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Antimony trioxide
CASRN 1309-64-4
Contents
0676
Antimony trioxide; CASRN 1309-64-4
Health assessment information on a chemical substance is included in IRIS only
after a comprehensive review of chronic toxicity data by U.S. EPA health
scientists from several Program Offices and the Office of Research and
Development. The summaries presented in Sections I and II represent a
consensus reached in the review process. Background information and
explanations of the methods used to derive the values given in IRIS are
provided in the Background Documents.
STATUS OF DATA FOR Antimony trioxide
File On-Line 09/01/1995
Category (section) Status Last Revised
----------------------------------------- -------- ------------
Oral RfD Assessment (I.A.) no data
Inhalation RfC Assessment (I.B.) on-line 09/01/1995
Carcinogenicity Assessment (II.) no data
_I. CHRONIC HEALTH HAZARD ASSESSMENTS FOR NONCARCINOGENIC EFFECTS
__I.A. REFERENCE DOSE FOR CHRONIC ORAL EXPOSURE (RfD)
Substance Name -- Antimony trioxide
CASRN -- 1309-64-4
Not available at this time.
__I.B. REFERENCE CONCENTRATION FOR CHRONIC INHALATION EXPOSURE (RfC)
Substance Name -- Antimony trioxide
CASRN -- 1309-64-4
Last Revised -- 09/01/1995
The inhalation Reference Concentration (RfC) is analogous to the oral RfD and
is likewise based on the assumption that thresholds exist for certain toxic
effects such as cellular necrosis. The inhalation RfC considers toxic effects
for both the respiratory system (portal-of-entry) and for effects peripheral
to the respiratory system (extrarespiratory effects). It is expressed in
units of mg/cu.m. In general, the RfC is an estimate (with uncertainty
spanning perhaps an order of magnitude) of a daily inhalation exposure of the
human population (including sensitive subgroups) that is likely to be without
an appreciable risk of deleterious effects during a lifetime. Inhalation RfCs
were derived according to the Interim Methods for Development of Inhalation
Reference Doses (EPA/600/8-88/066F August 1989) and subsequently, according to
Methods for Derivation of Inhalation Reference Concentrations and Application
of Inhalation Dosimetry (EPA/600/8-90/066F October 1994). RfCs can also be
derived for the noncarcinogenic health effects of substances that are
carcinogens. Therefore, it is essential to refer to other sources of
information concerning the carcinogenicity of this substance. If the U.S. EPA
has evaluated this substance for potential human carcinogenicity, a summary of
that evaluation will be contained in Section II of this file.
NOTE: ****SEE BENCHMARK CONCENTRATION IN DISCUSSION. Discussion of the
benchmark dose can be found in the Discussion of Principal and Supporting
Studies Section.
___I.B.1. INHALATION RfC SUMMARY
Critical Effect Exposures* UF MF RfC
-------------------- ----------------------- ----- --- ---------
Pulmonary toxicity, Benchmark Concentration: 300 1 2E-4
chronic interstitial See Conversion Factors mg/cu.m
inflammation and Assumptions and
Principal and Supporting
Rat 1-Year Inhalation Studies
Toxicity Study
Newton et al., 1994
*Conversion Factors and Assumptions: MW = 169.8. BMC = 0.87 mg/cu.m.
BMC(ADJ) = 0.87 +/- 6 hours/24 hours +/- 5 days/7 days = 0.16 mg/cu.m. The
BMC10(HEC) was calculated for a particle:respiratory effect in the thoracic
region. The RDDR(TH) = 0.46 for MMAD = 3.7 microns and sigma g = 1.7, based
on dosimetric modeling as described in U.S. EPA, 1994. BMC10(HEC) =
BMC10(ADJ) x RDDR = 0.074 mg/cu.m.
___I.B.2. PRINCIPAL AND SUPPORTING STUDIES (INHALATION RfC)
Newton, P.E., H.F. Bolte, I.W. Daly, et al. 1994. Subchronic and chronic
inhalation toxicity of antimony trioxide in the rat. Fund. Appl. Toxicol.
22: 561-576.
Newton et al. (1994) conducted a chronic study in which groups of 65
Fischer 344 rats/sex/group were exposed to target concentrations of 0, 0.05,
0.50, or 5.00 mg/cu.m (actual concentrations measured by atomic absorption
were 0, 0.06, 0.51, or 4.50 mg/cu.m, respectively) antimony trioxide for 6
hours/day, 5 days/week for 1 year (duration-adjusted concentrations = 0, 0.01,
0.09, or 0.80 mg/cu.m, respectively). The article by Newton et al. (1994) is
the published version of an earlier, more complete report (Bio/dynamics,
1990). In addition to the 1-year exposure, some animals were held for a 1-year
recovery period. Interim sacrifices were conducted on 5 animals/sex/group at
6 and 12 months of exposure and at the end of the first 6 months of the 12-
month postexposure recovery period. The remainder of the animals were
sacrificed at the end of the 12-month recovery period. The antimony trioxide
was determined to be 99.68% pure. The rats were exposed (whole body) in 6
cu.m stainless steel and glass chambers with a calculated air flow of 2,077-
2,280 L/min. The test atmosphere was generated with a Fluidized Bed Generator
(TSI, Inc., Model 3400 or 9310). The test atmosphere was analyzed by atomic
absorption spectrometry. Particle size distribution measurements were made
once at the beginning of weeks 4, 8, and 13, and months 6 and 12 using a TSI
Aerodynamic Particle Sizer. The particle size distribution at the high
concentration also was analyzed using a Delron DCI-6 (Battelle) cascade
impactor for comparative purposes. The MMAD was 3.7 microns, and sigma g was
1.7 for all concentrations. Body weights were measured weekly during the
first 3 months of exposure and monthly thereafter; hematology analyses were
conducted on 5 animals/sex/group at 12 and 18 months and on 10 rats/sex/group
at 24 months. Gross and histopathological evaluations were performed on all
animals. Microscopic examinations were performed on tissues of the larynx (1
section), lymph node [4 sections (peribronchial)], lungs (1 section from each
lung and 1 from the main stem bronchi), trachea (1 section), nasal turbinates
(4 sections), and heart for animals in all groups. The eyes, kidneys, liver,
prostrate, spleen, and urinary bladder were examined in the control and high-
exposure groups.
No difference between the control and exposed groups was noted in
survival, although an unexplained increase in the number of deaths was noted
in weeks 49-53. Body weight was not affected by exposure to antimony
trioxide.
