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Aramite
CASRN 140-57-8
Contents
0473
Aramite; CASRN 140-57-8
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 Aramite
File On-Line 06/01/1991
Category (section) Status Last Revised
----------------------------------------- -------- ------------
Oral RfD Assessment (I.A.) no data
Inhalation RfC Assessment (I.B.) no data
Carcinogenicity Assessment (II.) on-line 06/01/1991
_I. CHRONIC HEALTH HAZARD ASSESSMENTS FOR NONCARCINOGENIC EFFECTS
__I.A. REFERENCE DOSE FOR CHRONIC ORAL EXPOSURE (RfD)
Substance Name -- Aramite
CASRN -- 140-57-8
Not available at this time.
__I.B. REFERENCE CONCENTRATION FOR CHRONIC INHALATION EXPOSURE (RfC)
Substance Name -- Aramite
CASRN -- 140-57-8
Not available at this time.
_II. CARCINOGENICITY ASSESSMENT FOR LIFETIME EXPOSURE
Substance Name -- Aramite
CASRN -- 140-57-8
Last Revised -- 06/01/1991
Section II provides information on three aspects of the carcinogenic
assessment for the substance in question; the weight-of-evidence judgment of
the likelihood that the substance is a human carcinogen, and quantitative
estimates of risk from oral exposure and from inhalation exposure. The
quantitative risk estimates are presented in three ways. The slope factor is
the result of application of a low-dose extrapolation procedure and is
presented as the risk per (mg/kg)/day. The unit risk is the quantitative
estimate in terms of either risk per ug/L drinking water or risk per ug/cu.m
air breathed. The third form in which risk is presented is a drinking water
or air concentration providing cancer risks of 1 in 10,000, 1 in 100,000 or 1
in 1,000,000. The rationale and methods used to develop the carcinogenicity
information in IRIS are described in The Risk Assessment Guidelines of 1986
(EPA/600/8-87/045) and in the IRIS Background Document. IRIS summaries
developed since the publication of EPA's more recent Proposed Guidelines for
Carcinogen Risk Assessment also utilize those Guidelines where indicated
(Federal Register 61(79):17960-18011, April 23, 1996). Users are referred to
Section I of this IRIS file for information on long-term toxic effects other
than carcinogenicity.
__II.A. EVIDENCE FOR CLASSIFICATION AS TO HUMAN CARCINOGENICITY
___II.A.1. WEIGHT-OF-EVIDENCE CLASSIFICATION
Classification -- B2; probable human carcinogen
Basis -- Based on no human data and sufficient data from animal bioassays
including increased incidence of liver tumors and/or neoplastic nodules in
three strains of male and female rats and males of one strain of mice, and
extrahepatic biliary system tumors in dogs following chronic oral exposure.
___II.A.2. HUMAN CARCINOGENICITY DATA
None.
___II.A.3. ANIMAL CARCINOGENICITY DATA
Sufficient. Popper et al. (1960) (see also Oser and Oser, 1962) fed 50
FDRL rats/sex/group 100, 200 or 400 ppm aramite in the diet for 104 weeks.
Controls consisted of 100 rats/sex fed a basal diet containing no aramite.
Weight gain reportedly was similar in all groups. Survival in all groups was
95% or greater in the first year of the study. At the end of the study,
survival in the males was 59, 50, 46 and 46% in the control, low-, mid- and
high-dose groups, respectively. In females survival was 61, 64, 40 and 34%,
in the control, low-, mid-, and high-dose groups, respectively. Tumor
incidence data were not reported by sex; however, no sex differences were
noted in the pathology. There was a statistically significant dose-related
increase in the incidence of hyperplastic liver nodules: 2/193, 2/93, 3/100
and 20/90 in rats (male and female data combined) in the control, low-, mid-
and high-dose groups, respectively. The hyperplastic nodules described by
Popper et al. (1960) would now be classified as neoplastic liver nodules
(Baggs, 1990; Chiu and Singh, 1990). Also, in the high-dose group two liver
carcinomas and five bile duct adenomas were found; these tumor types were not
observed in any other groups. Rats with carcinomas also had neoplastic
nodules (hence were counted in the incidence data above), but it is unclear
whether the rats with the bile duct adenomas also had neoplastic liver
nodules.
