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Benzotrichloride
CASRN 98-07-7
Contents
0388
Benzotrichloride; CASRN 98-07-7
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 Benzotrichloride
File On-Line 07/01/1990
Category (section) Status Last Revised
----------------------------------------- -------- ------------
Oral RfD Assessment (I.A.) no data
Inhalation RfC Assessment (I.B.) no data
Carcinogenicity Assessment (II.) on-line 12/01/1990
_I. CHRONIC HEALTH HAZARD ASSESSMENTS FOR NONCARCINOGENIC EFFECTS
__I.A. REFERENCE DOSE FOR CHRONIC ORAL EXPOSURE (RfD)
Substance Name -- Benzotrichloride
CASRN -- 98-07-7
Not available at this time.
__I.B. REFERENCE CONCENTRATION FOR CHRONIC INHALATION EXPOSURE (RfC)
Substance Name -- Benzotrichloride
CASRN -- 98-07-7
Not available at this time.
_II. CARCINOGENICITY ASSESSMENT FOR LIFETIME EXPOSURE
Substance Name -- Benzotrichloride
CASRN -- 98-07-7
Last Revised -- 12/01/1990
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 inadequate human data and sufficient evidence of
carcinogenicity in animals; namely, significantly increased incidences of
benign and malignant tumors at multiple sites in one strain of female mice
treated orally, dermally, and by inhalation. There is also evidence of
mutagenicity in a variety of test systems.
___II.A.2. HUMAN CARCINOGENICITY DATA
Inadequate. Studies have shown that occupational exposure to the process
of benzoyl chloride production process, which involves benzotrichloride as a
major reaction intermediate, may increase the risk of cancer-induced
mortality. The available human data for benzotrichloride alone are considered
inadequate because the studies included small numbers of cancer deaths and
were based on exposure to mixtures of chlorinated compounds. In addition,
data on cigarette smoking were incomplete.
Sakabe et al. (1976) reported three cancer deaths among 41 workers
employed in a benzoyl chloride production plant in Japan between 1954 and
1972. Two of the deaths were from lung cancer, both in smokers in their
forties. The third cancer death was from maxillary malignant lymphoma in a
50-year-old worker not specified as a smoker or nonsmoker. A fourth case of
cancer diagnosed as squamous cell carcinoma of the lung was identified in a
nonsmoking worker still living at the time the analysis was undertaken in
1973. The number of years these four workers were employed in benzoyl
chloride production ranged from 6 to 15 years. The number of deaths from lung
cancer (2) was significantly higher than the number expected (0.06), based on
the Japanese national rates for death from lung cancer in males. In addition
to benzotrichloride and benzoyl chloride, these workers were exposed to
toluene, chlorine gas, hydrogen chloride, benzyl chloride, benzal chloride,
other chlorinated toluenes and polymerized products from the process.
However, the authors considered it highly possible that the four cancer cases
were produced by exposure to benzotrichloride or benzoyl chloride since these
are the major products of the two chemical reactions in the production
process. In addition, it was noted that these two chemicals have generally
been used as synthetic reagents because of their high chemical reactivity. In
a subsequent report, two lung cancer deaths were identified among workers
engaged in benzoyl peroxide and benzoyl chloride production at another plant,
in which the total number of workers ranged from 13 in 1952 to 40 in 1963
(Sakabe and Fukuda, 1977). The two individuals, one of whom was a smoker,
were in their forties and had worked in benzoyl chloride production for 6 to
18 years. The number of deaths expected among these workers was not reported.
Sorahan et al. (1983) conducted a study of cancer mortality among 953
workers at a British factory engaged in production of chlorinated toluenes.
As in the Japanese plants, there was exposure to toluene (the starting
material), benzotrichloride and benzoyl chloride (the major reaction
products), as well as benzyl chloride, benzal chloride and other materials.
The cohort of exposed workers consisted of 163 males employed for at least six
months between 1961 and 1970. Some of these individuals started employment as
early as 1923. Of the 10 deaths from cancer (25 total deaths) reported in
this group, 5 were due to digestive system cancers and 5 to respiratory
cancers, compared with 1.24 and 1.78 expected, respectively. The standarized
mortality ratio for each of these sites was significantly higher than
expected, based on mortality rates for England and Wales. A survival analysis
using the Cox Proportional Hazards model, adjusting for age at entry to the
survey and the time period when employment began, was also conducted. This
analysis showed a statistically significant association between estimated
cumulative exposure and deaths from cancer at all sites (but neither digestive
nor respiratory cancers individually), for persons first employed before 1951.
