United States
Environmental Protection
Agency
Office of Health and
Environmental Assessment
Washington. DC 20460
Research and Development
EPA/600/S8-84/026F July 1988
4>EPA Project Summary
Health Assessment
Document for Beryllium
The chemical and geochemical
properties of beryllium resemble
those of aluminum, zinc, and mag-
nesium. This resemblance is pri-
marily due to similar ionic potentials
that facilitate covalent bonding. The
three most common forms of
beryllium in industrial emissions are
the metal, the oxide, and the
hydroxide.
The main routes of beryllium
intake for man and animals are
inhalation and ingestion. While the
absorption of ingested beryllium is
probably quite small, the chemical
properties of beryllium are such that
inhaled beryllium has a long
retention time in the lungs and, thus,
a greater potential for absorption
and/or physical irritation. The tissue
distribution of absorbed beryllium is
characterized by depositions pri-
marily in the skeleton where the
biological half-time is fairly long.
The lung is the critical organ of
both acute and chronic non-
carcinogenic effects. However, unlike
most other metals, the lung effects
caused by chronic exposure to
beryllium may be combined with
systemic effects, of which one
common factor may be hypersen-
sitization. Certain beryllium com-
pounds have shown carcinogenic
activity in various experimental ani-
mals by various routes of exposure,
but not by ingestion per se.
Epidemiologic studies are inade-
quate to demonstrate or refute a
human carcinogenlcity potential. In
terms of the weight of evidence for
carcinogenicity. beryllium is judged
to be in Group B2 signifying that the
animal evidence for carcinogenicity
is sufficient and that beryllium and
its compounds are regarded as
probably carcinogenic for humans.
This Project Summary was
developed 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
The full report evaluates the effects
of beryllium on human health, with
particular emphasis on those effects that
are of most concern to the general U.S.
population. It is organized into chapters
that present in a logical order those
aspects of beryllium that relate directly to
human health risk. The chapters include:
an executive summary (Chapter 2);
background information on the chemical
and environmental aspects of beryllium,
including levels of beryllium in media
with which U.S. populations may come
into contact (Chapter 3); beryllium
metabolism, where absorption, biotrans-
formation, tissue distribution, and
excretion of beryllium are discussed with
reference to the element's toxicity
(Chapter 4); beryllium toxicology, where
the various acute, subacute, and chronic
health effects of beryllium in man and
animals are reviewed (Chapter 5);
beryllium mutagenesis, in which the
ability of beryllium to cause gene
mutations, chromosomal aberrations, and
sister-chromatid exchanges is
discussed (Chapter 6); and information
on beryllium carcinogenesis, which
includes a discussion of selected dose-
effect and dose-response relationships
(Chapter 7).
The full report is not an exhaustive
review of all the beryllium literature, but
is focused instead upon those data
thought to be most relevant to human
health risk assessment. Literature on
beryllium was collected and reviewed up
to January 1986. General information
pertaining to the calculation of unit risk
values was reviewed up to April 1987. In
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view of the fact that the full document is
to provide a basis for making decisions
regarding the regulation of beryllium as a
hazardous air pollutant under the
pertinent sections of the Clean Air Act,
particular emphasis is placed on those
health effects associated with exposure
to airborne beryllium. Health effects
associated with the ingestion of beryllium
or with exposure via other routes are also
discussed, providing a basis for possible
use of this document for multimedia risk
assessment purposes. The background
information provided on sources,
emissions, and ambient concentrations of
beryllium in various media is presented
to provide a general perspective for
viewing the health-effects evaluations
contained in later chapters of the
document. More detailed exposure
assessments will be prepared separately
for use in subsequent U.S. Environmental
Protection Agency (EPA) reports re-
garding regulatory decisions on beryl-
lium.
Results and Conclusions
Background
The industrial use of beryllium has
increased tenfold in the last 40 years.
