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Over six million people in nine districts of West Bengal, India are exposed to very high levels of arsenic primarily through their drinking water. More than 300,000 people showed arsenic-induced skin lesions in these districts. This is regarded as the greatest arsenic calamity in the world. Chronic arsenicosis causes varied dermatological signs ranging from pigmentation changes, hyperkeratosis to non-melanocytic cancer of skin, and also malignancies in different internal organs. Higher incidences of opportunistic infections are found in the arsenic-exposed individuals, indicating that their immune systems may be impaired somehow. We have thus investigated the effect of arsenic on T-cell proliferation and cytokine secretion in 20 individuals with arsenic-induced skin lesions and compared the results with 18 arsenic-unexposed individuals. A marked dose-dependent suppression of Concanavalin A (Con A) induced T-cell proliferation was observed in the arsenic-exposed individuals compared with the unexposed ( P < 0.001) individuals. This correlated with a significant decrease in the levels of secreted cytokines by the T cells (TNF-α, IFN-γ, IL2, IL10, IL5, and IL4) in the exposed individuals ( P < 0.001). Thus it can be inferred that arsenic exposure can cause immunosuppression in humans.

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Remediation aimed at reducing human exposure to groundwater arsenic in West Bengal, one of the regions most impacted by this environmental hazard, are currently largely focussed on reducing arsenic in drinking water. Rice and cooking of rice, however, have also been identified as important or potentially important exposure routes. Quantifying the relative importance of these exposure routes is critically required to inform the prioritisation and selection of remediation strategies. The aim of our study, therefore, was to determine the relative contributions of drinking water, rice and cooking of rice to human exposure in three contrasting areas of West Bengal with different overall levels of exposure to arsenic, viz. high (Bhawangola-I Block, Murshidibad District), moderate (Chakdha Block, Nadia District) and low (Khejuri-I Block, Midnapur District). Arsenic exposure from water was highly variable, median exposures being 0.02 μg/kg/d (Midnapur), 0.77 μg/kg/d (Nadia) and 2.03 μg/kg/d (Murshidabad). In contrast arsenic exposure from cooked rice was relatively uniform, with median exposures being 0.30 μg/kg/d (Midnapur), 0.50 μg/kg/d (Nadia) and 0.84 μg/kg/d (Murshidabad). Cooking rice typically resulted in arsenic exposures of lower magnitude, indeed in Midnapur, median exposure from cooking was slightly negative. Water was the dominant route of exposure in Murshidabad, both water and rice were major exposure routes in Nadia, whereas rice was the dominant exposure route in Midnapur. Notwithstanding the differences in balance of exposure routes, median excess lifetime cancer risk for all the blocks were found to exceed the USEPA regulatory threshold target cancer risk level of 10(-4)-10(-6). The difference in balance of exposure routes indicate a difference in balance of remediation approaches in the three districts.

In West Bengal, India, more than 300,000 arsenic-exposed people are showing symptoms of arsenic toxicity, which include cancers of skin and different internal organs. Since only 15-20% of the exposed population manifest arsenic-induced skin lesions, it is thought that genetic variation might play an important role in arsenic toxicity and carcinogenicity. A total of 422 unrelated arsenic-exposed subjects (244 skin-symptomatic and 178 asymptomatic) were recruited for this study. Cytogenetic damage, as measured by chromosomal aberrations in lymphocytes and micronuclei formation in oral mucosa cells, urothelial cells and binucleated lymphocytes, was studied in unexposed, skin-symptomatic and asymptomatic individuals with similar socioeconomic status. Identification of null mutations in GSTT1 and GSTM1 genes were carried out by PCR amplification. GSTP1 SNPs, implicated in susceptibility to various cancers, were assessed by PCR-RFLP method. Symptomatic individuals had higher level of cytogenetic damage compared to asymptomatic individuals and asymptomatic individuals had significantly higher genotoxicity than unexposed individuals. No difference in allelic variants in GSTT1 and GSTP1 was observed between these 2 groups. Incidence of GSTM1 null gene frequencies was significantly higher in the asymptomatic group. Individuals with GSTM1-positive (at least one allele) had significantly higher risk of arsenic-induced skin lesions (odds ratio, 1.73; 95% confidence interval, 1.24-2.22). These results show a protective role of GSTM1 null in arsenic toxicity. This study also indicates that asymptomatic individuals are sub clinically affected and are also significantly susceptible to arsenicinduced genotoxicity. ' 2005 Wiley-Liss, Inc.