United States
Environmental Protection
Agency
Environmental Criteria and
Assessment Office
Research Triangle Park NC 27711
Research and Development
EPA/600/S8-83/021F Aug. 1985
&ER& Project Summary
Health Assessment Document for
Inorganic Arsenic
Inorganic arsenic, predominantly the
tri- and pentavalent forms, is emitted
to the environment principally through
primary smelting activity, biocide use,
and glass manufacturing. Ambient air
monitoring data indicate a concentra-
tion equal to or less than 0.1 /tg/m* for
most locations. Major routes of absorp-
tion of inorganic arsenic in the general
population are inhalation and inges-
tion. Inhaled inorganic arsenic
deposited in the lungs is eventually ab-
sorbed. Most ingested soluble in-
organic arsenic is absorbed, whereas
insoluble forms pass through the gas-
trointestinal tract with negligible ab-
sorption. Inorganic arsenic metabolism
in man is complicated by biotransfor-
mation processes which include the
methylation and oxidation reduction in-
terconversion of inorganic arsenic.
Long-term accumulation of inorganic
arsenic does not generally occur in
physiologically active compartments in
the body; renal clearance appears to be
the major route of excretion of absorb-
ed inorganic arsenic. Acute symptoms
of inorganic arsenic poisoning include
severe gastrointestinal damage, facial
edema, cardiovascular reactions,
peripheral nervous system distur-
bances, and hematopoietic system ef-
fects. General population concerns
arising from longterm exposures to
moderate levels of inorganic arsenic in-
clude respiratory tract cancer, skin
cancer, noncancerous skin lesions,
peripheral neuropathological effects
and cardiovascular effects. There ap-
pears to be a nutritional requirement
for low levels of inorganic arsenic in
certain experimental animals;
however, this requirement has not yet
been established in man.
This Project Summary was devel-
oped by EPA's Environmental Criteria
and Assessment Office, Research
Triangle Park, NC, to announce key
findings of the research project that is
fully documented in a separate report
of the same title (see Project Report
ordering information at back).
Introduction
As a toxic agent, inorganic arsenic
possesses several unique properties. The
element exists in various chemical states;
e.g., tri- and pentavalent inorganic arsenic
and methylated organic arsenic, with each
having differing toxicological potential. In
man, experimental animals, and other
organisms, arsenic undergoes a variety of
transformations, the full significance and
mechanisms of which are, as yet, not well
understood. Furthermore, there appears to
be a nutritional requirement for low levels
of arsenic in certain experimental animals,
and this may also be the case for man. All
of these factors complicate the analyses of
the toxicological effects and the risk for
human health associated with environ-
mental exposure to arsenic compounds.
The following sections summarize these
factors which are presented in depth in the
document text.
Chemical/Physical Aspects
of Arsenic
Arsenic is encountered as a component
of sulfidic ores of metals such as copper,
cobalt, and nickel; the smelting of these
ores is associated with arsenic release to
the environment. Arsenic trioxide, ASjOa, a
lexicologically significant form, is a smelter
product arising from air roasting of the
sulfidic ores. It is only sparingly soluble in
water and other solvents which do not pro-
mote chemical transformation. This arsenic
compound dissolves in acidic or alkaline
aqueous media to yield either the free acid
or salts, soluble in a number of solvents.
The oxide readily sublimes (135°C), a factor
important in choosing analytical methods
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for measuring levels of the compound. The
pentavalent arsenic pentoxide, As206, may
be prepared by nitric acid oxidation of the
trioxide or the element itself. This form has
high solubility in water (63 g/100 g water),
forming the strongly oxidizing arsenic acid,
H3As04 (E° = 0.56V).
Stability of the valency forms of arsenic
in solution depends on the nature of the
medium. Oxygenated media and higher pH
favor the pentavalent form, while reducing
and/or acidic media favor the trivalent state.
The acids of both valency forms of
arsenic readily form alkali and alkaline metal
salts, with the former being more soluble
than the latter. Organic ester derivatives of
arsenic are quite labile to hydrolysis, and
this chemical behavior has biochemical/
toxicological implications in the postulated
role of arsenate ion in interfering with phos-
phorylation reactions.
Arsine (arsenic trihydride, AsH3) is the
most poisonous of the arsenicals, being a
strong hemolytic agent; it can be formed
under certain restricted conditions, e.g.,
reduction of the oxy compounds in the
presence of a strong hydrogen source.
