 References,
1999 & All Prior Years
Jump to references published in:
1999
Arsenic concentrations in well water and risk of bladder and kidney
cancer in Finland. Kurttio, Pivi, Eero Pukkala, Hanna Kahelin,
Anssi Auvinen, and Juha Pekkanen. Environmental Health Perspectives
Volume 107, Number 9, September 1999. [Abstract
available online.]
Arsenic field measurement - A field-deployable instrument for the
measurement and speciation of arsenic in potable water. Huilang Huang
and Purnendu K. Dasgupta. Analytica Chimica Acta 380 (1999) 27-37.
Arsenic groundwater contamination and sufferings of people in
Rajnandgaon district, Madhya Pradesh, India. D.Chakraborti, B.K.Biswas,
T.Roy Chowdhury, G.K. Basu, B.K. Mandal, U. K. Chowdhury, S.C. Mukherjee, J.P.
Gupta, S.R. Chowdhury, K.C. Rathore. Current Science, 77(4), 502-504.
Arsenic in drinking water. Washington, National Research Council.
Arsenic in Drinking Water. Commission on Life Sciences. National
Academy Press. [Whole
book online] (I haven't figured out yet if this and the previous reference
are to the same book ... could be.)
Arsenic in drinking water-problems and solutions. T.
Viraraghavan, K. S. Subramanian and J. A. Aruldoss. Wat. Sci. Technol. 40(2),
69-76. Abstract: "The current United States maximum
contaminant level for arsenic in drinking water is set at 50 µg/L. Because of
the cancer risks involved, Canada has already lowered the maximum contaminant
level to 25 µg/L; the United States Environmental Protection Agency is reviewing
the current allowable level for arsenic with a view of lowering it
significantly. Various treatment methods have been adopted to remove arsenic
from drinking water. These methods include 1) adsorption-coprecipitation using
iron and aluminum salts, 2) adsorption on activated alumina, activated carbon,
and activated bauxite, 3) reverse osmosis, 4) ion exchange and 5) oxidation
followed by filtration. Because of the promise of oxidation-filtration systems,
column studies were conducted at the University of Regina to examine oxidation
with KMnO4 followed by filtration using manganese greensand and iron-oxide
coated sand to examine the removal of arsenic from drinking water; these results
were compared with the data from ion exchange studies. These studies
demonstrated that As (III) could be reduced from 200 µg/L to below 25 µg/L by
the manganese greensand system. In the case of manganese greensand filtration,
addition of iron in the ratio of 20:1 was found necessary to achieve this
removal." [Abstract,
full text with password.]
Arsenic in soils of eastern Bangladesh. Stuart Rojstaczer and
Mohammed Riajul Islam,1999. Submitted to Environmental Sciences &
Technology.
Arsenic induced keratosis and squamous cell carcinoma. Rahman
M. 18th Annual Convention Indian Association for Cancer Research,
organized by All-India of Institute of Medical Science, New Delhi, 19-21th
February 1999 (proceedings). Abstract.
Arsenic levels and prevalence of skin lesions. Rahman
M. XI Meeting of International Epidemiological Conference, Florence
29 August - 4 September 1999 (proceedings). Abstract.
Arsenic poisoning in
the Ganges delta [brief communication]. Acharyya, S. K., P. Chakraborty, et
al. [Or: Chowdhury, T. R., G. K. Basu, et al.?]
Nature 401: 545.
Arsenic poisoning in the Ganges delta
[Reply]. McArthur, J. M. Nature 401: 546.
Arsenic treatment
considerations. Chen, H.-W., M. M. Frey, et al. Journal AWWA 91(3): 74-85.
Arsenicosis and deteriorating groundwater quality: Unfolding crisis in
central-east Indian region [Rajnandgaon district, Madhya Pradesh].
Piyush Kant Pandey, Ram Narayan Khare, Ramesh Sharma, Santosh Kumar Sar,
Madhurima Pandey, and Pramod Binayake. Current Science, Bangalore 77(5), 10 Sep
99, pp. 686-692.
Arsenicosis in a village in Bangladesh. Sk. Akhtar Ahmad, M.H.
Salim Ullah Sayed, Sk. Abdul Hadi, M.H. Faruquee, Manzurul Haque Khan, Md. Abdul
Jalil, Rukshana Ahmed, A. Wadud Khan. International Journal of Environmental
Health Research 9(3) September 1, 1999, 187-195. Abstract:
The study was carried out in a village in Jessore district, Bangladesh, to
identify the epidemiological characteristics of arsenicosis. Eighty-seven per
cent of the tubewells had arsenic concentration more than the WHO maximum
permissible limit of 0.05 mg l-1. The mean arsenic concentration was 0.240 mg
l-1 and the maximum concentration was 1.371 mg l-1. Of the total 3606 villagers,
10% (363) were found to be suffering from arsenicosis. Most of the arsenicosis
patients were between 10 to 39 years of age. There were more male patients
(52.6%). There were no patients among villagers who consumed tubewell water
having arsenic levels less than 0.082 mg l-1. The majority (93.4%) of the
patients were in the first and second stage of arsenicosis. With increasing
exposure to arsenic, a simultaneous increase in the severity of clinical
manifestations of arsenicosis was observed (F = 43.699; p = 0.000). The
time-weighted arsenic exposure varied from 0.248 to 5.482 mg day-1 and the mean
was 1.918 mg day-1. Melanosis was present in almost all the patients (99.5%) and
keratosis was present in 68.9%. Cancer (basal cell epithelioma) was present in
three (0.8%) patients. The duration of clinical manifestations of arsenicosis
varied from 1 to 12 years and the majority were suffering for 4-6 years. [At
Taylor & Francis.]
Arsenite methylation by methylvitamin B12 and glutathione does not
require an enzyme. Zakharyan RA, Aposhian HV. Toxicol Appl Pharmacol
1999 Feb 1;154(3):287-91. [Abstract]
Dietary exposure to inorganic arsenic. Schoof, R.A., J. Eickhoff, L.J. Yost, E.A. Crecelius, D.W. Cragin, D.M.
Meacher, D.B. Menzel. pp. 81-88. In: Proc. Third International Conference on Arsenic Exposure and
Health Effects. W.R. Chappell, C.O. Abernathy, and R.L. Calderon (eds). Elsevier Science Ltd.
Diabetes mellitus and arsenic exposure-results of three epidemiological
studies. Rahman
M, M Tondel, O Axelson. International conference on arsenic pollution
of ground water in Bangladesh: causes, effects and remedies, Dhaka, Bangladesh
(proceedings). Abstract.
Drinking water arsenic in Utah: a cohort mortality study.
Denise Riedel Lewis, J. Wanless Southwick, Rita Ouellet-Hellstrom, Jerry Rench,
and Rebecca L. Calderon. Environmental Health Perspectives 107(5), May. Abstract
The association of drinking water arsenic and mortality outcome was investigated
in a cohort of residents from Millard County, Utah. Median drinking water
arsenic concentrations for selected study towns ranged from 14 to 166 ppb and
were from public and private samples collected and analyzed under the auspices
of the State of Utah Department of Environmental Quality, Division of Drinking
Water. Cohort members were assembled using historical documents of the Church of
Jesus Christ of Latter-day Saints. Standard mortality ratios (SMRs) were
calculated. Using residence history and median drinking water arsenic
concentration, a matrix for cumulative arsenic exposure was created. Without
regard to specific exposure levels, statistically significant findings include
increased mortality from hypertensive heart disease [SMR = 2.20; 95% confidence
interval (CI), 1.36-3.36], nephritis and nephrosis (SMR = 1.72; CI, 1.13-2.50),
and prostate cancer (SMR = 1.45; CI, 1.07-1.91) among cohort males. Among cohort
females, statistically significant increased mortality was found for
hypertensive heart disease (SMR = 1.73; CI, 1.11-2.58) and for the category of
all other heart disease, which includes pulmonary heart disease, pericarditis,
and other diseases of the pericardium (SMR = 1.43; CI, 1.11-1.80). SMR analysis
by low, medium, and high arsenic exposure groups hinted at a dose relationship
for prostate cancer. Although the SMRs by exposure category were elevated for
hypertensive heart disease for both males and females, the increases were not
sequential from low to high groups. Because the relationship between health
effects and exposure to drinking water arsenic is not well established in U.S.
populations, further evaluation of effects in low-exposure populations is
warranted. [At
EHP Online.] From author Wanless's message
entitled, "Utah
Arsenic Research (1977 - 1997)" posted to the arsenic-medical
discussion group:
"We studied death patterns in Utah communities (which probably had the
highest levels of arsenic in drinking water of any United States communities).
Levels of over 150 parts per billion were common. Some drinking water tested
over 300 parts per billion. If the risks of dying of cancer from arsenic
in tap water were as great as described in the NRDC document, we should have
seen dozens of people who died of cancer from arsenic. Out of 2,203 deaths in
these communities, no evidence of arsenic caused cancers were found."
- J.
Wanless Southwick, Ph.D. [See also follow up message at http://groups.yahoo.com/group/arsenic-medical/message/14
]
Environmental pollution and chronic arsenicosis in Bangladesh.
Hasnat AH and M Rahman.
J Occup Health 1999;41:000-000 (in press).
Extremely high concentration of arsenic and its speciation in
groundwater from Bangladesh. Salminen, R., Islam, Md. R., and
Lahermo, P. Geological Survey of Finland, Special paper 27: 103 - 106.
Flow injection hydride generation atomic absorption spectrometry for
determination of arsenic in water and biological samples from arsenic affected
districts of West Bengal, India and Bangladesh. Samanta, T. Roy
Chowdhury, B. K. Mandal, B.K. Biswas, U.K. Chowdhury, G. K. Basu, R. Chanda, D.
Lodh and D. Chakraborti. Microchemical Journal, 62, 174-191. Abstract:
The increasing concern over human exposure to arsenic in West Bengal and
Bangladesh has necessitated the development of a rapid method for determination
of trace levels of arsenic in water and biological samples. We have developed a
simple indigenous flow injection hydride generation atomic absorption
spectrometry (FI-HG-AAS) system for the determination of arsenic in parts per
billion levels in water and biological samples. The technique is fast, simple,
and highly sensitive. The accuracy and precision of the method were evaluated by
spiking known amounts of arsenic and analyzing different types of environmental
and biological standard reference materials. The organic matter in a biological
sample was destroyed by acid digestion and dry ashing technique. We analyzed
thousands of tubewell water samples from the affected districts of West Bengal
and Bangladesh. Most of the water samples contained a mixture of arsenite and
arsenate and in none of them could we detect methylated arsenic. We also
analyzed thousands of urine (inorganic arsenic and its metabolites), hair, and
nail samples and hundreds of skin-scale and blood samples of people drinking
arsenic-contaminated water and showing arsenical skin lesions. Quality control
was assessed by interlaboratory analysis of hair samples. An understanding of
arsenic toxicity and metabolism requires quantitation of individual arsenic
species. The techniques we used for the determination and speciation of arsenic
are (i) separation of arsenite and arsenate from water by sodium
diethyldithiocarbamate in chloroform followed by FI-HG-AAS; (ii) determination
of arsenite in citrate/citric buffer at pH 3 and total arsenic in water in 5 M
HCl by FI-HG-AAS. Thus, arsenate is obtained from the difference; (iii) for
analysis of inorganic arsenic and its metabolites in urine FI-HG-AAS was used
after separation of the species with a combined cation-anion exchange column.
Total arsenic in urine was also determined by FI-HG-AAS after acid
decomposition. The species arsenite and arsenate are present in groundwater in
about a 1:1 ratio and about 90% of the total arsenic in urine is present as
inorganic arsenic and its metabolites.
Genesis of high arsenic
groundwater in the Bengal Delta Plains, West Bengal and Bangladesh. Mattias
von Brömssen. M.Sc. thesis 1999, Environmental Engineering, Royal School of Technology,
Stockholm. "Water samples from wells in Chakdaha, West-Bengal, India and
Bangladesh were analysed for a number of chemical parameters... This investigation
has produced no support for the first aerobic hypothesis ... [that] when
groundwater is withdrawn, oxygen may enter the aquifer and oxidise the
primary sulphides and subsequently releases arsenic and sulphate in groundwater.]
