1,2,4-Trichlorobenzene (CASRN 120-82-1)
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0119
1,2,4-Trichlorobenzene;
CASRN 120-82-1
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 1,2,4-Trichlorobenzene
File First On-Line 01/31/1987
Category (section) |
Status |
Last Revised |
---|---|---|
Oral RfD Assessment (I.A.) | on-line | 11/01/1996 |
Inhalation RfC Assessment (I.B.) | no data | 08/01/1993 |
Carcinogenicity Assessment (II.) | on-line | 03/01/1991 |
_I. Chronic Health Hazard Assessments for Noncarcinogenic Effects
_I.A. Reference Dose for Chronic Oral Exposure (RfD)
Substance Name — 1,2,4-Trichlorobenzene
CASRN — 120-82-1
Last Revised — 11/01/1996
The oral Reference Dose (RfD) is based on the assumption that thresholds
exist for certain toxic effects such as cellular necrosis. It is expressed
in units of mg/kg-day. In general, the RfD is an estimate (with uncertainty
spanning perhaps an order of magnitude) of a daily exposure to the human
population (including sensitive subgroups) that is likely to be without
an appreciable risk of deleterious effects during a lifetime. Please refer
to the Background Document for an elaboration of these concepts. RfDs
can also be derived for the noncarcinogenic health effects of substances
that are also 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.
__I.A.1. Oral RfD Summary
Critical Effect |
Experimental Doses* |
UF |
MF |
RfD |
---|---|---|---|---|
Increased adrenal Rat Reproductive Robinson et al., 1981 |
NOAEL: 100 ppm LOAEL: 400 ppm |
1000 |
1 |
1E-2 mg/kg/day |
*Conversion Factors: Doses were based on actual water consumption and body weights provided by Robinson et al. (1981) for rats 83 days old.
__I.A.2. Principal and Supporting Studies (Oral RfD)
Robinson, K.S., R.J. Kavlock, N. Chernoff and E. Gray. 1981. Multi-
generation study of 1,2,4-trichlorobenzene in rats. J. Toxicol. Environ.
Health. 8: 489-500.
The derivation of the oral RfD is based on a multigeneration reproductive
study. At birth of the F0 generation, litters (17-23 litters/dose group) were
randomly reduced to 4 males and 4 females. Male and female progeny were dosed
with 0, 25, 100 or 400 ppm of 1,2,4-trichlorobenzene (TCB) in the drinking
water. During the study maternal weights, litter size, neonate sex and
weight, and 24-hour food and water intake were recorded. Blood samples and
organs were collected on days 27 and 95 of age from selected rats from each
group for chemistry determinations (i.e., glucose, BUN, creatinine, Na, K, Cl,
uric acid, Ca, P, cholesterol, triglyceride, bilirubin, alkaline phosphatase,
SGOT, SGPT, LDH, CPK, protein, globulin and albumin), and organ weights (i.e.,
liver, kidney, uterus, adrenals, lungs, heart and gonads). Similar procedures
were performed with the F1 generation. The study ended when the F2 generation
was 32 days old. Fertility (as indexed by conception rate of dams) of the F0
and F1 generation rats was not affected by treatment. A LOAEL was derived
from a significant increase (11% in males, 13% in females) in adrenal gland
weights observed in the 400-ppm groups of males and females of the F0 and F1
generations.
The authors duplicated the increase in adrenal weights in an acute experiment
in which preweanling females were given three daily i.p. injections of TCB.
The acute experiment was performed to show that the adrenal enlargement was
not due to either estrogenic properties of TCB or to long-term stress. The
NOAEL was determined to be 100 ppm from the mid-dose group. The LOAEL was
determined to be 400 ppm on the basis of increased adrenal gland weight.
A 1-month study, which repeated part of the Robinson et al. (1981) study, was
performed by the U.S. EPA. Five rats/group were dosed with 53 mg/kg/day TCB
(the LOAEL from the Robinson study) in corn oil by gavage. Microscopic
examination of the TCB-treated rats showed moderate vacuolization of the zona
fasciculata; the control group showed only slight vacuolization. Twenty-four
hour urine and serum specimens were collected prior to post mortem
examination. A 14% increase in absolute adrenal gland weight was observed and
a 13% adrenal gland/body weight ratio was observed. This study indicated that
the increase in adrenal gland weight observed by Robinson et al. (1981) could
be associated with vacuolization of the zona fasciulata (Cicmanec, 1991). In
addition, the treated rats had decreased serum corticosterone levels when
compared with controls.
