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Arsenic Crisis News Feb 03 V3 N04

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  • dr_sara_bennett <acic@bicn.com>
    ===================================================================== Arsenic Crisis News February 2003 V3 N04
    Message 1 of 1 , Feb 11, 2003
      Arsenic Crisis News
      February 2003 V3 N04

      + From the Editor

      + Highlights

      + Upcoming Meetings & Conferences
      Updated Conference Web Pages & Sites

      + Selected Recent Media Articles Online

      + New & Newly-Discovered Scientific & Technical
      Publications On & Off Line

      + New & Newly-Discovered Web Sites & Web Pages
      Updated Web Sites & Web Pages

      + New & Newly Discovered Real World Stuff

      + Publication & Other Details


      ACN is published by the Arsenic Crisis Info Centre, (c) ACIC.
      Website http://www.bicn.com/acic. Editor Sara Bennett.

      Email addresses appear in this newsletter with a space before & after
      the @ symbol. To send email to an address, you must first remove the

      To visit long URLs that spill over onto more than one line, cut and
      paste the *entire* URL (all lines of it) into the address pane of
      your browser. Generally clicking on such URLs does *not* work.

      See end of message for how to subscribe, unsubscribe, submit, etc.


      I will be moving back to Canada from Bangladesh in June 2003. I know
      from the last time I lived in Canada in 2001-2 that, good intentions
      notwithstanding, I will not be able to create the arsenic newsletters
      nor maintain the website on a volunteer basis.

      Therefore, for ACN/ACIC to continue beyond June 2003, I need to find
      one or more partners. There are several possibilities, for example:

      - One or more individuals that would commit to a year term as
      volunteer editor(s) of one or more sections of the newsletter

      - An organization that would take ACN/ACIC on as a project (for which
      they could seek funding - most funding sources are closed to me as
      an individual)

      - Corporate sponsorship

      - A fundraising committee to help generate subscriber
      pledges/donations to pay the editor/webmaster (not necessarily
      me). Some subscribers have donated in the past to support
      a student intern and help cover some of the out-of-pocket
      website costs - for which I thank them again. New webtools
      have become available to accept online donations by credit card
      (eg http://gifttool.com/ ), which would facilitate mobilizing
      subscriber support

      If you are interested helping with any of the above; if you have an
      alternative suggestion; or if you would like to be part of a dialogue
      on how to continue ACIC/ACN past June 2003, please let me know. When
      I have some idea of the response, I will decide how to proceed. One
      possibility might be to open a small discussion group on this topic
      for interested persons.

      It may be time to see if ACIC/CAN can be transformed from a one-woman
      volunteer service to a broad-based stakeholder-driven effort. That
      would require stakeholders to take the lead in figuring out what it
      should be, how to do it, and then getting it set up.

      Then again, it may be that ACIC/ACN has fulfilled its purpose of
      getting the word out about the W Bengal/Bangladesh arsenic crisis.
      If so, letting it lapse in Jun 2003 would be appropriate.

      Sara Bennett


      Highlights of this issue include:

      - A Sylvia Mortoza editorial that appeared 14 Jan 03 in The
      Bangladesh Observer expressed "surprise to find the Government
      [of Bangladesh] has placed a ban on the marketing and
      distributing" of arsenic removal technologies.

      - A UN wire article reported the results of a four-year study of
      arsenic in Terai tubewells, in particular an estimate that
      "nearly half of Nepal's 22.3 million people are at risk of
      contracting diseases caused by arsenic-contaminated
      drinking water."

      - A study by Chakraborti et al. (2003) of 206 tubewells in the
      Middle Ganga Plain, Bihar, found 57% with arsenic levels
      above 50 µg/L and 20% above 300 µg/L. These findings
      suggest that "the possibility of contaminated groundwater
      at other sites in the Middle and Upper Ganga Plain merits

      - Hanchett et al.'s (2002) study of the impact of an arsenic
      public education program carried out under the 18 District
      Towns Project in Bangladesh, found many at-risk
      program-influenced respondents still drinking
      arsenic-contaminated water; widespread confusion about
      newly labeled 'unsafe' handpumps; and limited awareness
      of the dangers of arsenic consumption. These findings
      will clearly be significant in guiding the design of improved
      awareness building measures.

      - The topic of three of the articles listed in this issue is
      the role of dietary antioxidants (vitamin C, vitamin E,
      and in particular selenium) in mediating arsenic's health
      effects, and, conversely, of undernourishment in worsening
      them (Liu at al., 2001 and the accompanying 2001 Columbia News
      article; Wuyi et al., 2001; Hsueh et al. 1995) on. These
      articles are relevant to the discussions that have been
      going on at the arsenic-crisis newsgroup about the role
      of diet in arsenic sickness and treatment.


      Arsenic in Aquatic Environments and Systems at the 226th American
      Chemical Society National Meeting September 7-11, 2003, New York

      If you or a colleague is interested in presenting a paper, please
      submit a short abstract to the ACS online abstract system (OASYS) at
      http://oasys.acs.org/ by May 10, 2003.

      Xiaoguang Meng, Ph.D., P.E., Associate Professor
      Center for Environmental Engineering
      Dept. of Civil, Environmental & Coastal Engineering
      Stevens Institute of Technology
      Hoboken, NJ 07030

      Conference papers now online

      USGS Workshop on Arsenic in the Environment, Denver CO, 21-22
      February 2001

      Final abstracts available online at



      Articles from other sources than News From Bangladesh are presented
      first, then the NFB articles. Within these two categories article
      appear by publication date, most recent first.