On the contrary, it strongly forwards the second anaerobic hypothesis [that]
arsenic may be derived as a result of desorption and reductive dissolution of the surface reactive mineral phases such as hydrous ferric, aluminium
and manganese oxides (HFO, HAO and HMO) present as coatings in the aquifer
sediments." [Abstract and full text
online.]
Groundwater arsenic contamination and sufferings of people in
Bangladesh. U.K. Chowdhury, B. K. Biswas, R. K. Dhar, G. Samanta, B.K.
Mandal, T.Roy Chowdhury, D. Chakraborti, S.Kabir, S. Roy, pp. 165-182. In:
Arsenic Exposure and Health Effects, W. R. Chappell, C.O.Abernathy, R.L.
Calderon, eds. Elsevier, Amsterdam-Lausanne-New York-Oxford-Tokyo.
Groundwater arsenic contamination and sufferings of people in West
Bengal, India and Bangladesh: status report up to March 1998. B.K.
Mandal, B.K. Biswas, R.K. Dhar, T.Roy Chowdhury, G. Samanta. G.K. Basu, C.R.
Chanda, K.C. Saha, S. Kabir, S. Roy and D. Chakraborti, pp. 41-65. In: Metals
and Genetics, Bibudhendra Sarkar, ed., Kluwer Academic/Plenum Publishers,
New York.
Hydrogeological investigation
of ground water arsenic contamination in south Calcutta. Chatterjee, A. and A.
Mukherjee. Sci Total Environ
225(3): 249-62. Typical clinical symptoms of acute arsenic poisoning have been
detected in 1000 residents near a factory in P.N. Mitra Lane, Behala, South
Calcutta, located in a thickly populated area manufacturing copper acetoarsenite
(Paris-Green) an arsenical pesticide for the past 25 years. Soil around the
effluent dumping point of the factory was exceptionally contaminated, with
arsenic, copper and chromium concentrations of 20,100-35,500 mg kg-1,
33,900-51,100 mg kg-1 and 5300- 5510 mg kg-1. Arsenic and copper concentrations
in bore-hole soils collected up to a depth of 24.4 m at the effluent dumping
point, decreased with depth. Arsenous acid, arsenic acid, methylarsonic acid
(MA) and dimethylarsinic acid (DMA) were detected in bore-hole soils up to a
depth of 1.37 m, after which only inorganic arsenical compounds were present. A
positive correlation was established between arsenic and copper authenticated
the Paris-Green waste disposal site as the source of contamination. Mechanism of
ground water contamination from this disposal site had been probed by a
systematic hydrogeological survey and the arsenic content of the tube-well
waters in the surrounding areas. Hydraulic conductivity was maximum in the
central part. The site for disposal of the effluent was a ditch located in the
zone of discharge. Sparingly soluble Paris-Green cumulatively deposited in the
waste disposal site is decomposed by micro-organisms to water- soluble forms and
finally percolated to underground aquifers along with rain water through the
discharge zone. The contaminant is currently moving towards WNW with ground
water flow and the residents in the direction of encroaching contamination are
insecure due to penetration of the contaminant.
Hypertension and arsenic exposure
in Bangladesh. Rahman, M., M. Tondel, et al. Hypertension 33(1): 74-8. A prevalence comparison of
hypertension among subjects with and those without arsenic exposure through
drinking water was conducted in Bangladesh to confirm or refute an earlier
observation of a relation in this respect. Wells with and without present
arsenic contamination were identified, and we interviewed and examined 1595
subjects who were depending on drinking water from these wells for living, all
>/=30 years of age. The interview was based on a questionnaire, and arsenic
exposure was estimated from the history of well-water consumption and current
arsenic levels. Of the 1595 subjects studied, 1481 had a history of
arsenic-contaminated drinking water, whereas 114 had not. Time-weighted mean
arsenic levels (in milligrams per liter) and milligram-years per liter of
arsenic exposure were estimated for each subject. Exposure categories were
assessed as <0.5 mg/L, 0.5 to 1.0 mg/L, and >1.0 mg/L and alternatively as
<1.0 mg-y/L, 1.0 to 5.0 mg- y/L, >5.0 but </=10.0 mg-y/L, and >10.0
mg-y/L, respectively. Hypertension was defined as a systolic blood pressure of
>/=140 mm Hg in combination with a diastolic blood pressure of >/=90 mm
Hg. Corresponding to the exposure categories, and using "unexposed" as
the reference, the prevalence ratios for hypertension adjusted for age, sex, and
body mass index were 1.2, 2.2, 2.5 and 0.8, 1.5, 2.2, 3.0, in relation to
arsenic exposure in milligrams per liter and milligram- years per liter,
respectively. The indicated dose-response relationships were significant
(P<<0.001) for both series of risk estimates. These results suggest that
arsenic exposure may induce hypertension in humans.
Influence of microbes on the mobilization, toxicity and biomethylation of
arsenic in soil. Turpeinen, R., Panstar-Kallio, M., Haggblom, M., Kairesalo, T.
Science Total Environ 236: 173 - 180.E. Smith, R. Naidu and A.M. Alston. 1998. Arsenic in the soil
environment: A review. Advances in Agronomy, vol 64: 149 - 195.
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
online.]
A market basket survey of inorganic
arsenic in food. Schoof, R., L. Yost, et al. Food Chem Toxicol 37(8): 839-46.
Dietary arsenic intake
estimates based on surveys of total arsenic concentrations appear to be
dominated by intake of the relatively non-toxic, organic arsenic forms found in
seafood. Concentrations of inorganic arsenic in food have not been not well
characterized. Accurate dietary intake estimates for inorganic arsenic are
needed to support studies of arsenic's status as an essential nutrient, and to
establish background levels of exposure to inorganic arsenic. In the market
basket survey reported here, 40 commodities anticipated to provide at least 90%
of dietary inorganic arsenic intake were identified. Four samples of each
commodity were collected. Total arsenic was analysed using an NaOH digestion and
inductively coupled plasma-mass spectrometry. Separate aliquots were analysed
for arsenic species using an HCl digestion and hydride atomic absorption
spectroscopy. Consistent with earlier studies, total arsenic concentrations (all
concentrations reported as elemental arsenic per tissue wet weight) were highest
in the seafoods sampled (ranging from 160 ng/g in freshwater fish to 2360 ng/g
in saltwater fish). In contrast, average inorganic arsenic in seafood ranged
from less than 1 ng/g to 2 ng/g. The highest inorganic arsenic values were found
in raw rice (74 ng/g), followed by flour (11 ng/g), grape juice (9 ng/g) and
cooked spinach (6 ng/g). Thus, grains and produce are expected to be significant
contributors to dietary inorganic arsenic intake.
The relationship of arsenic levels in drinking water and the prevalence
rate of skin lesions in Bangladesh. Tondel M, M
Rahman, et al. Environmental Health Perspectives 1999; 107:727-729. Abstract:
To determine the relationship of arsenic-associated skin lesions and degree of
arsenic exposure, a cross-sectional study was conducted in Bangladesh, where a
large part of the population is exposed through drinking water. Four villages in
Bangladesh were identified as mainly dependent on wells contaminated with
arsenic. We interviewed and examined 1,481 subjects [Greater/equal to] 30 years
of age in these villages. A total of 430 subjects had skin lesions (keratosis,
hyperpigmentation, or hypopigmentation). Individual exposure assessment could
only be estimated by present levels and in terms of a dose index, i.e., arsenic
levels divided by individual body weight. Arsenic water concentrations ranged
from 10 to 2,040 microg/L, and the crude overall prevalence rate for skin
lesions was 29/100. After age adjustment to the world population the prevalence
rate was 30. 1/100 and 26.5/100 for males and females, respectively. There was a
significant trend for the prevalence rate both in relation to exposure levels
and to dose index (p < 0.05), regardless of sex. This study shows a higher
prevalence rate of arsenic skin lesions in males than females, with clear
dose-response relationship. The overall high prevalence rate in the studied
villages is an alarming sign of arsenic exposure and requires an urgent
remedy. [Abstract
online at MedLine.]
Possible arsenic contamination free groundwater source In Bangladesh.
D. Chakraborti, B. K. Biswas, G.K. Basu, U.K. Chowdhury, T. Roy Chowdhury, D.
Lodh, C.R. Chanda, B. K. Mandal, G. Samanta, A. K. Chakraborti, M. M. Rahman, K.
Paul, S. Roy, S. Kabir, B. Ahmed, R. Das, M. Salim, Q. Quamruzzaman. J.
Surface Sci. Technol., 15(3-4), 179-187. [Full
text available online.]
Prevention of cytotoxic effects
of arsenic by short-term dietary supplementation with selenium in mice in vivo.
Biswas, S., G. Talukder, et al. Mutation Research 441(1): 155-160. Interaction between selenium and
arsenic has been used to protect against the genotoxic effects of sodium
arsenite through dietary intervention by an equivalent amount (1/10 LD50) of
sodium selenite. The two salts were administered by gavaging to laboratory bred
Swiss albino mice sequentially and in combination. Cytogenetic endpoints,
including chromosomal aberrations (CA) and damaged cells (DC) were recorded 24 h
after exposure from chromosome spreads in bone marrow cells. Administration of
sodium selenite 1 h before sodium arsenite reduced the clastogenic effect of the
latter significantly. The protection was less when the salts were given together
and negative when arsenite was given before selenite. Histological changes were
recorded. Such reduction of arsenic toxicity through dietary intervention by
selenium is of significance in protecting against the widespread toxicity
observed in human populations exposed to arsenic through drinking water from
contaminated deep tubewells in West Bengal and Bangladesh.
Relations between exposure to arsenic,
skin lesions, and glucosuria. Rahman, M. and M. Tondel. Occupational and Environmental Medicine
56(4): 277-281. Objectives-Exposure to arsenic causes keratosis,
hyperpigmentation, and hypopigmentation and seemingly also diabetes mellitus, at
least in subjects with skin lesions. Here we evaluate the relations of arsenical
skin lesions and glucosuria as a proxy for diabetes mellitus. Methods-Through
existing measurements of arsenic in drinking water in Bangladesh, wells with and
without arsenic contamination were identified. Based on a questionnaire, 1595
subjects greater than or equal to 30 years of age were interviewed; 1481 had a
history of drinking water contaminated with arsenic whereas 114 had not. Time
weighted mean arsenic concentrations and mg- years/l of exposure to arsenic were
estimated based on the history of consumption of well water and current arsenic
concentrations. Urine samples from the study subjects were tested by means of a
glucometric strip. People with positive tests were considered to be cases of
glucosuria. Results-A total of 430 (29%) of the exposed people were found to
have skin lesions. Corresponding to drinking water with <0.5, 0.5- 1.0, and
>1.0 mg/l of arsenic, and with the 114 unexposed subjects as the reference,
the prevalence ratios for glucosuria, as adjusted for age and sex, were 0.8,
1.4, and 1.4 for those without skin lesions, and 1.1, 2.2, and 2.6 for those
with skin lesions. Taking exposure as <1.0, 1.0-5.0, >5.0-10.0 and
>10.0 mg-years/l of exposure to arsenic the prevalence ratios, similarly
adjusted, were 0.4, 0.9, 1.2, and 1.7 for those without and 0.8, 1.7, 2.1, and
2.9 for those with skin lesions. All series of risk estimates were significant
for trend, (p<0.01). Conclusions-The results suggest that skin lesions and
diabetes mellitus, as here indicated by glucosuria, are largely independent
effects of exposure to arsenic although glucosuria had some tendency to be
associated with skin lesions. Importantly, however, glucosuria (diabetes
mellitus) may occur independently of skin lesions.
The relationship of arsenic levels in drinking water and the prevalence
rate of skin lesions in Bangladesh. Tondel M.; Rahman M.; Magnuson A.;
Chowdhury I.A.; Faruquee M.H.; Ahmad Sk.A. Environmental Health Perspectives,
107(9), 727-729. "Abstract: To determine the
relationship of arsenic-associated skin lesions and degree of arsenic exposure,
a cross-sectional study was conducted in Bangladesh, where a large part of the
population is exposed through drinking water. Four villages in Bangladesh were
identified as mainly dependent on wells contaminated with arsenic. We
interviewed and examined 1481 subjects 30 years of age in these villages. A
total of 430 subjects had skin lesions (keratosis, hyperpigmentation, or
hypopigmentation). Individual exposure assessment could only be estimated by
present levels and in terms of a dose index, i.e., arsenic levels divided by
individual body weight. Arsenic water concentrations ranged from 10 to 2040 µg/L,
and the crude overall prevalence rate for skin lesions was 29/100. After age
adjustment to the world population the prevalence rate was 30.1/100 and 26.5/100
for males and females, respectively. There was a significant trend for the
prevalence rate both in relation to exposure levels and to dose index (p <
0.05), regardless of sex. This study shows a higher prevalence rate of arsenic
skin lesions in males than females, with clear dose-response relationship. The
overall high prevalence rate in the studied villages is an alarming sign of
arsenic exposure and requires an urgent remedy."