No significant changes in hematological parameters were observed that were
concentration-related or consistent across time periods. However, an increase
in mean corpuscular hemoglobin concentration was seen in both sexes exposed to
the high concentration for 12 months. This effect was not noted at other
exposure intervals.
An ophthalmoscopic examination was performed on all rats before the test
and at 6, 12, 18, and 24 months. Mild, compound-related ocular irritation was
noted at 6 months, but no indications of compound-related ocular disease were
noted at 12 or 18 months. Examination of all surviving rats at 24 months
revealed increases in the incidence of conjunctivitis (reported as
chromodacryorrhea secondary to dental abnormality, infectious disease, or
xerosis) and cataracts (females only; principally posterior subcapsular
cataracts). Statistical analysis of the cataract response observed at 24
months was performed for both male and female rats (Allen and Chapman, 1993).
Trend test and pairwise comparisons (Fishers Exact Test) revealed no
concentration-response relationship for the male rats. Incidence in the
females was 3/28, 8/21, 12/34, and 14/32 for the control and 0.06-, 0.51- and
4.50-mg/cu.m groups, respectively. Pairwise comparisons (Fishers Exact Test)
suggest marginally significant increases over controls (p < 0.05) in the low-
and mid-concentration groups (p values were between 0.03 and 0.04). When just
those two concentration groups and the controls were included in a trend test
analysis, the increases were determined not to be statistically significant (p
value was 0.09). At the high concentration, however, a statistically
significant increase in female cataracts was indicated by both the trend and
pairwise tests (p < 0.01). Based on information provided by the principal
investigators, this effect is not likely to be due to lack of cage rotation
(resulting in unequal exposure to light among the groups). However,
occupational studies that involved physical examinations and reported
respiratory effects in workers exposed to antimony trioxide have not reported
significant eye effects (Potkonjak and Pavlovich, 1983; Renes, 1953). There
is a great deal of uncertainty and judgment involved in the designation of
these lesions (Boorman, 1995). For this reason and because Newton et al.
(1994) did not observe a dose response in either sex, and because the lesions
attained statistical significance (trend test) only at the highest
concentration in the female rats at 24 months (increasing the potential for
confounding from spontaneous senile cataracts common among aging nocturnal
albino rodents), these results can not be considered an adequate basis for a
human risk assessment.
Microscopic lesions of the lungs revealed interstitial inflammation in
control and exposure groups at the end of 6, 12, 18, and 24 months.
Granulomatous inflammation and granulomas were observed in all exposure groups
at 18 and 24 months. An increase in the number of alveolar and intraalveolar
particle-laden macrophages was observed (at every exposure duration) in all
but the control groups. There is no indication given in the report that the
increases in particle-laden macrophages in the lungs of low- and mid-
concentration group rats were anything but normal, compensatory responses.
However, clearance half-times in the high-concentration groups were three
times greater than in the low- and mid-concentration groups, indicating that
clearance mechanisms may be compromised severely at this level of exposure.
It appears that this effect is largely due to the intrinsic toxicity of
antimony trioxide and not a general "particle overload" phenomenon. The rate
of clearance from lungs of deposited benign or slightly toxic insoluble
particles has been reported to be reduced by 50% at a dust volume of about
1000 nL (Muhle et al., 1990). Newton et al. (1994) report a 50% decrease in
clearance (or increase in half-time) at an antimony trioxide volume of about
270 nL in the high-exposure group. The disproportionate increase in antimony
trioxide retention in the high-exposure group can be seen by comparing the
exposure concentration ratios of 1:10:90 to the lung burden ratios of
1:11:138. Thus, the NOAEL for decreased rate of clearance is 0.51 mg/cu.m
[NOAEL(HEC) = 0.042 mg/cu.m].
With respect to interstitial inflammation and granulomatous inflammation,
statistical significance of incidence data was not reported in the study, but
the raw data from the original unpublished report (Bio/dynamics, 1990) were
evaluated using trend and pairwise (Fisher Exact) tests on the statistical
significance of increases in severity grades and incidence (Allen and Chapman,
1993). An evaluation of male and female graded responses for interstitial and
granulomatous inflammation using logistic regression techniques indicates no
effect in females at any concentration level and marginally significant
effects (for increased severity of interstitial inflammation) at the high-
concentration level for males during the exposure period (first 12 months).
However, in the second, follow-up year, significant (p < 0.05) increases in
the incidence and severity of these responses were evident at the high-
exposure level for both male and female rats that either died spontaneously or
were sacrificed at 18 and 24 months (Bio/dynamics, 1990). When incidence
alone was considered (regardless of severity), chronic interstitial
inflammation in the female rats that were either sacrificed or died
spontaneously was increased over controls in the mid-exposure group. However,
overall incidence is not considered an appropriate response measure for this
lesion due to the high rate (55%) of minimal to slight interstitial
inflammation in female controls and the fact that this increase was not seen
among sacrificed animals, but only among those female rats that died
spontaneously before normal sacrifice. When severity of these lesions is
taken into consideration, the analysis of Allen and Chapman (1993) indicates a
LOAEL of 4.50 mg/cu.m and a NOAEL of 0.51 mg/cu.m [NOAEL(HEC) = 0.042
mg/cu.m].
DERIVATION OF A BENCHMARK CONCENTRATION (BMC): Incidence of chronic
inflammation, granulomatous inflammation and fibrosis in male, female, and
combined male and female rats observed during the 1-year period were analyzed
for purposes of Benchmark Concentration (BMC) analysis. To minimize the
confounding rate of background lesions, only chronic inflammation given a
severity grade greater than 2 (slight) and granulomatous inflammation given a
severity grade greater than 1 (minimal) were considered in the BMC evaluation.
The concentrations associated with 1, 5, and 10% relative increases in the
probability of response were estimated using both Weibull and linear models.
Although limiting the response to specific severity grades decreased the
background rate, there was still enough of a response in the controls to cause
a slight difference in the results of models that calculate relative
(sometimes referred to as extra risk) vs. additional risk. A relative risk
model was selected as most appropriate, based on the conservative assumption
that the mechanisms causing the background response are independent of the
mechanisms causing the treatment-related response.