Despite this fact, increases in the
environmental concentrations of beryl-
lium have not been detected. Atmos-
pheric beryllium is primarily derived from
the combustion of coal.
Contamination of the environment
occurs almost entirely by the deposition
of beryllium from the air. Beryllium from
the atmosphere eventually reaches the
soil or sediments, where it is probably
retained in the relatively insoluble form of
beryllium oxide. Since the time of the
industrial revolution, it is likely that no
more than 0.1 ng Be/g has been added
to the surface of the soil, which has a
natural beryllium concentration of 0.6
pg/g. Distributed evenly throughout the
soil column, beryllium derived from the
atmosphere could account for not more
than one percent of the total soil
beryllium. Allowing for greater mobility of
atmospheric beryllium in soil than natural
beryllium, it is possible that 10 to 50
percent of the beryllium in plants and
animals may be of anthropogenic origin.
The typical American adult usually
takes in 400 to 450 ng Be/day, of which
50 to 90 percent comes from food and
beverages. Some of this beryllium found
in food may be derived from the
atmosphere; however, aside from
primary and secondary occupational
settings, air or dust has little impact on
total human intake.
Beryllium Metabolism
Inhalation and ingestion are the main
routes of beryllium intake for man and
animals. Percutaneous absorption is
insignificant. Due to the specific chemical
properties of beryllium compounds, even
primarily soluble beryllium compounds
are partly transformed to more insoluble
forms in the lungs. This can result in long
retention time in the lungs following
exposure to all types of beryllium
compounds. Like other paniculate matter,
dose and particle size are critical factors
that determine the deposition and
clearance of inhaled beryllium particles.
Of the deposited beryllium that is
absorbed, part will be rapidly excreted
and part will be stored in bone. Beryllium
is also transferred to regional lymph
nodes. Beryllium transferred from the
lungs to the gastrointestinal tract is
mainly eliminated in the feces with only a
minor portion being absorbed.
There are no quantitative data on
absorption of beryllium from the gastro-
intestinal tract in humans, but several
animal studies indicate that the
absorption of ingested beryllium is less
than one percent. The absorption of
beryllium through intact skin is very
small, as beryllium is tightly bound in the
epidermis.
Absorbed beryllium will enter the
blood, but there are no data on the
partitioning of beryllium between plasma
and erythrocytes. In plasma, there are
limited data to suggest that, at normally
occurring levels of beryllium, the main
binding is to various plasma proteins. In
animal experiments, it has been shown
that large doses of injected beryllium are
found in aggregates bound to phosphate.
The smaller the dose, the more beryllium
will be in the diffusible form. The data
are insufficient to permit an estimate of
the levels of beryllium normally occurring
in blood or plasma.
Absorbed beryllium is deposited in
the skeleton, with other organs
containing only very low levels. In the
liver, beryllium seems to be preferentially
taken up by lysosomes. There are not
enough data to permit any definitive
conclusions about the distribution and
amounts of beryllium normally present in
the human body. However, total body
burden is probably less than 50 tig.
Based on animal studies, beryllium
appears to have a long biological half-
time, caused mainly by its retention in
bone. The half-time in soft tissues is
relatively short, except in the lung.
Beryllium seems to be normally
excreted in small amounts in urine,
normal levels being only a
nanograms per liter. Animal data indicati
that some excretion occurs by way of th<
gastrointestinal tract.