Relationship between respiratory effects and skin lesions of chronic
arsenicosis in Bangladesh. Rahman
M and AH Milton. Occup Environ Med (submitted).
Requirements for a biologically realistic cancer risk assessment for
inorganic arsenic. Harvey J Clewell, P Robinan Gentry, Hugh A Barton,
Annette M Shipp, Janice W Yager, Melvin E Andersen. nternational Journal of
Toxicology, 18(2) March 1, 1999, 131-147. Abstract: A
remarkable feature of the carcinogenicity of inorganic arsenic (Asi) is the
observation that human exposures to Asi have been strongly associated with
increases in skin, lung, and internal cancers, but Asi does not typically cause
tumors in standard laboratory animal test protocols. Considerable controversy
has centered on whether there is epidemiological evidence of a ''threshold'' for
the carcinogenic effects of Asi , or at least of a highly nonlinear
dose-response Saturation of metabolism in the dose-range associated with tumors
does not appear to be adequate to produce a major impact on the dose-response
for carcinogenicity. If there is a strong nonlinearity, it results from the
nature of the carcinogenic mechanism(s) of Asi. However, no single hypothesis
for the mechanism of Asi carcinogenicity has widespread support. A biologically
realistic cancer risk assessment for Asi would require a quantitative
description of the dose of active arsenic species in target tissues, the
interactions between active arsenic and tissue constituents, and the manner in
which these interactions result in tumor formation in multiple organs in humans,
but not in experimental animals. Although Asi has only infrequently been
associated with tumors in animal studies, it has repeatedly been shown to act as
a comutagen in vitro and as a cocarcinogen in vivo. Asi is clastogenic, produci
ing chromatid aberrations, but does not produce point mutations at single gene
loci. Of particular interest, Asi has been shown to inhibit repair of DNA
single-strand breaks, a possible mechanism for its observed comutagenicity and
cocarcinogenicity. We propose a cocarcinogenic mode of action in which Asv acts
primarily on intermediate cells deficient in cell cycle control at a late stage
in a preexisting carcinogenic process. This interaction enhances genomic
fragility and accelerates conversion of premalignant lesions to more aggressive,
clinically observable tumors. An indirect effect of Asi on DNA repair is
consistent with the expectation of a nonlinear dose-response rather than the
linear dose-response traditionally assumed for mutagenic carcinogens. However,
defining the exact nature of this tumor dose-response will require further
experimental data on the dose-response for the cellular effects of Asi . Because
As carcinogenicity is unlikely to be observed in nor mal experimental animals
not exposed to other carcinogens, studies in animals and cell lines deficient in
cell cycle control should also be considered. Experimental studies specifically
designed to address the key mechanistic and dose-response issues for Asi
carcinogenicity are critically needed to support public health policy decisions
regarding current environmental exposures to Asi. [At
Taylor & Francis.]
Surface structural ion adsorption modeling of competitive binding
of oxyanions by metal (hydr)oxides. Hiemstra
T and W.H.Van Riemsdijk. Journal of Colloid and Interface Sci. 210,
182-193 (1999). [Application of CD-MUSIC model to arsenate phosphate
interaction covering most of the As binding literature.]
1998
Analytical chemistry of arsenic in drinking water. Andrew
Eaton, Hsaio Chiu Wang, Jack Northington. AWWARF Project #914, Catalog Order #
90729. Available
online through the AWWA Bookstore. Members / nonmembers price USD125 /
USD195. [Full description
online].
Anomalous arsenic concentrations in groundwaters of an island
community, Bowen Island, British Columbia. Boyle, D. R., R. J. W. Turner, et al.
Environmental Geochemistry and Health 20(4): 199-212. Recently,
occurrences of elevated arsenic concentrations in bedrock groundwaters used for
individual and municipal water supplies have been recognized along the mainland
coast of southern British Columbia, Canada. An area on Bowen Island (Queen
Charlotte Heights community) was chosen to investigate the source(s) of arsenic,
geochemical processes controlling its aqueous uptake, the role of geology and
structure in the formation of these waters, and the use of hydrogeochemical
survey methods for detecting arsenious groundwater regions. Pyrite-arsenopyrite-Cu
mineralisation in the Queen Charlotte Heights is present as veins associated
with NE-trending fault zones and as disseminations in marginal breccia and
stockwork zones of a rhyodacite porphyry stock. Near surface mineralisation was
later altered by supergene events to form minor pyrite-arsenopyrite in a matrix
of limonite and clay. Geochemical factors that control the concentration and
mobility of arsenic in these groundwaters include: (a) anion exchange of arsenic
from clay minerals during cation divalent/univalent exchange processes (water
softening) which leads to waters of high pH and high anion exchange capacities;
(b) desorption of arsenic from Fe and Al oxyhydroxide minerals during pronounced
shifts in pH from acid to alkaline conditions brought on by the water softening
process; and (c) stepwise oxidation of arsenopyrite mineralisation to form
arsenious sulphate-bearing groundwaters. The inconsistent behaviour of the As3+
and As5+ ions during the complex water-rock interaction processes described
above, precludes the use of detailed chemical analyses to predict relative
abundances of the more toxic As3+ species. For a full appreciation of the toxic
impact of groundwaters containing total arsenic concentrations that area above
regulatory guidelines an arsenic speciation analysis is required.
Arsenic and hypertension in Bangladesh. Tondel M, O
Axelson, IA Chowdhury, M Rahman.
Proceedings of Annual Doctor’s Conference at Gothenburg, Sweden 24-26th
November, 1998. Abstract.
Arsenic coprecipitation in
low-temperature pyrites; implications for bioremediation via sulfate reducing
bacteria. Thomas, R. C. and J. A. Saunders. In: Geological Society of America, 1998 annual meeting, Geological
Society of America (GSA). Boulder, CO, United States. 1998. To test for the
potential of biogenic sulfate reduction as a remediation technique for
arsenic-contaminated waters, two sites were studied that contained
low-temperature arsenic-bearing pyrite. The sites, with distinct depositional
histories, are: (1) pyrite replacing lignitized wood in terrace deposits along
Uphapee Creek (Macon County, Alabama), and (2) pyrite-rich calcite caprock from
the Hazlehurst Salt Dome (Copiah County, Mississippi). At Uphapee Creek, pyrite
replacing wood contains up to 1000 ppm As. It is proposed that weathering of
Piedmont metamorphic rocks continuously releases arsenic in low levels to
Uphapee Creek. Sorption reactions with oxyhydroxides led to the fixation of
arsenic on solid surfaces over a long time period. Deposition of oxyhydroxides
with woody material during a Pleistocene flood event created conditions for the
development of sulfate reducing bacterial communities once a shallow water table
developed in the alluvial deposits. Bacterial activity caused conditions around
logs and mediated the following general reaction: Fe (super 2+) + C (sub org) +
SO (sub 4) (super 2-) + H (sub 2) O + O (sub 2) --> FeS (sub 2) (py) + HCO
(super 3-) + CO (sub 2) . Reducing conditions led to the dissolution of iron
oxyhydroxides and release of sorbed arsenic. Based on textural and geochemical
evidence, the arsenic-bearing pyrite is believed to have precipitated directly
from solution. The pyrite-rich calcite caprock at Hazlehurst Salt Dome formed as
a result of biomediated reactions between oil-field brines and the underlying
anhydrite caprock. Pyrite at Hazlehurst formed via biogenic sulfidation of
precursor iron monosulfides and exhibits arsenic-rich (up to 4% As) bands.
Electron microprobe and x-ray diffraction analyses of Uphapee and Hazlehurst
pyrites indicate that arsenic apparently substitutes for iron in the pyrite
crystal lattice. These results suggest that arsenic may be sequestered into iron
sulfides at low temperatures in differing pathways of pyrite formation (direct
precipitation vs. sulfidation of iron monosulfides). It should be noted that the
presence of a local source of organic carbon to fuel the sulfate reduction
process is necessary. This has major implications for bioremediation focusing on
bacterial sulfate reduction as a means of metal removal from contaminated water.
An arsenic exposure model: probabilistic validation using empirical
data. Cohen, J.T., B.D. Beck, T.S. Bowers, R.L. Bornschein, and E.J. Calabrese. Hum. Ecol. Risk Assess. 4(2):341-377.
Arsenic in drinking water. How much
is too much? Rahman, M. and I. Chowdhury (1998). In Touch Feb(1-2).
Arsenic-induced keratosis and squamous cell carcinoma. Rahman
M, P Söderkvist P, BL Rozell, O Axelson. International Symposium
Workshop on Epidemiology and Prevention of Cancer, November 2-5, 1998,
Bangkok, Thailand (proceedings). Abstract.
Arsenic-laced water in
Chile [letter; comment] Biggs, M. L., R. Haque, et al. Science 281(5378): 785.
Arsenic levels in drinking water and the prevalence of skin lesions.
Rahman M, M Tondel,
IA Chowdhury. International Symposium Workshop on Epidemiology and Prevention
of Cancer, November 2-5, 1998, Bangkok, Thailand (proceedings). Abstract.
Arsenic levels in
drinking water and the prevalence of skin lesions in West Bengal, India.
Guha Mazumder, D. N., R. Haque, N. Ghosh, B.K. De, A. Santra, D. Chakraborti and
A. H. Smith. Int J Epidemiol 27(5): 871-7. Background: A cross-sectional survey was conducted
between April 1995 and March 1996 to investigate arsenic-associated skin lesions
of keratosis and hyperpigmentation in West Bengal, India, and to determine their
relationship to arsenic water levels. Methods: In all, 7683 participants were
examined and interviewed, and the arsenic levels in their drinking water
measured. RESULTS: Although water concentrations ranged up to 3400 µg/L of
arsenic, over 80% of participants were consuming water containing <500 µg/L.
The age-adjusted prevalence of keratosis was strongly related to water arsenic
levels, rising from zero in the lowest exposure level (<50 µg/L) to 8.3
per 100 for females drinking water containing >800 µg/L, and increasing
from 0.2 per 100 in the lowest exposure category to 10.7 per 100 for males in
the highest exposure level (> or =800 µg/L). However, 12 cases with
keratosis (2 females and 10 males) were drinking water containing <100 µg/L
of arsenic. Findings were similar for hyperpigmentation, with strong
dose-response relationships. Among those with hyperpigmentation, 29 cases were
exposed to drinking water containing <100 µg/L. Calculation by dose per
body weight showed that men had roughly two to three times the prevalence of
both keratosis and hyperpigmentation compared to women apparently ingesting the
same dose of arsenic from drinking water. Subjects who were below 80% of the
standard body weight for their age and sex had a 1.6 fold increase in the
prevalence of keratoses, suggesting that malnutrition may play a small role in
increasing susceptibility. Conclusion: The surprising finding of cases who had
arsenic-associated skin lesions with apparently low exposure to arsenic in
drinking water needs to be confirmed in studies with more detailed exposure
assessment. Further research is also needed concerning susceptibility factors
which might be present in the exposed population.
Arsenic poisoning of Bangladesh groundwater. R. Nickson, J.M.
McArthur, W.G. Burgess, M. Ahmed, P. Ravenscroft and M. Rahman. Nature, Volume 395,
page 338, 24th Sept, 1998. [Full text &
figures available online]. In Bangladesh and
West Bengal, alluvial Ganges aquifers used for public water supply are polluted
with naturally occurring arsenic, which adversely affects the health of millions
of people. Here we show that the arsenic derives from the reductive dissolution
of arsenic-rich iron oxyhydroxides, which in turn are derived from weathering of
base-metal sulphides. This finding means it should now be possible, by
sedimentological study of the Ganges alluvial sediments, to guide the placement
of new water wells so they will be free of arsenic.
Arsenic removal from geothermal
bore waters: the effect of mono-silicic acid. Swedlund, P. J. and J. G. Webster.