Both the Weibull and linear models gave the same goodness of fit for male
and female data. Although BMCs were not calculated and presented for all
endpoints, as per standard operating procedures, the best curve fits and the
lowest corresponding lower 95% confidence levels were obtained for chronic
inflammation in female rats. A previous chronic exposure study (Groth et al.,
1986) also determined female rats to be more sensitive to lung effects from
antimony trioxide exposure. Further, Allen and Chapman (1993) also concluded,
as a result of their analysis, that "males and females responded differently
to antimony trioxide exposure for the subacute/chronic interstitial
inflammation response, especially during the second, follow-up year." Because
it is possible that there is a biological basis for these reported sex
differences, the female data were evaluated separately. The studies by
Faustman et al. (1994) and Allen et al. (1994) suggest that the 10% incidence
level correlated with a NOAEL for one type of noncancer endpoint (quantal
developmental effects). Consequently, a 10% relative increase was chosen as a
benchmark response. The lower 95% confidence limit for the 10% relative
increase in the probability of response among this subset was determined to be
at 0.87 mg/cu.m. Although chronic inflammation can be considered a relatively
mild, potentially compensatory effect, a similar BMC10 analysis for
granulomatous inflammation and fibrosis (which can be considered to represent
further progression of the inflammatory aggravation) gives BMC10 estimates of
1.21 and 2.85 mg/cu.m, respectively. Thus, more serious lesions do occur at
only slightly higher concentrations. As stated earlier, when minimal and
slight interstitial inflammation are included, the overall incidence of
interstitial inflammation in female rats beyond the 12-month sacrifice was
increased at the mid-concentration over controls. However, the high rate of
minimal to slight inflammation in female controls and in animals that died
prior to sacrifice suggests that the BMC10 analysis of higher severity grades
is better representative of the true NOAEL. The BMC10 of 0.87 mg/cu.m was
chosen for RfC derivation, and a human equivalent concentration [BMC(HEC)] of
0.074 mg/cu.m was calculated.
___I.B.3. UNCERTAINTY AND MODIFYING FACTORS (INHALATION RfC)
UF -- An uncertainty factor of 10 is used for the protection of sensitive
human subpopulations. An uncertainty factor of 3 is used for interspecies
extrapolation because the dosimetric adjustments account for part of this area
of uncertainty. An uncertainty factor of 3 is applied for data base
inadequacies (principally, the lack of reproductive and developmental
bioassays). Although epidemiologic studies were not considered adequate for
use in a quantitative assessment, they provide qualitative support for the
health endpoint selected as the basis for the RfC and obviate the need for
toxicity data in a second species. Studies addressed in the next section
indicate the importance of exposure dose and duration on the dynamics of
reaching and maintaining a steady-state concentration and lung clearance.
There is no evidence that, at the lowest exposure level tested in the Newton
et al. (1994) study, the levels of antimony in the rat lungs reached a steady-
state concentration. Thus, an additional threefold uncertainty factor to
account for a less-than-lifetime exposure duration is applied. This is less
than the 10-fold uncertainty factor normally applied to adjust from subchronic
(90-day) to chronic studies because exposures lasted for 1 full year.
MF -- None
___I.B.4. ADDITIONAL STUDIES / COMMENTS (INHALATION RfC)
As studies addressed in this section illustrate, the disposition of an
antimony aerosol in the respiratory tract is dependent on the particle size,
distribution, and solubility of the compound. In general, aerosols containing
small particles (Felicetti et al., 1974a; Leffler et al., 1984; Thomas et al.,
1973) composed of antimony compounds with low water solubility (Leffler et
al., 1984) (e.g., particles of antimony oxides) are retained in the lungs for
a longer period of time than those containing larger particles with high water
solubility (e.g., particles of antimony tartrates). This is because particle
size and distribution determine the initial deposition in the respiratory
tract, and subsequent clearance depends on the deposition site, rate of
absorption, dissolution, extent of metabolism, and tissue distribution.
Retention reflects the difference between deposition and clearance. The toxic
effects of antimony compounds also will vary according to these and other
variables. Limited data on antimony trisulfide indicate that the critical
effect associated with exposure to this compound is cardiotoxicity, and that
effects may occur at similar, if not lower, exposure levels (Brieger et al.,
1954). Hence, the antimony trioxide RfC is not representative of the entire
class of antimony compounds and should not be used in this manner. Most
atmospheric releases of antimony result from high-temperature industrial
processes that produce antimony oxides. An RfC was derived separately for
antimony trioxide because it is the primary form of antimony in the atmosphere
(U.S. EPA, 1980), and because there are limited toxicologic data for other
forms of antimony.
Chronic occupational exposure to antimony (generally antimony trioxide) is
most commonly associated with "antimony pneumoconiosis" (Cooper et al., 1968;
McCallum, 1967; Potkonjak and Pavlovich, 1983; Renes, 1953). This condition
is characterized on X-rays by the presence of diffuse, densely distributed
punctate opacities that are round, polygonal, or irregular in shape; have a
diameter of usually <1 mm; and do not tend to conglomerate (Potkonjak
and Pavlovich, 1983).
Renes (1953) studied 78 employees of a mining company involved in either
antimony smelting operations or maintenance. The workers were exposed to an
average of 4.69 and 11.81 mg/cu.m antimony in two different work areas, and 69
of these men reported illness within the first 5 months of operation. The
smelter fume contained 35-68% antimony, 2-5% arsenic, 0.01-0.04% selenium,
0.04-0.30% lead, and 0.1-0.40% copper. Exposure to caustics (hydrogen sulfide
and sodium hydroxide) also was possible. Chest X-rays taken of six men who
were acutely ill revealed pneumonitis.
Cooper et al. (1968) examined 28 antimony smelter workers that had been
exposed to antimony ore and antimony trioxide dust for 1-15 years. Antimony
concentrations ranged from 0.08-138 mg/cu.m antimony, but particle size was
not specified. Pulmonary function studies were carried out on 14 of these
workers, and no consistent pattern of abnormalities was observed. However,
3/13 workers who underwent roentgenographic examination were found to have
antimony pneumoconiosis and 5 more were suspected of having pneumoconiosis.
McCallum (1963) reported that pneumoconiosis in antimony smelter workers
in the United Kingdom was generally benign (i.e., the workers were
symptomless). He reported a correlation between the degree of radiographic
abnormalities, amount of antimony retained in the lungs, and duration of
exposure; changes often were noted after just a few years of employment
(McCallum et al., 1971). Ambient antimony (as antimony trioxide)
concentrations measured 37 mg/cu.m antimony during tapping operations, and
averaged 5 mg/cu.m antimony in other areas; the particle size diameter was <1
micron. In a cross-sectional study of 274 antimony smelter workers in 1965-
1966, 26 new cases of pneumonoconiosis were found (McCallum, 1967).
