-------
Incidence of beryllium Induced lung cancers ranged from 0-100%. Generally,
a latency, period of at least 6 months and, preferably, 9 months was
required. These studies have been reviewed and evaluated In other recent
U.S. EPA (1986a,b) analyses. It 1s beyond the scope of this document to
reproduce these data, particularly since these data are not useful for risk
assessment. The most detailed studies of Intratracheal Injections of beryl-
lium were reported by Spencer et al. (1965, 1968, 1972). In these studies*
beryllium oxide fired at different temperatures was Injected Intratracheally
Into rats. The results showed that the beryllium oxide fired at the lowest
temperature (500°C) had the greatest carcinogenic potency. This beryllium
oxide also had the greatest surface area when compared to beryllium oxide
fired at 1100 or 1600'C.
Intravenous Injection and subperlosteal or Intraosseous Implantation of
beryllium and several of Its compounds have been shown to result In osteo-
sarcomas In rabbits (Nash, 1950; Outra and Largent, I960; Kawada, 1963;
Fodor, 1971; Komltowskl, 1969; Tapp, 1969; Yamaguchl and Katsura, 1963;
Gardner and Hesllngton, 1946; Barnes et al., 1950; Slssons, 1950; Cloudman
et al., 1949; Hoagland et al., 1950; Janes et al.. 1954; Kelly et al., 1961;
Hlgglns et al., 1964: Nazabraud, 1975) and mice (Cloudman et al., 1949).
The Incidence of osteosarcoma ranged from 0-100% by either route of adminis-
tration. A latency period of >9 months seemed to be required.
Beryllium has been studied 1n mutagenlclty assays. Beryllium sulfate
was negative In several tests conducted In Salmonella typhlmurlum both In
the presence and absence of S9 (Simmon, 1979a; Rosenkranz and Polrler, 1979;
Arlauskas et al., 1985; Simmon et al., 1979). Beryllium was also negative
In the pol assay (Rosenkranz and Lelfer, 1980) and the HP2 system (Ishlzawa,
1979) 1n Escher1ch1a coll and In Saccharomvces cerevlslae 03 (Simmon et al.,
0113h -24- 07/20/87
-------
1979; Simmon. 1979b). Positive reports In microorganisms Include the
fluctuation test 1n S. typhlmurlum strain TA100 (Arlauskas et al., 1985),
the rec assay In Bacillus subtnis (Kanematsu et al.f 1980; Kada et al.,
1980) and the Induction of DNA protein adducts 1n E.. coll (Kub1nsk1 et al..
1981).
Other studies of the genotoxlc potential of beryllium In cultured
mammalian cells have been reported. Mlyakl et al. (1979) demonstrated the-
Induction of 8-azaguan1ne-res1stant mutants by beryllium chloride In Chinese
hamster V79 cells. Hsle et al. (1979a,b) reported the Induction of
8-azaguan1ne-res1stant mutants In CHO cells exposed to beryllium sulfate.
Larramendy et al. (1981) reported that beryllium sulfate Induced chromosomal
aberrations In Syrian hamster embryo cells and In human lymphocytes and that
beryllium sulfate caused a dose-dependent Increase In sister-chromatld
exchanges In both Syrian hamster cells and human lymphocytes. These
results, however, showed Increases In slster-chromatld exchanges that were
<2-fold, so that the dose-response relationship suggested by Larramendy et
al. (1981) may be somewhat tenuous.
Williams et al. (1982) found that beryllium sulfate did not Induce
unscheduled DNA synthesis In rat primary hepatocyte cultures. Beryllium
sulfate also resulted 1n no chromosomal effects In human flbroblasts (UI 38
cells) (Paton and Allison, 1972). In. vitro exposure of rat liver cells to
beryllium resulted In Us binding to phosphorylated non-hlstone proteins
(Parker and Stevens, 1979). Perry et al. (1982) found that exposure of
cultured rat hepatosomal cells to beryllium reduced the glucocortlcold
Induction of tyros1r»e transamlnase activity. In a DNA fidelity assay,
beryllium Increased the mlslncorporatlon of nucleotlde bases In the daughter
strand of DNA synthesized In vitro from polynucleotlde templates (Zakour et
0113h -25- 07/20/87
-------
al., 1981). Beryllium has also been Investigated for Its effect on the'
transcription of calf thyrous DMA and phage T^ DNA by RNA polymerase (from
E_. colD under controlled conditions. Beryllium Inhibited overall tran-
scription but Increased RNA Initiation, Indicating the Interaction of the
metal with the DNA template (Nlyogl et al., 1981).
