Family correlations of arsenic methylation patterns in children and parents exposed to high concentrations of arsenic in drinking water.

We investigated the evidence of a familial contribution to urinary methylation patterns in families ingesting arsenic in drinking water. Arsenic methylation can be assessed by measuring urinary levels of inorganic arsenic (InAs) and its methylated metabolites, monomethylarsonate (MMA), and dimethylarsinate (DMA). Methylation activity is reflected in the ratios: InAs/methylated arsenic (InAs/metAs) and MMA/DMA. Eleven families from Chile were selected because of their long-term exposure to very high levels of arsenic in drinking water (735-762 microg/L). Each family consisted of a father, a mother, and two children. We measured urinary arsenic and its methylated metabolites for each participant (n = 44). The intraclass correlation coefficients showed that 13-52% of the variations in the methylation patterns were from being a member of a specific family. Family correlations were calculated for father-mother, parent-child, and sibling-sibling pairs. Methylation patterns correlated strongly between siblings [r = 0.78 for InAs/metAs, 95% confidence interval (CI), 0.34-0.94; r = 0.82 for MMA/DMA, 95%CI, 0.43-0.95] compared to lower correlations in father-mother pairs (r = 0.18, r = -0.01, respectively), after adjustment for total urinary arsenic, age, and sex. Family correlations were not notably altered when adjustments were made for specific blood micronutrients (methionine, homocysteine, folate, vitamin B6, selenium, and vitamin B12 potentially related to methylation. We also report on a family pedigree with high prevalence of arsenic-induced effects. Participants from this family had low InAs/metAs values, which is consistent with increased toxicity of trivalent methylated arsenic species. Despite our small sample size, we observed that methylation patterns aggregate in families and are correlated in siblings, providing evidence of a genetic basis for the variation in arsenic methylation. Larger studies with more extensive pedigrees will need to be conducted to confirm these findings

Gastric adenocarcinoma in a patient re-infected with H. pylori after regression of MALT lymphoma with successful anti-H. pylori therapy and gastric resection: a case report

BACKGROUND: Helicobacter pylori (H. pylori) has been etiologically linked with primary gastric lymphoma (PGL) and gastric carcinoma (GC). There are a few reports of occurrence of both diseases in the same patient with H. pylori infection. CASE PRESENTATION: We report a patient with PGL in whom the tumor regressed after surgical resection combined with eradication of H. pylori infection. However, he developed GC on follow up; this was temporally associated with recrudescence / re-infection of H. pylori. This is perhaps first report of such occurrence. CONCLUSIONS: Possible cause and effect relationship between H. pylori infection and both PGL and GC is discussed. This case also documents a unique problem in management of PGL in tropical countries where re-infection with H. pylori is supposed to be high

Role and Mechanism of Arsenic in Regulating Angiogenesis

Arsenic is a wide spread carcinogen associated with several kinds of cancers including skin, lung, bladder, and liver cancers. Lung is one of the major targets of arsenic exposure. Angiogenesis is the pivotal process during carcinogenesis and chronic pulmonary diseases, but the role and mechanism of arsenic in regulating angiogenesis remain to be elucidated. In this study we show that short time exposure of arsenic induces angiogenesis in both human immortalized lung epithelial cells BEAS-2B and adenocarcinoma cells A549. To study the molecular mechanism of arsenic-inducing angiogenesis, we find that arsenic induces reactive oxygen species (ROS) generation, which activates AKT and ERK1/2 signaling pathways and increases the expression of hypoxia-inducible factor 1 (HIF-1) and vascular endothelial growth factor (VEGF). Inhibition of ROS production suppresses angiogenesis by decreasing AKT and ERK activation and HIF-1 expression. Inhibition of ROS, AKT and ERK1/2 signaling pathways is sufficient to attenuate arsenic-inducing angiogenesis. HIF-1 and VEGF are downstream effectors of AKT and ERK1/2 that are required for arsenic-inducing angiogenesis. These results shed light on the mechanism of arsenic in regulating angiogenesis, and are helpful to develop mechanism-based intervention to prevent arsenic-induced carcinogenesis and angiogenesis in the future

Effect of drinking arsenic-contaminated water in children

Chronic arsenic toxicity due to drinking of arsenic-contaminated water has been a major environmental health hazard throughout the world including India. Although a lot of information is available on health effects due to chronic arsenic toxicity in adults, knowledge of such effect on children is scanty. A review of the available literature has been made to highlight the problem in children. Scientific publications on health effects of chronic arsenic toxicity in children with special reference to psychological issues are reviewed. The prevalence of skin abnormalities such as pigmentation change and keratosis, the diagnostic signs of chronic arsenic toxicity, vary in various arsenic-exposed children population in different regions of the world. The occurrence of chronic lung disease including pulmonary interstitial fibrosis has been described in arsenic-exposed children in Chile. Affection of intellectual function has also been reported to occur in arsenic-exposed children studied in Thailand, Bangladesh, and India. Methylation patterns of arsenic in children aggregate in families and are correlated in siblings, providing evidence of a genetic basis for the variation in arsenic methylation. Chronic arsenic toxicity due to drinking of arsenic-contaminated water causes significant morbidity in children resulting in skin lesions, lung disease, and defect in intellectual function

Microbial arsenic transformations: towards cause and mitigation of the arsenic problem

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Review on arsenic contamination in inland open water ecosystems.

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Effect of safe water on arsenicosis: A follow-up study

Background: Arsenic pollution in groundwater, used for drinking purposes, has been envisaged as a problem of global concern. Treatment options for the management symptoms of chronic arsenicosis are limited. Mitigation option available for dealing with the health problem of ground water arsenic contamination rests mainly on supply of arsenic safe water in arsenic-endemic region of Indo-Bangladesh subcontinent. Limited information is available regarding the long-term effect of chronic arsenic toxicity after stoppage of consumption of arsenic-containing water. Objective: The current study was, therefore, done to assess, objectively, the effect of drinking arsenic safe water (<50 μg/L) on disease manifestation of arsenicosis. Results: Manifestations of various skin lesions and systemic diseases associated with chronic arsenic exposure were ascertained initially by carrying on baseline study on 208 participants in Nadia (Cohort-I, with skin lesion and Cohort-II, without skin lesion) using a scoring system, as developed by us, and compared objectively at the end of each year for 3 year follow-up period. All the participants who had arsenic contaminated drinking water source in their houses were supplied with arsenic removal filters for getting arsenic-free water during the follow-up period. In participants belonging to Cohort-I, the skin score was found to improve significantly at the end of each year, and it was found to be reduced significantly from 2.17 ± 1.09 to 1.23 ± 1.17; P < 0.001 at the end of 3 year′s intervention study indicating beneficial effect of safe water on skin lesions. The systemic disease symptom score was also found to improve, but less significantly, at the end of 3 years in both the cohorts. Most important observation during the follow-up study was persistence of severe symptoms of chronic lung disease and severe skin lesion including Bowen′s disease in spite of taking arsenic-safe water. Further, death could not be prevented to occur because of lung cancer and severe lung disease. Conclusion: It is, therefore, an urgent need to make arrangement for availability of safe water source among the arsenic-affected people in the district. Many of the people in the affected villages are not aware of contamination of their home tube wells with arsenic. Awareness generation and motivation of the people for testing their drinking water sources for arsenic and environmental interventions like rain water harvesting, ground water recharge, and restricting excessive use of ground water for domestic and agricultural purposes are also important to prevent further exposure of arsenic to these people