__I.A.3. Uncertainty and Modifying Factors (Oral RfD)
UF — An uncertainty factor of 10 was used to account for extrapolation
from laboratory studies to humans. An additional factor of 10 was used to
allow for sensitive subpopulations among humans. An additional factor of 10
was used to account for a lack of chronic studies. This results in a total
uncertainty factor of 1000 for this substance.
MF — None
__I.A.4. Additional Studies/Comments (Oral RfD)
Toxicokinetic studies by Smith and Carlson (1980) have shown that initially,
adrenal glands have the highest concentration of TCB immediately following a
single oral dose of radiolabeled compound. Later during the first week
following dosing, only abdominal fat, kidney and liver showed higher
concentrations than the adrenal gland. It has been demonstrated that dosing
with pentachlorobenzene can induce increased adrenal weights in test rats
(Linder et al., 1980). Inhalation studies with monochlorobenzene showed
increased adrenal weights, attributed to vacuolization of the zona
fasciculata, a significant adverse effect (Dilley, 1977). Other chlorinated
aromatic compounds, including o-chlorotoluene and beta-chloronapthalene, have
a critical effect on adrenal gland weight. On the basis of this information
for structurally similar compounds, the EPA determined that the occurrence of
increased adrenal weights following administration of TCB is a significant
adverse effect. Coate et al. (1977) reported a study in which rats, rabbits
and cynomolgus monkeys were exposed by inhalation to TCB for 26 weeks at
concentrations of 0, 25, 50 or 100 ppm (0, 186, 371 or 741 mg/cu.m) for 7
hours/day, 5 days/week. Thirty rats, 6 rabbits and 9 cynomolgus monkeys were
assigned to each dose group.
Pulmonary function tests, operant behavior tests and opthalmoscopic
examinations, as well as serum chemistry determinations (i.e., BUN, LDH
isozymes, SGOT, SGPT, and alkaline phosphatase), were performed on monkeys.
Microscopic examination of rat tissues were made at 4, 13 and 26 weeks.
Although hepatocytomegaly, hepatic vacuolization, biliary hyperplasia, and
granuloma formation were observed at 4 and 13 weeks, none of these changes
were observed in rats killed at 26 weeks. Hyaline degeneration was present in
the renal cortex at 4 and 13 weeks but not at 26 weeks. Adrenal glands were
not examined. The authors felt that since it has not been shown that humans
have a similar adaptive mechanism for long-term exposure, an occupational TLV
of 5 ppm should be recommended on the basis of this study. A LOAEL was not
established. No adverse effect was defined for rabbits or monkeys from this
study.
Watanabe et al. (1977) reported the results of a subchronic inhalation study
in which rats were exposed to TCB for 6 hours/day, 5 days/week for 90 days.
The exposure concentrations tested were 0, 3 and 10 ppm (0, 22.3 and 74.2
mg/cu.m). The results showed a very weak sporatic increase in urinary
porphyrins at 10 ppm. The 10-ppm exposure was considered a LOAEL and 3 ppm
was considered a NOAEL.
Carlson (1977) reported a study in which induction of porphyria by
hexachlorobenzene, dichlorobenzene and trichlorobenzene was investigated.
Doses of 0, 50, 100 and 200 mg/kg/day of each compound were administered
orally to female rats. Liver weights, hepatic porphyrins, and urinary
porphyrins were determined at 30, 60, 90 and 120 days. The study demonstrated
that hexachlorobenzene induced porphyria but that dichlorobenzene and
trichlorobenzene did not.
In the study reported by Carlson and Tardiff (1976) male CD rats (6/dose) were
dosed orally with TCB at 0, 10, 20 or 40 mg/kg/day. The investigators
evaluated the effect upon weight gain, liver weight, hemoglobin, hematocrit
and indicators of xenobiotic metabolism including cytochrome C reductase,
detoxification, cytochrome P-450, glucoronyl transferase, benzopyrene
hydroxylase and azoreductase activity. The dose of 10 mg/kg/day induced some
enzymatic changes but did not affect liver-to-body weight ratios or blood
parameters. For many of the enzymes tested change was dose-related. At 40
mg/kg/day, liver-to-body weight ratios were increased. Although enzyme
induction is a sensitive endpoint, it is not an adverse effect. For this
study 20 mg/kg/day is considered a NOAEL and 40 mg/kg/day is considered a
LOAEL.