Potkonjak and Pavlovich (1983) investigated 51 antimony smelter workers
that had been employed for 9-31 years. The workers (aged 51-54 years) were
examined (physical examination, laboratory analysis, chest X-ray, and
pulmonary function studies) 2-5 times over the 25-year period. The airborne
dust concentrations measured 17-86 mg/cu.m, and analysis of the dust revealed
0.82-4.72% free silica, 38.73-88.86% antimony trioxide, and 2.11-7.82%
antimony pentoxide. Other agents present in the dust included 0.90-3.81%
ferric trioxide and 0.21-6.48% arsenic oxide. More than 80% of the particles
were <5 microns in diameter. X-ray findings considered positive were
characterized by the presence of diffuse, densely distributed punctate
opacities having a diameter <1 mm and concentrated in the mid-lung region and
were found in many of the workers employed for over 9 years.
A subchronic study was performed (Newton et al., 1994; Bio/dynamics, 1985)
in which groups of 50 Fischer 344 rats/sex were exposed to target
concentrations of 0, 0.2, 1.0, 5.0, or 25.0 mg/cu.m antimony trioxide (actual
concentrations were 0, 0.25, 1.08, 4.92, or 23.46 mg/cu.m, respectively) for 6
hours/day, 5 days/week for 13 weeks (duration-adjusted concentrations = 0,
0.05, 0.19, 0.88, or 4.20 mg/cu.m, respectively). The antimony trioxide was
determined to be 99.93% pure. In addition, some animals were held for a 27-
week recovery period. Interim sacrifices were conducted on 5
animals/sex/group at exposure weeks 1, 2, 4, 8, and 13 and at recovery weeks
1, 3, 10, 18, and 28. The protocol for exposure and the test atmosphere
analysis were the same as described previously for the 1-year bioassay (Newton
et al., 1994). The MMAD was 2.9, 3.9, 2.9, and 3.4 microns for the 0.25-,
1.08-, 4.92-, and 23.46-mg/cu.m levels, respectively, and sigma g was 1.6,
1.5, 1.6, and 1.5 for the four concentrations, respectively. Body weights
were measured weekly during both exposure and recovery, and hematology and
clinical chemistry analyses were conducted on five animals/sex/group at
exposure weeks 1, 2, 4, 8, and 13 and at recovery weeks 1, 2, 4, 8, and 13.
Complete gross and histopathological evaluations were conducted of all major
organ tissues, including the lungs and heart, for all animals.
No exposure-related deaths occurred. Corneal irregularities and alopecia
were observed in all groups (including controls) with higher incidence in the
high-concentration group. Body weight was statistically significantly reduced
at the two highest concentrations in both the males and the females during
exposure and most of the recovery period. No significant changes in
hematological parameters were observed that were concentration related or
consistent across time periods. An exposure-related significant increase in
aspartate transaminase was seen in the males exposed to the two highest
concentrations of antimony trioxide during exposure. Mean and absolute lung
weights were significantly increased in both males and females exposed to the
two highest concentrations during exposure and the early part of the recovery
period. Gross necropsy revealed lung discoloration in the 4.92- and 23.46-
mg/cu.m groups during exposure and in the 23.46-mg/cu.m group during recovery.
Microscopic lesions of the lungs observed in all animals exposed to antimony
trioxide included particle-laden macrophages, degenerating macrophages, and
cellular debris in the lumen of the alveoli. Multifocal pneumonocyte
hyperplasia, nonsuppurative alveolitis, and focal alveolar wall thickening
also were observed in both males and females exposed to 4.92 and 23.46
mg/cu.m. The macrophages, pneumonocyte hyperplasia, and alveolar wall
thickening were still present after 27 weeks of recovery. No histopathologic
findings were reported in any other tissues examined, including cardiac
tissue. From these results, a NOAEL of 1.08 mg/cu.m [NOAEL(HEC) = 0.096
mg/cu.m], based on pulmonary effects from subchronic exposure, can be
estimated.
Watt (1983) exposed groups of 50 female Wistar rats and 3 female Sinclair
S-1 miniature swine to antimony trioxide for 6 hours/day, 5 days/week for 1
year. The exposure concentrations were 0, 1.9, and 5.0 mg/cu.m (duration-
adjusted concentrations = 0, 0.3, and 0.9 mg/cu.m, respectively). The
particle size (Ferret's diameter) was 0.44 and 0.40 microns for the low and
high concentrations, respectively, and standard deviations were 2.23 and 2.13,
respectively. No exposure-related effects on survival, hematology, or
clinical chemistry were noted. The body weights of the exposed animals were
consistently higher than the controls throughout the study. No consistent
pattern of abnormalities were detected in electrocardiograms taken from swine
at preexposure, after 6 months of exposure, and at the end of exposure. Lung
weight was increased in both species. Nonneoplastic pulmonary effects
observed in all exposed animals included focal fibrosis, adenomatous
hyperplasia, multinucleated giant cells, cholesterol clefts, pneumonocyte
hyperplasia, and pigmented macrophages. The severity of these effects
increased with concentration and duration of exposure. Postmortem findings
that appeared to be treatment related included discoloration and increased
pulmonary alveolar-intralveolar macrophages in the mid- and high-exposure
groups and focal subacute-chronic interstitial inflammation and granulomatous
inflammation in the high-exposure group. The incidence of lung tumors
(scirrhous carcinomas, squamous cell carcinomas, and bronchoalveolar adenomas)
was statistically significantly increased in the animals exposed to 5.0
mg/cu.m only. No other nonneoplastic or neoplastic lesions were observed in
the exposed rats, and no microscopic, exposure-related changes were observed
in the swine. Based on the occurrence of pulmonary effects in rats, a LOAEL
of 1.9 mg/cu.m can be estimated from this study.
Cooper et al. (1968) exposed two groups of 10 Sprague-Dawley rats/sex to
powdered antimony ore or antimony trioxide at a concentration of 1,700 mg/cu.m
for 1 hour, 1-6 times every 2 months. This exposure regimen continued for 66-
311 days for the ore and 66-366 days for the antimony trioxide. No control
animals were included in the study. The powdered ore induced mild and
transient edema and lung congestion after the first exposure. Both the ore
and the trioxide exposure resulted in a phagocytic response that became
apparent 66 days after the first exposure and increased in intensity with
continuing exposure. The authors noted that no signs of chronic pneumonitis
were apparent at 311 days for the trioxide and 366 days for the ore. As the
duration of exposure increased, scattered particles with moderate
reticuloendothelial proliferation was noted in the spleen. No exposure-
related effects were seen in the liver or kidney. No controls were used, and
details regarding protocol (e.g., number of animals sacrificed at the end of
the study) and results (e.g., incidence data) were lacking.