Monomethyl and dimethyl arsenic arise
by both environmental and in vivo trans-
formation processes.
In high-temperature processes, arsenic is
released as a vapor which is then adsorbed
or condensed onto small particles. Such
adherence to particles of 1-2 /im or less may
result in enhanced health risk from the
agent since particles in this size range are
inhaled and deposited in the deepest part of
the respiratory tract.
Arsenic compounds tend to form insolu-
ble complexes with soils and sediments. In
the case of soils, the interaction occurs
with amorphous aluminum or iron oxides.
The Environmental
Cycling of Arsenic
Primary smelting, biocide use, and glass
manufacturing are major sources of arsenic
in the environment. Of an estimated total
release of approximately 10,000 short tons
annually in the United States, smelter ac-
tivity accounts for 50 percent; use of
biocide (pesticide, fungicide, herbicide), 32
percent; and glass production contributes
about 7.0 percent; various other sources
release the remainder.
The atmosphere is a major conduit for
arsenic emitted from anthropogenic
sources via wet and dry precipitation pro-
cesses to the other environmental media.
Dry and wet arsenic falling on soils may be
followed by movement through soils either
into groundwater or surface water. Passage
of arsenic into surface waters may be
followed by its transfer to sediments. Such
cycling is made complex by chemical and
biological transformations, which have
been reported as occurring in the various
environmental compartments.
Trivalent arsenic in the atmosphere or in
aerated surface waters can undergo oxida-
tion to the pentavalent state, while pen-
tavalent arsenic in media which are below
pH 7.0 and contain oxidizable material can
be reduced to the trivalent form.
Biological transformations of arsenic
have been documented as occurring via
both sedimentary bacteria and suspended
marine algae. Reduction and mythylation of
inorganic arsenic occur only to a limited ex-
tent in soils, one report noting a conversion
of only 1-2 percent over a period of months.
The annual environmental burden of
arsenic indicates that approximately 90 per-
cent of arsenic is deposited on land, with
the atmosphere accounting for eight per-
cent and the smallest quantity deposited in
waters.
Levels of Arsenic
in Various Media
Available data on levels of arsenic in
various media with which man interacts are
generally presented as total arsenic, with
limited information available for identifying
specific chemical forms of arsenic.
Levels of Arsenic in Ambient Air
Based on the comprehensive data for
U.S. air levels of arsenic obtained by the
U.S. EPA's National Air Sampling Net-
work, air levels of arsenic in the U.S.
generally do not exceed 0.1 /*g/m3.
Generally, airborne arsenic adheres to
particulate matter. Although the immediate
areas around smelters may contain some
arsenic in the vapor form, available data in-
dicate rapid adherence to particulate matter
when sampling 2-3 km from these emission
sites.
The specific chemical form(s) of airborne
arsenic is still unclear. Generally, in most
urban/suburban areas, arsenic occurs
mainly in the form of a mixture of inorganic
arsenic in the tri- and pentavalent states.
Only in areas where methylated arsenic is
used agriculturally, or where biotic trans-
formation can occur, has methylated
arsenic been found in air samples.
Levels of Arsenic
in Drinking Water
The National Interim Primary Drinking
Water Regulations, promulgated under the
Safe Drinking Water Act, set the Maximum
Contaminant Level (MCL) for arsenic in
U.S. public water supplies at 50
general, arsenic is not found in drinkin
water at levels exceeding this MCL. W*
waters in the western U.S. and Alask;
however, may have much higher levels ov
ing to geochemical enrichment. In Lar
County, Oregon, recent analyses repo
levels up to 2.2 ppm (2.2 mg/liter), whi
the highest figure in Alaska was 10 ppm (1
mg/liter), representing both natural an
mining residue contributions.
It is reasonable to assume that the chii
chemical form of arsenic in most publ
water supplies would be the pentavalent ir
organic form, owing to both aeration an
chlorination. Similarly, well waters i
Alaska and the western U.S. are reporte
to mainly contain pentavalent inorgan
arsenic.
Arsenic in Food
The most recent data base for the arson
content of foods is the 1975-1976 surve
carried out by the U.S. Food and Drug Ac
ministration. Shellfish and other marir
foods have the highest levels on a foe
category basis. Overall, the total dietary it
take of arsenic in 1975-1976 was appro:
imately 50 fig (elemental arsenic), repn
senting an increase from the precedin
years. Whether this increase represents
trend or merely reflects analytical variatic
in sampling from year to year is still to t
determined.