      Arsenic reducing techniques and unwarranted hurdles
      By Sylvia Mortoza. From The Bangladesh Observer 14 Jan 2003 / NFB 10
      Feb 2003.

      The human body can excrete arsenic only at a certain maximum rate.
      This rate may vary with the individual but when arsenic is ingested
      at a rate greater than can be excreted by the kidneys, it will build
      up in the liver, spleen and blood because arsenic is a cumulative
      poison. However it is possible to help people if arsenic can be
      excluded from the diet altogether, in which case whatever has
      accumulated in the body, this will be excreted within a matter of
      days or weeks with the exception of the portion that has been
      sequestered in the nails and hair. What this means in practical
      terms is, if the patient is able to drink only arsenic-free water,
      and provided the victim has not reached the point of no return, he
      will be put back on the road to good health. This is why
      technologies for reducing the amount of arsenic in the water are so
      important, at least until a permanent solution can be found....

      We know that scientists and others are working round the clock to
      find solutions. As such it comes as a surprise to find the
      government has placed a ban on the marketing and distributing of such
      technologies. Whereas we agree there is a genuine need to assess all
      possible technologies and put them through their paces, to place any
      restriction on technologies that have been properly tested is to our
      minds, immoral especially when Bangladesh is struggling to mitigate
      the arsenic toxicity in the drinking water. Surely a more sensible
      approach is called for when nearly 80 million people are at risk? And
      as this dreadfully toxic element is in the food chain too, we cannot
      afford to waste time. Unfortunately, according to reports, people
      without scruples are busy making money at the expense of the
      afflicted and this is quite untenable. How people can profit on
      other people's misery is beyond our comprehension but when genuine
      people who have kept in mind the special needs of Bangladeshi people
      like efficiency and the appropriateness of the technology, are being
      handicapped by red tape, we despair for our nation. The process of
      testing tubewells is also too slow for us to drag our feet where
      technology is concerned. Therefore the process of certification must
      be speeded up.

      Already the official mitigation project has earned a bad name and
      been termed "weak-kneed and lacking in coordination" (between
      implementing agencies and donors). It has also been said that some
      western marketing companies, aided and abetted by some of the donor
      agencies, are taking full advantage of the situation and are carving
      out a market for their arsenic filtration devices. This too must not
      be allowed more especially when there are some promising home-grown
      technologies that are economically viable and socially acceptable
      available. In other words once a technique has been field tested and
      found suitable there is no logical reason for not releasing it to the

      [ http://www.bangladesh-web.com/news/feb/10/d10022003.htm#A2 ]

      Nepal: warnings of arsenic contamination in Terai

      Source: UN Wire, 15 Jan 2003, http://www.unfounda
      tion.org/unwire/2003/01/15/current.asp#31423 , by way of Source
      Weekly No. 3-4, 27 January 2003.

      Nearly half of Nepal's 22.3 million people are at risk of contracting
      diseases caused by arsenic-contaminated drinking water, according to
      a four-year study by a nongovernmental organisation and experts from
      UNICEF and the World Health organisation (WHO). Tests on about 10% of
      the 200,000 shallow tubewells in the country's Terai region, where
      47% of the population lives, indicate arsenic levels above WHO
      standards, said Prasant Chaudhary of the NGO, the Public Health
      Concern Center....

      Nepalese Health Department official Ram Sharan Duwadi said villagers
      in the region, 90% of whom get their water from the wells, often
      complain of dizziness and hearing problems. He added that because
      such incidents are comparatively recent, "most people are ignorant
      about the matter."

      The measurements in the affected areas of Nepal have revealed
      concentrations almost double the highest measured in Bangladesh. A
      National Arsenic Steering Committee (NASC) was formed in the
      beginning of year 2001, and shortly after the Non Government
      Organisations' Informal Group for Arsenic Mitigation (NIGAM) was

      Web address: Arsenic Contamination in Nepal,

      Contact: Mr. G.P. Shresta, DWSS, dwss @ nmip.mos.com.np, or Mr. H.
      Spruijt, UNICEF, hspruijt @ unicef.org

      [None since 2002-12-30, reported in the previous issue of ACN]


      Sorted by year (newest first), alphabetical by title within each year.


      Arsenic groundwater contamination in Middle Ganga Plain, Bihar,
      India: A Future Danger? Chakraborti, Dipankar, Subhash C. Mukherjee,
      Shyamapada Pati, Mrinal K. Sengupta, Mohammad M. Rahman, Uttam K.
      Chowdhury, Dilip Lodh, Chitta R. Chanda, Anil K. Chakraborti, and
      Gautam K. Basu. Environmental Health Perspectives 2003, in press.