Guinea pigs (n = 24) were exposed to antimony trioxide at a concentration
of 45.4 mg/cu.m (38.1 mg/cu.m antimony) for 2 hours/day, 7 days/week for 2
weeks, followed by 3 hours/day for the duration of the experiment (8-265
days). The particle size was assumed to be less than or equal to 1 micron
(Dernehl et al., 1945). The authors assumed that lung retention of antimony
was 50% and calculated a daily average retention of 1.6 mg. Interstitial
pneumonitis was observed in all 24 guinea pigs, and, of the four deaths that
occurred, two were from pneumonia. Increased lung weight was observed at
necropsy, and subpleural petechial hemorrhages were observed in animals
exposed for greater than or equal to 30 days. Increased liver weight, cloudy
swelling of the liver, and fatty degeneration in 73% of the animals exposed
for greater than or equal to 48 days were observed. Decreased white blood
counts were reported in the exposed animals, and splenic hyperplasia and
hypertrophy also were noted in half of the exposed animals.
Electrocardiograms were taken of three guinea pigs, and no exposure-related
abnormalities were noted.
In two separate studies, Gross et al. (1952, 1955) exposed 50 male
Sprague-Dawley rats to antimony trioxide dust at a concentration of 100-125
mg/cu.m (84-105 mg/cu.m antimony) for 100 hours/month for up to 14.5 months.
No experimental controls were included in the 1952 study, and animals exposed
to 25 mg/cu.m dust containing 1% antimony trioxide (90% calcium phosphate)
served as controls in the 1955 study. The authors determined by electron
microscopy that the average particle size was 0.6 microns. Death due
primarily to pneumonia occurred in many of the animals. On gross examination,
the lungs appeared mottled, and swelling, proliferation, and desquamation of
the alveolar macrophages were observed early in the experiment and were
followed by fatty degeneration, necrosis, and cell death as the exposure
duration increased. Alveolar fibrosis also was observed. The authors
characterized these pulmonary changes as "endogenous lipid pneumonia."
Rabbits administered the same levels of antimony trioxide, according to the
same treatment regimen, exhibited similar pulmonary effects. However, the
interstitial pneumonia was more pronounced in the rabbits, and the fibrosis
was less diffuse (Gross et al., 1955). Considerable deposits of antimony
trioxide were found in the lymph nodes, but there was no fibrosis. This
prompted the authors to postulate that the lung damage observed was secondary
to metabolic disturbances, fatty degeneration, and necrosis of alveolar
macrophages, resulting in lipid deposits that, in turn, cause fibrosis (Gross
et al., 1952, 1955).
In a study sponsored by NIOSH, groups of 90 male and female Wistar rats
were exposed to dusts of antimony trioxide or antimony ore for 7 hours/day, 5
days/week for up to 52 weeks (Groth et al., 1986). The exposure
concentrations were 45 mg/cu.m antimony trioxide (37.8 mg/cu.m antimony) and
36-40 mg/cu.m antimony ore (17.5 mg/cu.m antimony). Rats exposed to filtered
air served as controls. The duration adjusted concentrations were 9.4 mg/cu.m
and approximately 7.9 mg/cu.m antimony ore, respectively. The MMADs for the
two test atmospheres were 2.80 (antimony trioxide) and 4.78 (antimony ore);
the sigma g values were not reported. Interim sacrifices were performed on 5
animals/sex/group at 6, 9, and 12 months, and the remainder of the animals
were held for an additional 20 weeks after the termination of exposure.
Slight but statistically significant decreases in mean body weight were
observed in both the males exposed to antimony trioxide (6.2%) and the females
exposed to antimony ore (6.4%). Slightly elevated, confluent, white and
yellow foci were grossly visible on the pleural surfaces of the lungs from all
exposed animals. Histologically, interstitial fibrosis, alveolar-wall cell
hypertrophy and hyperplasia, and cuboidal and columnar cell metaplasia of the
lungs were observed in the exposed animals after 6 months of exposure. These
effects increased with respect to the size of the area affected after 12
months of exposure, and the extent of fibrosis increased after 4-5 months of
recovery. Cholesterol clefts also were seen in the lungs of the exposed
animals. None of these effects were seen in the control animals, and no other
exposure-related nonneoplastic effects were observed. An increase in the
incidence of lung tumors (squamous-cell carcinomas, bronchoalveolar adenomas,
bronchoalveolar carcinomas, and scirrhous carcinomas) was seen in 27% of the
females exposed to antimony trioxide and 25% of the females exposed to
antimony ore. Based on the results of this study, a LOAEL(HEC) of 5 mg/cu.m
(assumes a sigma g of 2) for antimony trioxide can be estimated for effects in
the thoracic region of the respiratory tract.
Quantitative data regarding the disposition of inhaled antimony oxides in
humans or laboratory animals are not available. However, antimony has been
detected in the blood and urine of smelters, with and without lung changes,
who were chronically exposed to antimony trioxide; urine levels of antimony
often remained elevated for extended periods after exposure had terminated
(Bailly et al., 1991; Brieger et al., 1954; Cooper et al., 1968; Ludersdorf et
al., 1987; McCallum, 1963). This provides evidence that antimony oxides are
absorbed by humans following inhalation exposure.
Data obtained from both live and deceased smelter workers indicate that
antimony is retained in the lungs for long periods of time (Gerhardsson et
al., 1982; McCallum, 1967; McCallum et al., 1971; Vanoeteren et al.,
1986a,b,c). Gerhardsson et al. (1982) measured the antimony content of the
lungs of 40 deceased smelter workers and found that the antimony levels in the
exposed men (316 mg/kg) were 12-times greater (p < 0.001) than the levels of
antimony measured in nonexposed referents. Furthermore, antimony
concentration in the lungs did not tend to decrease with increasing period
after cessation of exposure, which indicates that lung antimony has a long
biological half-life. A series of studies conducted by Vanoeteren et al.
(1986a,b,c) support the observation that antimony accumulates in lung and is
retained for long periods of time.
