The surprising finding of cases who had arsenic-associated skin lesions with apparently low exposure to arsenic in drinking water needs to be confirmed in studies with more detailed exposure assessment. Further research is also needed concerning susceptibility factors which might be present in the exposed population.

We have demonstrated hepatic fibrosis due to long-term arsenic toxicity in an animal model. Initial biochemical evidence of hepatic membrane damage, probably due to reduction of glutathione and antioxidant enzymes, may be seen by 6 months. Continued arsenic feeding resulted in fatty liver with serum aminotransferase and alanine aminotransferase elevated at 12 months and hepatic fibrosis at 15 months. The murine model is proposed as relevant to epidemic human toxicity in areas of arsenic contamination.

Current arsenic concentrations in urine, which reflect all sources of recent exposure, including water and food, were associated with small decrements in intellectual testing in school-aged children in West Bengal. We did not see associations between long-term water arsenic concentrations and intellectual function.

Various systemic manifestations are reported to be caused by chronic arsenic exposure in the population living in the Indo-Bangladesh subcontinent. This study from West Bengal assesses the likelihood of occurrence of hypertension (HTN) in individuals resident in an area of high groundwater contamination with arsenic (Nadia district) compared to those from a non-contaminated area (Hoogly district) in West Bengal, India. Two hundred and eight study participants (Group 1) were recruited from a cross-sectional study in six villages in the Nadia district and 100 controls (Group 2) from a village in the Hoogly district. The two groups were evenly matched in regard to age and sex. History taking and clinical examination including blood pressure measurement were undertaken in each participant. Water samples from current and previous drinking water sources and hair and urine samples from each participant were collected for estimation of arsenic. The present study shows evidence of increased association of HTN in individuals resident in arsenic endemic region compared to those from a non-endemic region in West Bengal. There were increased odds ratios for HTN [Adjusted Odds Ratio, OR, 2.87 (95 %CI = 1.26-4.83)] in Group- 1 participants compared to Group- 2 people. Within Group 1, there was no difference in prevalence of HTN between those with and without skin lesion. There was a dose-effect relationship seen with increasing cumulative arsenic exposure and arsenic level in hair and HTN in participants living in arsenic endemic region.The findings reported here support an association between arsenic exposure and HTN. More work is needed to characterize the link further.