4.4. HEIGHT OF EVIDENCE
Beryllium has been shown to be clearly carcinogenic In laboratory
animals following Inhalation exposure and Injection (see Sections 4.2.2. and
4.3.). Epidemiology studies of Inhalation exposure (see Section 4.1.2.) are
suggestive but have been judged Inadequate to demonstrate or refute a
carcinogenic potential 1n humans.
From the available data, IARC (1980) concluded that there 1s sufficient
evidence that beryllium Is carcinogenic In animals, but ep1dem1olog1cal
evidence that occupational exposure to beryllium may lead to an Increased
lung cancer risk Is only limited. This description Is consistent with the
IARC Group 2B classification.
Applying the U.S. EPA (1986d) guidelines for carcinogen risk assessment,
the evidence from the Inhalation animal studies 1s judged to be sufficient
that bery'illjm Is an animal carcinogen. U.S. EPA (1986a) concluded that the
human evidence Is "Inadequate"; therefore* according to the guidelines for
evaluating the weight of evidence of carclnogenlclty to humans, beryllium 1s
most appropriately classified 1n Group B2, a probable human carcinogen (U.S.
EPA, 1986a). The weight of evidence for beryllium's carcinogenic potential
from oral exposure Is much less certain given that there are only two
studies thai: provide only suggestive evidence of carcinogenic activity. The
data presented In these studies contain Inconsistencies that give low
confidence to quantitative analysis. The U.S. EPA Carcinogen Assessment
Group lus stated that Ingested beryllium may be capable of Inducing a human
0113h -26- 07/20/87
-------
carcinogenic response (unlike some other metal for which carcinogenic
activity has not been detected) and therefore caution should be exercised
until further research Is available to define the oral carcinogenic
potential of beryllium.
0113h -27- 07/20/87
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5. REGULATORY STANDARDS AND CRITERIA
Occupational standards for beryllium and compounds have been developed.
The ACGIH (1986) TLV-TWA for beryllium and compounds Is 0.002 jig/m3 (2
mg/m*,) based primarily on Industrial experience. The ACGIH committee 1s
currently reviewing the data regarding beryllium. OSHA (1985) standards for
beryllium are 2 ug/m3 as the 8-hour TWA, 5 yg/m3 as the celling-
limit and 25 yg/m3 as the maximum peak above the celling concentration
to which an Individual can be exposed for 30 minutes during an 8-hour shift.
A number of ambient water quality criteria values for beryllium have
been derived. U.S. EPA (1980a, 1982), using the statistically Insignifi-
cant excess of grossly observed tumors at all sites 1n male rats from the
Schroeder and Kitchener (1975a) study and the linearized multistage model,
determined that a water concentration of 68 ng/i corresponds to a risk
level of 10~><> This value Is based on a dally Intake of 2 l of water
and 6.5 g fish and shellfish for a 70 kg human, and a BCF of 19. This value
was also presented In a more recent U.S. EPA (1986b) analysis. A toxlclty-
based ambient water level of 17.8 yg/l was also calculated from the
Schroeder and MHchener (1975a) study by using the 5 ppm drinking water
level as a NOAEL (U.S. EPA. 1980a, 1982). An equivalent dose of 0.538
mg/kg/day was estimated by assuming water consumption of 0.035 I/day and
estimating the body weight of exposed rats at 0.325 kg. Th? water concen-
tration from this NOAEL 1s equivalent to 0.0377 mg/day for a 70 kg human.
An RfD of 5.0xlO~» mg/kg/day (0.377 mg/day) based on the 5 ppm NOAEL In
the Schroeder and Kitchener, 1975a) study has been derived by the U.S. EPA
(1986c).