The association was not significant for all entry cohorts combined.
Interpretation of this study is limited by several factors, including possible
bias in assignment of exposure categories, exposure to multiple compounds and
lack of data on smoking.
Another retrospective mortality study reported on a cohort of 697 male
workers who were exposed to benzyl chloride, benzotrichloride and benzoyl
chloride at a chlorination plant (Wong and Morgan, 1984). The length of
employment at the plant ranged from 1 year to >35 years. Seven deaths from
respiratory cancer were found in the total cohort compared with 2.84 expected
deaths based on U.S. mortality rates for males. Five of these deaths occurred
in workers employed for at least 15 years. This was significantly greater
than the 1.32 deaths expected for this subgroup. The results of this study
were confounded by multiple exposures and lack of data on smoking.
In summary, because of small sample sizes, lack of data on cigarette
smoking and the fact that exposure was to a mixture of halogenated
intermediates, the available human data are insufficient to determine the
potential carcinogenicity of benzotrichloride exposure.
___II.A.3. ANIMAL CARCINOGENICITY DATA
Sufficient. The animal data consist of oral, inhalation and skin painting
studies in female mice of a single strain.
Groups of 40 nine-week-old female ICR mice were gavaged with 0.043, 0.17,
0.7, or 2.7 mg benzotrichloride of unknown purity in 0.1 mL sesame oil twice
weekly for 25 weeks (Fukuda et al., 1978). The 40 control animals were
untreated. Surviving animals were killed and examined histologically 18
months after the start of treatment. Mortality was significantly increased in
the two highest dose groups, reaching 50% at 6.5 months in the highest dose
group and at 16.5 months in the second highest dose group. Forestomach
squamous cell carcinoma was observed in 0/35, 0/37, 2/38, 22/40, and 24/35
animals in the control to high-dose groups, respectively. The incidence was
significantly increased at the two highest dose levels. Lung adenocarcinoma
was reported in 0/35, 1/37, 9/38, 16/40, and 10/35 animals; the incidences
were significantly increased in the three highest dose groups. Lung adenoma
was observed in approximately equal proportions to carcinoma (1/35, 0/37, 6/38
17/40, and 10/35; significantly increased at the two highest dose levels).
Thymoma incidence (0/35, 0/37, 1/38, 2/40, and 7/35) was significantly
increased only at the highest dose.
Yoshimura et al. (1979, 1986) exposed 37 5-week-old female ICR-JCL mice to
an average concentration of 1.6 ppm (12.8 mg/cu.m) benzotrichloride of unknown
purity vaporized at room temperature, twice weekly for 30 minutes for 12
months. Surviving animals were observed for an additional 0 to 3 months.
Thirty control animals were maintained for 12 months only. In the 10 treated
mice that died before 12 months, the following tumor incidences were observed:
7 lung adenomas, 1 lung adenocarcinoma, and 1 skin papilloma. Ten treated
mice were sacrificed at 12 months; lung adenoma was found in 5, adenocarcinoma
in 4, skin papilloma in 3 and skin carcinoma in 1. Lung adenoma was observed
in 3/30 of the control animals that died or were killed at 12 months. Of 8
treated mice that died from 12 to 15 months, 3 had lung adenoma, and 3
adenocarcinoma. None had skin tumors. The remaining 9 mice were killed at 15
months; 2 had lung adenomas, 5 had adenocarcinomas, 2 had skin papillomas, and
3 had skin carcinomas. Thus, the proportion of malignant tumors at these
sites increased with time. During the first 12 months, 3 malignant lymphomas
were observed, and 1 was observed between 12 and 15 months. The overall
incidence of tumors was 30/37 (81%) for the lung (compared to 3/30 in
controls), 10/37 (27%) for the skin (0/30 in controls), and 4/37 (11%) for
malignant lymphoma (0/30 in controls). The incidence at each of these sites
was significantly elevated compared to the control incidence. Yoshimura et
al. (1979) noted that all treated animals had severe bronchitis and bronchial
pneumonia.
