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8. What has happened in areas where drinking water is heavily contaminated?

    The source document for this Digest states:

    In nature, arsenic-bearing minerals undergo oxidation and release arsenic to water. This could be one explanation for the problems of arsenic in the groundwater of West Bengal and Bangladesh. In these areas the groundwater usage is very high. It has been estimated that there are about 4–10 million tube wells in Bangladesh alone. [It was thought that] the excessive withdrawal and lowering of the water table for rice irrigation and other requirements lead to the exposure and subsequent oxidation of arsenic-containing pyrite in the sediment. As the water table recharges after rainfall, arsenic leaches out of the sediment into the aquifer.

    However, recent studies seem to favour the reduction of Fe/As oxyhydroxides as the source for arsenic contamination in groundwater. Arsenic forms co-precipitates with ferric oxyhydroxide. Burial of the sediment, rich in ferric oxyhydroxide and organic matter, has led to the strongly reducing groundwater conditions. The process has been aided by the high water table and fine-grained surface layers which impede the penetration of air to the aquifer. Microbial oxidation of organic carbon has depleted the dissolved oxygen in the groundwater. The highly reducing nature of the groundwater explains the presence of arsenite (< 50%) in the water. The "pyrite oxidation" hypothesis is therefore unlikely to be a major process, and the "oxyhydroxide reduction" hypothesis is probably the main cause of arsenic contamination in groundwater. Although the oxyhydroxide reduction hypothesis requires further validation, there is no doubt that the source of arsenic in West Bengal and Bangladesh is geological, as none of the explanations for anthropogenic contamination can account for the regional extent of groundwater contamination.

    Source & ©: IPCS "Environmental Health Criteria for Arsenic and Arsenic compounds", 
    EHC 224, Chapter 3: section 3.1 natural sources, paragraphs 4-5

    Although arsenic levels in natural waters are usually low (a few µg/litre), there are several areas in the world where humans consume drinking-water containing > 100 µg As/litre resulting from natural geochemical activity. In the West Bengal region of India it was estimated that over 1 000 000 people consume drinking-water containing > 50 µg/litre (up to 3.7 mg/litre) arising from normal geochemical processes. In the areas of West Bengal and Bangladesh, 38% of groundwaters sampled in 27 districts were > 50 µg/litre. Natural geochemistry resulted in the pre-1970 exposure of about 100 000 people in the south-western coastal region of Taiwan to variable but high (10–1800 µg/litre, mean 500 µg/litre) concentrations of arsenic in drinking-water. A similar problem was reported in Chile where 100 000 people consumed drinking-water containing 800 µg As/litre between 1959 and 1970, when the concentration was lowered to about 50 µg/litre. About 200 000 people in north central Mexico were reported to be exposed to >50 µg/litre arsenic in drinking-water (410 µg/litre in at least one village).

    Source & ©: IPCS "Environmental Health Criteria for Arsenic and Arsenic compounds", 
    EHC 224, Chapter 5: Section 5.2.3 Drinking-water, paragraph 4

    Chronic skin effects of arsenic, including pigmentation changes, hyperkeratosis and skin cancer, from medicinal use but also from drinking-water, were reported as early as the 19th century. A large number of case series on arsenical skin cancer after exposure via drinking-water were published from Argentina, Chile, Mexico and Taiwan in the early 1900s.

    An endemic peripheral vascular disease, known as wu chiao ping or blackfoot disease, leading to progressive gangrene of the legs, has been known in Taiwan since the 1920s. It has increased in prevalence since the 1950s, and has been the subject of intense investigation since the late 1950s.

    Source & ©: IPCS "Environmental Health Criteria for Arsenic and Arsenic compounds", 
    EHC 224, Chapter 8: section 8.2 long-term effects: a historical introduction

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