Popper et al. (1960) (see also Oser and Oser, 1962) also fed groups of 50
CFN rats/sex and 50 Sprague-Dawley rats/sex 100, 200 or 400 ppm aramite in the
diet for 104 weeks. Controls consisted of 100 rats/sex/strain fed a diet
containing no aramite. Tumor incidence data were not reported by sex. CFN
rats showed a dose-related increased incidence of neoplastic nodules; 5/180,
3/93, 10/90 and 22/96 in the 0, 100, 200 or 400 ppm groups, respectively. No
liver carcinomas were observed in CFN rats, but the incidences of bile duct
adenomas were 0/180, 2/93, 1/200 and 2/96 in the control, 100, 200 and 400 ppm
groups, respectively. It is unclear whether these rats also had neoplastic
liver nodules. Only Sprague-Dawley rats dying after 1 year were examined.
High mortality (about 60%) (unrelated to treatment) in the ninth and tenth
months due to respiratory infections in the Sprague-Dawley rats precluded
evaluation for late-developing tumors. Respiratory infections also caused
many deaths in CFN rats (about 20%) (unrelated to treatment) after 6 months.
Oser and Oser (1960) fed groups of 20-21 FDRL rats (approximately
10/sex/group) diets containing 0, 500, 1580 or 5000 ppm aramite for 24-96
weeks. All rats fed the 5000 ppm diet died by 96 weeks of treatment, and
survival was reduced in the other treated groups, compared with controls.
Tumor incidence data were not reported by sex. The authors reported a
significantly increased incidence of liver tumors: 0/20, 0/20, 2/21 and 6/20
in rats fed 0, 500, 1580 and 5000 ppm, respectively. Tumors in rats fed the
5000 ppm diet were described as hepatomas or cholangiomas; tumors in rats fed
the 1580 ppm diet were described as malignancies. One rat fed the 500 ppm
diet had neoplastic liver nodules. Neoplastic nodules were not observed in
the controls; the incidence of nodules in rats fed higher doses of aramite was
not reported.
Male Wistar rats were fed diets containing aramite at 0 (20 rats) or 5000
ppm (33 rats) for 56 weeks (Truhaut et al., 1975, 1978; Blanc et al., 1978).
Neither survival nor liver tumor incidence data were reported for the
controls. At 56 weeks, 19/33 treated rats were alive and all (19/19) had
liver tumors.
Radomski et al. (1965) fed 50 ppm aramite alone in the diet or 50 ppm
aramite mixed with three other pesticides in the diet to 50 Osborne-Mendel
rats/sex/group for 2 years. In a second experiment, 30 Osborne-Mendel
rats/sex/group were fed 80 ppm aramite alone in diet or 80 ppm aramite mixed
with three other pesticides in the diet for 2 years. Deichmann et al. (1967)
fed 200 ppm aramite either alone or mixed with three other pesticides in the
diet to 30 Osborne-Mendel rats/sex/group for 24-27 months. Although actual
data were not provided, both studies stated that survival and weight gain were
not affected by the dietary addition of aramite either alone or in combination
[except for decreased weight gain in the group that was fed the mixture of
four pesticides in the Deichmann et al. (1967) report]. In both reports,
tumors were detected by gross examination at autopsy; all tumors and several
body organs, including the liver, were examined histologically. There were no
increases in the tumor incidence in rats fed aramite alone or in combination
with other pesticides. Since the MTD was not reached in either study, both
studies are considered inadequate.
Oser and Oser (1962) fed groups of 50 C3H mice/sex and 50 C57BL mice/sex
100, 200 or 400 ppm aramite in the diet for 2 years. Controls consisted of
100 mice/sex/strain fed a diet containing no aramite. There was no evidence
of a neoplasia reported in either strain of mice.
In an extended regimen, B6C3F1 mice and B6AKF1 mice (16 mice/sex/strain)
received aramite in 0.5% gelatin by gavage at 464 mg/kg/day from 7 days after
birth until weaning at 4 weeks (Innes et al., 1969). After weaning, aramite
was administered in the diet at 1112 ppm for approximately 80 weeks. A
significant increase (6/16) in hepatomas was observed in male
(C57BL/6xC3H/Anf)F1 mice compared with the incidence in controls (8/73).
Tumor incidences in the female mice of this strain and in both sexes of the
B6AKF1 strain were not increased by comparison to controls.