Water-Rock Interaction-9. G. B.
Arehart and J. R. Hulston. Rotterdam, Balkema: 947-950.
Association between the clastogenic effect in peripheral lymphocytes
and human exposure to arsenic through drinking water. Maki-Paakkanen J
et al. Environ. Molecular Mutagenesis 32(4):301-313.
Abstract: "Consumption of arsenic-contaminated well water has been
previously associated with the development of cancer. In this study, the authors
showed a relationship between consumption of arsenic-contaminated well water and
the development of chromosomal aberrations among residents of Finland. The
chromosomal aberrations were of a type associated with a future risk of cancer,
and were most highly correlated with arsenic exposure among current well-water
ingestors. This work adds to scientific work indicating that arsenic is an
important carcinogen with specific implications for populations that have
arsenic-contaminated well water (e.g. deep well users in the U.S., and large
populations of Taiwan, Chile, and Bangledesh)."
Calcutta's industrial pollution: groundwater arsenic
contamination in a residential area and sufferings of people due to industrial
effluent discharge - An eight-year study report. D. Chakraborti, G.
Samanta, B.K. Mandal, T. Roy Chowdhury, C.R. Chanda, B.K. Biswas, R.K. Dhar, G.K.
Basu and K.C. Saha. Current Science 74(4), 346-355.
Cancer mortality trends in a blackfoot disease endemic community of Taiwan following water source
replacement. Tsai SM, TN Wang, YC Ko J. Toxicol Environ Health A 1998 Nov 27;55(6):389-404.
[Abstract]
Chronic arsenic
toxicity in west Bengal--the worst calamity in the world. Guha
Mazumder, D. N., J. Das Gupta, et al. J Indian Med
Assoc 96(1): 4-7, 18. Since 1983 large number of people are being encountered
with arsenic toxicity due to drinking of arsenic contaminated water (0.05-3.2
mg/l) in 6 districts of West Bengal. Clinical and various laboratory
investigations were carried out on 156 patients to ascertain the nature and
degree of morbidity and mortality that occurred due to chronic arsenic toxicity.
All the patients studied had typical rain drop like skin pigmentation (being
inclusion criteria) while thickening of palm and sole were found in 65.5%
patients. Other features included weakness (70%), gastro-intestinal symptoms
(58.6%), involvement of respiratory system (57.08%) and nervous system (50.6%).
Lung function tests showed restrictive lung disease in 53% (9/17) and combined
obstructive and restrictive lung disease in 41% (7/17) of patients. Abnormal
electromyography was found in 34.8% (10/29) and altered nerve conduction
velocity in 34.8% (10/29) of cases. Enlargement of liver was found in 120 cases
(76.9%) while splenomegaly in 31.4% cases. Liver function test showed elevated
globulin level in 15.8% and alkaline phosphatase in 51.3%, alanine amino
transferase (ALT) in 11.8% and aspartate amino transferase (AST) in 27.6% of
cases. Evidence of portal hypertension was found in 33.3% patients. Liver biopsy
reports of 45 patients showed non-cirrhotic portal fibrosis in 41, cirrhosis in
2 and normal histology in 2 cases. There was no correlation between the quantity
of arsenic taken through water and the level of arsenic in hair, nail, liver
tissues and the degree of fibrosis. There were 5 deaths of which one had skin
cancer. The various non-cancer manifestations which were observed in these
patients were much severe than those reported in similar cases in other parts of
the world.
Chronic arsenicism and squamous cell carcinoma- a case report.
Rahman M, M Tondel,
O Axelson. International Symposium Workshop on Epidemiology and Prevention
of Cancer, November 2-5, 1998, Bangkok, Thailand (proceedings). Abstract.
Considerations in arsenic
analysis and speciation. Edwards, M., S. Patel, et al. Journal AWWA 90(3): 103-113.
Arsenic in drinking
water is often talked about as if it were a single, uniform material. To the
contrary, it wears several faces. It may be organic or inorganic; inorganic
arsenic may be dissolved, colloidal, or particulate; dissolved arsenic may be
arsenite [As(III)] or arsenate [As(V)]. In order to make well-grounded treatment
decisions about arsenic-a regulated substance in drinking water-managers must
know the concentration of total arsenic plus the character and quantity of each
arsenic component in the supply. Determining total arsenic is fairly
straightforward. Several methods are in use, and all work well in the hands of a
careful technician. Because organic arsenic rarely is present at concentrations
above 1 µg/L, it is not considered further. Most inorganic arsenic is
dissolved. However, in some water more than half the total arsenic is in the
form of very fine particulates that can be removed by filters. The presence of
colloidal or particulate arsenic may produce falsely high measurements of As(III).
To help suppliers identify arsenic species, an anion exchange method was
modified for use in the field. The method requires no preservation, provides
results in 4 minutes, is easy to use, and costs about $10 per sample.
Discussions about regulating arsenic will be based on national surveys of
arsenic occurrence. If these surveys use methods that give incorrect results,
little will be gained. Techniques described in this article will lead to more
accurate analyses and ultimately to a better regulation.
Cost to utilities of a lower MCL for arsenic (Journal Article).
Chowdhury, Z.K.; Edwards, M.A.; Frey, M.M.; Owen, D.M.; Raucher, R.S.; Hagler Bailly
Services -Boulder, CO, US In: Journal American Water Works Association;
vol. 90, no. 3 (1998); p. 89-102 : 6 fig., 8 tab.. - 35 ref.
Dearsenation of drinking water by means of coagulation in Bangladesh
(Report, unpublished document). Liang, Q.; Technical University of Denmark -Lyngby, DK. -
Lyngby, Denmark, Technical University of Denmark, 1998.
- xi, 81 p. + 15 appendixes (37 p.) : 38 fig., 20 tab. C958419 65 ref.
- Master Thesis.
Detailed study report of Samta, one of the arsenic-affected villages of Jessore District,
Bangladesh. Biggs, M. L., R. Haque, et al. [or Bhajan K. Biswas, Ratan
K. Dhar, Gautam Samanta, Badal K. Mandal, Imtiaz Faruk, Kazi Saiful Islam, Md.
Moniruzzaman Chowdhury, Ashraful Islam and Shibtosh Roy and Dipankar Chakraborti.?]
Current Science 74(2): 134-145.
In Bangladesh, arsenic in
groundwater above 0.05 mg/l, the maximum permissible limit laid down by WHO, was
found in 41 out of 64 districts. People suffering from arsenicosis have been
identified in 20 districts out of the 21 districts we have surveyed so far. To
know the magnitude of the calamity, it was necessary to survey thousands of
villages in the 41 districts. To get an idea about the situation, we surveyed in
detail one village, Samta, in Jessore district, having a population of 4841. All
the tubewells in the village were analysed for arsenic. A few hundred hair, nail
and urine samples were analysed as well to know the arsenic burden on the
population. Furthermore, 600 people were examined for arsenical dermatosis. We
have attempted a statistical interpretation of the data.
Diabetes mellitus associated with
arsenic exposure in Bangladesh. Rahman, M., M. Tondel, et al. Am J Epidemiol 148(2): 198-203.
The
objective of this study was to assess whether arsenic exposure is a risk factor
for diabetes mellitus as indicated in a few earlier studies. Arsenic in drinking
water is known to occur in western Bangladesh, and in 1996, two of the authors
conducted a survey of the prevalence of diabetes mellitus among 163 subjects
with keratosis taken as exposed to arsenic and 854 unexposed individuals.
Diabetes mellitus was determined by history of symptoms, previously diagnosed
diabetes, glucosuria, and blood sugar level after glucose intake. The crude
prevalence ratio for diabetes mellitus among keratotic subjects exposed to
arsenic was 4.4 (95% confidence interval 2.5-7.7) and increased to 5.2 (95%
confidence interval 2.5-10.5) after adjustment for age, sex, and body mass
index. On the basis of a few earlier measurements of arsenic concentrations in
drinking water by the authorities in Bangladesh and another 20 new ad hoc
analyses, approximate time- weighted exposure levels to arsenic in drinking
water could be estimated for each subject. Three time-weighted average exposure
categories were created, i.e., less than 0.5, 0.5-1.0, and more than 1.0
mg/liter. For the unexposed subjects, the corresponding prevalence ratios were
1.0, 2.6, 3.9, and 8.8, representing a significant trend in risk (p < 0.001).
The result corroborates earlier studies and suggests that arsenic exposure is a
risk factor for diabetes mellitus.
Diabetes mellitus - some epidemiological observation with regard
to arsenic exposure. Rahman
M. Proceedings of Diabetes and Endocrine Conference 1998, BIRDEM, Dhaka,
Bangladesh. Abstract.
Dietary arsenic intake in Taiwanese districts with elevated arsenic in drinking water.
Schoof, R.A., L.J. Yost, E. Crecelius, K. Irgolic, H.-R. Guo, and H.L. Greene. Hum. Ecol. Risk Assess. 4(1):117-136.
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
online.]
Exposure to inorganic arsenic
metabolites during early human development. Concha, G., G. Vogler, et al.
Toxicol Sci 44(2): 185-90.
Because of the lack of data on the exposure to and toxic effects of inorganic
arsenic during early human development, the transfer of arsenic to the fetus and
suckling infant was studied in a native Andean population, living in the village
San Antonio de los Cobres in the North west of Argentina, where the drinking
water contains about 200 micrograms/liter. The concentration of arsenic in cord
blood (median, 9 micrograms/liter) was almost as high as in maternal blood
(median, 11 micrograms/liter), and there was a significant correlation between
the two. Thus, at least in late gestation, arsenic is easily transferred to the
fetus. The median concentration of arsenic in the placenta was 34 micrograms/kg,
compared with 7 micrograms/kg previously reported for nonexposed women.
Interestingly, essentially all arsenic in the blood plasma of both the newborns
and their mothers was in the form of dimethylarsinic acid (DMA), the end product
of inorganic arsenic metabolism. Similarly, about 90% of the arsenic in the
urine of both the newborns and mothers in late gestation was present as DMA,
compared with about 70% in nonpregnant women (p < 0.001). This may indicate
that methylation of arsenic is increased during pregnancy and that DMA is the
major form of arsenic transferred to the fetus. The increased methylation in
late gestation was associated with lower arsenic concentrations in blood and
higher concentrations in urine, compared with a few months postpartum. The
arsenic concentrations in the urine of the infants decreased from about 80
micrograms/liter during the first 2 days of life to less than 30
micrograms/liter at 4.4 months (p = 0.025). This could be explained by the low
concentrations of arsenic in the breast milk, about 3 micrograms/kg.
Factors controlling As and U in
shallow ground water, southern Carson Desert, Nevada. Welch, A. H. and M. S.
Lico. Appl. Geochem 13(4):
521-539. Unusually high As and U concentrations (>100
µg/L) are widespread
in shallow ground water beneath the southern Carson Desert. The high
concentrations, which locally exceed 1000 µg/L, are of concern from a human
health standpoint because the shallow ground water is used for domestic supply.
Possible affects on wildlife are also of concern because the ground water flows
into shallow lakes and marshes within wildlife refuges. Arsenic and U
concentrations in ground water of the southern Carson Desert appear to be
affected by evaporative concentration, redox reactions, and adsorption. The
relation of these elements with Cl suggest that most of the high concentrations
can be attributed to evaporative concentration of Carson River water, the
primary source of recharge. Some ground water contains higher As and U
concentrations that cannot be explained by evaporative concentration alone.
Oxidation-reduction reactions, involving metal oxides and sedimentary-organic
matter, appear to contribute As, U, inorganic C, Fe and Mn to the ground water.
Arsenic in Fe-oxide was confirmed by chemical extraction and is consistent with
laboratory adsorption studies. Uranium in both sedimentary-organic C and
Fe-oxide coatings has been confirmed by fission tracks and petrographic
examination. Arsenic concentrations in the ground water and chemical extracts of
aquifer sediments are broadly consistent with adsorption as a control on some
dissolved As concentrations. An apparent loss of As from some ground water as
evaporative concentration proceeds is consistent with adsorption as a control on
As. However, evidence for adsorption should be viewed with caution, because the
adsorption model used values for the adsorbent that have not been shown to be
valid for the aquifer sediments throughout the southern Carson Desert.