Beryllium Toxicology
Subcellular and Cellular Aspects
of Beryllium Toxlcity
It is not well known in what form c
through which mechanism beryllium i
bound to tissue. Beryllium can bind t
lymphocyte membranes, which ma
explain the sensitizing properties of th
metal. A number of reports describ
various in vivo and in vitro effects c
beryllium compounds on enzymes
especially alkaline phosphatase, to whic
beryllium can bind. Effects on protei
and nucleic acid metabolism have bee
shown in many experimental studie;
however, the doses in these studies hav
been large and parenterally administers*
Because such administrative routes hav
less practical application to humans, th
data from these studies have limite
utility in advancing an understanding i
human effects, which are mainly on tt-
lung. Beryllium particles retained in th
lung are found in the macrophages, ar
the understanding of how these and oth<
pulmonary cells metabolize beryllium
probably of most relevance to the u
derstanding of chronic beryllium diseas
An important aspect of berylliu
toxicology is that beryllium can cau:
hypersensitivity which is essential
cell-mediated. There are species d
ferences; humans and guinea pigs c;
be sensitized to beryllium, whereas tl
present data indicate that no sue
mechanism exists for the rat. There a
also strain differences among guinea pit
indicating that a genetic component mi
be operative. Patch tests have been usi
to detect beryllium hypersensitivity
humans, but these tests are no long
used since they were shown to cause
reactivation of latent beryllium disea;
Presently, the lymphoblast transformatii
test is regarded as the most useful test
detect hypersensitivity to beryllium.
Pulmonary and Systemic
Toxicity of Beryllium in Man an
Animals
There are no data indicating tl
moderate beryllium exposure by o
administration causes any local
systemic effects in humans or anim.
Respiratory effects, occasionally co
bined with systemic effects, constit
the major health concern of beryllii
exposure, with hypersensitization lik
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laying an important role in the
manifestation of the systemic effects.
Respiratory effects may occur as either a
nonspecific acute disease or as a more
specific chronic beryllium disease.
The most acutely toxic beryllium
compounds are probably beryllium
oxides fired at low temperatures, e.g.,
500°C, and some salts, such as the
fluoride and the sulfate. The latter forms
of beryllium are acidic, and part of the
toxic reactions caused by these com-
pounds may be due to the acidity of the
particles. Acute effects have generally
occurred at concentrations above 100 pg
Be/m3. The main feature of such effects
is a chemical pneumonitis which may
lead to pulmonary edema and even
death. In animal experiments, concen-
trations of more than 1 mg/m3 have
generally been needed to produce acute
effects, but effects have been reported at
lower levels of exposure. In most cases,
the acute disease will regress, but it may
take several weeks or months before
recovery is complete. If there is no
further excessive exposure to beryllium,
it is generally believed that acute disease
will not lead to chronic beryllium disease.
The amount initially deposited during
acute exposure and an individual's pre-
disposition are probably the main factors
leading to later sequelae.
Acute beryllium poisoning was quite
common in the 1940's, but since the
present standards were established in
1949, the number of new cases reported
has been relatively small.
Chronic beryllium disease occurred
as an epidemic in the 1940's, which led
to the establishment of the "Beryllium
Case Registry" (BCR), a file for all cases
of acute and chronic beryllium disease.
Chronic beryllium disease is char-
acterized by dyspnea, cough, and weight
loss. It is sometimes associated with
systemic effects in the form of
granulomas in the skin and muscles, as
well as effects on calcium metabolism.
There are many similarities between
chronic beryllium disease and sar-
coidosis, but in sarcoidosis the systemic
effects are much more prominent. In
most cases of chronic beryllium disease,
there are only lung effects without
systemic involvement. Pathologically, the
disease is a granulomatous interstitial
pneumonitis in which eventually there
may be fibrosis, emphysema, and also
cor pulmonale. Deaths from chronic
beryllium disease are often due to cor
pulmonale. A long latency time is typical;
sometimes there may be more than 20
years between last exposure and the
diagnosis of the disease.
It has been very difficult to establish
the levels of beryllium in air that may
cause the disease. One reason for this
difficulty is that exposure data have not
always been obtainable. Another factor is
that hypersensitization may cause the
occurrence of the disease in people with
relatively low exposures, whereas in
nonsensitized people with much higher
exposures there may be no effects.
Diagnosis of the disease is obtained by
X-ray examinations, but vital capacity
may decrease before roentgenological
changes are seen. Hypersensitization
can be detected by the lymphoblast
transformation test.