Oser and Oser (1960) fed mongrel dogs (3/group, sex not stated) a basal
diet containing 0, 500 or 1580 ppm aramite. The dogs were sacrificed after 1
year of study. Autopsies showed degeneration of the liver; however, no tumors
were reported. This study is inadequate due to small number of animals and
the short duration of the experiment.
Sternberg et al. (1960) (see also Oser and Oser, 1962) identified tumors
in the extrahepatic biliary tract of dogs exposed to aramite in the diet. A
total of 40 mongrel dogs (17 male and 23 female) were fed diets containing
aramite at 0, 500 or 828-1429 ppm for 811-1220 days (low-dose group) and for
462-1206 days (high-dose group). Seven of the 12 low-dose dogs and 12/16
high-dose dogs appeared moribund or died during treatment and were necropsied
and examined for tumors. The control dogs and the remaining low-dose dogs
appeared healthy and were not autopsied. Extrahepatic biliary system
adenocarcinomas were found in 7/7 low-dose dogs and in 7/12 high-dose dogs
subjected to necropsy (extrahepatic biliary system adenocarcinomas were
observed in all of the 7 high-dose dogs surviving more than 715 days on
study). Neoplastic nodules in the liver parenchyma (3/7 and 3/12 in the low-
dose and high-dose dogs, respectively), and hyperplasia and adenocarcinomas of
liver bile ducts (6/7 and 7/12 in the low-dose and high-dose dogs,
respectively) were also observed in both treated groups. Five of the 12 high-
dose dogs died early in the experiment (before 715 days) with no signs of
cancer. No statistical analyses were reported.
Hodge et al. (1966) administered a single subcutaneous injection of 10 mg
aramite in the vehicle trioctanonin to 50 C3H/Anf mice/sex. Vehicle controls,
50 C3H/Anf mice/sex, were injected with trioctanonin only. The body weights
of aramite-injected and vehicle-control groups did not differ significantly.
Among the male groups the mean survival times were not significantly
different. The mean survival times of aramite-injected females (401 days)
were greater than their corresponding vehicle-controls (337 days). (The
statistical significance of this reduction in survival was not reported.)
Many of these deaths were due to pneumonitis. In aramite-injected mice there
was no evidence of injection-site tumors during gross examination or of
neoplasia during histological examination.
In a dermal application study, Hodge et al. (1966) applied either 0.1 mg
of aramite or 10 mg of aramite in acetone weekly to the shaved skins of 50
C3H/Anf mice/sex. Two acetone control groups/sex (one corresponding to each
dose) were also utilized. The mice were housed 12-13/cage. The mean survival
time of the low-dose males (426 days) was equivalent to those of their
corresponding controls (430 days). The mean survival time of all other groups
differed significantly from corresponding control groups; the mean survival
time for high-dose males was 452 days vs. 386 in the appropriate controls, for
low-dose females it was 328 days vs. 393 in the appropriate controls, and for
high-dose females it was 441 days vs. 313 in the appropriate controls. Many
of these deaths were due to pneumonitis and were not the result of chemical-
related toxicity. No gross evidence of tumor formation in the skins of
control or treated mice was detected.
___II.A.4. SUPPORTING DATA FOR CARCINOGENICITY
Aramite was negative for mutagenicity expressed as a dominant lethal
effect when administered as a single intraperitoneal injection of 200 or 500
mg/kg dose into 7 and 9 male ICR Ha Swiss mice, respectively (Epstein et al.,
1972).
__II.B. QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM ORAL EXPOSURE
___II.B.1. SUMMARY OF RISK ESTIMATES
Oral Slope Factor -- 2.5E-2 per (mg/kg)/day
Drinking Water Unit Risk -- 7.1E-7 per (ug/L)
Extrapolation Method -- Linearized multistage procedure, extra risk
Drinking Water Concentrations at Specified Risk Levels:
Risk Level Concentration
------------------------------------
E-4 (1 in 10,000) 1E+2 ug/L
E-5 (1 in 100,000) 1E+1 ug/L
E-6 (1 in 1,000,000) 1E+0 ug/L
___II.B.2. DOSE-RESPONSE DATA (CARCINOGENICITY, ORAL EXPOSURE)
Tumor Type -- neoplastic liver nodules and carcinomas
Test Animals -- rat/FDRL, male and female
Route -- diet
Reference -- Popper et al., 1960; Oser and Oser, 1962
---------------- Dose ------------------
Transformed Human
Administered Animal Equivalent Tumor
(ppm) (mg/kg)/day (mg/kg)/day Incidence
------------ ----------- ----------- ---------
0 0 0 2/193
100 5 0.78 2/93
200 10 1.57 3/100
400 20 3.14 20/90
___II.B.3. ADDITIONAL COMMENTS (CARCINOGENICITY, ORAL EXPOSURE)
This study yielded the most appropriate quantitative estimate of cancer
risk for aramite. Carcinoma and neoplastic hyperplastic liver nodule
incidences were combined; however, carcinomas were observed only in two rats
in the high-dose group.