In a related study, 32 5-week-old female ICR mice were exposed by
inhalation to an average concentration of 6.8 ppm (54.8 mg/cu.m)
benzotrichloride of unknown purity, vaporized at 50C (Takemoto et al., 1978;
Yoshimura et al., 1986). The animals were exposed twice weekly for 30 minutes
for 5 months, followed by a 1- to 5-month observation period. The control
group of 30 animals was observed for 12 months; no results were reported. Of
12 treated mice that died during the exposure period, 2 had lung adenomas; 6
had malignant lymphoma. At the end of the treatment, 6/11 mice had developed
lung adenomas and 1/11 had squamous-cell carcinoma of the skin. After 10
months, 8/9 had lung adenomas, 1/9 had lung adenocarcinoma, 3/9 had skin
carcinoma, 4/9 had skin papillomas, and 2/9 had malignant lymphoma. The
overall tumor incidence was 17/32 (53%) for the lung, 8/32 (25%) for the skin,
and 8/32 (25%) for malignant lymphoma, compared with 3/30 lung adenomas and no
other tumors in the controls. Benzoyl chloride administered under the same
conditions to 7 mice induced 2 skin papillomas by 10 months, and 3 lung tumors
(1 adenoma, 2 carcinomas) by 14 months.
Fukuda et al. (1981) conducted a series of three skin-painting studies on
specific pathogen-free ICR mice, using benzotrichloride (reagent grade) at
successively smaller doses for longer periods. The compound was administered
undiluted or dissolved in benzene. The animals were housed at about 10 per
cage. In the first experiment, three groups of 19 to 22 14-week-old female
ICR mice received skin applications of 25 uL benzene (vehicle control), 25 uL
benzotrichloride (34.3 mg), or 25 uL of a 50% solution of benzotrichloride
(17.1 mg) in benzene. The doses were given twice weekly for 3 weeks, then
once weekly until the mice were killed at 7.2 months. Assuming a total of 34
doses, the high dose corresponded to a total of approximately 1165 mg (average
dose rate of 5.4 mg/day) and the low dose to 582.4 mg (average dose rate of
2.7 mg/day). Mortality at the termination of the experiment was 0, 10, and
46% in the control, low- and high-dose groups, respectively. The number of
mice with tumors was 0/20, 17/19, and 21/22 in the control, low-dose, and
high-dose groups, respectively. The reported incidence of tumors at specific
sites for low- and high-dose groups was 6/19 and 12/22 for skin carcinomas,
10/19 and 9/22 for lung adenoma/carcinoma, and 1/19 and 6/22 for thymus
lymphoma.
Similar results were obtained in the second experiment in which three
groups of 9 to 10 3-week-old female ICR mice received dermal application of 10
uL of benzene (vehicle control), 10 uL benzotrichloride or 10 uL of a 50%
benzotrichloride:benzene solution 3 times/week for 4 weeks then twice weekly
thereafter until sacrifice at 9.8 months. The mice in the high-dose group
were sacrificed at 5.7 months because of high mortality and morbidity. The
high dose thus represented a total of 740 mg and the low dose 603 mg (4.3 and
2.1 mg/day, respectively). Mortality at termination was 0, 60, and 80% for
the control, low-dose, and high-dose groups, respectively. The number of mice
with tumors was 0/10, 10/10, and 8/9 in the control, low-dose, and high-dose
groups, respectively. Reported tumor incidences at specific sites for the
low- and high-dose groups was 7/10 and 4/9 for skin carcinomas, 10/10 and 3/9
for lung adenoma/adenocarcinoma, and 3/10 and 5/9 for thymus lymphoma. In
addition, two squamous-cell carcinomas of the lips and one squamous-cell
carcinoma of the forestomach were reported in the low-dose mice. These tumors
were assumed to result from the ingestion of benzotrichloride caused by
licking of the skin.
In the third experiment, 2 groups of 20 7-week-old female ICR mice
received skin applications of 25 uL benzene (controls) or 25 uL of a 9.2%
solution of benzotrichloride in benzene twice weekly for 11.7 months. The
total dose was approximately 315 mg (0.9 mg/day). Surviving mice were
sacrificed at 18.7 months (controls) or at 13.3 months (benzotrichloride-
treated). Mortality at termination was 20% in the controls compared with 35%
in the treated group. In the control group, 2/20 mice had lung adenomas while
in the treated group, 13/19 had skin carcinoma and 11/19 had lung
adenoma/carcinoma. Nineteen other tumors, attributed to licking, were
observed in the lips, tongue, esophagus, forestomach and glandular stomach of
the treated mice.
