Literature DB >> 12504762

Chromosomal aberrations and sister chromatid exchanges in individuals exposed to arsenic through drinking water in West Bengal, India.

J Mahata1, A Basu, S Ghoshal, J N Sarkar, A K Roy, G Poddar, A K Nandy, A Banerjee, K Ray, A T Natarajan, R Nilsson, A K Giri.   

Abstract

Arsenic contamination in groundwater has become a worldwide problem. Currently an unprecedented number of people in West Bengal, India and Bangladesh are exposed to the ubiquitous toxicant via drinking water in exposure levels far exceeding the maximum recommended limit laid down by WHO. This arsenic epidemic has devastated nine districts of West Bengal encompassing an area of 38,865 km(2) leading to various clinical manifestations of chronic arsenicosis. We conducted a human bio-monitoring study using chromosomal aberrations (CA) and sister chromatid exchanges (SCE) as end points to explore the cytogenetic effects of chronic arsenic toxicity in the population of North 24 Parganas, one of the arsenic affected districts in West Bengal. Study participants included 59 individuals residing in this district where the mean level (+/-S.E.) of arsenic in drinking water (microg/l) was 211.70+/-15.28. As age matched controls with similar socio-economic status we selected 36 healthy, asymptomatic individuals residing in two unaffected districts--Midnapur and Howrah where the mean arsenic content of water (microg/l) was 6.35+/-0.45. Exposure was assessed by standardized questionnaires and by detecting the levels of arsenic in drinking water, nails, hair and urine samples. In the exposed group the mean arsenic concentrations in nails (microg/g), hair (microg/g) and urine (microg/l) samples were 9.04+/-0.78, 5.63+/-0.38 and 140.52+/-8.82, respectively, which were significantly high (P<0.01) compared to the corresponding control values of 0.44+/-0.03, 0.30+/-0.02 and 5.91+/-0.49, respectively. Elevated mean values (P<0.01) of the percentage of aberrant cells (8.08%) and SCEs per cell (7.26) were also observed in the exposed individuals in comparison to controls (1.96% and 5.95, respectively). The enhanced rates of CAs and SCEs among the residents of North 24 Parganas are indicative of the cytogenetic damage due to long term exposure to arsenic through consumption of contaminated water.

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Year:  2003        PMID: 12504762     DOI: 10.1016/s1383-5718(02)00255-3

Source DB:  PubMed          Journal:  Mutat Res        ISSN: 0027-5107            Impact factor:   2.433


  18 in total

1.  Precancerous and non-cancer disease endpoints of chronic arsenic exposure: the level of chromosomal damage and XRCC3 T241M polymorphism.

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Review 7.  The mechanistic basis of arsenicosis: pathogenesis of skin cancer.

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9.  BRCA2-dependent homologous recombination is required for repair of Arsenite-induced replication lesions in mammalian cells.

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10.  Epigallocatechin gallate attenuates arsenic induced genotoxicity via regulation of oxidative stress in balb/C mice.

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