0113h -28- 07/20/87
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The U.S. EPA (19865) derived the following HAs for beryllium:
1-day HA for a 10 kg child. 26 mg/i
1-day HA for a 70 kg adult. 96 mg/i
10-day HA for a 10 kg child. 2.6 mg/t
10-day HA for a 70 kg adult, 9.6 mg/i
An RfO of 0.005 mg/kg/day has also been derived based on the Schroeder and
Kitchener (1975a) rat study (U.S. EPA 1986c).
0113h -29- 07/20/87
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6. RISK ASSESSMENT
6.1 SUBCHRONIC REFERENCE DOSE (RfD$)
6.1.1. Oral (RfO-g). Beryllium has been shown to be clearly
carcinogenic by other routes of exposure, although for the oral route the
evidence Is less certain. A plausible upper bound estimate of q, * has
been calculated. Therefore, H 1s not appropriate to derive an RfDcn
oU
value for beryllium or Us compounds.
6.1.2. Inhalation (RfD-,). Numerous experiments using laboratory
animals have Indicated that beryllium 1s carcinogenic following Inhalation
exposure; therefore, an RfDej value will not be derived.
6.2. REFERENCE OOSE (RfD)
6.2.1. Oral (RfOQ). Beryllium has been shown to be clearly
carcinogenic by other routes of exposure, and a q,* has been calculated
for oral exposure. Therefore. It 1s not appropriate to derive an RfO.
value.
6.2.2. Inhalation (RfD.). Beryllium has been shown to be carcinogenic
1n laboratory animals by the Inhalation route; therefore, an RfD, value
will not be derived.
6.3. CARCINOGENIC POTENCY (q^)
6.3.1. Oral. Beryllium has been shown to be clearly carcinogenic
following Inhalation exposure, Intratracheal Injection. Intravenous
Injection and Implantation. To what extent beryllium Is carcinogenic by the
oral route 1s largely uncertain, due to the fact that oral absorption data
are conflicting. Hyslop et al. (1943), Crowley et al. (1949) and Furchner
et al. (1973) Indicate that absorption Is <1X, while Reeves (1965) estimated
that absorption may range from 10-40% of the Ingested dose. If beryllium Is
absorbed following oral exposure, evidence from other routes of exposure
Indicate that It Is also likely to be a carcinogen by the oral route. The
0113h -30- 07/20/87
-------
hypothesis Is that beryllium's solubility In the gastrointestinal system may
be the key to better characterizing the oral carcinogenic risk of beryllium
and Its salts. This hypothesis, however, has not been fully developed.
Because beryllium may pose a carcinogenic risk by the oral route of
exposure, a default position has been adopted for calculating a q,*
despite the clear presence of significant tumor Incidences 1n the two
chronic oral studies. The presumption Is that the risk would not be any
higher than that estimated from a nonsignificant (negative) study and that
the value derived 1s of lower confidence In estimating an upper limit of
possible risk. The derived estimate 1s thought to be only a plausible upper
bound due to the hypothesis that the solubility of beryllium salts may be a
differentiating factor In beryllium's cancer risk from oral exposure.
In the Schroeder and Kitchener (1975a,b) studies, rats and mice were
provided with drinking water containing 5 ppm beryllium sulfate throughout
their lifetime. Male rats showed a statistically Insignificant Increase In
the Incidence of grossly observed tumors, while female mice showed a small
Insignificant excess of lymphoma leukemlas. In an unpublished study by
Horgareldge et al. (1975), rats were exposed to beryllium at concentrations
of 5, 50 or 500 ppm 1n the diet for 2 years. The data from this study were
analyzed by U.S. EPA (1986b), which found a significantly higher number of
retlculum cell sarcomas In the two lower dose male groups. The relationship
between the dose and response was Inverse; the most significant response
occurred at 5 ppm, and no significant response occurred at 500 ppm. Because
of the lack of dose-response, the limitations In design and execution of the
study and because these results have never been published, the Horgareldge
et al. (1975) study cannot be used to calculate a q *; however, the study
does provide evidence that beryllium 1s carcinogenic following oral exposure.
0113h -31- 07/20/87
-------
U.S. EPA (1986b), using Global 82 (Howe and Crump, 1982), calculated a
q * from the nonsignificant tumor Incidence data In male rats from the
Schroeder and Kitchener (1975a) study. The data used to calculate the q,*
of 4.86 (mg/kg/day)"1 1s presented 1n Table 6-1. The water Intake value
derived to determine the dose level used 1n the q,* calculation was not
provided.