Stoner et al. (1986) administered benzotrichloride (at least 99% purity)
in tricaprylin to both sexes of A/J mice (11 to 15/group) by intraperitoneal
injection at doses of 12, 30, or 60 mg/kg, 3 times/week for 8 weeks. Total
doses were 287, 719, or 1440 mg/kg. The mice were observed for 16 weeks
following the exposure period. Lung adenomas were observed in 4/15 vehicle-
treated controls of each sex, while 100% of the animals in all treated groups
developed lung adenomas. The tumor incidence was significantly increased in
each group compared with controls, and there was a significant dose-related
trend in the average number of tumors per mouse. In other organs, only tumors
observed as gross lesions at necropsy were further examined. In the highest
dose group, three lymphomas and two kidney sarcomas, which reportedly occur
rarely in this strain, were observed.
___II.A.4. SUPPORTING DATA FOR CARCINOGENICITY
Results of mutagenicity testing of benzotrichloride in bacterial systems
are equivocal. Positive results were obtained in a rec assay in Bacillus
subtilis and in reverse mutation assays in Escherichia coli and Salmonella
typhimurium when a metabolic activation system was present (Yasuo et al.,
1978). In another study, negative results were found for reverse mutation in
S. typhimurium and for forward mutation in Saccharomyces cerevisiae in the
absence and presence of metabolic activation (Jagannath, 1978). Koshi and
Fukuda (1986) reported slight increases in chromosomal aberrations in bone
marrow cells of rats exposed to 1 ppm benzotrichloride for 6 hours/day, 5
days/week, during 1-, 3- and 6-month periods. A significantly increased
frequency of sister chromatid exchanges in peripheral lymphocytes was also
observed.
The predominant metabolite of benzotrichloride in the rat is benzoic acid,
which is excreted in the urine (greater than 90%) following conjugation with
glycine and formation of hippuric acid (Yu and Nietschmann, 1980). Benzoic
acid has been tested for mutagenicity and results have been consistently and
unequivocally negative (U.S. EPA, 1987).
Benzyl chloride and benzal chloride, which are also intermediates in the
benzoyl chloride production process, are structural analogues of
benzotrichloride and have been shown to be carcinogenic in animals
(Preussmann, 1968; Fukuda et al., 1981). (Benzyl chloride is classified as
B2.) Both of these compounds have also demonstrated mutagenic activity (Yasuo
et al., 1978; Rosenkranz and Poirier, 1979).
__II.B. QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM ORAL EXPOSURE
___II.B.1. SUMMARY OF RISK ESTIMATES
Slope Factor for use with Dietary Intakes -- 1.3E+1 per (mg/kg)/day
Drinking Water Unit Risk -- 3.6E-4/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) 3E-1 ug/L
E-5 (1 in 100,000) 3E-2 ug/L
E-6 (1 in 1,000,000) 3E-3 ug/L
___II.B.2. DOSE-RESPONSE DATA (CARCINOGENICITY, ORAL EXPOSURE)
Tumor Type -- lung, adenocarcinoma
Test Animals -- mouse/ICR, female
Route -- gavage, sesame oil
Reference -- Fukuda et al., 1978
Administered Dose Transformed Animal Human Equivalent Tumor
Dose (mg/mouse) Dose (mg/kg)/day) Dose (mg/kg)/day) Incidence
----------------- ------------------ ----------------- ---------
0 0 0 0/35
0.043 0.131 0.004 1/37
0.17 0.52 0.017 9/38
0.7 2.1 0.068 16/40
2.7 8.2 0.262 10/35
___II.B.3. ADDITIONAL COMMENTS (CARCINOGENICITY, ORAL EXPOSURE)
No model fit adequately using all five doses; therefore, the high dose was
dropped in deriving the slope factor.
Transformed animal doses were calculated by dividing the experimental dose
by the reference mouse body weight of 0.03 kg and by multiplying by 2 days/7
days and by 25 weeks (length of treatment)/78 weeks (length of experiment).
The human equivalent doses were calculated by multiplying the animal doses by
the cube root of the ratio of the mouse body weight to the reference human
body weight (70 kg). Since the length of the experiment in mice was less than
the lifespan of mice, the doses were further corrected by the cube of 78
(length of experiment)/104 (lifespan of animal).
