humans is associated with chronic exposure to inorganic arsenic in medication, contaminated water, and the workplace. Arsenic-induced skin cancer is frequently characterized by lesions over the entire body, mostly in unexposed areas such as the trunk, palms, and soles. More than one type of skin cancer may occur in a patient. Most of the Taiwanese who developed skin cancer in association with ingestion of arsenic-contaminated drinking water had multiple cancer types.
The most commonly reported types, in order of decreasing frequency, were intraepidermal carcinomas (Bowen disease), squamous cell carcinomas, basal cell carcinomas, and “combined forms. ” Seventy-two percent of the Taiwanese with skin cancer also had hyperkeratosis, and 90% had hyperpigmentation. Some hyperkeratinized lesions can develop into intraepidermal carcinoma, which may ultimately become invasive. The lesions are sharply demarcated round or irregular plaques that tend to enlarge; they may vary in size from 1 millimeter to ;10 centimeters.
Arsenical basal cell carcinomas most often arise from normal tissue, are almost always multiple, and frequently occur on the trunk. The superficial spreading lesions are red, scaly, atrophic, and are often indistinguishable from Bowen disease by clinical examination. Arsenic-associated squamous cell carcinomas are distinguished from UV-induced squamous cell carcinomas by their tendency to occur on the extremities (especially palms and soles) and trunk rather than on sun-exposed areas such as the head and neck. However, it may be difficult to distinguish other arsenic-induced skin lesions from those induced by other causes.
Epidemiological studies indicate that a dose-response relationship exists between the level of arsenic in drinking water and the prevalence of skin cancers in the exposed population. Excessive mortality rates due to arsenic-induced skin cancer have also been observed in vineyard workers with dermal and inhalation exposure.
Lung Cancer: In arsenic-exposed workers, there is a systematic gradient in lung cancer mortality rates, depending on duration and intensity of exposure. An association between lung cancer and occupational exposure to inorganic arsenic has been confirmed in several epidemiologic studies. A higher risk of lung cancer was found among workers exposed predominantly to arsenic trioxide in smelters and to pentavalent arsenical pesticides in other settings. Neither concomitant exposure to sulfur dioxide nor cigarette smoke were determined to be essential co-factors in these studies.