6.3.2. Inhalation. Beryllium has been found to be carcinogenic Irv
numerous animal studies. Unfortunately, the animal studies are not well-
documented and many were conducted at one dose level. The U.S. EPA (1986a)
has used data from 10 studies to calculate potency estimates. These esti-
mates are presented In Table 6-2. Except for the Reeves and Deltch (1969)
study, the estimates were derived using the linear nonthreshold dose-
response model, which provides conservative risk estimates. The risk
estimate from the Reeves and Deltch (1969) study was calculated using a
multistage model AOOLLI-83 developed by Crump and Howe (1984). All risk
estimates were calculated with and without surface area correction. The
surface area correction Is used to correct for higher metabolic rates In
smaller animals. Because beryllium seems to be sequestered In the lungs and
the dose may not be affected by metabolism. It Is uncertain whether the
surface area correction should be used. Using both methods, q * values of
4.9x10"* to 4.3 (ug/mT1 were derived. The magnitude of the q^
value appears to depend, as a function of Its solubility, on the form of
beryllium used In the experiment. Beryl ore 1s the least potent of the four
compounds, while beryllium sulfate Is the most potent.
The U.S. EPA (1980a) has recommended a q^* from human epidemiology
data. However, this Is an external review draft currently undergoing
revision by the Agency. This ep1dem1olog1cal data has been judged to be
Inadequate for demonstrating or refuting a carcinogenic effect.
0113h -32- 07/20/87
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TABLE 6-1
Derivation of q-j* for Beryllium3
Reference: Schroeder and Kitchener, 1975a
Species/sex: rat/male
Route/vehicle: oral/drinking water
Length of exposure (1e) =1126 days
Length of experiment (LE) = 1126 days
Llfespan of animal (L) = 1126 days
Body weight * 0.325 kg (measured)0
Tumor site and type: gross tumors, all sites
Experimental
Exposure
0
5 mg/l
Human q-j* * 4.86
Transformed Dosec
(mg/kg/day)
0
0.455
(mg/kg/day)"1
Incidence
No. Responding/No. Tested
4/26
9/33
aSource: U.S. EPA, 19866
DBody weight average for both sexes estimated from tabular data provided
by Investigator.
cEst1mat1on based on the assumption that rats consumed 0.35 i of water/day.
0113h -33- 07/20/87
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The usual approach In risk assessment 1s to accept the most conservative
estimate of carcinogenic risk, which In this case would be 4.3
(vg/m*)"1, calculated from the rat study by Vorwald et al. (1966).
The U.S. EPA (1986a) suggested that the use of this animal potency estimate
would overestimate the human risk and Is not consistent with human experi-
ence In the beryllium Industry. Therefore, U.S. EPA (1986a) recommends
2.4xlO~3 (vg/m3)"1 as the estimate of risk associated with \
ng/m3 of beryllium 1n air. This estimate 1s the geometric mean of eight
q.j*s calculated on the basis of human data under various assumptions
(Table 6-3). The estimate of 2.4x10"" dig/m*)"1 could be considered
to be an upper-bound estimate of the cancer risk because low dose linearity
Is assumed In the extrapolation and the 95X upper confidence limits of the
relative risks are used In the calculations. Transforming to units of
(mg/kg/day)"1, the unit risk of 2.4xlO~» Ug/m")"1 Is equivalent
to 8.4 (mg/kg/day)"1.
Because the carcinogenic potency seems to be related to beryllium's
solubility, the U.S. EPA (1986a) cautions that beryllium species
Identification Is likely to be a very Important aspect of properly
characterizing the possible oral or Inhalation exposure risk to humans.
U.S. EPA (1986a) Is an external draft document that Is currently undergoing
revision, therefore a final recommended unit risk (q,* value) will have to
await the flnallzatlon of this document.