      Abstract: The pandemic of arsenic poisoning due to contaminated
      groundwater in West Bengal, India and all of Bangladesh has been
      thought limited to the Ganges Delta (the Lower Ganga Plain) despite
      early survey reports of arsenic contamination in groundwater in the
      Union Territory of Chandigarh and its surroundings in the
      northwestern Upper Ganga Plain and recent findings in the Terai area
      of Nepal. Anecdotal reports of arsenical skin lesions in villagers
      led us to evaluate arsenic exposure and sequelae in the Semria Ojha
      Patti village in the Middle Ganga Plain, Bihar, where tube wells
      replaced dug wells about 20 years ago. Analyses of the arsenic
      content of 206 tube wells (95% of the total) showed 56.8% to exceed
      arsenic concentrations of 50 µg/L with 19.9% >300 µg/L, the
      concentration predicting overt arsenical skin lesions. On medical
      examination of a self-selected sample of 550 (390 adults; 160
      children), 13% of the adults and 6.3% of the children had typical
      skin lesions, an unusually high involvement for children, except in
      extreme exposures combined with malnutrition. The urine, hair, and
      nail concentrations of arsenic correlated significantly (r=0.72-0.77)
      with drinking water arsenic concentrations up to 1654 µg/L. On
      neurological examination, arsenic-typical neuropathy was diagnosed in
      63% of the adults, a prevalence previously seen only in severe,
      subacute exposures. We also observed an apparent increase in fetal
      loss and premature delivery in the women with the highest drinking
      water arsenic. The possibility of contaminated groundwater at other
      sites in the Middle and Upper Ganga plain merits investigation.

      [Abstract currently available at http://dx.doi.org/, DOI=
      10.1289/ehp.5966 . Permanent URL will be http://e
      hpnet1.niehs.nih.gov/docs/2003/5966/abstract.html ]

      Hair and toenail arsenic concentrations of residents living in areas
      with high environmental arsenic concentrations. Andrea L. Hinwood,
      Malcolm R. Sim, Damien Jolley, Nick de Klerk, Elisa B. Bastone, Jim
      Gerostamoulos, and Olaf H. Drummer. Environ Health Perspect
      111:187-193 (2003).

      Abstract: Surface soil and groundwater in Australia have been found
      to contain high concentrations of arsenic. The relative importance
      of long-term human exposure to these sources has not been
      established. Several studies have investigated long-term exposure to
      environmental arsenic concentrations using hair and toenails as the
      measure of exposure. Few have compared the difference in these
      measures of environmental sources of exposure. In this study we
      aimed to investigate risk factors for elevated hair and toenail
      arsenic concentrations in populations exposed to a range of
      environmental arsenic concentrations in both drinking water and soil
      as well as in a control population with low arsenic concentrations in
      both drinking water and soil. In this study, we recruited 153
      participants from areas with elevated arsenic concentrations in
      drinking water and residential soil, as well as a control population
      with no anticipated arsenic exposures. The median drinking water
      arsenic concentrations in the exposed population were 43.8 µg/L
      (range, 16.0-73 µg/L) and median soil arsenic concentrations were
      92.0 mg/kg (range, 9.1-9,900 mg/kg). In the control group, the
      median drinking water arsenic concentration was below the limit of
      detection, and the median soil arsenic concentration was 3.3 mg/kg.
      Participants were categorized based on household drinking water and
      residential soil arsenic concentrations. The geometric mean hair
      arsenic concentrations were 5.52 mg/kg for the drinking water
      exposure group and 3.31 mg/kg for the soil exposure group. The
      geometric mean toenail arsenic concentrations were 21.7 mg/kg for the
      drinking water exposure group and 32.1 mg/kg for the high-soil
      exposure group. Toenail arsenic concentrations were more strongly
      correlated with both drinking water and soil arsenic concentrations;
      however, there is a strong likelihood of significant external
      contamination. Measures of residential exposure were better
      predictors of hair and toenail arsenic concentrations than were local
      environmental concentrations.

      [ http://ehpnet1.niehs.nih.gov/docs/2003/5455/abstract.html ]

      Prevalence of non-insulin-dependent diabetes mellitus and related
      vascular diseases in southwestern arseniasis- endemic and nonendemic
      areas in Taiwan. Shu-Li Wang, Jeng-Min Chiou, Chien-Jen Chen,
      Chin-Hsiao Tseng, Wei-Ling Chou, Cheng-Chung Wang, Trong- Neng Wu,
      and Louis W. Chang. Environmental Health Perspectives 111(2)
      155-159, February 2003.

      Abstract: There is evidence indicating that ingestion of arsenic may
      predispose the development of diabetes mellitus in arsenic-endemic
      areas in Taiwan. However, the prevalence of diabetes and related
      vascular diseases in the entire southwestern arseniasis-endemic and
      nonendemic areas remains to be elucidated. We used the National
      Health Insurance Database for 1999-2000 to derive the prevalence of
      non-insulin- dependent diabetes and related vascular diseases by age
      and sex among residents in southwestern arseniasis-endemic and
      nonendemic areas in Taiwan. The study included 66,667 residents
      living in endemic areas and 639,667 in nonendemic areas, all 25 years
      of age. The status of diabetes and vascular diseases was ascertained
      through disease diagnosis and treatment prescription included in the
      reimbursement claims of clinics and hospitals. The prevalence of
      non-insulin-dependent diabetes, age- and gender-adjusted to the
      general population in Taiwan, was 7.5% (95% confidence interval,
      7.4-7.7%) in the arseniasis- endemic areas and 3.5% (3.5-3.6%) in the
      nonendemic areas. Among both diabetics and nondiabetics, higher
      prevalence of microvascular and macrovascular diseases was observed
      in arseniasis-endemic than in the nonendemic areas. Age- and
      gender-adjusted prevalence of microvascular disease in endemic and
      nonendemic areas was 20.0% and 6.0%, respectively, for diabetics, and
      8.6% and 1.0%, respectively, for nondiabetics. The corresponding
      prevalence of macrovascular disease was 25.3% and 13.7% for
      diabetics, and 12.3% and 5.5% for nondiabetics. Arsenic has been
      suggested to increase the risk of non- insulin-dependent diabetes
      mellitus and its related micro- and macrovascular diseases.