The transformed animal dose was calculated by multiplying the administered
dose (in ppm) by the food factor, assumed to be 0.05 for rats. The human
equivalent dose was calculated by multiplying the transformed animal dose by
the cube route of the ratio of the body weight of the rats (estimated at 0.270
kg) to the assumed body weight of humans (70 kg).
The unit risk should not be used if the water concentration exceeds 1E+4
ug/L, since above this concentration the slope factor may differ from that
stated.
___II.B.4. DISCUSSION OF CONFIDENCE (CARCINOGENICITY, ORAL EXPOSURE)
The key study was conducted with a sufficient number of animals of both
sexes using a relevant route of exposure and control plus three doses, the
highest of which was only slightly below the maximum tolerated dose, for the
lifetime of the animals. The data demonstrated a dose relationship for tumor
incidence. Data from dog studies indicate that this species may be more
sensitive to the carcinogenic effects of aramite, but poor survival precluded
the use of dog data for quantitation of risk.
__II.C. QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM INHALATION EXPOSURE
___II.C.1. SUMMARY OF RISK ESTIMATES
Inhalation Unit Risk -- 7.1E-6 per (ug/cu.m)
Extrapolation Method -- Linearized multistage procedure, extra risk
Air Concentrations at Specified Risk Levels:
Risk Level Concentration
-------------------- -------------
E-4 (1 in 10,000) 1E+1 ug/cu.m
E-5 (1 in 100,000) 1E+0 ug/cu.m
E-6 (1 in 1,000,000) 1E-1 ug/cu.m
___II.C.2. DOSE-RESPONSE DATA FOR CARCINOGENICITY, INHALATION EXPOSURE
The inhalation estimates are derived from the oral exposure data presented
in Section II.B.2.
___II.C.3. ADDITIONAL COMMENTS (CARCINOGENICITY, INHALATION EXPOSURE)
The inhalation unit risk and risk-specific concentrations in air were
estimated from the oral data (see Section II) because inhalation data were not
located. The observation of tumors at sites (the liver and extrahepatic
biliary tract) distant from the digestive tract in oral studies in rats, mice
and dogs supports the unit risk.
The unit risk should not be used if the air concentration exceeds 1E+4
ug/cu.m, above this concentration the unit risk may differ from that stated.
___II.C.4. DISCUSSION OF CONFIDENCE (CARCINOGENICITY, INHALATION EXPOSURE)
Data from inhalation exposures were not located; pharmacokinetic data are
insufficient to predict whether the fates of inhaled and ingested aramite are
similar.
__II.D. EPA DOCUMENTATION, REVIEW, AND CONTACTS (CARCINOGENICITY ASSESSMENT)
___II.D.1. EPA DOCUMENTATION
Source Document -- U.S. EPA, 1989
The 1989 Health and Environmental Effects Document on Aramite has received
external peer review and Agency review.
___II.D.2. REVIEW (CARCINOGENICITY ASSESSMENT)
Agency Work Group Review -- 12/06/1990, 01/10/1991
Verification Date -- 01/10/1991
___II.D.3. U.S. EPA CONTACTS (CARCINOGENICITY ASSESSMENT)
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).
_VI. BIBLIOGRAPHY
Substance Name -- Aramite
CASRN -- 140-57-8
Last Revised -- 06/01/1991
__VI.A. ORAL RfD REFERENCES
None
__VI.B. INHALATION RfD REFERENCES
None
__VI.C. CARCINOGENICITY ASSESSMENT REFERENCES
Baggs, R.B. 1990. University of Rochester Medical Center, Rochester, NY.
Memorandum to P.F. Goetchius, Syracuse Research Corporation, Syracuse, NY,
December 20. Critical review of the "hyperplastic nodules" as described by
Popper et al., and Oser and Oser.