0113h -36- 07/20/87
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TABLE 6-3
Upper-Bound Cancer Potency Estimates Calculated
Under Various Assumptions3
Beryllium
Concentration
In Workplace f/L
(vg/m3)
100 1
0.25
1000 1
0.25
Effective
Doseb
Ug/m3)
21.92
5.48
219.18
54.79
95X Upper -Bound
Estimate of
Relative Risk
1.98
2.09
1.98
2.09
1.98
2.09
1.98
2.09
Cancer Potency0
Ug/m3)'1
1.61xlO"3
1.79xlO"»
6.44x10"'
7.16xlO"3
1.61x10"*
1.79x10"*
6.44x10"*
7.16x10"*
^Source: U.S. EPA, 1986a
^Effective dose Is calculated by multiplying the beryllium concentration
In the workplace by the factor (8/24)x(240/365)x(f/L) (f - years exposed;
L - years at risk).
cFor a given effective dose (d) and a relative risk (R), the carcinogenic
potency 1s calculated by the formula B = (R-l) x 0.036/d, where 0.036 Is
the estimated lung cancer mortality rate In the United States population.
0113h
-37-
07/20/87
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7. REFERENCES
ACGIH (American Conference of Governmental Industrial Hyglenlsts). 1986.
Documentation of Threshold Limit Values and Biological Exposure Indices, 5th
ed. Cincinnati, OH. p. 56-57.
Andrews, J.L., H. Kazeml and H.L. Hardy. 1969. Patterns of lung dysfunction-
In chronic beryllium disease. Am. Rev. Resplr. 01s. 100: 791-800. (Cited
In U.S. EPA, 1986a)
Arlauskas, A., R.S. Baker, A.N. Bonln, K.R. Tandon, P.T. Crisp and J. Ellis.
1985. NutagenlcUy of metal Ions In bacteria. Environ. Res. 36(2):
379-388.
Barna, B.P., T. Chiang, S.G. P1llar1sett1 and S.D. Deodhar. 1981. Immuno-
loglc studies of experimental beryllium lung disease In the guinea pig.
Cl1n. Immunol. Immunopathol . 29: 402-411. (Cited 1n U.S. EPA, 1986a)
Barnes, J.N., F.A. Oenz and H.A. Slsson. 1950. Beryllium bone sarcomata In
rabbits. Br. J. Cancer. 4: 212-222. (Cited In U.S. EPA, 1980a. 1986b)
, O.L. and U.S. Lalnhart. 1972. Mortality patterns 1n beryllium
production workers. Presented at the Am. Ind. Hygiene Assoc. Conf. OSHA
Exhibit No. 66. Docket No. H005. (Cited 1n U.S. EPA, 1986a,b)
0113h -38- 11/03/86
-------
Bayllss, D.L. and J.K. Wagoner. 1977. Bronchogenlc cancer and cardlo-
resplratory disease mortality among white males employed In a beryllium
production facility. OSHA Beryllium Hearing, 1977, Exhibit 13.F. (Cited In
U.S. EPA, 1986a,b)
Bayllss. O.L., U.S. Lalnhart, L.J. Crally, R. Llgo, H. Ayer and F. Hunter.
1971. Mortality patterns In a group of former beryllium workers. In.:.
Trans. 334rd Ann. Meeting AGCIH, Toronto, Canada, p. 94-107. (Cited 1n
U.S. EPA, 1986a,b)
Bencko, V., E.V. VoslHevo and K. Symon. 1980. Immunologlcal aspects of
exposure to emissions from burning coal of high beryllium content. Environ.
Res. 22: 439-449. (Cited In U.S. EPA. 1986a)
Berg, J.W. and F. Burbank. 1972. Correlations between-carcinogenic trace
metals In water supply and cancer mortality. Ann. N.Y. Acad. Sc1. 199:
249-261. (Cited 1n U.S. EPA. 1980a, 1986b)
Chlapplno, 6., A. Clrla and E.C. V1g11on1. 1969. Delayed-type hypersensl-
tlvlty reactions 1n beryllium compounds: An experimental study. Arch.
Pathol. 87: 131-140.
Cloudman, A.M., D. Vlnlng, S. Barkulls and J.J. Nlckson. 1949.. Bone
changes following Intravenous Injections of beryllium. Am. J. Pathol. 25:
810-811. (Cited 1n U.S. EPA, 1980a, 1986b)
0113h -39- 03/05/87
-------
Constantlnldls, K. 1978. Acute and chronic beryllium disease. Br. J.
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