      [Abstract at http://ehpnet1.niehs.nih.gov/docs/200
      3/5457/abstract.html ]


      Note: The entire 7 July 2002 issue of Toxicology Letters (Vol. 133
      No. 1) is devoted to arsenic-related topics. Some (but not all) of
      the articles from this issue appear below. The Table of Contents for
      this issue is available at


      Arsenic contamination of groundwater in West Bengal (India): build-up
      in soil-crop systems. S. K. Sanyal and S. K. T. Nasar. Paper
      presented to the International Conference on Water Related Disasters
      held in Kolkata on 5-6 December 2002.

      Abstract: A large part of the Bengal delta basin bound by the rivers
      Bhagirathi and Padma is affected by arsenic contamination of
      groundwater of geogenic origin. The exact sequence of geochemical
      reactions releasing arsenic from the aquifer sediments is still
      debated. Only less than 10% of the total groundwater accounts for
      drinking purpose while more than 90% is used for crop-irrigational
      requirements. The present communication deals with the source of
      arsenic contamination in groundwater, accumulation of the toxin in
      soils and crops in the affected belt of West Bengal irrigated with
      contaminated groundwater, and in animal tissues and products, and
      demonstrates the pathways, other than drinking water, through which
      arsenic may have access to human, animal and crop systems. The
      retention of arsenic by the soil organic fraction in the affected
      sites has been demonstrated, so also the release potential of As from
      the resulting organo-As complexes by the competing oxyanions such as
      phosphate and nitrate. The application of FYM [sic] and phosphate was
      found to have opposing effect on release of native and applied
      arsenic in the contaminated soils, with FYM reducing such release,
      thereby tending to moderate the toxic effect of arsenic in soil-plant
      system. This agreed well with the findings of a rice pot-culture
      experiment. Different crop plants raised in a crop cafeteria
      experiment exhibited varying tendencies to accumulate arsenic in
      different plant parts in the following sequence: r
      oot>stem>leaf>economic produce. The inclusion of pulses/other
      legumes/green manure crops in cropping sequences, coupled with
      organic manuring, was found to moderate arsenic build-up in soil and
      plant parts. Among the microorganisms, two genera of blue-green
      algae (Anabaena sp. and Nostoc sp.), and four different types of
      bacteria showed promise of As-decontamination ability. However,
      arsenic concentration bio-magnified as one passed from the
      groundwater to crop plants via soil.

      [Paper can be downloaded from http://groups.yahoo
      2002-As-GW-W-Bengal-soil-crop.doc . The referring page is
      http://groups.yahoo.com/group/arsenic-crisis/files/ . ]

      Arsenic removal from water using advanced oxidation processes. Zaw,
      Myint, and Maree T. Emett. Toxicology Letters, 133(1), 7 July 2002,

      Abstract: Consumption of groundwaters containing natural arsenic at
      several hundred g/l (ppb) in countries such as Bangladesh has lead to
      the increased occurrence of many cancers particularly those of the
      skin and bladder, while concerns in the USA and Australia regarding
      the unknown health impact of drinking water containing tens of ppb of
      arsenic is leading to increasingly stringent maximum contaminant
      levels. The anaerobic conditions of these groundwaters result in the
      arsenic being present in its reduced form, hence the use of an
      oxidant is necessary if the arsenic is to be successfully removed by
      precipitation or ion exchange methods. Advance oxidation methods
      which utilise ultraviolet light and a photo absorber have been
      developed and patented, in which both iron salts and sulphite can be
      used as the photoabsorber. The former absorber has been developed
      for arsenic removal in rural areas of Bangladesh and the latter for
      groundwaters in countries such as the USA.

      [Abstract at http://www.sciencedirect.com/science?
      4a68d67950fe59a1c2b0dc1f ]

      Arsenic toxicity and potential mechanisms of action. Hughes, Michael
      F. Toxicology Letters 133(1), 7 July 1-16 2002.

      Abstract: Exposure to the metalloid arsenic is a daily occurrence
      because of its environmental pervasiveness. Arsenic, which is found
      in several different chemical forms and oxidation states, causes
      acute and chronic adverse health effects, including cancer. The
      metabolism of arsenic has an important role in its toxicity. The
      metabolism involves reduction to a trivalent state and oxidative
      methylation to a pentavalent state. The trivalent arsenicals,
      including those methylated, have more potent toxic properties than
      the pentavalent arsenicals. The exact mechanism of the action of
      arsenic is not known, but several hypotheses have been proposed. At a
      biochemical level, inorganic arsenic in the pentavalent state may
      replace phosphate in several reactions. In the trivalent state,
      inorganic and organic (methylated) arsenic may react with critical
      thiols in proteins and inhibit their activity. Regarding cancer,
      potential mechanisms include genotoxicity, altered DNA methylation,
      oxidative stress, altered cell proliferation, co- carcinogenesis, and
      tumor promotion. A better understanding of the mechanism(s) of action
      of arsenic will make a more confident determination of the risks
      associated with exposure to this chemical.

      [Abstract at http://www.sciencedirect.com/science?
      42e3236082957fd069024b5 ]

      Increasing awareness of arsenic in Bangladesh: lessons from a public
      education programme. Hanchett, Suzanne, Qumrun Nahar, Astrid Van
      Agthoven, Cindy Geers and MD Ferdous Jamil Rezvi. Health Policy and
      Planning, 2002, 17(4): 393-401.