The chemical forms of arsenic in fooc
are varied and complex. Crustaceans ar
other marine life store arsenic in compk
organoarsenical forms which, based on n
cent reports, are assimilated by man ar
generally excreted intact. Toxicologicall
these forms are comparatively inert.
Arsenic in Soils
Background soil arsenic levels ranc
from less than 1 ppm to over 40 ppm, tf
latter reflecting agricultural practices <
well as air fallout. Soil arsenic is usual
bound to clay surfaces, and its mobility is
function of soil pH, phosphate levels, ire
and aluminum content, and soil type. Tl
mobile fraction, usually in the pentavale
form, is of concern in terms of moveme
to plants and water. Little reducth
methylation occurs in most soils.
Other Sources of Arsenic
Limited data on arsenic content of toba
co suggest that more recent values rant
from around 1.5 ppm or less, while in tl
past (1945), values up to 40 ppm we
measured. This decrease reflects reduct
use of arsenical biocides in tobacco produ
tion.
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Aggregate Exposure Levels to
Arsenic in the U.S. Population
Among individuals of the general popula-
tion (not occupational^ exposed to
arsenic), the main routes of exposure to
arsenic are typically via ingestion of food
and water, with lesser exposures occurring
via inhalation. Representative intake figures
are presented in Table 1. Intake by inhala-
tion is augmented among smokers in pro-
portion to the level of smoking.
Assuming a daily ventilation rate of 20
m3, and a national population inhalation
average of 0.006 /*g/m3/As, the total daily
inhalation exposure for arsenic can be pro-
jected to be approximately 0.12 fig. Assum-
ing 30 percent absorption, approximately
0.03 /tg of arsenic would be absorbed on a
daily average.
Contribution of tobacco-borne arsenic to
the respiratory burden would depend upon
the rate of cigarette smoking. Assuming a
mass of 1 gram/cigarette and an average
tobacco value of 1.5 ppm, this yields 1.5 fig
arsenic/cigarette. With 20 percent of this
amount in mainstream smoke, the inhaled
amount for each pack of cigarettes would
be approximately 6 /*g arsenic, and of this
amount, 40 percent would be deposited in
the respiratory tract. Assuming an absorp-
tion of 75 percent of the deposited fraction,
approximately 2 g/pack of cigarettes would
be absorbed. This represents a factor of 10
to 100 times greater than intake for
nonsmokers in given ambient air settings.
The rates of absorption for trivalent and
pentavalent arsenic in the respiratory tract
are assumed to be equivalent.
Since drinking water arsenic is mainly in
a soluble form (arsenate or arsenite), vir-
tually all of it is absorbed in the Gl tract.
Thus, assuming an average daily consump-
tion of two liters of water containing at
most 10 ing As/liter as an outside high
figure, it can be estimated that the total
arsenic absorbed from drinking water
would be approximately 20 fig/day. Most
individuals would, in reality, take in much
less than this amount, while those in the
Western U.S. with well water supplies
much higher in arsenic content would
assimilate proportionately more.
Food arsenic values taken from the 1976
FDA survey indicate a daily total dietary in-
take of approximately 50 /*g elemental
arsenic. The major portion (80 percent) of
food arsenic would be absorbed, resulting
in a net daily food arsenic absorption of 40
lig total.
Thus, a nonsmoker would have a total
daily absorption from all exposure media of
approximately 60 HQ arsenic/day or less. Of
this, the diet would be the major con-
Table 1. Routes of Daily Human Arsenic Intake
Route/Level Rate
Total Intake
Absorbed Amount
Ambient air/ 0.006 ng/m3 (a)
Drinking water/ < 10 ng/ liter
Food/SO ng daily (elemental As)
Cigarettes/ 6 ng in mainstream smoke/ pack le)
Total: < 60 fig nonsmokers
20m3
2 liters
Vi pack
1 pack
2 pack
0. 12 pg
50 M
3/i9
6119
12 W
0.036 ft
40 it
0.9 n
1.8 p
2.7 f.
p!c!
g(1)
gtt)
{a]National Average for 1981.
lbl'Assumes 30 percent respiratory absorption.
M Assumes total absorption.
ldl'Assumes 80 percent absorption.
