Reportedly, 300 million people worldwide are affected by the consumption of arsenic contaminated groundwater. India prominently figures amongst them and the state of Bihar has shown an upsurge in cases affected by arsenic poisoning. Escalated arsenic content in blood, leaves 1 in every 100 human being highly vulnerable to being affected by the disease. Uncontrolled intake may lead to skin, kidney, liver, bladder, or lung related cancer but even indirect forms of cancer are showing up on a regular basis with abnormal arsenic levels as the probable cause. But despite the apparent relation, the etiology has not been understood clearly. Blood samples of 2000 confirmed cancer patients were collected from pathology department of our institute. For cross-sectional design, 200 blood samples of subjects free from cancer from arsenic free pockets of Patna urban agglomeration, were collected. Blood arsenic levels in carcinoma patients as compared to sarcomas, lymphomas and leukemia were found to be higher. The geospatial map correlates the blood arsenic with cancer types and the demographic area of Gangetic plains. Most of the cancer patients with high blood arsenic concentration were from the districts near the river Ganges. The raised blood arsenic concentration in the 2000 cancer patients strongly correlates the relationship of arsenic with cancer especially the carcinoma type which is more vulnerable. The average arsenic concentration in blood of the cancer patients in the Gangetic plains denotes the significant role of arsenic which is present in endemic proportions. Thus, the study significantly correlates and advocates a strong relation of the deleterious element with the disease. It also underlines the need to address the problem by deciphering the root cause of the elevated cancer incidences in the Gangetic basin of Bihar and its association with arsenic poisoning.

Exposure of 10-d-old spinach (Spinacea oleracea L.) plants to excess (500 µM) concentrations of Co, Ni, Cu, Zn and Cd in sand culture inhibited growth, induced toxicity symptoms, oxidative damage and changes in the antioxidant defense system. The severity of the metal-induced effects varied with the metals and the duration of exposure to excess supply of the metals. Each metal induced chlorosis. In addition, excess Co, Ni and Cd also produced metal specific toxic effects. Excess supply of each metal caused lipid peroxidation (TBARS). Their effectiveness in producing oxidative damage was in the order: Ni > Co > Cd > Cu >Zn. Of all the metals, Ni was also most effective in lowering the concentration of the chloroplast pigments (Chl, Car). While each metal increased the concentration of ascorbate and activated the key enzymes of the ascorbate-glutathione cycle, excess Cd and Zn were more effective in this regard. Each metal increased the activity of SOD and POD and decreased the activity of CAT. Enhancement in SOD activity and inhibition of CAT activity suggested high build-up of H 2 O 2 , possibly the main cause of oxidative stress, induced in response to excess supply of the heavy metals.

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