      Abstract: Experts are making a major effort to find technical
      solutions to the serious public health problems posed by arsenic in
      drinking water in Bangladesh, but public education strategies receive
      less systematic attention. This article presents the findings of a
      study evaluating the impact of a 1999 campaign by the 18 District
      Towns Project to educate the public about the arsenic problem in six
      Bangladesh towns, where half of the population was estimated to be
      using arsenic-contaminated domestic water: (1) Water users were
      advised not to consume arsenic-affected tube-well water; (2) A
      simple, temporary water treatment method was recommended for those
      using such water, if they had no safe alternative source; (3)
      Caretakers of tube-wells having arsenic-free water were advised to
      share their water sources with others. This evaluation study,
      utilizing a combination of quantitative and qualitative social
      research methods, found those influenced by the programme to have
      higher awareness levels and significantly lower levels of risk
      behaviour than others. Yet more than half of the at-risk,
      programme-influenced survey respondents were found still to be
      drinking (57%) or cooking with (54%) arsenic-affected water. Despite
      the fact that the campaign did not have a satisfactory public health
      impact, the experience can inform future efforts to educate the
      Bangladeshi public about arsenic. One finding is widespread
      confusion about trusted tube-well water being newly labelled as
      'unsafe'. Some think the problem is in the hand pumps themselves.
      Awareness of life threatening danger from arsenic contamination was
      found to be low. Learning points from this experience are: the value
      of explaining together with water testing; giving people
      opportunities to ask questions; repeating messages; continuing to
      educate children about the serious risks of consuming surface water;
      conducting community-wide education programmes for people of all
      ages; and evaluating the impact of specific public education
      strategies. Respecting such principles in public information
      campaigns will greatly help the public to benefit from future
      technical developments.

      [Abstract at http://heapol.oupjournals.org/cgi/con
      tent/abstract/17/4/393 ]

      A review of animal models for the study of arsenic carcinogenesis.
      Wang, Jian Ping, Lixia Qi, Michael R. Moore and Jack C. Ng.
      Toxicology Letters 133(1), 7 July, 17-31 2002.

      Abstract: As inorganic arsenic is a proven human carcinogen,
      significant effort has been made in recent decades in an attempt to
      understand arsenic carcinogenesis using animal models, including
      rodents (rats and mice) and larger mammals such as beagles and
      monkeys. Transgenic animals were also used to test the carcinogenic
      effect of arsenicals, but until recently all models had failed to
      mimic satisfactorily the actual mechanism of arsenic carcinogenicity.
      However, within the past decade successful animal models have been
      developed using the most common strains of mice or rats. Thus
      dimethylarsinic acid (DMA), an organic arsenic compound which is the
      major metabolite of inorganic arsenicals in mammals, has been proven
      to be tumorigenic in such animals. Reports of successful cancer
      induction in animals by inorganic arsenic (arsenite and arsenate)
      have been rare, and most carcinogenetic studies have used organic
      arsenicals such as DMA combined with other tumor initiators.
      Although such experiments used high concentrations of arsenicals for
      the promotion of tumors, animal models using doses of arsenicals
      species closed to the exposure level of humans in endemic areas are
      obviously the most significant. Almost all researchers have used
      drinking water or food as the pathway for the development of animal
      model test systems in order to mimic chronic arsenic poisoning in
      humans; such pathways seem more likely to achieve desirable results.

      [Abstract at http://www.sciencedirect.com/science?
      726f089134d21fb30e3f797 ]


      Induction of oxyradicals by arsenic: implication for mechanism of
      genotoxicity. Su X. Liu, Mohammad Athar, Istvan Lippai, Charles
      Waldren, and Tom K. Hei. Proc. Natl. Acad. Sci. USA, Vol. 98, Issue
      4, 1643-1648, February 13, 2001

      Abstract: Although arsenic is a well-established human carcinogen,
      the mechanisms by which it induces cancer remain poorly understood.
      We previously showed arsenite to be a potent mutagen in human-hamster
      hybrid (AL) cells, and that it induces predominantly multilocus
      deletions. We show here by confocal scanning microscopy with the
      fluorescent probe 5',6'-chloromethyl-2',7'- dichlo
      rodihydrofluorescein diacetate that arsenite induces, within 5 min
      after treatment, a dose-dependent increase of up to 3-fold in
      intracellular oxyradical production. Concurrent treatment of cells
      with arsenite and the radical scavenger DMSO reduced the fluorescent
      intensity to control levels. ESR spectroscopy with
      4-hydroxy-2,2,6,6-tetramethyl-1-hydroxypiperidine (TEMPOL-H) as a
      probe in conjunction with superoxide dismutase and catalase to quench
      superoxide anions and hydrogen peroxide, respectively, indicates that
      arsenite increases the levels of superoxide-driven hydroxyl radicals
      in these cells. Furthermore, reducing the intracellular levels of
      nonprotein sulfhydryls (mainly glutathione) in AL cells with
      buthionine S-R-sulfoximine increases the mutagenic potential of
      arsenite by more than 5-fold. The data are consistent with our
      previous results with the radical scavenger DMSO, which reduced the
      mutagenicity of arsenic in these cells, and provide convincing
      evidence that reactive oxygen species, particularly hydroxyl
      radicals, play an important causal role in the genotoxicity of
      arsenical compounds in mammalian cells.