The absorption and retention of antimony following inhalation exposure has
been studied in laboratory animals, and the results support the observations
made in humans that antimony can be retained in the lung (Newton et al., 1994;
Felicetti et al., 1974a; Leffler et al., 1984; Thomas et al., 1973). These
investigators have demonstrated that the extent of deposition and subsequent
clearance and retention of antimony from the lung depends primarily on
solubility (Leffler et al., 1984) and particle size (Felicetti et al., 1974a;
Leffler et al., 1984; Thomas et al., 1973). Thomas et al. (1973) exposed mice
to aerosols of radiolabeled trivalent antimony as a tartrate complex for 10
minutes. The aerosols were generated at three different temperatures (100,
500, and 1100 F) that yielded particle sizes (activity median aerodynamic
diameter) of 1.6, 0.7, and 0.3 microns, respectively (with sigma g's of 1.9,
1.8, and 1.3, respectively). Whole-body scintillation counting was conducted
immediately after exposure and at various intervals thereafter; serial
sacrifices to determine tissue distribution were conducted at 0, 2, 4, 8, 16,
and 32 days postexposure. The results of the serial whole-body counts
revealed that antimony was cleared rapidly at first, and this initial, rapid
phase was followed by a slower, steady decrease in antimony content. The
aerosol generated at 100 F was more soluble than those generated at 500 and
1100 F; the more soluble material was cleared from the lung and absorbed into
the systemic circulation at a higher rate (to be preferentially accumulated in
the bone) than the aerosols generated at higher temperatures. Consequently,
the less soluble and smaller particles that were generated at higher
temperatures tended to be retained in the lung for long periods of time.
Similar results were obtained in dogs exposed to antimony aerosols generated
at 100, 500, and 1100 F having particle sizes of 1.3, 1.0, and 0.3 microns,
respectively (Felicetti et al., 1974a). The largest-sized particles
demonstrated relatively rapid clearance from the upper respiratory tract, due
in part, perhaps, to solubilization and absorption in the lung and rapid
excretion via the urine. The smaller sized, less soluble particles were
retained to a higher degree and for a longer duration in both the lungs and
the whole body.
Leffler et al. (1984) reported that solubility had the greatest influence
on the degree of lung retention of antimony in hamsters following
intratracheal instillation. They treated hamsters with both copper smelter
dust (volume median diameter of 5.0 microns with a sigma g of 2.1 microns),
which contained 1.6% (by weight) antimony, or with pure antimony trioxide
(volume median diameter of 7.0 microns with a sigma g of 2.2 microns). The
results of these experiments were compared with experiments in which arsenic
containing dust and pure arsenic trioxide were instilled intratracheally.
Arsenic dust and arsenic trioxide are much more soluble than antimony dust or
antimony trioxide. Lung clearance was characterized by two phases. In the
initial phase, approximately 20% of the instilled pure antimony trioxide and
approximately 35% of the instilled antimony dust were eliminated from the
lungs during the first 20 hours (half-life of elimination was approximately
equal to 40 hours for pure antimony and 30 hours for antimony dust). The
second phase was slow, with half-lives of elimination of 20-40 days for both
forms of antimony. The authors also instilled various particle sizes of
antimony trioxide and found that, although there was a somewhat lower lung
retention of antimony at larger particle sizes, the solubility of the
particles was more influential in determining lung retention. The more
soluble arsenic dust and arsenic trioxide were cleared much more quickly than
antimony.
Antimony trioxide levels were measured in the chronic study conducted by
Newton et al. (1994). The rate at which antimony trioxide was cleared by the
lungs depended on the dose, with clearance half-times of 2.3, 3.6, and 9.5
months for the low-, mid-, and high-concentration groups. These results
suggest that clearance is dependent on lung burden. Substantial amounts of
antimony were found in the lungs of these animals after 1 year of exposure
(10.6, 120, and 1460 micrograms/g lung tissue in the three exposure groups,
respectively).
Data obtained from humans indicate that, as discussed above, inhaled
antimony tends to accumulate in the lung, but is relatively rapidly cleared
from other tissues. Gerhardsson et al. (1982) found no difference in antimony
levels in either liver or kidney in deceased smelter workers, as compared with
nonexposed referents.
Experiments in laboratory animals have shown that aerosols of trivalent
antimony (tartrate) are distributed primarily to the lung, bone, liver, pelt,
and thyroid following inhalation exposure and are excreted both in the feces
and in the urine (Felicetti et al., 1974a; Thomas et al., 1973). Significant
levels of antimony were found in the lungs and RBCs of animals inhaling
antimony trioxide (Newton et al., 1994). Felicetti et al. (1974b) compared
the distribution of trivalent vs. pentavalent antimony inhaled as tartrate in
hamsters. The liver accumulated more of the trivalent than the pentavalent
form, whereas the opposite was true for the skeleton. Trivalent antimony in
blood concentrated almost exclusively in the RBCs, whereas pentavalent
antimony in blood was found to a greater extent in the plasma during the first
2 hours postexposure, after which, pentavalent antimony also concentrated in
the RBCs. In an English abstract of a Russian study, Chekunova (1971)
reported that high levels of antimony were found in blood and lungs, with the
levels in liver, kidneys, spleen, and pancreas being similar following
"chronic poisoning of rats by inhalation of antimony pentachloride and
pentafluoride."
Bailly et al. (1991) studied the metabolism and excretion of antimony
following parenteral administration of antimony trichloride to rats, in a
woman who attempted suicide by ingesting antimony trisulfide, and in workers
occupationally exposed to antimony pentoxide. No methylation of antimony was
found in humans or animals. Antimony is excreted primarily in bile
(conjugated to glutathione) and in urine. Urinary excretion of pentavalent
antimony in exposed workers correlated with the level of exposure.
Gynecological examinations were performed on women (number not specified)
occupationally exposed to dust containing metallic antimony, antimony
trioxide, and antimony pentasulfide over a period of 2 years (Belyaeva, 1967).
These women were compared with a group of control women, who, presumably, were
not exposed. The level of exposure was not specified, and it is not known how
the control group was selected, whether several important confounding
variables were controlled for, or whether concurrent exposure to other
potentially toxic substances occurred. A higher incidence of "various sexual
disturbances" was reported in the exposed women as compared with controls
(77.5% vs. 56.0%); these included disturbances of the menstrual cycle in 61.2%
of the exposed women (as compared with 35.7% of the controls), inflammatory
disease in 30.4% (as compared with 55.3% of the controls), and other ailments
of the sexual organs in 8.4% of the exposed workers. Antimony was detected in
the blood of the exposed workers at levels 10 times higher than in the
controls. Antimony also was measured in the urine, breast milk, amniotic
fluid, placental tissue, and umbilical cord blood of the exposed workers. The
incidence of spontaneous abortions was 12.5% in the exposed women as compared
with 4.1% in the controls, and the incidence of premature births was 3.4%
(1.2% in the controls). The birth weights of children born to the exposed
women were comparable to those of children born to the controls, but body
weight of the children of exposed women began to lag considerably after 1
year.
