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      A review on exposure and effects of arsenic in passerine birds

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      Science of The Total Environment
      Elsevier BV

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          Mechanisms of arsenic biotransformation.

          Inorganic arsenic, a documented human carcinogen, is methylated in the body by alternating reduction of pentavalent arsenic to trivalent and addition of a methyl group from S-adenosylmethionine. Glutathione, and possibly other thiols, serve as reducing agents. The liver is the most important site of arsenic methylation, but most organs show arsenic methylating activity. The end metabolites are methylarsonic acid (MMA) and dimethylarsinic acid (DMA). These are less reactive with tissue constituents than inorganic arsenic and readily excreted in the urine. However, reactive intermediates may be formed. Absorbed arsenate (As(V)) is fairly rapidly reduced in blood to As(III), which implies increased toxicity. Also, intermediate reduced forms of the methylated metabolites, MMA(III) and DMA(III), have been detected in human urine. In particular MMA(III) is highly toxic. To what extent MMA(III) and DMA(III) contribute to the observed toxicity following exposure to inorganic arsenic remains to be elucidated. There are marked differences in the metabolism of arsenic between mammalian species, population groups and individuals. There are indications that subjects with low MMA in urine have faster elimination of ingested arsenic, compared to those with more MMA in urine.
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            Marked increase in bladder and lung cancer mortality in a region of Northern Chile due to arsenic in drinking water.

            Studies in Taiwan and Argentina suggest that ingestion of inorganic arsenic from drinking water results in increased risks of internal cancers, particularly bladder and lung cancer. The authors investigated cancer mortality in a population of around 400,000 people in a region of Northern Chile (Region II) exposed to high arsenic levels in drinking water in past years. Arsenic concentrations from 1950 to the present were obtained. Population-weighted average arsenic levels reached 570 microg/liter between 1955 to 1969, and decreased to less than 100 microg/liter by 1980. Standardized mortality ratios (SMRs) were calculated for the years 1989 to 1993. Increased mortality was found for bladder, lung, kidney, and skin cancer. Bladder cancer mortality was markedly elevated (men, SMR = 6.0 (95% confidence interval (CI) 4.8-7.4); women, SMR = 8.2 (95% CI 6.3-10.5)) as was lung cancer mortality (men, SMR = 3.8 (95% CI 3.5-4.1); women, SMR = 3.1 (95% CI 2.7-3.7)). Smoking survey data and mortality rates from chronic obstructive pulmonary disease provided evidence that smoking did not contribute to the increased mortality from these cancers. The findings provide additional evidence that ingestion of inorganic arsenic in drinking water is indeed a cause of bladder and lung cancer. It was estimated that arsenic might account for 7% of all deaths among those aged 30 years and over. If so, the impact of arsenic on the population mortality in Region II of Chile is greater than that reported anywhere to date from environmental exposure to a carcinogen in a major population.
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              Trace metal concentrations in aquatic invertebrates: why and so what?

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                Author and article information

                Journal
                Science of The Total Environment
                Science of The Total Environment
                Elsevier BV
                00489697
                April 2015
                April 2015
                : 512-513
                :
                : 506-525
                Article
                10.1016/j.scitotenv.2015.01.069
                65fdf3fc-f5df-4e81-b172-67107352ccb7
                © 2015
                History

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