Chronic arsenic toxicity in Bangladesh and West Bengal, India--a review and commentary - PubMed
Review
doi: 10.1081/clt-100108509.
U K Chowdhury, S C Mukherjee, B K Mondal, K Paul, D Lodh, B K Biswas, C R Chanda, G K Basu, K C Saha, S Roy, R Das, S K Palit, Q Quamruzzaman, D Chakraborti
Affiliations
- PMID: 11778666
- DOI: 10.1081/clt-100108509
Review
Chronic arsenic toxicity in Bangladesh and West Bengal, India--a review and commentary
M M Rahman et al. J Toxicol Clin Toxicol. 2001.
Abstract
Fifty districts of Bangladesh and 9 districts in West Bengal, India have arsenic levels in groundwater above the World Health Organization's maximum permissible limit of 50 microg/L. The area and population of 50 districts of Bangladesh and 9 districts in West Bengal are 118,849 km2 and 104.9 million and 38,865 km2 and 42.7 million, respectively. Our current data show arsenic levels above 50 microg/ L in 2000 villages, 178 police stations of 50 affected districts in Bangladesh and 2600 villages, 74 police stations/blocks of 9 affected districts in West Bengal. We have so far analyzed 34,000 and 101,934 hand tube-well water samples from Bangladesh and West Bengal respectively by FI-HG-AAS of which 56% and 52%, respectively, contained arsenic above 10 microg/L and 37% and 25% arsenic above 50 microg/L. In our preliminary study 18,000 persons in Bangladesh and 86,000 persons in West Bengal were clinically examined in arsenic-affected districts. Of them, 3695 (20.6% including 6.11% children) in Bangladesh and 8500 (9.8% including 1.7% children) in West Bengal had arsenical dermatological features. Symptoms of chronic arsenic toxicity developed insidiously after 6 months to 2 years or more of exposure. The time of onset depends on the concentration of arsenic in the drinking water, volume of intake, and the health and nutritional status of individuals. Major dermatological signs are diffuse or spotted melanosis, leucomelanosis, and keratosis. Chronic arsenicosis is a multisystem disorder. Apart from generalized weakness, appetite and weight loss, and anemia, our patients had symptoms relating to involvement of the lungs, gastrointestinal system, liver, spleen, genitourinary system, hemopoietic system, eyes, nervous system, and cardiovascular system. We found evidence of arsenic neuropathy in 37.3% (154 of 413 cases) in one group and 86.8% (33 of 38 cases) in another. Most of these cases had mild and predominantly sensory neuropathy. Central nervous system involvement was evident with and without neuropathy. Electrodiagnostic studies proved helpful for the diagnosis of neurological involvement. Advanced neglected cases with many years of exposure presented with cancer of skin and of the lung, liver, kidney, and bladder. The diagnosis of subclinical arsenicosis was made in 83%, 93%, and 95% of hair, nail and urine samples, respectively, in Bangladesh; and 57%, 83%, and 89% of hair, nail, and urine samples, respectively in West Bengal. Approximately 90% of children below 11 years of age living in the affected areas show hair and nail arsenic above the normal level. Children appear to have a higher body burden than adults despite fewer dermatological manifestations. Limited trials of 4 arsenic chelators in the treatment of chronic arsenic toxicity in West Bengal over the last 2 decades do not provide any clinical, biochemical, or histopathological benefit except for the accompanying preliminary report of clinical benefit with dimercaptopropanesulfonate therapy. Extensive efforts are needed in both countries to combat the arsenic crisis including control of tube-wells, watershed management with effective use of the prodigious supplies of surface water, traditional water management, public awareness programs, and education concerning the apparent benefits of optimal nutrition.
Comment in
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Arsenic exposure and health effects.
Guha Mazumder DN. Guha Mazumder DN. J Toxicol Clin Toxicol. 2002;40(4):527-8; author reply 529-30. J Toxicol Clin Toxicol. 2002. PMID: 12217011 No abstract available.
Comment on
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Guha Mazumder DN, De BK, Santra A, Ghosh N, Das S, Lahiri S, Das T. Guha Mazumder DN, et al. J Toxicol Clin Toxicol. 2001;39(7):665-74. doi: 10.1081/clt-100108507. J Toxicol Clin Toxicol. 2001. PMID: 11778664 Clinical Trial.
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Kannan GM, Tripathi N, Dube SN, Gupta M, Flora SJ. Kannan GM, et al. J Toxicol Clin Toxicol. 2001;39(7):675-82. doi: 10.1081/clt-100108508. J Toxicol Clin Toxicol. 2001. PMID: 11778665
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