MAssumes 20 percent of cigarette content in inhaled smoke.
w Assumes 30 percent absorption of inhaled amount.
tributor, assuming levels in water much
below 10 /tg/liter. For cigarette smokers, 2
jig/arsenic/pack of cigarettes smoked daily
would have to be added.
If aggregate intake is viewed not in terms
of total arsenic intake but in terms of tox-
icologically significant forms of the ele-
ment, then much of the dietary fraction, for
reasons given earlier, such as complex
organoarsenicals being present, becomes
relatively less important than the forms in
water and air as well as in cigarette smoke.
Arsenic forms in such media include pen-
tavalent arsenic in most water supplies,
variable mixtures of tri- and pentavalent
arsenic in ambient air, and probably an
arsenic oxide in cigarette smoke. From this
viewpoint, utilizing the examples already
given above, nonsmokers would absorb 20
fig or less daily of lexicologically significant
arsenic. Heavy smokers having otherwise
very low air and water exposure, con-
ceivably could receive their major exposure
via cigarettes.
Significant Human Health
Effects Associated With
Ambient Exposure Acute
Exposure Effects
Serious acute effects and late sequelae
from exposure to arsenic will appear after
single or short-term respiratory or oral ex-
posures to large amounts of arsenic.
Available data indicate that inorganic
trivalent compounds of arsenic are general-
ly more acutely toxic than inorganic pen-
tavalent compounds, which in turn are
more toxic than organic arsenic com-
pounds. Serious effects will also appear
after long-term exposure to respiratory or
oral doses of arsenic.
The acute symptoms following oral ex-
posure consist of gastrointestinal disturb-
ances, which may be so severe that secon-
dary cardiovascular effects and shock may
result and cause death. Also, direct toxic
effects on the liver, blood-forming organs,
the central and pheripheral nervous
systems, and the cardiovascular system
may appear. Some symptoms, especially
those from the nervous system, may ap-
pear a long time after exposure has ceased
and may not be reversible, whereas the
other effects seem to be reversible. Infants
and young children especially are suscepti-
ble with regard to effects on the central ner-
vous system. A Japanese study on milk
poisoned with arsenic showed that per-
sisting damage, especially mental retarda-
tion and epilepsy, is a late sequela in
children of short-term oral exposure to
large doses of inorganic arsenic. Among
adults, the central nervous system is not as
susceptible, but peripheral neuropathy has
been a common finding.
Both in adults and children, acute oral
exposure has resulted in dermal changes,
especially hyperpigmentation and kera-
tosis, as a late sequela.
Acute inhalation exposures have also
resulted in irritation of the upper respiratory
tract, even leading to nasal perforations.
Direct dermal exposure to arsenic may
lead to dermal changes; allergic reactions
may also be involved.
Chronic Exposure Effects
Both carcinogenic and non-carcinogenic
effects are associated with long-term ex-
posures, which do not cause any obvious
immediate effects. Chronic effects ger-
mane to the general population can be
ranked as follows:
1. Respiratory tract cancer
2. Skin cancer
3. Non-cancerous skin lesions
4. Peripheral neuropathological effects
5. Cardiovascular changes
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Cancer of the respiratory system is
clearly associated with exposure to ar-
senic via inhalation. This association has
been especially noted among smelter
workers where there is a consistency of
findings across different studies in dif-
ferent countries, high relative risk, and
dose-response by length and intensity of
exposure. Excess risk of lung cancer has
also been found among arsenical pesti-
cide manufacturing workers. Based on
this information, the Carcinogen Assess-
ment Group (CAG) of the U.S. Environ-
mental Protection Agency has concluded
that there is sufficient evidence that
inorganic arsenic compounds are lung
carcinogens in humans.
Cancer of the skin was found to have a
dose-related effect in a population in
Taiwan who had lifetime exposure to
arsenic in well water. Cancer of the skin
has also been found among people treated
with large doses of arsenite for skin
disorders. The CAG has concluded that
there is sufficient evidence that inorganic
arsenic compounds are skin carcinogens
in humans.
Hyperkeratosis and hyperpigmentation,
sometimes with precancerous changes,
have been a common finding in persons in-
gesting arsenic. These skin lesions, as well
as the manifest cancer, develop on skin sur-
faces usually unexposed to sunlight. In
studies in the United States, an association
between skin lesions or skin cancer has not
been demonstrated. These studies have
been limited, however, by sample sizes too
small to be able to detect the dose response
seen in studies outside the U.S.