      [Full text at http://www.pnas.org/cgi/content/full/98/4/1643%5d

      NB see also the 'Columbia News' science journalism article about this
      paper immediately below.

      Free Radicals Mediate Arsenic's Harmful Effects - Columbia News 15
      Feb 2001

      Arsenic, a cancer-causing metal that poisons millions of people
      worldwide, exerts its harmful effects by boosting the body's
      production of damaging chemicals called free radicals, Columbia
      researchers report.

      The new research, published in the Feb. 13 issue of "Proceedings of
      the National Academy of Sciences," adds to growing evidence that
      nutrients called antioxidants, which eliminate free radicals, may
      help prevent cancer and other illnesses caused by such environmental
      toxins as arsenic, cadmium, and asbestos. Sources of antioxidants
      include vitamins and micronutrients commonly found in the human diet,
      such as vitamin C, vitamin E and selenium.

      "Arsenic is among the top environmental contaminants on the EPA
      Superfund list," says Tom K. Hei, the lead author of the study.
      "This piece of research provides the first clear-cut evidence that an
      environmental carcinogen acts predominantly through a free-radical
      pathway." Hei is professor of radiation oncology and public health
      at the Center for Radiological Research at Columbia's College of
      Physicians and Surgeons.

      "If we understand how arsenic causes cancer, we'll have better means
      of prevention." Antioxidants are a leading candidate for such
      preventive measures, he said.

      The study, which also involved P&S dermatology researchers and
      researchers at Albert Einstein College of Medicine and Colorado State
      University, showed that cells cultured in the laboratory sharply
      increased their free radical production within five minutes of being
      exposed to an arsenic compound. The compound, sodium arsenite -- the
      main toxic form of arsenic in the environment -- also boosted the
      rate of mutations among the cells. Mutations are a key step in
      cancer development. The mutation rate shot up still higher when
      researchers added a chemical that reduced the cells' production of
      natural antioxidants. This was consistent with previous research
      suggesting that antioxidants can protect cells from arsenic-induced
      genetic damage.

      Close to a million U.S. residents are exposed to unsafe levels of
      arsenic, especially in the Southwest, says Hei. And the problem is
      substantially worse in some other countries. One study showed
      arsenic contaminates 27 percent of drinking wells in certain parts of
      Bangladesh and India, at levels more than 10 to 20 times higher than
      the maximum level the EPA has deemed safe.

      Arsenic, a natural component of the Earth's crust, can enter the body
      primarily in two ways. One is through ingestion, such as through
      contaminated water, food, or drugs. Another is by inhalation,
      usually resulting from workplace exposure in industries such as ore
      smelting, semiconductor and glass manufacturing, and the burning of
      arsenic-tainted coal. Diseases associated with chronic arsenic
      exposure include lung, skin, bladder, and liver cancers, diabetes,
      atherosclerosis, kidney failure, liver and nervous system damage, and
      keratosis, a skin disease.

      "In addition to the gene and chromosomal mutations that we have
      illustrated in this study, the oxidative damage is likely to
      contribute to other arsenic-associated human diseases as well. This
      includes cardiovascular and renal abnormalities," says Hei.

      How arsenic induces human cancer has been somewhat of a mystery for
      two reasons. First, arsenic is an oddball among human carcinogens in
      that it has not been shown to cause cancer in laboratory animals.
      Second, laboratory research on the mutagenic effect of arsenic in
      mammalian cells has turned up nothing. This has puzzled scientists
      because epidemiological studies have established that arsenic is a
      human carcinogen, and mutations are generally a crucial first step in
      the development of cancer.

      Hei and colleagues believe rodents such as those used for research
      have cellular mechanisms that protect them from arsenic damage. They
      also speculate that the types of mutations induced by arsenic are
      large chromosomal losses that are hard to detect with conventional
      mutation assays. When arsenic deletes the monitored gene, it also
      might delete crucial genes nearby, thus killing the cells.

      To circumvent these problems, Hei and colleagues used a line of
      hybrid human-animal cells. These are hamster ovary cells containing
      a copy of human chromosome No. 11 in addition to their own
      chromosomes. Since these cells can live despite damage to the human
      chromosome, the number of mutants can be measured by the absence or
      presence of surface antigens that are coded by the human chromosome.

      Using these and other techniques, Hei and colleagues developed data
      suggesting arsenic acts through a series of chemical reactions in the
      cell that produce free radicals. Free radicals form naturally in the
      body during oxygen metabolism, but their levels rise with the
      presence of some toxins. They are harmful because they tend to
      interact strongly with nearby molecules, changing the structure of
      cellular components such as DNA.

      Using a spin trapping assay, Hei's team showed that arsenic acts by
      first spurring production of superoxide, a very unstable free radical
      species that is rapidly being converted into hydrogen peroxide by
      enzymes in the cells. The hydrogen peroxides are in turn converted
      into hydroxyl radicals, extremely reactive and damaging free radicals
      that attack cell membranes and DNA to create mutations.

      "As such, antioxidants could be an interventional approach in
      patients who have been subjected to chronic arsenic exposure," says
      Hei. He plans to extend the study to determine the source of these
      radical species, in particular the role of mitochondria in mediating
      the genotoxic effects of arsenic.

      [ http://www.columbia.edu/cu/news/01/02/arsenic.html ]

      Prevention of endemic arsenism with selenium. Wang Wuyi, Yang
      Linsheng, Hou Shaofan, Tan Jian'an and Li Hairong. Current Science,
      Vol. 81, No. 9, 10 November 2001 1215-1218.