Hydrologic and geochemical conditions in the Carson Desert are similar to other
areas with high As and U concentrations in ground water, including the Salton
Sea basin and southern San Joaquin Valley of California. Hydrologic and
geochemical conditions that produced some sandstone-type U-ore deposits,
including those in the non-marine, closed-basin sediments of the Morrison
Formation near Grants, New Mexico, suggest that the Carson Desert may be a
modern analog for those systems.
Feasibility of New Epidemiologic Studies of Low Level Arsenic.
Allan H. Smith. AWWARF Project #288, Catalog #90755. Available online at
the AWWA
Bookstore. Price members / nonmembers USD125 / USD195. [Full
description online.]
Geochemical mapping and speciation of arsenic in
the groundwater of Faridpur municipality, Bangladesh. Ullah, S. S.
Journal of
Bangladesh Academy of Sciences 22(1): 143-147. A detailed mapping of Faridpur
municipality. Over 500 samples were collected and measured for arsenic,
including speciation. GPS was used to record well locations. Highest
concentrations were invariably found in shallow wells. Distinct local patterns
were observed: the highest concentrations lay almost in a straight line parallel
to the old bank of the Ganges. There were also a few small hot spots.
Granular ferric hydroxide -- a new adsorbent for the removal of arsenic from
natural water. W. Driehaus, M. Jekel, U. Hildebrandt
Journal of Water Science, Research and Technology --Aqua Vol. 47, pp. 30-35.
[The article is on a new treatment method. The described media is available
and is used successfully for arsenic removal in Germany.]
Human exposures to arsenic
from consumption of well water in West Bengal, India. Subramanian, K. S. and M. J.
Kosnett.
Int J Occup Environ
Health 4(4): 217-30. The authors visited the State of West Bengal, India, in
August 1996, as consultants to the World Health Organization (WHO). The general
mandate of the mission was to formulate recommendations to the Government of
India regarding its efforts to assist the Government of West Bengal in remedying
health problems arising from the presence of arsenic in groundwater in excess of
the WHO guideline limit of 0.05 mg/L in eight districts of the State. The
authors held discussions with Government of India and Government of West Bengal
officials, as well as scientists, engineers, and physicians studying the
analytic, medical, engineering, and hydrogeologic facets of the problem. They
conducted field visits to arsenic-affected villages; inspected health centers,
including the laboratories conducting the analytic and clinical studies; and
interviewed and examined local lay people, including many arsenic- poisoned
patients. This overview of the arsenic contamination problem in West Bengal is
based upon a review of the scientific literature and government reports and the
authors direct, firsthand assessment. The authors hope that their
recommendations will assist in the development of a comprehensive infrastructure
and plan of action, which are necessary to control the epidemic of chronic
arsenic poisoning now afflicting West Bengal.
Immobilization mechanism of
arsenic in waste solidified using cement and lime. Dutre, V. and C.
Vandecasteele. Environmental Science and Technology 32(18):
2782-2787. The material studied, a waste fly ash from the
metallurgical industry, contains the toxic element As in high concentrations,
ranging from 23% to 47% (wt %). Besides As, Sb and Pb are present in the waste
material. The waste was solidified with inorganic materials such as cement and
pozzolanic materials in order to reduce the leachability of the contaminants
from the waste. The optimal solidification recipe lowered the As concentration in
the leachate of the extraction test DEIN 38 414 S4 from ca. 5 g/l to ca. 5 mg/l.
In this paper, it was shown that this enormous reduction in As concentration was
due to the formation of CaHAsO3 in the leachate, in the presence of Ca(OH)2.
Formation of CaHASO3 alone cannot lower the arsenic concentration beneath ca. 55
mg/l, as was calculated with the speciation program MINTEQA2.
Impact of safe water for
drinking and cooking on five arsenic-affected families for 2 years in West
Bengal, India. Mandal, B. K., T. R. Chowdhury, G. Samanta, D.P.
Mukherjee, C.R. Chanda, K.C. Saha, D. Chakraborti. Sci Total Environ 218, 185-201.
The groundwater in
seven districts of West Bengal, India, covering an area of 37,000 km2 with a
population of 34 million, has been contaminated with arsenic. In 830
villages/wards more than 1.5 million people, out of the total population, drink
the arsenic-contaminated water. Safe water from a source having <0.002 mg
1(-1) arsenic has been supplied for 2 years to five affected families comprising
17 members (eight of them with arsenical skin-lesions) of different age groups
for impact assessment study in terms of loss of arsenic through urine, hair and
nail. The study indicates random observable fluctuations of arsenic
concentration in urine among members on different scheduled sampling days with a
declining trend, particularly during the first 6 months. Furthermore, the
investigation showed that despite having safe water for drinking and cooking,
the study group could not avoid an intake of arsenic, time and again, through
edible herbs grown in contaminated water, food materials contaminated through
washing, and the occasional drinking of contaminated water. After minimizing the
level of contamination, a noteworthy declining trend after 8 months was observed
in urine, hair and nails in all the cases, but not to that level observed in a
normal population, due to prevailing elevated background level of arsenic in the
area. The eight members, who had already developed skin lesions, are far from
recovering completely, indicating a long-lasting damage. Statistical
interpretation of the data are considered.
Intake of inorganic arsenic in the North American diet. Yost,
L.J., R.A. Schoof, and R. Aucoin. 1998. Hum. Ecol. Risk Assess. 4:137-152.
Likelihood ratio analysis of skin cancer prevalence associated with arsenic in
drinking water in the USA. Valberg, P.A., B.D. Beck, P.D. Boardman, and
J.T. Cohen. Env. Geochemistry and Health 20(2):61-66.
Low-level arsenic excretion in
breast milk of native Andean women exposed to high levels of arsenic in the
drinking water. Concha, G., G. Vogler, et al. Int Arch Occup Environ Health 71(1): 42-6.
Objective: To
investigate the excretion of arsenic in breast milk of lactating native Andean
women living in a village in northwestern Argentina with high concentrations of
arsenic in the drinking water (about 200 micrograms/l) and to assess the
exposure of children to arsenic during the very first period of life. Methods:
The study included ten lactating women and two nursing babies.
Hydride-generation atomic absorption spectrometry (HG-AAS) was used to determine
the concentration of arsenic in samples of human milk, drinking water, blood,
and urine. Results: The concentrations of arsenic detected in maternal blood
(total arsenic) and urine (metabolites of inorganic arsenic) were high,
averaging 10 and 320 micrograms/l, respectively. In subjects without known
exposure to arsenic the average concentrations found in blood and urine are 1-2
and about 10 micrograms/l, respectively. The metabolites of inorganic arsenic
constituted more than 80% of the total arsenic in the urine, which shows that
inorganic arsenic was the main form of arsenic ingested. The average
concentration of arsenic detected in human milk was 2.3 micrograms/kg fresh
weight (range 0.83-7.6 micrograms/kg). Although data on background levels of
arsenic in human breast milk are scarce, the present concentrations seem to be
slightly elevated. However, considering the high levels of arsenic exposure in
the mothers, the total arsenic concentrations measured in human milk were low.
In concordance with the low concentrations of arsenic found in the milk, the
concentrations of arsenic metabolites measured in the urine of two of the
nursing babies were low: 17 and 47 micrograms/l, respectively. Conclusions: The
low concentrations of arsenic detected in the breast milk and urine of the two
nursing babies in relation to the high level of maternal exposure to arsenic
indicate that inorganic arsenic is not excreted in breast milk to any
significant extent. This is a very important reason for long breast-feeding
periods.
Lung and kidney cancer mortality associated with arsenic in drinking
water in Cordoba, Argentina. Hopenhayn-Rich C, ML Biggs. Int J
Epidemiol Aug;27(4):561-9. [Abstract]
Main Report Phase I,
Groundwater Studies of Arsenic Contamination in Bangladesh. British
Geological Survey and Mott-MacDonald International Ltd. (BGS/MMI) [See ACIC's
version of the executive summary for an explanation of the editions/versions
available.]
Marked increase in bladder
and lung cancer mortality in a region of Northern Chile due to arsenic in
drinking water. Smith, A. H., M. Goycolea, et al. Am J Epidemiol 147(7): 660-9.
[Abstract]
Studies in Taiwan and
Argentina suggest that ingestion of inorganic arsenic from drinking water
results in increased risks of internal cancers, particularly bladder and lung
cancer. The authors investigated cancer mortality in a population of around
400,000 people in a region of Northern Chile (Region II) exposed to high arsenic
levels in drinking water in past years. Arsenic concentrations from 1950 to the
present were obtained. Population-weighted average arsenic levels reached 570 µg/L between 1955 to 1969, and decreased to less than 100 µg/L
by 1980. Standardized mortality ratios (SMRs) were calculated for the years 1989
to 1993. Increased mortality was found for bladder, lung, kidney, and skin
cancer. Bladder cancer mortality was markedly elevated (men, SMR = 6.0 (95%
confidence interval (CI) 4.8-7.4); women, SMR = 8.2 (95% CI 6.3-10.5)) as was
lung cancer mortality (men, SMR = 3.8 (95% CI 3.5-4.1); women, SMR = 3.1 (95% CI
2.7-3.7)). Smoking survey data and mortality rates from chronic obstructive
pulmonary disease provided evidence that smoking did not contribute to the
increased mortality from these cancers. The findings provide additional evidence
that ingestion of inorganic arsenic in drinking water is indeed a cause of
bladder and lung cancer. It was estimated that arsenic might account for 7% of
all deaths among those aged 30 years and over. If so, the impact of arsenic on
the population mortality in Region II of Chile is greater than that reported
anywhere to date from environmental exposure to a carcinogen in a major
population.
Metabolism of inorganic arsenic
in children with chronic high arsenic exposure in northern Argentina.
Concha, G., B. Nermell, et al. Environ Health Perspect 106(6): 355-9. This study concerns the metabolism of
inorganic arsenic (As) in children in three villages in northern Argentina: San
Antonio de los Cobres and Taco Pozo, each with about 200 microg As/l in the
drinking water, and Rosario de Lerma, with 0.65 microg As/l. Findings show that
the concentrations of As in the blood and urine of the children in the two
As-rich villages were on average 9 and 380 µg/L, respectively, the highest
ever recorded for children. The concentrations were about 10 and 30 times higher
for blood and urine, respectively, than in Rosario de Lerma. Total As in urine
was only slightly higher than the sum of metabolites of inorganic As (U-Asmet),
i.e., inorganic As, methylarsonic acid (MMA), and dimethylarsinic acid (DMA);
this shows that inorganic As was the main form of As ingested. In contrast to
previous studies on urinary metabolites of inorganic As in various population
groups, the children and women in the present study excreted very little MMA.
Thus, there seems to be a polymorphism for the enzymes (methyltransferases)
involved in the methylation of As. Interestingly, the children had a
significantly higher percentage of inorganic As in urine than the women, about
50% versus 32%. Also, the percentage of inorganic As in the children is
considerably higher than in previous studies on children (about 13% in the two
studies available) and adults (about 15-25%) in other population groups. This
may indicate that children are more sensitive to As-induced toxicity than
adults, as the methylated metabolites bind less to tissue constituents than
inorganic As. In the children, the percentage inorganic arsenic in urine
decreased, and the percentage of DMA increased with increasing U-Asmet,
indicating an induction of As methylation with increasing exposure. [Paper
available online.]