The effects on the peripheral nervous
system range from sensory disturbances to
motor weakness and even paralysis. The
more severe signs have been noted in
subacute poisonings, but more subtle
changes after long-term low-level exposure
have been found by using electromy-
ography or measuring nerve conduction
velocity. These subclinical effects are slow
in recovery and may persist for years after
cessation of exposure. In a study in
Canada, electromyographic (EMG)
changes were noted when water concen-
trations of arsenic exceeded 0.05 mg/l.
Cardiovascular effects have been noted
especially in Taiwan, where Blackfoot
disease (peripheral vasculopathy) occurred
after long-term exposure to arsenic in well
water. However, the presence of ergota-
mine-like compounds raises the possibility
of vascular effects from these agents.
Peripheral vascular changes were also
found among German vintners who were
exposed both occupationally, by spraying
arsenic-containing pesticides, and orally.
by drinking wine with elevated arsenic
levels. Studies on occupationally exposed
persons have been inconclusive in showing
that arsenic causes an increase in mortality
from cardiac disease.
Dose-Effect/Dose-Response
Relationships
The general question of how to define
and employ a dose factor in attempts at
quantitative assessments of human health
risk for any toxicant is highly dependent
upon: 1) the available information on the
body's ability to metabolize the agent, and
2) the assessment of the relative utility of
various internal indices of exposure.
The time period over which a given total
intake occurs is highly important. For ex-
ample, intake of one gram of arsenic over a
period of years would be quite different
pathophysiologically from assimilating this
amount at one time, the latter probably
having a lethal outcome. This time-
dependent behavior is related in part to the
relative ability of the body to detoxify in-
organic arsenic by methylation as a func-
tion of both dose and time.
In cases of acute and subacute exposure,
indicators of internal exposure such as
blood or urine arsenic levels are probably
appropriate for assessing the intensity of
exposure.
With chronic, low-level exposure, how-
ever, the available data would indicate that
the total amount assimilated is probably
more important than an indicator concen-
tration without knowledge of the total ex-
posure period. An added problem is the
background level of arsenic found in these
indicators due to dietary habits. For exam-
ple, in acute exposures, levels in blood or
urine would be greatly elevated over
background values while low-level chronic
exposures would only result in moderate in-
creases over background.
In regard to hair arsenic levels as an in-
dicator of internal arsenic exposure, no
reliable methods exist for distinguishing ex-
ternal contamination levels from those ac-
cumulated via absorption and metabolic
distribution. Hair arsenic levels cannot,
therefore, be employed as reliable in-
dicators of either current or cumulative
long-term exposures for individual subjects,
but rather may provide only a rough overall
indication of group exposure situations.
Given the above considerations and
limitations concerning the use of blood,
urinary, or hair arsenic concentrations as in-
ternal indices of cumulative, long-term low-
level arsenic exposures of concern here, the
dose-effect/dose-response relationships
summarized below are done so mainly in
terms of external arsenic exposure levels v
either inhalation or ingestion.
It is difficult to define a precise acul
lethal dose of arsenic for man, becaus
such exposure situations rarely allow a<
curate determination of the effectiv
amounts. However, for trivalent arsenii
the figure is believed to range from 70 1
180 milligrams.
For subacute exposure, it appears thi
for children, about one gram assimilate
over a period of 3-4 weeks will induce deal
with severe effects in survivors, while f<
adults, that dose will occasion significar
clinical effects. In one poisoning episodi
intake of approximately 50 milligrams over
period as short as two weeks resulted i
clinically demonstrable effects in adults.
From available data, the Carcinoge
Assessment Group (CAG) has estimate
carcinogenic unit risks for both air an
water exposures to arsenic. The quar
titative aspect of carcinogen risk asses:
ment is included here because it may be c
use in setting regulatory priorities
evaluating the adequacy of technology
based controls, and other aspects of th
regulatory decision-making process
However, the imprecision of present
available technology for estimating canct
risks to humans at low levels of exposui
should be recognized. At best, the line;
extrapolation model used provides a roug
but plausible estimate of the upper limit c
risk—that is, with this model it is not like
that the true risk would be much more tha
the estimated risk, but it could be cor
siderably lower. The risk estimate
presented below should not be regardec
therefore, as accurate representations <
true cancer risks even when the exposure
involved are accurately defined. Th
estimates presented may, however, be fai
tored into regulatory decisions to the exter
that the concept of upper-risk limits
found to be useful.