      Abstract: Arsenism is a disease with severe damage to human health
      resulting from long-term exposure to high arsenic levels in the
      environment. Selenium was used to prevent the accumulation of
      arsenic in the human body and rectify the damages in the experiment.
      After the administration of 100-200 mg Se/day for 14 months, 75.0 and
      55.0% of the patients served as patients for selenium-therapy group
      in clinical examination and symptom, and 25.6% and 24.4% as control
      group. In the Se-therapy group, liver function, hepatic
      ultrasonotomography, electrocardiogram and electron microscope
      observation of erythrocyte reversed significantly than the control as
      80%, 60%, 72.22%, 84.78% versus 46.15%, 30.7%, 0%, 44.83%,
      respectively. Arsenic concentration in blood, urine and hair of the
      Se-group decreased much more than that of the control group.

      [http://tejas.serc.iisc.ernet.in/~currsci/nov102001/1215.pdf ]


      A longitudinal investigation of solid-food based dietary exposure to
      selected elements. Scanlon KA, MacIntosh DL, Hammerstrom KA, Ryan
      PB. J Expo Anal Environ Epidemiol Sep-Oct 1999; 9(5):485-93.

      Abstract: As part of a longitudinal investigation of environmental
      exposures to selected chemical contaminants, the National Human
      Exposure Assessment Survey (NHEXAS), food consumption and duplicate
      diet samples were obtained in each of six sampling cycles from up to
      80 individuals in Maryland during 1995-1996. Duplicate diet samples
      were weighed and analyzed for arsenic, cadmium, chromium and lead and
      were used to derive average daily intakes of each element. Mean
      log-transformed concentrations of arsenic and cadmium in duplicate
      diet samples and derived intakes of chromium were found to vary
      significantly among sampling cycles. Repeated observations of
      dietary exposure metrics from the same individual over time were
      highly variable. The results suggest that distributions of dietary
      exposure to arsenic and cadmium do vary for a population within a
      1-year period, while those for chromium and lead do not. This may
      result in single measurements of exposure being sufficient to
      characterize population variability for these latter two elements.
      However, even for those elements not displaying statistically
      significant temporal variability for the population, a single dietary
      exposure measurement may still not be sufficient to characterize
      accurately chronic dietary exposure levels for individuals.

      [Abstract http://www.ncbi.nlm.nih.gov:80/entrez/qu
      ery.fcgi?cmd=Retrieve&db=PubMed&list_uids=10554150&dopt=Abstract ]

      Dimercaptosuccinic acid (DMSA), a non-toxic, water-soluble treatment
      for heavy metal toxicity. AL Miller. Altern Med Rev 1998

      Abstract: Heavy metals are, unfortunately, present in the air,
      water, and food supply. Cases of severe acute lead, mercury,
      arsenic, and cadmium poisoning are rare; however, when they do occur
      an effective, non-toxic treatment is essential. In addition,
      chronic, low- level exposure to lead in the soil and in residues of
      lead-based paint, to mercury in the atmosphere, in dental amalgams
      and in seafood, and to cadmium and arsenic in the environment and in
      cigarette smoke is much more common than acute exposure. Meso-
      2,3-dimercaptosuccinic acid (DMSA) is a sulfhydryl-containing,
      water-soluble, non-toxic, orally-administered metal chelator which
      has been in use as an antidote to heavy metal toxicity since the
      1950s. More recent clinical use and research substantiates this
      compound s efficacy and safety, and establishes it as the premier
      metal chelation compound, based on oral dosing, urinary excretion,
      and its safety characteristics compared to other chelating

      [Abstract http://www.ncbi.nlm.nih.gov:80/entrez/qu
      ery.fcgi?cmd=Retrieve&db=PubMed&list_uids=9630737&dopt=Abstract ]


      Dietary exposures to selected metals and pesticides. David L.
      MacIntosh, John D. Spengler, Halûk Özkaynak, Ling-hui Tsai, and
      P. Barry Ryan. Environmental Health Perspectives 104:202-209 (1996).

      Abstract: Average daily dietary exposures to 11 contaminants were
      estimated for approximately 120,000 U.S. adults by combining data on
      annual diet, as measured by a food frequency questionnaire, with
      contaminant residue data for table-ready foods that were collected as
      part of the annual U.S. Food and Drug Administration Total Diet
      Study. The contaminants included in the analysis were four heavy
      metals (arsenic, cadmium, lead, mercury), three organophosphate
      pesticides (chlorpyrifos, diazinon, malathion), and four
      organochlorine pesticides (dieldrin, p,p´-DDE, lindane, heptachlor
      epoxide). Dietary exposures to these contaminants were highly
      variable among individuals, spanning two to three orders of
      magnitude. Intraindividual exposures to the metals,
      organophosphates, and organochlorines were estimated to be strongly
      correlated; Pearson's correlation coefficients ranged from 0.28 for
      lindane:dieldrin to 0.84 for lead:mercury. For some of the compounds
      (e.g., arsenic and dieldrin), a substantial fraction of the
      population was estimated to have dietary intakes in excess of
      health-based standards established by the EPA. Before use for risk
      assessment or epidemiologic purposes, however, the validity of the
      exposure estimates must be evaluated by comparison with biological
      indicators of chronic exposure. Because of their low detection rate
      in table-ready foods, the estimated distributions of exposures for
      dieldrin, p,p´-DDE, heptachlor epoxide, lindane, diazinon, and
      chlorpyrifos were found to be sensitive to assumed values for
      nondetect samples. Reliable estimates of the population distribution
      of dietary exposures to most other contaminants cannot be made
      currently, due to their low rate of detection in table-ready foods.
      Monitoring programs that use more sensitive study designs and
      population-based assessments for other subpopulations should be a
      priority for future research.