Blanc, F., V. Ngoc-Huyen, J.M. Warnet, J-R. Claude and R. Truhaut. 1978.
Carcinogenic effect, on the liver, of an insectide: Aramite. Toxicol. Eur.
Res. 1(1): 13-21.
Chiu, A. and D. Singh. 1990. U.S. EPA. Memorandum to P. McGinnis, Syracuse
Research Corporation, Cincinnati, OH, December 18. Review of CRAVE cover
sheet for Aramite.
Deichmann, W.B., M. Keplinger, F. Sala and E. Glass. 1967. Synergism among
oral carcinogens. IV. The simultaneous feeding of four tumorigens to rats.
Toxicol. Appl. Pharmacol. 11(1): 88-103.
Epstein, S.S., E. Arnold, J. Andrea, W. Bass and Y. Bishop. 1972. Detection
of chemical mutagens by the dominant lethal assay in the mouse. Toxicol.
Appl. Pharmacol. 23: 288-325.
Hodge, H.C., E.A. Maynard, W.L. Downs, J.K. Ashton and L.L. Salerno. 1966.
Tests on mice for evaluating carcinogenicity. Toxicol. Appl. Pharmacol.
9(3): 583-596.
Innes, J.R.M., B.M. Ulland, M.G. Valerio, et al. 1969. Bioassay of
pesticides and industrial chemicals for tumorigenicity in mice: A preliminary
note. J. Natl. Cancer Inst. 42(6): 1101-1114.
Oser, B.L. and M. Oser. 1960. 2-(p-tert-Butylphenoxy)isopropyl 2-chloroethyl
sulfite (aramite). I. Acute, subacute, and chronic oral toxicity. Toxicol.
Appl. Pharmacol. 2: 441-457.
Oser, B.L. and M. Oser. 1962. 2-(p-tert-Butylphenoxy)isopropyl 2-chloroethyl
sulfite (aramite). II. Carcinogenicity. Toxicol. Appl. Pharmacol. 4: 70-88.
Popper, H., S.S. Sternberg, B.L. Oser and M. Oser. 1960. The carcinogenic
effect of aramite in rats: A study of hepatic nodules. Cancer. 13(5): 1035-
1046.
Radomski, J.L., W.B. Deichmann, W.E. MacDonald and E.M. Glass. 1965.
Synergism among oral carcinogens. I. Results of the simultaneous feeding of
four tumorigens to rats. Toxicol. Appl. Pharmacol. 7(5): 652-656.
Sternberg, S.S., H. Popper, B.L. Oser and M. Oser. 1960. Gallbladder and
bile duct adenocarcinomas in dogs after long term feeding of aramite. Cancer.
13(4): 780-789.
Truhaut, R., J-R. Claude, V.N. Huyen, J.M. Warnet and F. Blanc. 1975. Primary
liver carcinogenesis in rats after feeding of a pesticide 2,4-tert
butylphenoxy-1-methylethyl-2-chloroethyl sulfite aramite. C.R. Hebd Seances
Acad. Sci. Ser. Sci. Nat. 281(9): 599-604.
Truhaut, R., J.R. Claude, J.M. Warnet, V.N. Huyen and F. Blanc-Habets. 1978.
Aramite: Experimental carcinogenicity and metabolism. Meded. Fac. Landbouww.
Rijksuniv. Gent. 43(2): 1225-1231.
U.S. EPA. 1989. Health and Environmental Effects Document for Aramite.
Prepared by the Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH for the Office of Solid Waste,
Washington, DC.