The air estimates were based on dal
obtained in five separate studies involvin
three independently exposed worker pop
ulations. Both linear and quadratic absc
lute risk and relative risk models wer
fitted to the data. It was found that for th
models that fit the data at the p = 0.01 c
better level, the corresponding unit ris
estimates ranged from 1.05x10~4to1.3
x 10~2. Linear models were found to f
better than quadratic models, and absc
lute risk models better than relative ris
models. Restricting their unit risk esi
imates to those obtained from linee
absolute risk models gave a range of 1.2
x 10"3to 7.6 x 10"3. A weighted average c
the five estimates in this range gave
composite estimate of 4.3 x 10~3.
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The unit risk estimates for water were
based on an extensive drinking water study
which was conducted in a rural area of
Taiwan. An association between arsenic in
well water and skin cancer was observed in
the study population. Using the male
population, who appeared to be more
susceptible, the CAG estimated that the
unit risk associated with drinking water
contaminated with 1 yug/l of arsenic was
4.3 x 10'4
To compare the air and water unit risks,
the CAG converted the exposure units in
both cases to mg/kg/day absorbed doses,
which resulted in unit risk estimates of 50.1
and 15.0, respectively.
The potency of arsenic compared to
other carcinogens was evaluated by noting
that an arsenic potency of 2.25 x 10*3
(mMol/kg/day)"' lies in the first quartile of
the 52 suspect carcinogens that have been
evaluated by the CAG.
The U.S. EPA is presently examining in-
formation from studies on both patient and
general populations which have been ex-
posed to arsenic via medicinals or drinking
water, respectively, in order to determine
whether quantitative dose-response rela-
tionships can be established for non-
cancerous skin lesions.
While the qualitative evidence for
peripheral neurological effects and car-
diovascular changes in arsenic-exposed
populations is well established, the data are
insufficient for determining quantitative
dose-response relationships at the present
time.
Populations at Special Risk to
Health Effects of Arsenic
From a Japanese study, which reported
on the poisoning of children exposed to
arsenic in infant milk formula, young
children may be considered at risk for acute
exposure to arsenic. From the clinical
reports published at the time of the mass
poisoning, as well as those from follow-up
studies, a number of signs of central ner-
vous system involvement were noted at
both the time of the episode and much
later, with the follow-up studies showing
behavioral problems, abnormal brain wave
patterns, marked cognitive deficits, and
severe hearing loss.
Because children consume more water
per unit body weight than do adults, the
daily intake of arsenic via drinking water per
kilogram body weight would be greater in
children. This might have implications
regarding chronic exposure effects in
children. However, it should be noted that
serious health effects due to chronic ex-
posure of arsenic in drinking water have not
been found at a greater frequency in
children than adults.
Individuals residing in the vicinity of cer-
tain arsenic-emitting sources, e.g., certain
types of smelters, may be at risk for in-
creased arsenic intake because of both
direct exposure to arsenic in air and indirect
exposure via arsenic secondarily deposited
from air onto soil or other human exposure
media. The relative contribution from such
indirect exposures to increased risk would
be difficult to define, however.
A less defined group at risk would be
cigarette smokers due to some arsenic in
tobacco, but it is not clear just what the
quantitative increase in risk would be.
^U.S.GOVERNMENTPRINTINGOFFia 1985/559-111/20661
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This Project Summary was prepared by staff of Environmental Criteria and
Assessment Office, U.S. Environmental Protection Agency, Research Triangle
Park, NC 27711.
Donna J. Sivulka is the EPA Project Officer (see below).
The complete report, entitled "Health Assessment Document for Inorganic
Arsenic," (Order No. PB 84-190 891; Cost: $23.50, subject to change) will be
available only from:
National Technical Information Service
5285 Port Royal Road
Springfield. VA 22161
Telephone: 703-487-4650
The EPA Project Officer can be contacted at:
Environmental Criteria and Assessment Office
U.S. Environmental Protection Agency
Research Triangle Park, NC27711
United States
Environmental Protection
Agency
Center for Environmental Research
Information
Cincinnati OH 45268
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EPA/600/S8-83/021F
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CHICAGO
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