There are limited data on levels of
beryllium found in lung tissue in cases of
acute and chronic beryllium disease, and
these data do not allow for conclusions
about dose-effect relationships.
New cases of chronic beryllium
disease are still being reported due to
the fact that, in some instances, the
occupational standards have been ex-
ceeded. In industries where the average
exposure generally has been below 2
ng/m3, there have been very few new
cases of chronic beryllium disease.
There have also been a large
number of "neighborhood" cases of
beryllium disease. Neighborhood cases
are those in which chronic beryllium
disease occurs in people living in the
vicinity of beryllium-emitting plants. The
air concentrations of beryllium in such
areas at the time when the disease
occurred have probably been around 0.1
iig/m3, but considerable exposure via
dust transferred to homes on workclothes
likely contributed to the occurrence of
the disease. No new "neighborhood"
cases of beryllium disease have
occurred since standards of 0.01 iig/m3
were set for the ambient air and the
practice of washing workers' clothes in
the plants was initiated. Presently,
ambient air levels are generally below 1
Ng/m3, although a few urban areas report
values between 1 and 6 Ng/m3.
Dermatological Effects of
Beryllium Exposure
Contact dermatitis and some other
dermatological effects of beryllium have
been documented in occupationally
exposed persons, but there are no data
indicating that such reactions have
occurred, or may occur, in the general
population.
Teratogenic and Reproductive
Effects of Beryllium Exposure
Available information on the
teratogenic or reproductive effects of
beryllium exposure is limited to three
animal studies. The information from
these studies is not sufficient to
determine whether beryllium compounds
have the potential to produce adverse
reproductive or teratogenic effects.
Further studies are needed in this area.
Mutagenic Effects of Beryllium
Exposure
Beryllium has been tested for its
ability to cause gene mutations in
Salmonella typhimurium, Escherichia
co//', yeast, cultured human lymphocytes,
and Syrian hamster embryo cells; DNA
damage in Escherichia co//; and
unscheduled DNA synthesis in rat
hepatocytes.
Beryllium sulfate and beryllium
chloride have been shown to be
nonmutagenic in all bacterial and yeast
gene mutation assays. However, this may
be due to the fact that bacterial and yeast
systems generally are not sensitive to
metal mutagens. In contrast, gene
mutation studies in cultured mammalian
cells, Chinese hamster V79 cells, and
Chinese hamster ovary (CHO) cells have
yielded positive mutagenic responses of
beryllium. Similarly, chromosomal aber-
ration and sister-chromatid exchange
studies in cultured human lymphocytes
and Syrian hamster embryo cells have
also resulted in positive mutagenic
responses of beryllium. In DNA damage
and repair assays, beryllium was
negative in pol, rat hepatocyte, and
mitotic recombination assays, but was
weakly positive in the rec assay. Based
on available information, beryllium
appears to have the potential to cause
mutations.
Carcinogenic Effects of
Beryllium Exposure
Animal Studies
Experimental beryllium carcino-
genesis has been induced by intravenous
or intramedullary injection of rabbits and
by inhalation exposure or by intratracheal
injection of rats and monkeys. With one
possible exception, beryllium carcino-
genesis has not been induced by
ingestion. Carcinogenic responses have
been induced by a variety of forms of
beryllium including beryllium sulfate,
phosphate, oxide, and beryl ore. The
carcinogenic evidence in mice (intra-
venously injected or exposed via
inhalation) and guinea pigs and hamsters
(exposed via inhalation) is equivocal.
Osteosarcomas are the predominant
types of tumors induced in rabbits. These
tumors are highly invasive, metastasize
-------
readily, and are judged to be
histologically similar to human osteo-
sarcomas. In rats, pulmonary adenomas
and/or carcinomas of questionable
malignancy have been obtained,
although pathological endpoints have not
been well documented in many cases.