_VII. REVISION HISTORY
Substance Name -- Aramite
CASRN -- 140-57-8
-------- -------- --------------------------------------------------------
Date Section Description
-------- -------- --------------------------------------------------------
06/01/1991 II. Carcinogenicity assessment on-line
06/01/1991 VI. Bibliography on-line
01/01/1992 IV. Regulatory Action section on-line
VIII. SYNONYMS
Substance Name -- Aramite
CASRN -- 140-57-8
Last Revised -- 06/01/1991
140-57-8
SULFUROUS ACID, 2-(p-t-BUTYLPHENOXY)-1-METHYLETHYL-2-CHLOROETHYL ESTER
Sulfurous acid, 2-(p-tert-butylphenoxy)-1-methylethyl 2-chloroethyl ester
Sulfurous acid, 2-chloroethyl 2-(4-(1,1-dimethylethyl)phenoxy)-1-methylethyl
ester
2-p-tert-butylphenoxyisopropyl 2-chloroethyl sulfite
Acaracide
AI3-16519
Aracide
Aramit
Aramite
Aramite-15W
ARAMITEARARAMITE-15W
Aratron
beta-CHLOROETHYL-beta-(p-t-BUTYLPHENOXY)-alpha-METHYLETHYL SULPHITE
beta-CHLOROETHYL-beta'-(p-t-BUTYLPHENOXY)-alpha'-METHYLETHYL SULFITE
Butylphenoxyisopropyl chloroethyl sulfite
Caswell No. 131
CES
Compound 88R
ENT 16,519
EPA Pesticide Chemical Code 062501
ETHANOL, 2-CHLORO-, ESTER WITH 2-(p-tert-BUTYLPHENOXY)-1-METHYLETHYL SULFITE
ETHANOL, 2-CHLORO-, 2-(p-t-BUTYLPHENOXY)-1-METHYLETHYL SULFITE
Niagaramite
NSC 404155
Ortho-Mite
SULFUROUS ACID, 2-(P-T-BUTYLPHENOXY)-1-METHYLETHYL-2-CHLOROETHYL ESTER
SULFUROUS ACID, 2-(P-TERT-BUTYLPHENOXY)-1-METHYLETHYL 2-CHLOROETHYL ESTER
SULFUROUS ACID, 2-CHLOROETHYL 2-(4-(1,1-DIMETHYLETHYL)PHENOXY)-1-METHYLETHYL
ESTER
SULFUROUS ACID, 2-CHLOROETHYL-, 2-(4-(1,1-DIMETHYLETHYL)PHENOXY)-1-METHYLETHYL
ESTER
2-(p-butylphenoxy)-1-methylethyl 2-chloroethyl sulfite
2-(p-Butylphenoxy)isopropyl 2-chloroethyl sulfite
2-(p-t-BUTYLPHENOXY)-1-METHYLETHYL SULPHITE of 2-CHLOROETHANOL
2-(p-t-BUTYLPHENOXY)-1-METHYLETHYL 2-CHLOROETHYL ESTER of SULPHUROUS ACID
2-(p-t-BUTYLPHENOXY)-1-METHYLETHYL 2'-CHLOROETHYL SULPHITE
2-(p-t-BUTYLPHENOXY)-1-METHYLETHYL-2-CHLOROETHYL SULFITE
2-(p-t-butylphenoxy)isopropyl 2'-chloroethyl sulfite
2-(p-t-butylphenoxy)isopropyl 2'-chloroethyl sulphite
2-(p-terc.BUTYLFENOXY)ISOPROPYL-2'-CHLORETHYLESTER KYSELINY SIRICITE [Czech]
2-(p-tert-Butylphenoxy)-1-methylethyl sulfite of 2-chloroethanol
2-(p-tert-Butylphenoxy)-1-methylethyl 2-chloroethylsulfite
2-(p-tert-Butylphenoxy)-1-methylethyl 2'-chloroethyl sulfite
2-(p-tert-Butylphenoxy)-1-methylethyl-2-choroethyl sulfite
2-(p-tert-Butylphenoxy)isopropyl 2-chloroethyl sulfite
2-(4-t-BUTYLPHENOXY)ISOPROPYL-2-CHLOROETHYL SULFITE
2-(4-t-butylphenoxy)isopropyl-2-chloroethyl sulphite
2-(4-tert-Butylphenoxy)isopropyl 2-chloroethyl sulfite
2-(4-tert-Butylphenoxy)isopropyl-2-chloroethyl sulfite
2-Chloroethyl sulfite of 1-(p-t-butylphenoxy)-2-propanol
2-CHLOROETHYL SULPHITE of 1-(p-t-BUTYLPHENOXY)-2-PROPANOL
2-CHLOROETHYL 1-METHYL-2-(p-t-BUTYLPHENOXY)ETHYL SULPHATE
2-Chloroethyl 1-methyl-2-(p-tert-butylphenoxy)ethyl sulfite
2-PROPANOL, 1-(p-t-BUTYLPHENOXY)-, 2-CHLOROETHYL SULFITE
2-Propanol, 1-(p-tert-butylphenoxy)-, 2-chloroethyl sulfite
88-R
88R
Last updated: 5 May 1998
URL: http://www.epa.gov/iris/SUBST/0473.HTM
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