      [Abstract at http://ehpnet1.niehs.nih.gov/docs/199
      6/104-2/macintoshabs.html ]


      Multiple risk factors associated with arsenic-induced skin cancer:
      effects of chronic liver disease and malnutritional status. Hsueh
      YM, Cheng GS, Wu MM, Yu HS, Kuo TL, Chen CJ. Br J Cancer 1995

      Abstract: In order to evaluate the prevalence and multiple risk
      factors of arsenic-induced skin cancer among residents in Taiwanese
      villages in which chronic arseniasis is hyperendemic, a total of 1571
      subjects aged 30 or more years were recruited between September 1988
      and March 1989. All of them were interviewed personally by a public
      health nurse using a structured questionnaire, and 1081 interviewed
      study subjects, including 468 men and 613 women, participated in
      physical examination, giving a participation rate of 68.8%. The
      overall prevalence of skin cancer was as high as 6.1%, showing an
      increase with age in both men and women. There was a significant
      dose-response relation between skin cancer prevalence and chronic
      arsenic exposure as indexed by duration of residence in the endemic
      area, duration of consumption of high-arsenic artesian well water,
      average arsenic exposure in parts per million (p.p.m.) and cumulative
      arsenic exposure in p.p.m.-years. Chronic carriers of hepatitis B
      surface antigen with liver dysfunction had an increased prevalence of
      skin cancer. Undernourishment, indexed by a high consumption of
      dried sweet potato as a staple food, was also significantly
      associated with an increased prevalence of arsenic-induced skin
      cancer. All these risk factors remained statistically significant in
      the multiple logistic regression analysis. Consistent with animal
      experiments, the findings imply that liver function and nutritional
      status may affect the metabolism of inorganic arsenic and the
      development of subsequent skin cancers.

      [Abstract at http://www.ncbi.nlm.nih.gov:80/entrez
      /query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7819025&dopt=Abstract ]


      Estimating human exposure through multiple pathways from air, water,
      and soil. McKone TE, Daniels JI. Regul Toxicol Pharmacol 1991

      Abstract: This paper describes a set of multipathway, multimedia
      models for estimating potential human exposure to environmental
      contaminants. The models link concentrations of an environmental
      contaminant in air, water, and soil to human exposure through
      inhalation, ingestion, and dermal-contact routes. The relationship
      between concentration of a contaminant in an environmental medium and
      human exposure is determined with pathway exposure factors (PEFs). A
      PEF is an algebraic expression that incorporates information on human
      physiology and lifestyle together with models of environmental
      partitioning and translates a concentration (i.e., mg/m3 in air,
      mg/liter in water, or mg/kg in soil) into a lifetime-equivalent
      chronic daily intake (CDI) in mg/kg-day. Human, animal, and
      environmental data used in calculating PEFs are presented and
      discussed. Generalized PEFs are derived for air----inhalation,
      air----ingestion, water----inhalation, water----ingestion,
      water----dermal uptake, soil----inhalation, soil----ingestion, and
      soil----dermal uptake pathways. To illustrate the application of the
      PEF expressions, we apply them to soil-based contamination of
      multiple environmental media by arsenic, tetrachloroethylene (PCE),
      and trinitrotoluene (TNT).

      [Abstract at http://www.ncbi.nlm.nih.gov:80/entrez
      /query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2024045&dopt=Abstract ]


      USGS Arsenic Study Group Searchable Bibliography

      This bibliography contained 2000 references as of August 2001 (about
      2% of all arsenic references they say), and more will be added over
      time. See http://arsenic.cr.usgs.gov/

      U.S. Agency for Toxic Substances and Disease Registry (ATSDR)
      Case Studies in Environmental Medicine: Arsenic Toxicity (Oct 2000)

      "The goal of the CSEM is to increase the primary care provider's
      knowledge of hazardous substances in the environment and to aid in
      the evaluation of potentially exposed patients.

      "After completion of this educational activity, the reader should be
      able to discuss the major exposure route for arsenic, describe two
      potential environmental and occupational sources of arsenic exposure,
      give two reasons why arsenic is a health hazard, describe three
      factors contributing to arsenic toxicity, identify evaluation and
      treatment protocols for persons exposed to arsenic, and list two
      sources of information on arsenic.

      "Continuing education credit is available free of charge!"

      See http://www.atsdr.cdc.gov/HEC/CSEM/arsenic/index.html

      Environmental Health Criteria 18: Arsenic.

      The full text of this 1981 book from the WHO EHC series
      (International Programme on Chemical Safety, a joint effort of
      WHO/ILO/UNEP) is now available online, at:


      Environmental Health Criteria 224: Arsenic And Arsenic Compounds

      This 2001 publication in the WHO EHC series (IPCS) is also available


      The webpage doesn't exactly make clear what the relationship is
      between EHC 224 and EHC 18. It doesn't explicitly say that 224
      supercedes 18, anyway.

      Arsenic Keratosis

      Article at emedicine.com covering clinical diagnosis, workup,
      treatment, etc of arsenic keratosis. At



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