Mobilization of mercury and arsenic in humans by sodium
2,3-dimercapto-1-propane sulfonate (DMPS). Aposhian HV. Environ Health
Perspect 1998 Aug;106 Suppl 4:1017-25. [Abstract]
Randomized
placebo-controlled trial of 2,3-dimercaptosuccinic acid in therapy of chronic
arsenicosis due to drinking arsenic-contaminated subsoil water. Guha
Mazumder, D. N., U. C. Ghoshal, et al. J Toxicol
Clin Toxicol 36(7): 683-90. Introduction: Chronic arsenic toxicity producing
various clinical manifestations is currently epidemic in West Bengal, India,
Bangladesh, and other regions of the world. Animal studies have indicated that
2,3-dimercaptosuccinic acid can be used as an oral chelating agent. A
prospective, double-blind, randomized controlled trial was carried out to
evaluate the efficacy and safety of 2,3-dimercaptosuccinic acid for chronic
arsenicosis due to drinking arsenic-contaminated (> or = 50 micrograms/L)
subsoil water in West Bengal. Method: Twenty-one consecutive patients with
chronic arsenicosis were individually randomized (random number; assignment made
by individual not evaluating patients) into 2 groups: 11 patients (10 male, age
25.5 +/- 8 years) received 2,3-dimercaptosuccinic acid 1400 mg/d (1000 mg/m2) in
the first week and 1050 mg/d (750 mg/m2) during the next 2 weeks with a repeat
course 3 weeks later. The other 10 patients (all male, age 32.2 +/- 9.7 years)
were given placebo capsules for the same schedule. The clinical features were
evaluated by an objective scoring system before and after treatment. Routine
investigations including liver function tests, arsenic concentrations in urine,
hair, and nails, and skin biopsy evaluations were also completed. Results:
Though there was improvement in the clinical score of 2,3-dimercaptosuccinic
acid- treated patients, similar improvement was observed in the placebo- treated
group. There were no statistical differences in the clinical scores between the
2 groups at the beginning and at the end of treatment. Similarly, no differences
were found for the other investigated parameters. Conclusion: Under the
conditions of this study, 2,3-dimercaptosuccinic acid was not effective in
producing any clinical or biochemical benefit or any histopathological
improvement of skin lesions in patients with chronic arsenicosis.
Selenium and arsenic in the
environment in Finland. Lahermo, P., G. Alfthan, et al. J Environ Pathol Toxicol Oncol 17(3-4): 205-16.
A
characteristic feature of glaciated Precambrian environments is their low
selenium content, as a chalcophile element, Se, replaces sulfur in many of the
sulfide minerals, for example, pyrite, chalcopyrite, pyrrhotite, and pentlandite.
The average Se concentration in rocks and related till deposits in Finland is in
the range of 0.01 to 0.2 mg/kg. Due to geologicalconditions, Se concentrations
in surface and ground water are low in Finland compared with other countries. In
a nationwide study dealing with the hydrogeochemistry of headwater streams, the
median Se concentration in streams during August to September 1990 was 30 to 180 µg/L. For comparison, Se concentrations in shallow well waters are generally
in the range of 50 to 1000 µg/L. The Se concentrations in stream sediments
varied from 0.03 to 3.94 mg/kg. There was a highly significant correlation
between the Se concentrations in stream water and in stream sediment. The
streams with Se concentrations exceeding the general level in both water and
sediment were most common in southern Finland. A speciation study on Finnish
stream waters revealed that there were equal proportions of Se complexed with
humic substances (36%) and Se as a selenate species (36%), whereas selenite
accounted for less than 10% of total Se. About 8% of the Se in stream water
occurred in particulate form. In an effort to enhance the Se intake of Finns
through diet, Se-supplemented fertilizers have been used nationwide since 1985.
While greatly improving Se levels in the population, the measure has raised
concerns about undesirable environmental effects. Therefore, the amount of Se
added to fertilizers has been reduced since 1991. Differing in behavior from Se,
arsenic is considered one of the most toxic metals derived from the natural
environment. Alarm has been triggered in Finland by the recent lowering from 50 µg/L to 10 µg/L of the upper level of As permissible in potable water,
the recent information of high As concentrations in water from drilled bedrock
wells, and the findings of international medical studies suggesting that As is a
carcinogen. The most important source of As is arsenopyrite (FeAsS). Hence, high
As concentrations most frequently occur in areas of sulfide mineralization,
often in connection with occurrences of mafic rocks such as gabbros,
amphibolites, and peridotites. The As concentrations in till fines, the most
common glaciogenic soil type in Finland, reflect those in bedrock. The
concentrations in groundwater are controlled by the chemical composition of the
bedrock and the soil and prevailing hydrogeochemical conditions, for example, pH
and Eh levels. Arsenic concentrations are lowest in surface water and swiftly
flowing shallow ground water discharged by springs and are somewhat higher in
shallow wells dug into overburden. By far, the highest As concentrations are to
be found in wells drilled into bedrock (maximum 1 to 2 mg/L), although the
concentrations vary by several orders of magnitude from well to well. The
highest probability of encountering deleteriously arsenious well water is in
areas with characteristic As anomalies in the till and bedrock. Hence, it is
important to understand local geological conditions, particularly in the case of
wells drilled into bedrock. The risk of deleteriously high As concentrations
occurring in captured springs and shallow wells is slight.
Using biogeochemistry of trace arsenic
contamination in groundwater in Zimapan, Mexico. Crawford, S., H. Mango, et al.
In: Geological Society of
America, Northeastern Section, 33rd annual meeting; abstracts, Geological
Society of America (GSA). Boulder, CO, United States.
1997
The arsenic calamity in Bangladesh (Journal Article). Dahi, E.; DANIDA
-Copenhagen, DK In: ITN Bangladesh newsletter; no. 2 (1997); p. 1-6 : 1
fig., 4 tab.. - 14 ref.
Arsenic contamination in ground water and arsenicosis in Bangladesh. Sk.
Akhtar Ahmad, Don Bandaranayake, Abdul Wadud Khan, Sk. Abdul Hadi Giasuddin, Md.
Abdul Halim. International Journal of Environmental Health Research, 7(4)
December 1, 1997, 271-276. Abstract: Arsenic contamination
of ground water has been found in Rajarampur village in the Nawabgonj district
of north-western Bangladesh. A recent survey has indicated that 11% of tubewell
water contains arsenic in the range 0.01 mg/l to 0.05 mg/l, and 29% above the
WHO maximum permissible limit of 0.05 mg/l. None of the water samples from
tubewells of less than 60 ft depth showed arsenic levels above 0.05 mg/l. Of the
1273 people exposed to this contaminated water supply, 7.5% showed clinical
manifestations of arsenicosis. The majority of these (59.4%) were female. There
were no cases below 7 years of age. The most frequently seen clinical
manifestations were melanosis (98.9%), keratosis (92.7%), hyperkeratosis
(45.8%), depigmentation (29.2%), anorexia (26.0%) and cough (25.0%).
Hepatomegaly was detected in 3.2% of the population and there was one case of
squamous-cell carcinoma. The article also describes the use of a validated field
test for the detection of arsenic in water. [At
Taylor & Francis.]
Arsenic contamination of groundwater and its remedial action plan
in West Bengal. AIIH&PH. In: Consultation on arsenic in
drinking water and resulting arsenic toxicity in India and Bangladesh,
WHO,
New Delhi, 1997.
Arsenic in drinking water and incidence of urinary cancers. Guo
HR, HS Chiang, H Hu, SR Lipsitz, RR Monson. Epidemiology
Sep;8(5):545-50. [Abstract]
Arsenic in drinking water and resulting arsenic toxicity in India
and Bangladesh - recommendations for action. WHO Regional Office
for South-East Asia, New Delhi. WHO pamphlet SEA/EH/505 [Full
text available online].
Arsenic in groundwater - geological overview. S. K. Acharyya.
In: Consultation on arsenic in drinking water and resulting arsenic
toxicity in India and Bangladesh, WHO, New Delhi, 1997.
Arsenic in groundwater in Bangladesh. P L Smedley. In:
Consultation
on arsenic in drinking water and resulting arsenic toxicity in India and
Bangladesh, WHO, New Delhi, 1997.
Arsenic in groundwater in six districts of West Bengal. Dipankar
Das, Gautam Samanta, B K Mandal, T R Chowdhury, C R Chanda, P P Chowdhury,
Gautam Basu and D Chakraborti. In: Consultation on arsenic in drinking
water and resulting arsenic toxicity in India and Bangladesh, WHO,
New Delhi, 1997.
Arsenic in groundwater in six districts of West Bengal, India-the
biggest arsenic calamity in the world: the status report up to August,
1995. Tarit Roy Chowdhury, Badal Kr. Mandal, Gautam Samanta, Gautam
Kr. Basu, Partha P.Chowdhury, Chitta R.Chanda, Nirmal Kr.Karan, Dilip Lodh,
Ratan Kr.Dhar, Dipankar Das, K.C.Saha and Dipankar Chakraborti. In: Arsenic -
Exposure
and Health Effects, edited by C.O.Abernathy, R.L. Calderon and W.R.
Chappell Chapter 9: 91-111, 1997; Publisher: Chapman & Hall.
Arsenic in groundwater in six districts of West Bengal, India:
the biggest arsenic calamity in the world: the status report up to August
1995. T. R. Chowdhury, B. K. Manal, G. Samanta, G. K. Basu, P.
P. Chowdhury, C. R. Chanda, N. K. Karan, D. Lodh, R. K. Dhar, D. Das, K.
C. Saha and D. Chakroborti. In: Consultation on arsenic in drinking
water and resulting arsenic toxicity in India and Bangladesh, WHO,
New Delhi, 1997.
Arsenic in ground water in West Bengal. S. P. Sinha Ray.
In: Consultation on arsenic in drinking water and resulting arsenic
toxicity in India and Bangladesh, WHO, New Delhi, 1997.
Arsenic management in drinking water. Saumyendra Nath
Mukherji. In: Consultation on arsenic in drinking water and resulting
arsenic toxicity in India and Bangladesh, WHO, New Delhi, 1997.
Arsenic occurrence and speciation in groundwater, Hanford, CA:
Implications for health effects and treatment options. Janet G.
Hering and Van Q. Chiu. In: CSCE/ASCE Environmental Engineering Conference,
Edmonton,
1997.
Arsenic pollution of groundwater in Samta village, Jessore, Bangladesh.
Hiroshi Yokota, Kimiko Tanabe, Yashuhiro Akiyoshi, Kazuyuki Kawahara, Mitsuo
Hashiguchi, Wadud Kahn, Akhtar Ahmad and Abdul Hadi. Miyazaki University,
AAN, NIPSOM, Dhaka, 1997.
Arsenic removal from drinking water during coagulation.
Janet Hering, Pen-Yuang Chen, Jennifer A. Wilkie and Menachem Elimelech.
Journal
of Environmental Engineering, 123 (8): 800-807, 1997.
Chronic arsenic toxicity in West Bengal. B.K. Mandal,
T. Roy Chowdhury, G.Samanta, G.K.Basu, P.P.Chowdhury, C.R.Chanda, D.Lodh,
N.K.Karan, R.K.Dhar, D.T.Tamili, D.Das, K.C.Saha and D.Chakraborti. Current
Science, 72(2), 114-117, 1997.
Chronic neuropathy due to arsenic intoxication from geo-chemical
source - a 5-year follow-up. D Basu, J Das Gupta, A Mukherjee and
D N Guha Mazumder. In: Consultation on arsenic in drinking water and
resulting arsenic toxicity in India and Bangladesh, WHO, New Delhi,
1997.
DMPS-arsenic challenge test. I: Increased urinary excretion of
monomethylarsonic acid in humans given dimercaptopropane sulfonate. Aposhian
HV, Arroyo A, Cebrian ME, del Razo LM, Hurlbut KM, Dart RC, Gonzalez-Ramirez D,
Kreppel H, Speisky H, Smith A, Gonsebatt ME, Ostrosky-Wegman P, Aposhian MM. J
Pharmacol Exp Ther 1997 Jul;282(1):192-200. [Abstract]
Enzymatic methylation of arsenic species and other new approaches to
arsenic toxicity. Aposhian HV. Annu Rev Pharmacol Toxicol
1997;37:397-419. [Abstract]
Evaluation of the validity of the US EPA‘s cancer risk assessment
of arsenic for low-level exposures: a likelihood ratio approach. How-Ran
Guo, Environmental Geochemistry and Health 19 (9):133-142, 1997.
Excerpts from "Arsenic contamination of drinking water in Bangladesh".
J.M.
Dave. In: Consultation on arsenic in drinking water and resulting arsenic
toxicity in India and Bangladesh,
WHO, New Delhi, 1997.
Excerpts from "Technical report and action plan for arsenic in
drinking water in Bangladesh focusing on health". Allan H. Smith.
In: Consultation on arsenic in drinking water and resulting arsenic
toxicity in India and Bangladesh, WHO, New Delhi, 1997.
Experiences with large scale arsenic toxicity in other parts of
the world. Allan Smith. In: Consultation on arsenic in drinking
water and resulting arsenic toxicity in India and Bangladesh, WHO,
New Delhi, 1997.