Although, individually, many of the
reported animal studies have
methodological and reporting limitations
compared to current standards for
bioassays, collectively the studies
provide reasonable evidence for
carcinogenicity. Responses have been
noted in multiple species at multiple sites
and, in some cases, afford evidence of a
dose response. On this basis, using EPA
Guidelines for Carcinogen Risk
Assessment to classify the weight of
evidence for carcinogenicity in experi-
mental animals, there is "sufficient"
evidence to conclude that beryllium is
carcinogenic in animals. Since positive
responses were seen for a variety of
beryllium compounds, all forms of
beryllium are considered to be
carcinogenic.
Human Studies
Epidemiologic studies provide
equivocal conclusions on the carcin-
ogenicity of beryllium and beryllium
compounds. Early epidemiologic studies
of beryllium-exposed workers do not
report positive evidence for increased
cancer incidence. However, recent
studies do report a significantly
increased risk of lung cancer in exposed
workers. The absence of beryllium ex-
posure levels and a demonstrated
concern about possible confounding
factors within the workplace make the
reported positive correlations between
beryllium exposure and increased risk of
cancer difficult to substantiate. This
relegates the reported statistically sig-
nificant increases of lung cancer to, at
best, an elevated incidence that is not
statistically significant. Because of these
limitations, the EPA considers the
available epidemiologic evidence to be
"inadequate" to support or refute the
existence of a carcinogenic hazard for
humans exposed to beryllium.
This designation of the epi-
demiologic data as "inadequate" differs
from that of the International Agency for
Research on Cancer (IARC) which con-
cluded that the epidemiologic data
provide "limited" evidence for the
carcinogenicity of beryllium. In the EPA
evaluation, more recent unpublished
tabulations and analysis of the earlier
study cohorts that correct for errors in
the data base and the National Institute
for Occupational Safety and Health
(NIOSH) Life-Table program were
included. Use of this newer data provides
a basis to change the weight-of-
evidence conclusion for the human data.
Qualitative Carcinogenicity
Using the EPA weight-of-evidence
criteria for evaluating both human and
animal evidence, beryllium is most
appropriately classified in Group 82,
indicating that, on the strength of animal
studies, beryllium should be considered
a probable human carcinogen. This
category is reserved for chemicals
having "sufficient" evidence for carcin-
ogenicity in animal studies and
"inadequate" evidence in human studies.
In this particular case, the animal
evidence demonstrates that all beryllium
species should be regarded as probably
being carcinogenic for humans.
Human Health Risk Assessment
of Beryllium
Exposure Aspects
In the general U.S. population, the
dietary intake of beryllium is probably
less than 1 ng a day, and due to its
chemical properties, very little is
available in the gut for absorption.
Approximately half of the absorbed
beryllium enters the skeleton.
For most people, the daily amount of
beryllium inhaled is only a few
nanograms. However, it is likely that
much of this is retained in the lungs. The
available data indicate that the beryllium
lung burden in the average adult ranges
from 1 to 10 pg. Since beryllium occurs
in cigarettes, it is possible that smokers
will inhale and retain more beryllium than
nonsmokers. Unfortunately, the data on
beryllium concentrations in mainstream
smoke are, at present, uncertain.
Relevant Health Effects
Occupational exposure to various
beryllium compounds has been as-
sociated with acute respiratory disease
and chronic beryllium disease (in the
form of granulomatous interstitial pneu-
monitis). Some systemic effects have
also been noted and a hypersensitization
component probably plays a major role
in the manifestation of these effects. In
the past, chronic beryllium disease was
found in members of the general
population living near beryllium-emitting
plants, but past exposures were relatively
high compared to present levels of
beryllium in the ambient air. Con-
taminated workclothes brought home for
washing contributed to these exposures.
No "neighborhood" cases of chronf
beryllium disease have been reported i
the past several years.
