=====================================================================
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
spaces.

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.

=====================================================================
FROM THE EDITOR

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
Editor


=====================================================================
HIGHLIGHTS OF THIS ISSUE

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
   investigation."

- 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.


=====================================================================
UPCOMING MEETINGS & CONFERENCES AND UPDATED CONFERENCE WEBPAGES &
SITES

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.

Sincerely,
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
http://attila.stevens-tech.edu/~xmeng


-----------------------------------------------------------------
Conference papers now online

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

Final abstracts available online at

http://wwwbrr.cr.usgs.gov/Arsenic/finalabstracts.htm


=====================================================================
SELECTED RECENT MEDIA ARTICLES ONLINE

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
public.

[ 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
formed.

Web address: Arsenic Contamination in Nepal,
http://www.msnepal.org/reports_pubs/arsenic/index.htm

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


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


=====================================================================
NEW & NEWLY DISCOVERED SCIENTIFIC/TECHNICAL PUBLICATIONS ON & OFF LINE

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

-----------------------------------------------------------------
2003
-----------------------------------------------------------------

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 ]


-----------------------------------------------------------------
2002
-----------------------------------------------------------------

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

http://www.sciencedirect.com/science?_ob=IssueURL&
_tockey=%23TOC%235177%232002%23998669998%23321457%
23FLA%23display%23Volume_133,_Issue_1,_Pages_1-118
_(7_July_2002)%23tagged%23Volume%23first%3D133%23I
ssue%23first%3D1%23Pages%23first%3D1%23last%3D118%
23date%23(7_July_2002)%23&_auth=y&_acct=C000050221
&_version=1&_urlVersion=0&_userid=10&md5=b291c7fad
fd9bf2b04ba13fd291d510e


-----------------------------------------------------------------
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.
com/group/arsenic-crisis/files/India-Sanyal-Nasar-
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,
113-118.

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?
_ob=ArticleURL&_udi=B6TCR-45NY3NM-3&_user=10&_cove
rDate=07%2F07%2F2002&_rdoc=11&_fmt=summary&_orig=b
rowse&_srch=%23toc%235177%232002%23998669998%23321
457!&_cdi=5177&_sort=d&_docanchor=&_acct=C00005022
1&_version=1&_urlVersion=0&_userid=10&md5=4427e42d
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?
_ob=ArticleURL&_udi=B6TCR-45TTSGH-2&_user=10&_cove
rDate=07%2F07%2F2002&_rdoc=1&_fmt=summary&_orig=br
owse&_srch=%23toc%235177%232002%23998669998%233214
57!&_cdi=5177&_sort=d&_docanchor=&_acct=C000050221
&_version=1&_urlVersion=0&_userid=10&md5=b1117797b
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?
_ob=ArticleURL&_udi=B6TCR-45TTSGH-3&_user=10&_cove
rDate=07%2F07%2F2002&_rdoc=2&_fmt=summary&_orig=br
owse&_srch=%23toc%235177%232002%23998669998%233214
57!&_cdi=5177&_sort=d&_docanchor=&_acct=C000050221
&_version=1&_urlVersion=0&_userid=10&md5=ebc65d46c
726f089134d21fb30e3f797 ]


-----------------------------------------------------------------
2001
-----------------------------------------------------------------

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]

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 ]


-----------------------------------------------------------------
1999
-----------------------------------------------------------------

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 ]

-----------------------------------------------------------------
1998
-----------------------------------------------------------------
Dimercaptosuccinic acid (DMSA), a non-toxic, water-soluble treatment
for heavy metal toxicity.  AL Miller.  Altern Med Rev 1998
Jun;3(3):199-207

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
substances.

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


-----------------------------------------------------------------
1996
-----------------------------------------------------------------

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 ]

-----------------------------------------------------------------
1995
-----------------------------------------------------------------

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
Jan;71(1):109-14

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 ]


-----------------------------------------------------------------
1991
-----------------------------------------------------------------

Estimating human exposure through multiple pathways from air, water,
and soil. McKone TE, Daniels JI. Regul Toxicol Pharmacol 1991
Feb;13(1):36-61

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 ]


=====================================================================
NEW & NEWLY DISCOVERED WEB SITES & WEB PAGES
UPDATED WEBSITES & WEB PAGES

-----------------------------------------------------------------
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:

http://www.inchem.org/documents/ehc/ehc/ehc018.htm


-----------------------------------------------------------------
Environmental Health Criteria 224:  Arsenic And Arsenic Compounds

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

http://www.inchem.org/documents/ehc/ehc/ehc224.htm

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

http://www.emedicine.com/derm/topic36.htm


=====================================================================
NEW & NEWLY DISCOVERED REAL WORLD STUFF

Offline-only print publications & newsletters, videos, research in
progress, test kits, removal technologies, etc.

-----------------------------------------------------------------
[none this issue]


=====================================================================
PUBLICATION & OTHER DETAILS

+ ACN is published by Sara Bennett from Dhaka.  Publication schedule:
irregular.

+ ACN items may be freely reprinted with this attribution:
   "Source:  ACN Arsenic Crisis News - web http://bicn.com/acic
   - email acic @ bicn.com"

+ ACIC/ACN encourages all arsenic crisis stakeholders to submit
   information by email to acic @ bicn.com

+ Other arsenic information services:

   Discussion group at egroups.com -
       arsenic-crisis - combines former groups arsenic-source,
           arsenic-safewater, and arsenic-medical

   Website -
       http://www.bicn.com/acic

       Includes links to conferences, major media coverage,
          research results, individual researchers, projects,
          organizations, etc. with site search capability.

+ SUPPORT ACIC/ACN at no extra cost or effort to you

   Commissions from your purchases automatically go to ACIC when you -

   Buy from amazon.com or amazon.ca through these links:

     http://www.amazon.com/exec/obidos/subst/home/h
ome.html/104-2598657-7351167
     http://www.amazon.ca/exec/obidos/tg/browse/-/9
15398/702-0164432-5297635

   Buy from Barnes & Noble online through this link (copy & paste both
   parts of the URL into the address pane of your browser):

     http://service.bfast.com/bfast/click?bfmid=218
1&sourceid=32390&categoryid=rn_home

   Sign up for website hosting that is high quality, affordable, with
   excellent, friendly customer support, with the company that hosts
   ACIC, WSO.net:

     http://www.wso.net/referral.mv?wso00834

+ ACN email newsletter subscribers:  1127 (-94 since the last issue).

+ Visitors to ACIC website since inception (Apr 98): 142,428
   (+2598 since the last issue).

=====================================================================