Groundwater arsenic calamity in Bangladesh. Ratan K. Dhar,
Bhajan Kr. Biswas, Gautam Samanta, Badal Kr. Mandal, D. Chakraborti, Shibtosh
Roy, Abu Jafar, Ariful Islam, Gulshan Ara, Saiful Kabir, A. Wadud Khan,
S. Akther Ahmed and S. Abdul Hadi Current Science, Vol. 73, No.
1, 48-59, 1997.
Health effects of arsenic toxicity. Wadud Abdul Khan.
In: Consultation on arsenic in drinking water and resulting arsenic
toxicity in India and Bangladesh, WHO, New Delhi, 1997.
Inorganic arsenic: a need and an opportunity to improve risk assessment.
Chappell WR, B.D. Beck, K.G. Brown, R. Chaney, C. Richard Cothern,
K.J. Irgolic, D.W. North, I. Thornton, and T.A. Tsongas. Env. Health Persp. 105(10):1060-1067.
October. Abstract
available online.
Manganese greensand for removal of arsenic in drinking water. K.S.
Subramanian, T. Viraraghavan, T. Phommavong and S. Tanjore. Water Quality
Research Journal of Canada, 32(3): 551-561. Abstract: "The
present study was initiated to identify treatment techniques suitable for the
removal of As from small community groundwater supplies below the current
interim maximum acceptable (IMAC) concentration of 25 µg/L prescribed in the
Guidelines for Canadian Drinking Water Quality. The effectiveness of manganese
greensand filtration (MGSF), including the effect of Fe(II) in the influent, was
studied in batch (intermittent) and column (continuous) modes. Batch studies
based on the Freundlich adsorption isotherm model showed that the percent
removal efficiency of arsenic by MGSF to the IMAC value was 60 for 24-h
equilibration. Column studies gave an overall percent removal efficiency of 41.
However, in the presence of Fe(II), especially at an Fe/As concentration ratio
of 20, manganese greensand gave an overall efficiency of 83% and a throughput
volume of 1,440 L. Results showed that at a Fe/As ratio of at least 20 and in
the presence of Fe(II), manganese greensand is capable of removing As to below
the IMAC value, under continuous mode of operation and when the influent As
concentration is <200 µg/L."
Metabolic methylation is a possible genotoxicity-enhancing process of
inorganic arsenics. Yamanaka K., Hayashi. H., Tachikawa M., Kato K., Hasegawa A., Oku N.,and
Okada S. Mutat. Res., 394:95-101.
Non-cancer effects of chronic arsenicosis with special reference to
liver damage. N. Guha Mazumder, J. Das Gupta, A. Santra, A. Pal, A.
Ghose, S. Sarkar, N. Cattopadhaya and D. Chakraborti, pp. 112-123. In: Arsenic
- Exposure and Health Effects, C.O.Abernathy, R.L. Calderon, and
W.R.Chappell, eds., Chapman & Hall, New York.
Non-cancer effects of chronic arsenicosis with special reference
to liver damage. D.N. Guha Mazumder, J. Das Gupta, A. Santra, A.
Pal, A. Ghose, S. Sarkar, N. Chattopadhaya and D. Chakroborti. In: Consultation
on arsenic in drinking water and resulting arsenic toxicity in India and
Bangladesh, WHO, New Delhi, 1997.
Occurrence of arsenic contaminated groundwater in alluvial aquifers
from Delta Plains, Eastern India: Options for safe drinking water supply.
P.
Bhattacharya, D. Chatterjee, and G. Jacks. Int. Jour. Water Resources
Management, 13(1): 79-92.
Report of study of the impact of the Bangladesh Rural Electrification
Program on groundwater quality. NRECA. Dhaka, 1997.
Subsurface arsenic occurrence and depth of contamination in Bangladesh.
Karim,
M. M., Y. Komori, and M. Alam, J. of Environmental Chemistry, 7(4),
783-792. [Abstract
available online]
Working paper on arsenic in drinking water in Bangladesh and its
intervention. DPHE. Department of Public Health Engineering, Dhaka,
1997.
World Health Organization guideline value for arsenic in drinking
water. Hend Galal-Gorchev. In: Consultation on arsenic in drinking
water and resulting arsenic toxicity in India and Bangladesh, WHO,
New Delhi, 1997.
1996
Adsorption of arsenic onto hydrous ferric oxide: effects of adsorbate/adsorbent
ratios and co-occurring solutes. Jennifer A. Wilkie and Janet G.
Hering. Colloids and Surfaces: Physiochemical and Engineering Aspects,
107
97-110,
1996.
Arsenic calamity due to ground water pollution in West Bengal.
D.
N. Guha Mazumder. In: Consultation on arsenic in drinking water and
resulting arsenic toxicity in India and Bangladesh, WHO, New Delhi,
1996.
Arsenic in groundwater in seven districts of West Bengal, India
- the biggest arsenic calamity in the world. B K Mandal, T R Chowdhury,
G Samanta, G K Basu, P P Chowdhury, C R Chanda, N K Lodh, N K Karan, R
K Dhar, D K Tamili, K C Saha and D Chakraborti. Current Science,
70
(11):
976-987, 1996.
Arsenic in groundwater in seven districts of West Bengal,India-The
biggest arsenic calamity in the world. Badal K.Mandal, Tarit Roy
Chowdhury, Gautam Samanta, Gautam K.Basu, Partha Pratim Chowdhury, Chitta
R. Chanda, Dilip Lodh, Nirmal K.Karan, Ratan K.Dhar, Dipak K.Tamili, Dipankar
Das, K.C.Saha & D.Chakraborti. Current Science, 70(11),976-986,
June 1996.
Arsenic in ground water in six districts of West Bengal, India.
Dipankar Das, Gautam Samanta, Badal Kumar Mondal, Chitta R. Chanda, Partha
Pratim Chowdhury, Gautam Kumar Basu & Dipankar Chakraborti. Environmental
Geochemistry & Health,18(1),5-15,1996. [Full text & graphics
available online: see HTML
version (415k total for text + linked graphics) republished permission EGH.
EGH's 5.2Mb Acrobat .PDF file is not currently available online.]
Arsenic removal by enhanced coagulation and membrane processes.
Janet G. Hering and Menachem Elimelech. AWWARF Catalog Order # 90706. Available
online at the AWWA
Bookstore. Price members / nonmembers USD125 / USD195. [Full
description online].
Arsenic removal. 18DTP, Dhaka, 1996.
Arsenic removal by ferric chloride. Janet G. Hering, Pen
Yuan Chen, Jennifer A. Wilkie, Menachem Elimelech and Sun Liang. Journal
American Water Works Association, 88 (4): 155-167, 1996. Abstract:
Laboratory studies on arsenic removal were carried out to compare coagulation
with ferric chloride and adsorption onto preformed hydrous ferric oxide.
Adsorption was found to be an important (though not the sole) mechanism
governing arsenic removal during coagulation. Better removal was observed
with arsenic (V) [As(V)] than with arsenic (III) [As(III)] in both coagulation
and adsorption. The effect of variations in pH and in the presence of sulphate
was investigated.
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
online.]
Drinking water without arsenic : a review of treatment technologies
(Books/Monographs). Subramanian, K.S.; Swaninathan, T.V.; Viraraghavan,
T.; ENSIC -Bangkok, TH. - Bangkok, Thailand, Environmental Systems Information
Center, 1996. - 35 p.: 14 tab.. - (Environmental systems reviews; no. 37,
1994) 77 ref. Abstract: Arsenic, a known carcinogen, finds its way into
the water supply systems due to industrial discharges, geothermal activities
and agricultural runoffs. The carcinogenic property of arsenic has forced
environmental regulatory agencies around the world to review their maximum
acceptable concentration (MAC) in drinking water supplies, one of the main
sources of human intake. With stricter regulations likely to be in place,
it is necessary to review the treatment processes adopted for the removal
of arsenic and identify a suitable treatment technique, which is efficient
and economical, for reducing the concentration below the MAC. This paper
presents a review of the treatment techniques being employed for the removal
of arsenic from water supplies. These include: coagulation; lime softening;
activated alumina (AA) systems; adsorption; ion exchange; reverse osmosis
(RO); and filtration.
Health : Arsenic Poisoning - India (Journal Article) (Down to earth,
vol. 4, no. 23, April 30, 1996, p. 11). Abstract: The National Human Rights
Commission (NHRC) has sought an updated and detailed report on arsenic
poisoning in six districts - Nadia, Murshidabad, Malda, Burwan and the
24 Parganas (North and South). This came in response to a petition filed
by a Delhi-based advocate and a British human rights activist who have
asked the Commission to look into reported incidents of hundreds of thousands
of people getting disabled or dying because they have to drink water from
contaminated wells as no other source has been provided by the government.
Implications of arsenic genotoxicity for dose-response of carcinogenic
effects. Rudel, R., T.M. Slayton, and B.D. Beck. Reg. Tox. Pharm. 23:87-105
Issues in arsenic cancer risk assessment. Slayton, T.M., B.D.
Beck, K.A. Reynolds, S.D. Chapnick, P.A. Valberg, L.J. Jost, R.A. Schoof, T.D.
Gauthier, and L. Jones. Environ. Health Perspec. 104(10):1012-1014.
Options to safeguard groundwater from arseniferous aquifers in
West Bengal, India. P. Bhattacharya, D. Chatterjee, and G. Jacks.
In: Reaching the Unreached-Challenges for the 21st Century, Proceedings
of the 22nd WEDC Conference, New Delhi, India (eds J. Pickford, S.
House, D. Miles, J. Ockelford, J. Parr, D. Saywell, R. Shaw, B. Skinner,
I. Smout and R. Stear) pp. 258-261.
A surface structural approach to ion adsorption: the charge
distribution model. Hiemstra
T and W.H.Van Riemsdijk. Journal of Colloid and Interface Sci. 179,
488-508 (1996). [CD-MUSIC model of surface complexation, helpful in understanding
the behaviour of As etc. binding to mineral surfaces.]
Toenail trace element levels and breast cancer: a prospective study. M
Garland, JS Morris, GA Colditz, MJ Stampfer, VL Spate, CK Baskett, B Rosner, FE
Speizer, WC Willett and DJ Hunter. Am J Epidemiol 144(7):653-660. [Abstract]
Water technology : Arsenic Removal (Journal Article) - (Down to earth,
vol. 5, no. 1, May 31, 1996, p. 7). Abstract: French researchers, led by
Marc Leblanc from the French national research agency CNRS at the University
of Montpellier, have discovered two strains of bacteria which convert the
soluble form of arsenic into a less toxic precipitate. A stream flowing
through the abandoned Carnoules lead and zinc mine in the Cevennes mountains
in southern France was found to be the home of these bacteria. The researchers
believe that the bacteria could belong to the Thiobacillus and Leptotrix
strains. The discovery may have potential for use in the treatment of drinking
water. (NB) Marc Leblanc, Geofluides-Bassins-Eau (CNRS-Montpellier 2), France, tel.:
+33-467 1445 69, fax: +33-467 1447 74, E-mail: Leblanc@dstu.univ-montp2.fr
1995
Arsenic contamination in groundwater within multilevel aquifer system
of Indo-gangetic delta plains: A case study from West Bengal, eastern India.
P.
Bhattacharya, D. Chatterjee, and G. Jacks. 5th Seminar on Hydrogeology
and Environmental Geochemistry, B. Bølviken Seminar-95; November
9-10, 1995, Norges Geologiske Undersøkelse, Report 95.138, 8-9.
Arsenic in ground water in six districts of West Bengal, India:
the biggest arsenic calamity in the world. Part 1. Arsenic Species in drinking
water and urine of the affected people. Amit Chatterjee, Dipankar
Das, Badal K. Mandal, Tarit Roy Chowdhury, Gautam Samanta and Dipankar
Chakraborti. The Analyst, Royal Society of Chemistry,UK,120,3,643-650,1995.
Arsenic in ground water in six districts of West Bengal, India:
the biggest arsenic calamity in the world. Part 2. Arsenic concentration
in drinking water, hair, nails, urine, skin-scale and liver tissue (biopsy)
of the affected people. Dipankar Das, Amit Chatterjee, Badal Mandal,
Gautam Samanta, Bhabatosh Chanda & Dipankar Chakraborti. The Analyst,
Royal Society of Chemistry,UK,120,3,917-924,1995.