Balyaeva (1967) also exposed female rats to antimony trioxide dust by
inhalation for a total of 1.5-2.0 months at a concentration of 250 mg/cu.m
(210 mg/cu.m antimony) for 4 hours/day. Exposure began 3-5 days before estrus
and continued through mating and gestation until 3-5 days prior to delivery.
Only 16/24 exposed rats became pregnant; 10/10 control rats were pregnant.
The average litter size was smaller in the exposed rats (6.2 vs. 8.3 in the
controls). No teratogenic effects were seen in the fetuses of the exposed
animals. No data were presented on the incidence of resorption or fetal
deaths. In addition, no fetal abnormalities were seen in animals given a
single dose of metallic antimony (50 mg/kg) 3-5 days prior to mating.
___I.B.5. CONFIDENCE IN THE INHALATION RfC
Study -- Medium
Data Base -- Medium
RfC -- Medium
Medium confidence is placed in the critical study because, although it
used an adequate number of animals, adequately characterized the exposure
atmosphere, and thoroughly examined the respiratory tract, it was not a
chronic, lifetime study. Medium confidence is placed in the data base because
no adequate developmental or reproductive toxicity studies are available,
although the human studies do suffice for toxicity data in a second species.
A medium confidence in the RfC follows.
___I.B.6. EPA DOCUMENTATION AND REVIEW OF THE INHALATION RfC
Source Document -- This assessment is not presented in any existing U.S. EPA
document.
This assessment was peer reviewed by external scientists. This review was
completed on August 31, 1993. Their comments have been carefully evaluated
and considered in the revision and finalization of this IRIS summary. A
record of these comments is included in the IRIS documentation files.
Other EPA Documentation -- U.S. EPA, 1980, 1985, 1987, 1989
Agency Work Group Review -- 02/09/1993, 09/23/1993, 05/10/1995
Verification Date -- 05/10/1995
___I.B.7. EPA CONTACTS (INHALATION RfC)
Please contact the Risk Information Hotline for all questions concerning this
assessment or IRIS, in general, at (513)569-7254 (phone), (513)569-7159 (FAX)
or RIH.IRIS@EPAMAIL.EPA.GOV (internet address).
_II. CARCINOGENICITY ASSESSMENT FOR LIFETIME EXPOSURE
Substance Name -- Antimony trioxide
CASRN -- 1309-64-4
This substance/agent has not undergone a complete evaluation and determination
under US EPA's IRIS program for evidence of human carcinogenic potential.
_VI. BIBLIOGRAPHY
Substance Name -- Antimony trioxide
CASRN -- 1309-64-4
Last Revised -- 09/01/1995
__VI.A. ORAL RfD REFERENCES
None
__VI.B. INHALATION RfC REFERENCES
Allen, B.C. and M. Chapman. 1993. Statistical analysis of lung and cataract
responses in rats exposed to antimony trioxide. (Unpublished material prepared
for J.S. Gift, Environmental Criteria and Assessment Office, Office of Research
and Development, U.S. EPA.)
Allen, B.C., R.J. Kavlock, C.A. Kimmel and E.M. Faustman. 1994. Dose-
response assessment for developmental toxicity. II. Comparison of generic
benchmark dose estimates with no observed adverse effect levels. Fund. Appl.
Toxicol. 23(4): 487-495.
Bailly, R., R. Lauwerys, J.P. Buchet, P. Mahieu and J. Konings. 1991.
Experimental and human studies on antimony metabolism: Their relevance for
the biological monitoring of workers exposed to inorganic antimony. Br. J.
Ind. Med. 48:(2):93-7.
Belyaeva, A.P. 1967. The effect of antimony on reproduction. Gig. Truda.
Prof. Zabol. 11(1): 32-37. (Russian)
Bio/dynamics. 1985. A three month inhalation toxicity study of antimony
trioxide in the rat followed by a recovery period. East Millstone, NJ.
Project No. 83-7646.
Bio/dynamics. 1990. A one year inhalation toxicity study of antimony
trioxide in the rat (with a one year recovery period). East Millstone, NJ.
Project No. 83-7647.
Boorman, G. 1995. National Institute for Environmental Health and Safety.
Telephone communication with Gary Foureman, National Center for Environmental
Assessment, U.S. EPA, Research Triangle Park, NC.
Brieger, H., C.W. Semisch III, J. Stasney and D.A. Piatnek. 1954. Industrial
antimony poisoning. Ind. Med. Surg. 23: 521-523.
Chekunova, M.P. 1971. On the fate of antimony halogen compounds in the
organism. Gig. Tr. Prof. Zabol. 15(3): 31-34. (Rus. trans.)
Cooper, D.A., E.P. Pendergrass, A.J. Vorwald, et al. 1968. Pneumoconiosis
among workers in an antimony industry. Am. J. Roentgenol. Radium Ther. Nucl.
Med. 103(3): 495-508.
Dernehl, C.U., C.A. Nau and H.H. Sweets. 1945. Animal studies on the
toxicity of inhaled antimony trioxide. J. Ind. Hyg. Toxicol. 27(9): 256-262.
Faustman, E.M., B.C. Allen, R.J. Kavlock and C.A. Kimmel. 1994. Dose-
response assessment for developmental toxicity. I. Characterization of
database and determination of no observed effect levels. Fund. Appl. Toxicol.
23(4): 478-486.
Felicetti, S.W., R.G. Thomas and R.O. McClellan. 1974a. Retention of inhaled
antimony-124 in the beagle dog as a function of temperature of aerosol
formation. Health Phys. 26(6): 525-531.
Felicetti, S.A., R.G. Thomas and R.O. McClellan. 1974b. Metabolism of two
valence states of inhaled antimony in hamsters. Am. Ind. Hyg. Assoc. J.
35(5): 292-300.
Gerhardsson, L., D. Brune, G.F. Nordberg and P.O. Wester. 1982. Antimony in
lung, liver, and kidney tissue from deceased smelter workers. Scand. J. Work
Environ. Health. 8(3): 201-208.
Gross, P., J.H.U. Brown and T.F. Hatch. 1952. Experimental endogenous lipoid
pneumonia. Am. J. Pathol. 28: 211-221.
Gross, P., M.L. Westrick, J.H.U. Brosn, R.P. Srsic, H.H. Schrenk and T.F.