Using the data from Fukuda et al. (1978), slope factors were derived for
the incidence of forestomach squamous-cell carcinoma (6.0 per (mg/kg)/day) and
thymoma (1.4 per (mg/kg)/day) in female mice. Since the slope factor derived
from the data on adenocarcinomas of the lungs is higher than that generated
from the data on tumors in the forestomach and thymus, it was recommended as
the risk estimate. (Because individual pathology data were not presented, the
tumors could not be pooled across sites to derive the risk estimate.)
The slope factor for benzotrichloride is approximately 2 orders of
magnitude greater than that for benzyl chloride (1.7E-1 per(mg/kg)/day), a
structurally similar and process-related chemical.
The unit risk should not be used if the water concentration exceeds 3E+1
ug/L, since above this concentration the slope factor may differ from that
stated.
___II.B.4. DISCUSSION OF CONFIDENCE (CARCINOGENICITY, ORAL EXPOSURE)
A sufficient number of animals was used for analysis of late-developing
tumors. Benzotrichloride was administered by a relevant route of exposure at
several doses for a significant portion of the animals' lifespan.
Histological examination was comprehensive. There is uncertainty associated
with adjusting for an experimental dose administered for a relatively short
exposure duration over the lifetime of the animal. The uncertainty relates
both to the method by which risk estimation is carried out and the mechanism
by which the agent may cause cancer.
__II.C. QUANTITATIVE ESTIMATE OF CARCINOGENIC RISK FROM INHALATION EXPOSURE
Not available.
__II.D. EPA DOCUMENTATION, REVIEW, AND CONTACTS (CARCINOGENICITY ASSESSMENT)
___II.D.1. EPA DOCUMENTATION
Source Document -- U.S. EPA, 1986, 1987
The 1986 Health and Environmental Effects Profile for Benzotrichloride has
received Agency review.
___II.D.2. REVIEW (CARCINOGENICITY ASSESSMENT)
Agency Work Group Review -- 04/05/1989, 05/03/1989, 05/30/1989, 08/02/1989
Verification Date -- 08/02/1989
___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 -- Benzotrichloride
CASRN -- 98-07-7
Last Revised -- 07/01/1993
__VI.A. ORAL RfD REFERENCES
None
__VI.B. INHALATION RfD REFERENCES
None
__VI.C. CARCINOGENICITY ASSESSMENT REFERENCES
Fukuda, K., H. Matsushita and K. Takemoto. 1978. Carcinogenicity of orally
administered benzotrichloride (J-4774). In: Proc. 52nd Ann. Meet. Japanese
Ind. Health Assoc. TSCA 8E Submission Document No. 88-8000360, Fiche #204867.
p. 516-517.
Fukuda, K., H. Matsushita, H Sakabe and K. Takemoto. 1981. Carcinogenicity
of benzyl chloride, benzal chloride, benzotrichloride and benzoyl chloride in
mice by skin application. Gann. 72: 655-664.
Jagannath, D.R. 1978. Mutagenicity Evaluation of Benzotrichloride in the
Ames Salmonella/Microsome Plate Test. Litton Bionetics, Inc., Kensington, MD.
Project 20988, Genetic Assay 3566. TSCA FYI Submission Doc. No. 1180-0107 IN.
Koshi, K. and K. Fukuda. 1986. Cytogenetic and morphological findings in
rats exposed to benzotrichloride. Mutat. Res. 164: 272.
Preussmann, R. 1968. Direct alkylating agents as carcinogens. Food Cosmet
Toxicol. 6(5): 576-577.
Rosenkranz, H.S. and L.A. Poirier. 1979. Evaluation of the mutagenicity and
DNA-modifying activity of carcinogens and noncarcinogens in microbial systems.
J. Natl. Cancer Inst. 62(4): 873-892.
Sakabe, H. and K. Fukuda. 1977. An updating report on cancer among benzoyl
chloride manufacturing workers. Ind. Health. 15(3-4): 173-174.
Sakabe, H., H. Matsushita and S. Koshi. 1976. Cancer among benzoyl chloride
manufacturing workers. Ann. NY. Acad. Sci. 271: 67-70.
Sorahan, T., J.A.H. Waterhouse, M.A. Cooke, E.M.B. Smith, J.R. Jackson and L.
Temkin. 1983. A mortality study of workers in a factory manufacturing
chlorinated toluenes. Ann. Occup. Hyg. 27(2): 173-182.