Arsenic removal by coagulation (Journal Article). Do, H.D.; Green,
J.F.;
McLean, S.J.; Scott, K.N.; Metropolitan Water District of Southern California
-La Verne, CA, US In: Journal American Water Works Association; vol. 87,
no. 4 (1995); p. 114-126: 5 fig., 10 tab.. - 24 ref.
Case-control study of bladder cancer and arsenic in drinking water. MN
Bates, AH Smith and KP Cantor. Am J Epidemiol 141(6):523-530. [Abstract]
Diabetes mellitus among Swedish art glass workers - an effect
of arsenic exposure? Mahfazur Rahman, Gun Wingren and Olav Axelson.
Scandinavian
Journal of Work and Environmental Health, 22 146-149, 1995.
Diabetes mellitus and arsenic exposure: a second look at case-control
data from a Swedish copper smelter. Mahfazur Rahman and Olav Axelson.
Occupational
and Environmental Medicine, 52 773-774, 1995.
Ingested arsenic and internal cancer: a historical cohort study
followed for 33 years. T Tsuda, A Babazono, E Yamamoto, N Kurumatani, Y
Mino, T Ogawa, Y Kishi and H Aoyama. Am J Epidemiol 141(3):198-209. [Abstract]
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
online.]
Plant uptake and determination of arsenic species in soil solution under
flooded conditions.
Onken, B. M., and Hossner, L. R. Journal of Environmental Quality, 24: 373 - 381.
Soluble arsenic removal at water treatment plants (Journal Article).
Edwards, M.; McNeil, L.S.; University of Colorado -Boulder, CO, US In:
Journal American Water Works Association; vol. 87, no. 5 (1995); p. 105-113:
6 fig., 4 tab.. - 9 ref.
Source of the Arsenious Sediments at Kachua and Itina, Habra Block,
North 24 Parganas, West Bengal - A Case Study. Subhasis Ghosh and
Sahadeb De. Indian Journal of Earth Sciences, 22 (4): 183-189,
1995.
1994
Arsenic contamination in six districts of West Bengal, India: the
biggest arsenic calamity in the world. Dipankar Das, Amit Chatterjee,
Gautam Samanta, B K Mandal, T R Chowdhury, Gopal Samanta, P P Chowdhury,
C R Chanda, Gautam Basu, Dilip Lodh, Swarup Nandi, Tushar Chakroborty,
Swapan Mandal, Sanjit Mohan Bhattacharya and D Chakraborti. Analyst,
119
(Dec.):
168-170, 1994.
Arsenic in ground water in six districts of West Bengal: The biggest
arsenic calamity in the world. D.Das, Amit Chatterjee, G.Samanta,
D.Chakraborti, et. al., The Analyst, Royal Society of Chemistry,
UK, 119 (12) Dec. 1994, N-168-N-170.
Arsenic in the Environment, Part I: Cycling and Characterization.
Ed. J.O. Nriagu. Wiley, New York, 1994. [Ordering.]
Arsenic in the Environment, Part II: Human Health and Ecosystem
Effects. Ed. J.O. Nriagu. Wiley, New York, 1994. [Description
& ordering.]
Chemistry of arsenic removal during coagulation and Fe-Mn oxidation.
M Edwards. Journal of American Water Works Association, 86 (9):
64-78, 1994.
Enhanced coagulation for arsenic removal (Journal Article).
Beuhler,
M.D.; Cheng, R.C.; Sun Liang; Wang, H.-C.; Metropolitan Water District
of Southern California -La Verne, CA, US In: Journal American Water Works
Association; vol. 86, no. 9 (1994); p. 79-90: 8 fig., 11 tab.. - 23 ref.
Health implications of arsenic in drinking water (Journal Article).
Brown, K.G.; Chien-Jen Chen; Pontius, F.W.; AWWA -Denver, CO, US In: Journal
American Water Works Association; vol. 86, no. 9 (1994); p. 52-63: 3 fig.,
5 tab.. - 85 ref.
The hydrogeochemistry of alluvial aquifers in central Bangladesh, J.
Davies. In: Groundwater Quality; H.Nash and GJH McCall (eds). Chapman
Hall.
Ingested inorganic arsenic and prevalence of diabetes mellitus.
MS Lai, YM Hsueh, CJ Chen, MP Shyu, SY Chen, TL Kuo, MM Wu and TY Tai. Am J
Epidemiol 139(5):484-492. [Abstract]
Metal-induced developmental toxicity in mammals: a review. Domingo
JL. J Toxicol Environ Health 1994 Jun;42(2):123-41. [Abstract]
Studies on the concentrations of arsenic, selenium, copper, zinc, and
iron in the hair of blackfoot disease patients in different clinical stages.
Wang C.T., Chang W.T., et. al. Eur. J. Clin. Chem. Clin. Biochem.
,32:107-11.
1990-3
1993
Arsenic and its compounds (Books/Monographs); Canada. Environment Canada
-CA; Canada. Health and Welfare Canada (CA. - Ottawa, Ont, Canada, Ministry
of Supply and Services Canada, 1993. - vii, 56 p.: 4 fig., 4 tab. - (Priority
substances list assessment report) ISBN 0662204883 Bibliography: p. 36-56.
Removal of arsenic(III) from contaminated ground waters by Ganga
sand. R C Vaishya and I C Agarwal. Journal of Indian Water Works
Association, 25 (3): 249-253, 1993.
Selenium in Nutrition. Revised edition. [Whole
book online]
A Study of Ground Water Contamination by Arsenic in the Residential
Area of Behala, Calcutta due to Industrial Pollution. Amit Chatterjee,
Dipankar Das & D.Chakraborti; Environmental Pollution, 80 (1), 57-65, 1993.
1992
Arsenic ingestion and internal cancers: a review. MN Bates, AH
Smith and C Hopenhayn-Rich. Am J Epidemiol 135(5): 462-476. [Abstract]
Environmental biochemistry of arsenic. Tamaki, S., and Frankenberger, W. T.
Rev. Environ. Contamination Toxicol. 124:79 - 110.
Environmental pollution and chronic arsenicosis in South Calcutta.
D. N. Guha Mazumder, J. Das Gupta, A. K. Chakroborty, A. Chatterjee, D.
Das and D. Chakroborty. Bulletin of the World Health Organizatoin,
70
(4):
481-485, 1992.
Hydrochemical character of the main aquifer units of central and
north-eastern Bangladesh and possible toxicity of groundwater to fish and
humans, J. Davies and C Exley. BGS Technical Report WD/92/43R.
1991
Arsenic pollution in groundwater in West Bengal. PHED.
In: Consultation on arsenic in drinking water and resulting arsenic
toxicity in India and Bangladesh, WHO, New Delhi, 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
online.]
Removal of arsenic from groundwater by lime softening with powdered
coal additive. A Dutta and M Chaudhuri. Aqua, 41 (1):
25-29, 1991. High levels of arsenic in tubewell drinking-water in West Bengal, India,
have been linked to arsenical dermatosis and skin cancer. A laboratory
lime softening test was carried out to remove arsenic from groundwater
samples collected from one of the affected areas. At a lime dose of 1250
mg/l and pH 11.8, maximum removal was 90% whereby arsenic concentration
was reduced from 0.68-0.70 mg/l (arsenic (III) 0.59-0.60 mg/l) to 0.07
mg/l. With powdered bituminous coal additive (2 g/l), residual arsenic
level below the WHO guideline level of 0.05 mg/l was achieved at a lime
dose of 800 mg/l and pH 11.5. The magnesium-hydroxide precipitate played
a more significant role in removing arsenic, particularly arsenic (III)
than calcium carbonate.
1990
Removal of arsenic (III) from groundwater by low-cost materials (Journal
Article). Chaudhuri, M.; Ghua, S.; Indian Institute of Technology -Kanpur,
IN In: Asian environment; vol. 12, no. 1 (1990); p. 42-50: fig., tab..
- Includes references
1980-9
1989
Arsenic, selenium and zinc in patients with blackfoot disease. Lin SM, Yang
MH. Biol Trace Elem Res 15:213-222.
Arsenic in groundwater under oxidizing conditions, south-west United
States. Frederick N. Robertson. Environmental Geochemistry and
Health, 11 171-185, 1989.
Dose-response relation between arsenic concentration in well water and
mortality from cancers and vascular diseases. MM Wu, TL Kuo, YH Hwang
and CJ Chen. Am J Epidemiol, 130(6):1123-1132, 1989. [Abstract]
1988
Arsenic in ground water of the western United States.
Alan H. Welch, Michael S. Lico and Jennifer L. Hughes. Ground Water,
26
(3):
333-347, 1988.
The biochemistry of arsenic. Knowles, F.C. and Benson, A.A. Trends
Biochem. Sci. 8, 178-180
Chronic arsenic toxicity from drinking tubewell water in rural
West Bengal. D.N. Guha Mazumder, A. K. Chakroborty, A. Ghose, J.
Das Gupta, D. Chakroborti, S. B. Dey and N. Chattopadhaya. Bulletin
of the World Health Organization, 64 (4): 499-506, 1988.
Special report on ingested inorganic arsenic - skin cancer, nutritional
essentiality. U.S. Environmental Protection Agency. USEPA, EPA-625/3-87-013.
Washington, D.C., 1988.
1987
Lead, mercury, cadmium and arsenic in the environment.
Ed. T.C. Hutchinson and K.M. Meena. Wiley, New York, 1987
1986
Arsenical dermatosis from tube well water in West Bengal. A K
Chakraborty and K C Saha. Indian Journal of Medical Research 1987,
accepted August 1986.
1985
1984
Chronic arsenic poisoning from tubewell water. Goriar, R,
Chakraborty, K., Pyne, R., 1984. J. Indian Med. Assoc., 82, pp. 34-35.
Arsenic: industrial, biomedical, environmental perspectives.
Ed. W.H. Lederer and R.J. Fensterheim. Van Nostrand Reinhold, New York,
1984
1983
Biological and environmental effects of arsenic. Ed. B.A.
Fowler. Elesevier, Amsterdam, 1983
Chronic arsenic poisoning in the north of Mexico. M E
Cebrian, A Albores, M Aquilar and E Blakely. Human Toxicology, 2
121-133,
1983.
1982
1981
 Environmental Health Criteria 18: Arsenic. WHO. World
Health Organization, Geneva, 1981. [Full
text available online.]
1980
Ground-water geochemistry: arsenic in landfills. A W Hounslow.
Ground
Water, 18 (4): 331-333, 1980.
1970-9
1979
Synergistic toxicity between arsenic and methylated selenium compounds.
Kraus RJ, Ganther H. Biol Trace Elem Res 20:105-113. Schrauzer GN, 1979: Trace elements in carcinogenesis. Advances in
Nutritional Research, ed. HH Draper. C:219-244. Summary: Overview on
essentiality, mutagenicity, antimutagenicity, carcinogenicity etc., of selenium, arsenic, iodine, zinc, cadmium, lead, nickel, chromium, copper,
manganese.
1978
1977
Arsenic: Medical and Biological Effects of Environmental Pollutants (1977).
Commission on Life Sciences. National Academy Press. [Whole
book online]
Effects and dose-response relationships of skin cancer and blackfoot
disease with arsenic. W.P. Tseng. Environmental Health Perspectives,
19
109-119,
1977.
1976
Arsenic stability in contaminated soils. R.E. Hess and
R.W. Blanchar. Soil Soc. Am. J., 40 847-852, 1976.
1975
1974
Biological cycles for toxic elements in the environment.
J. M. Wood. Science, 183 (March): 1049-1052, 1974.
Before 1970
Prevalance of skin cancer in an endemic area of chronic arsenicism
in Taiwan. W P Tseng, H M Chu, S W How, J M Fong, C S Lin and S
Yeh. Journal of the National Cancer Institute, 40 (3): 453-463,
1968.
Geochemistry of arsenic. Y. Onishi and E.B. Sandell. Geochimica
et Cosmochimica Acta, 7, 1-33, 1955.
Selenium metabolism, V: studies on the distribution of Se in rats given arsenic.
Levander OA, Bauman CA. Toxicol. Appl. Pharmacol. 9:98-105. Summary: Interaction of retentions of Selenium
and Arsenic in subacute dosages - presence of one of them makes the body excrete the other more efficiently.
Contact information for Current Science:
Editorial Office, Current Science
C.V. Raman Avenue
Bangalore 560 080, India
Tel 91-80-3342310
Fax: 91 80 3346094
Email: currsci@ias.ernet.in
|