Hatch. 1955. Toxicologic study of calcium halophosphate phosphors and
antimony trioxide. II. Pulmonary studies. Arch. Ind. Health. 11: 479-486.
Groth, D.H., L.E. Stettler, J.R. Burg, W.M. Busey, G.C. Grant and L. Wong.
1986. Carcinogenic effects of antimony trioxide and antimony ore concentrate
in rats. J. Toxicol. Environ. Health. 18(4): 607-26.
Leffler P., L. Gerhardsson, D. Brune and G.F. Nordberg. 1984. Lung retention
of antimony and arsenic in hamsters after the intratracheal instillation of
industrial dust. Scand. J. Work Environ. Health. 10(4): 245-251.
Ludersdorf, R., A. Fuchs, P. Mayer, G. Skulsuksai and G. Schacke. 1987.
Biological assessment of exposure to antimony and lead in the glass-producing
industry. Int. Arch. Occup. Environ. Health. 59(5): 469-474.
McCallum, R.I. 1963. The work of an occupational hygiene service in
environmental control. Ann. Occup. Hyg. 6: 55-64.
McCallum, R.I. 1967. Detection of antimony in process workers' lungs by X-
radiation. Trans. Soc. Occup. Med. 17: 134-138.
McCallum, R.I., M.J. Day, J. Underhill and E.G.A. Aird. 1971. Measurement of
antimony oxide dust in human lungs in vivo by X-ray spectrophotometry. In:
Walton, W.H., ed. Inhaled Particles III. Old Woking, UK, Unwin Bros. p.
611-619.
Muhle, H., B. Bellmann, O. Creutzenberg, U. Henrich, M. Ketkar and R.
Mermelstein. 1990. Dust overloading of lungs after exposure of rats to
particles of low solubility: Comparative studies. J. Aerosol Sci. 21(3):
374-377.
Newton, P.E., H.F. Bolte, I.W. Daly, et al. 1994. Subchronic and chronic
inhalation toxicity of antimony trioxide in the rat. Fund. and Appl. Tox.
22: 561-576.
Potkonjak, V. and M. Pavlovich. 1983. Antimonosis: A particular form of
pneumonoconiosis. I. Etiology, clinical and X-ray findings. Int. Arch.
Occup. Environ. Health. 51: 199-207.
Renes, L.E. 1953. Antimony poisoning in industry. Arch. Ind. Hyg. Occup.
Med. 7: 99-108.
Thomas, R.G., S.W. Felicetti, R.V. Lucchino, and R.O. McClellan. 1973.
Retention patterns of antimony in mice following inhalation of particles
formed at different temperatures. Proc. Soc. Exp. Biol. Med. 144(2):
544-550.
U.S. EPA. 1980. Ambient Water Quality Criteria Document for Antimony.
Prepared by the Environmental Criteria and Assessment Office, Cincinnati, OH
for the Office of Water Regulations and Standards, Washington, DC. EPA 440/5-
80-020.
U.S. EPA. 1985. Health and Environmental Effects Profile for Antimony
Oxides. Prepared by the Environmental Criteria and Assessment Office,
Cincinnati, OH for the Office of Solid Waste and Emergency Response,
Washington, DC. EPA/600/X-85/271.
U.S. EPA. 1987. Health Effects Assessment for Antimony and Compounds.
Prepared by the Environmental Criteria and Assessment Office, Cincinnati, OH
for the Office of Solid Waste and Emergency Response, Washington, DC.
EPA/600/8-88/018.
U.S. EPA. 1989. Ambient Water Quality Criteria Document Addendum for
Antimony. Prepared by the Environmental Criteria and Assessment Office,
Cincinnati, OH for the Office of Water Regulations and Standards, Washington,
DC.
U.S. EPA. 1994. Interim Methods for Development of Inhalation Reference
Concentrations. Prepared by the Environmental Criteria and Assessment Office,
Research Triangle Park, NC. October 1994. EPA/600/8-90/066A. (Final Draft)
Vanoeteren, C., R. Cornelis and R. Dams. 1986a. Evaluation of trace elements
in human lung tissue. II. Recovery and analysis of inhaled particulates.
Sci. Total Environ. 54(0): 231-236.
Vanoeteren, C., R. Cornelis and P. Versieck. 1986b. Evaluation of trace
elements in human lung tissue. I. Concentration and distribution. Sci. Total
Environ. 54(0): 217-230.
Vanoeteren, C., R. Cornelis and P. Verbeeck. 1986c. Evaluation of trace
elements in human lung tissue. III. Correspondence analysis. Sci. Total
Environ. 54(0): 237-245.
Watt, W.D. 1983. Chronic inhalation toxicity of antimony trioxide:
Validation of the threshold limit value. Dissertation, Wayne State
University, Detroit, MI. Avialable from Microfilms International, Ann Arbor,
MI.
__VI.C. CARCINOGENICITY ASSESSMENT REFERENCES
None
_VII. REVISION HISTORY
Substance Name -- Antimony trioxide
CASRN -- 1309-64-4
-------- -------- --------------------------------------------------------
Date Section Description
-------- -------- --------------------------------------------------------
03/01/1993 I.B. Inhalation RfC now under review
11/01/1993 I.B. Work group review date added
06/01/1995 I.B. Work group review date added
09/01/1995 I.B. Inhalation RfC summary on-line
09/01/1995 VI.B. Inhalation RfC references on-line
VIII. SYNONYMS
Substance Name -- Antimony trioxide
CASRN -- 1309-64-4
Last Revised -- 03/01/1993
1309-64-4
Antimony oxide
Diantimony trioxide
A 1530
A 1582
A 1588LP
AMSPEC-KR
Antimonious oxide
Antimony peroxide
Antimony sesquioxide
Antimony trioxide
ANTIMONY WHITE
ANTIMONY(3+) OXIDE
ANTOX
ANZON-TMS
AP 50
BLUE STAR
C.I. PIGMENT WHITE 11
C.I. 77052
CHEMETRON FIRE SHIELD
CI PIGMENT WHITE 11
CI 77052
DECHLORANE A-O
Exitelite
Extrema
FLOWERS of ANTIMONY
HSDB 436
NCI-C55152
Nyacol A 1510LP
NYACOL A 1530
Senarmontite
Thermoguard B
Thermoguard S
Timonox
TWINKLING STAR
Valentinite
Weisspiessglanz [German]
WHITE STAR
Last updated: 5 May 1998
URL: http://www.epa.gov/iris/SUBST/0676.HTM
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