Stoner, R.D., M. You, M. Morgan and M. Superczynski. 1986. Lung tumor
induction in Strain A mice with benzotrichloride. Cancer Lett. 33: 167-173.
Takemoto, K., H. Yoshimura and S. Matsushita. 1978. Experiment of pulmonary
tumorigenicity of benzotrichloride. Proc. 51st Ann. Meet. Japan Assoc. of
Ind. Health. TSCA 8e Submission Document No. 88-8000360, Fiche # 204867.
p. 514-515.
U.S. EPA. 1986. Health and Environmental Effects Profile for
Benzotrichloride. Prepared by the Office of Health and Environmental
Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH for
the Office of Solid Waste, Washington, DC.
U.S. EPA. 1987. Health and Environmental Effects Document for Benzoic Acid.
Prepared by the Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH for the Office of Solid Waste
and Emergency Response, Washington, DC.
Wong, O. and R.W. Morgan. 1984. Final Report. A Cohort Mortality Study of
Employees at the Velsicol Chattanooga Plant, 1943-1982. Prepared for
Velsicol Chemical Corp. by Environmental Health Associates, Inc. TSCA 8e
submission 8EHQ-0884-0522, 88-8400657.
Yasuo, K., S. Fujimoto, M. Katoh, Y. Kikuchi and T. Kada. 1978. Mutagenicity
of benzotrichloride and related compounds. Mutat. Res. 58(2-3): 143-150.
Yoshimura, H., H. Katayama, K. Takomoto and S. Matsushita. 1979.
Experimental lung tumors induced by exposure to benzotrichloride. [2] Proc.
of Japan Assoc. of Ind. Health. TSCA 8e Submission Document No. 88-8000360,
Fiche # 204867. p. 332-333.
Yoshimura, H., K. Takemoto, K. Fukuda and H. Matsushita. 1986.
Carcinogenicity in mice by inhalation of benzotrichloride and benzoyl
chloride. Jap. J. Ind. Health. 28: 352-359. (translation).
Yu, C.C. and D.A. Nietschmann. 1980. Pharmacokinetics and Metabolism of
Benzotrichloride in Rats. Velsicol Chemical Corp., Chicago, Il, Project
482448, Report NO. 6, TSCA FYI Submission Doc. No. FYI-OTS-1180-0107 IN.
_VII. REVISION HISTORY
Substance Name -- Benzotrichloride
CASRN -- 98-07-7
-------- -------- --------------------------------------------------------
Date Section Description
-------- -------- --------------------------------------------------------
07/01/1990 II. Carcinogen assessment on-line
07/01/1990 VI. Bibliography on-line
12/01/1990 II. Text edited
01/01/1992 IV. Regulatory Action section on-line
07/01/1993 VI.C. References alphabetized correctly
VIII. SYNONYMS
Substance Name -- Benzotrichloride
CASRN -- 98-07-7
Last Revised -- 07/01/1990
98-07-7
AI3-02583
BENZENE, (TRICHLOROMETHYL)-
BENZENYL CHLORIDE
BENZENYL TRICHLORIDE
BENZOIC TRICHLORIDE
BENZOTRICHLORIDE
BENZOTRICLORURO [SPANISH]
BENZYLIDYNE CHLORIDE
BENZYL TRICHLORIDE
CHLORURE DE BENZENYLE [FRENCH]
CHLORURE DE BENZYLIDYNE [FRENCH]
HSDB 2076
OMEGA,OMEGA,OMEGA-TRICHLOROTOLUENE
PHENYL CHLOROFORM
PHENYLCHLOROFORM
PHENYLTRICHLOROMETHANE
RCRA WASTE NUMBER U023
TOLUENE TRICHLORIDE
TOLUENE, ALPHA,ALPHA,ALPHA-TRICHLORO-
TRICHLOORMETHYLBENZEEN (DUTCH)
TRICHLORMETHYLBENZOL (GERMAN)
TRICHLOROMETHYLBENZENE
(TRICHLOROMETHYL)BENZENE
1-(TRICHLOROMETHYL)BENZENE
TRICHLOROPHENYLMETHANE
ALPHA,ALPHA,ALPHA-TRICHLOROTOLUENE
TRICLOROMETILBENZENE (ITALIAN)
TRICLOROTOLUENE (ITALIAN)
UN 2226
Last updated: 5 May 1998
URL: http://www.epa.gov/iris/SUBST/0388.HTM
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