Numerous animal studies have bee
performed to determine whether or n<
beryllium and beryllium-containin
substances are carcinogenic. Althoug
some of these studies have limitation!
the overall evidence from animal studie
is considered to be "sufficient" usin
EPA Guidelines for Carcinogen Ris
Assessment. The IARC has also cor
eluded that the evidence from anim;
studies is "sufficient." Human studies c
beryllium carcinogenicity have deficiei
cies that limit any definitive conclusic
that a true association between berylliui
exposure and cancer exists. Neve
theless, it is possible that a portion of tr
excess cancer risks reported in thej
studies may, in fact, be due to berylliui
exposure. Although IARC concluded th
beryllium and its compounds should t
classified as having "limited" humj
evidence of carcinogenicity, the EPA
Carcinogen Assessment Group (CAC
has concluded that the direct hurm
evidence is "inadequate."
Dose-Effect and Dose-
Response Relationships of
Beryllium
As previously stated, beryllium a
act upon the lung in two ways, eith
through a direct toxic effect on pi
monary tissue or through hype
sensitization. Even if reliable and detaili
exposure data were available, it wot
still be difficult to establish dose-effe
and dose-response relationships due
this hypersensitization factor. No adver
non-cancerous effects have been not
in industries complying with the 2 pg/r
standard set by the Occupational Safe
and Health Administration (OSH/
therefore, it appears that this level
beryllium in air provides good protecti
with regard to non-cancer respiratc
effects. It is unknown whether exposur
to the maximum permissible pe
standard (25 pg/m3) can cause delay
effects.
From available data, the Agen
assessment document has discussed 1
estimation of carcinogenic unit risks
inhalation exposure to beryllium. T
quantitative aspect of carcinogen r
assessment is included here because
may be of use in setting regulate
priorities and in evaluating the adequc
of technology-based controls and otl
aspects of the regulatory decisii
making process. However, the meth<
ologic uncertainties associated w
estimating cancer risks to humans at
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svels of exposure should be recognized.
The linear extrapolation procedures used
typically provide a rough but plausible
estimate of the upper limit of risk-that is,
it is not likely that the true risk would be
much higher than the estimated risk, but
it could be considerably lower. In the
case of beryllium, the uncertainty
introduced by specific characteristics of
the data base may be best thought of as
affecting the confidence in the upper-
limit estimates. These risk estimates
should not be regarded, therefore, as
accurate representations of true cancer
risks. The estimates presented may,
however, be factored into regulatory
decisions to the extent that the concept
of upper-limit risks are found to be
useful.
Both animal and human studies have
been used to examine the carcinogenic
potency of beryllium. For quantitative risk
assessment purposes the animal data
present some difficult analytical prob-
lems because of weaknesses in the de-
sign and the reporting of the studies.
Despite the weaknesses of the individual
studies, however, there is little doubt that
beryllium induces cancer in laboratory
animals.
An additional difficulty in the use of
animal data for quantitative assessment
is that not only did many of the animal
studies utilize different forms of beryllium
than those commonly present in the
ambient environment, but the car-
cinogenic response varied with the
beryllium compound used. Moreover, the
form most common in ambient air is
beryllium oxide and, although all the
animal studies were deficient in some
respects, the ones utilizing beryllium
oxide were more deficient, as a group,
than those utilizing beryllium salts.
Nevertheless, it was felt that the quan-
titative analysis should focus upon the
form of beryllium humans are most likely
to be exposed to.
While the available beryllium oxide
studies were individually weak, a cor-
relation of estimates from several data
sets would be expected to increase
confidence in the results. Potency factors
were thus calculated using data from
eight beryllium oxide animal studies. The
results were reasonably consistent and
the geometric mean of all eight potency
factors was 2.1 x 1Q.-3/(ng/m3), which
agreed quite well with the potency factor
derived from the human epidemiologic
data.
The question of beryllium potency
by ingestion is debatable due to the
equivocal or negative results from in-
gestion studies. From a weight-of-
evidence point of view, the potential for
human carcinogenicity by this route
cannot be dismissed given the know-
ledge that some beryllium (<1%) would
be absorbed from the gastrointestinal
tract, and intravenous injection of
beryllium produced distant site tumors.
For practical purposes, however, the
potency of beryllium via ingestion must
be considered as largely unknown, al-
though an upper bound risk estimate is
provided.
Even though the epidemiologic
studies have been judged to be
qualitatively inadequate to assess the
potential of carcinogenicity for humans,
these studies can be analyzed to
determine the largest plausible risk that
is consistent with the available epidemi-
ologic data. This upper bound is a risk
estimate and can be used to evaluate the
reasonableness of estimates derived
from animal studies. Information from a
published epidemiologic study and the
industrial hygiene reviews by NIOSH and
other investigators have been combined
to estimate a plausible upper bound for
incremental cancer risk associated with
exposure to air contaminated with
beryllium oxide. The epidemiologic data,
while being useful for estimating the
cancer potency of beryllium, nev-
ertheless, also has interpretative lim-
itations because of the uncertainties
regarding exposure levels. In the
occupational exposure studies upon
which the risk analysis is based, the
narrowest range for median exposure
that could be obtained on the basis of
available information was 100 to 1,000
iig/m3. Furthermore, an assumption was
made that the ratio of exposure duration
to years at risk ranged from 0.25 to 1.0.
The geometric mean of the potency
factors derived using these assumptions
equals 2.4 x 1p-3/(iig/m3).
The unit risks from the animal data
sets are best viewed as a sensitivity
analysis, as opposed to a collection of
reasonable upper-bound risk values.
The sensitivity relates to the beryllium
species tested, and for beryllium oxide,
perhaps to firing temperature. Because
of the need to assume exposure levels,
the risk estimate derived from the human
epidemiology data is, in effect, also the
result of a sensitivity analysis.
With these noted caveats, the GAG
feels that a recommendation for a
specific upper-bound estimate of risk is
warranted, even though it does evolve
from less than ideal data, in order to
provide a crude measure of the potential
for public health impact if, in fact,
beryllium is a human carcinogen. Taken
together the notable comparability of the
animal and human based estimates
encourages one to consider these es-
timates as being of some utility. Given
the correlation of animal and human
estimates, the upper-bound incremental
lifetime cancer risk associated with 1
iig/m3 of beryllium, after rounding to one
significant figure, is 2 x 10-3. This value
is based on the assumption that
beryllium is present in the environment in
the oxide form. If, however, the form of
beryllium present includes more than a
small fraction of beryllium salts, then this
potency value may underestimate the
upper limit and consideration should be
given to the animal estimates based on
exposure to beryllium sulfate. The
incremental upper-limit risk, 2 x 10'3/
(ng/m3), places beryllium in the lower
part of the third quartile of 58 suspect
carcinogens evaluated by the GAG.
Populations at Risk
In terms of exposure, persons
engaged in handling beryllium in
occupational environments obviously
have a higher potential for risk than the
general public. With regard to the
population at large, there may be some
risk for people living near beryllium-
emitting industries. However, the risk for
such individuals may not be from
ambient air levels of beryllium, but rather
from beryllium-contaminated dust within
the household. There are no data that
allow an estimate of the number of
people that may be at such risk, but it is
reasonable to assume that it is a very
small group. It should be noted that no
new "neighborhood" cases of beryllium
disease have been reported since the
1940s.
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Donna Slvulka is the EPA Project Officer (see below).
The complete report, entitled "Health Assessment Document for Beryllium,"
(Order No. PB 88-179 2051 AS; Cost: $25.95, 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, NC 27711
United States /-
Environmental Protection
Agency /
Center for Environmental Research
Information
Cincinnati OH 45268
Official Business
Penalty for Private Use $300
EPA/600/S8-84/026F
PS
CHICAGO
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