In the study reported by Kociba et al. (1981), male rats, rabbits and dogs
were exposed to 0, 30 or 100 ppm (0, 223 or 742 mg/cu.m) for 44 days. No
significant effects were observed for body weight gain, hematologic
parameters, serum biochemical tests or microscopic appearance of tissues. A
reversible increase in urinary excretion of porphyrins was noted. The authors
interpreted this change as being a compound-specific physiologic effect rather
than a sign of toxicity.
Smith et al. (1978) performed a study in which rhesus monkeys were dosed
orally with 0, 25, 90, 125 and 173.6 mg/kg. The 25-mg/kg doses were nontoxic.
Doses of 90 mg/kg caused hepatic induction as evidenced by a shift in the
urinary pattern of chloroguanide metabolites and increased clearance of i.v.
doses of labelled TCB. Doses of 173.6 mg/kg were lethal within 30 days.
Monkeys receiving this dose exhibited severe weight loss and had fine tremors.
At termination they had elevated levels of BUN, Na, K, CPK, SGOT, SGPT, LDH
and ALK T'ase, hypercalcemia and hyperphosphatemia, but jaundice was not
present. Clinical symptoms and biochemical changes were reversed when
treatment was discontinued.
Kitchin and Ebron (1980) examined the maternal reproductive and hepatic
effects of TCB upon CD-1 rats that were dosed with 0, 36, 120, 360 or 1200
mg/kg/day of TCB on days 9-13 of gestation. Among the treatment groups of 9
dams/group, alteration of embryonic parameters was noted only in the 360
mg/kg/day group. (All of the dams in the 1200 mg/kg/day group died.) The
observed changes included significant retardation of all four growth criteria
(i.e., head length, crown-rump length, somite number, and protein content).
TCB did not cause increased resorptions, embryolethality or teratogenicity.
This study also demonstrated significantly increased xenobiotic hepatic enzyme
activity at 120 and 360 mg/kg/day.
In the development toxicity study of Black et al. (1983) pregnant Wistar rats
received doses ranging from 75-600 mg/kg/day of 1,2,4-, 1,2,3-, and 1,3,5-TCB
on days 6-15 of gestation. No abnormal teratogenic changes were observed
except mild osteogenic changes. This paper was available only in abstract
form and the dosage at which the changes were observed was not stated.
__I.A.5. Confidence in the Oral RfD
Study — Medium
Database — Medium
RfD — Medium
A medium degree of confidence for the RfD is chosen since the multi- generation study of Robinson et al. (1981) provides sufficient data with multiple endpoints. The study used appropriate group sizes. A medium to low confidence rating is given to the database since no chronic exposure study is available. Medium confidence in the RfD follows.
__I.A.6. EPA Documentation and Review of the Oral RfD
Source Document — U.S. EPA, 1985
Other EPA Documentation — U.S. EPA, 1988
Agency Work Group Review — 02/26/1986, 05/26/1988, 09/11/1991, 12/12/1991
Verification Date — 12/12/1991
Screening-Level Literature Review Findings — A screening-level review conducted by an EPA contractor of the more recent toxicology literature pertinent to the RfD for 1,2,4-Trichlorobenzene conducted in November 2001 did not identify any critical new studies. IRIS users who know of important new studies may provide that information to the IRIS Hotline at hotline.iris@epa.gov or (202)566-1676.
__I.A.7. EPA Contacts (Oral RfD)
Please contact the IRIS Hotline for all questions concerning this assessment or IRIS, in general, at (202)566-1676 (phone), (202)566-1749 (FAX) or hotline.iris@epa.gov (internet address).
_I.B. Reference Concentration for Chronic Inhalation Exposure (RfC)
Substance Name — 1,2,4-Trichlorobenzene
CASRN — 120-82-1
Not available at this time.
_II. Carcinogenicity Assessment for Lifetime Exposure
Substance Name — 1,2,4-Trichlorobenzene
CASRN — 120-82-1
Last Revised — 03/01/1991
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 Human Carcinogenicity
__II.A.1. Weight-of-Evidence Characterization
Classification — D; not classifiable as to human carcinogenicity
Basis — A dermal exposure study in mice was found inadequate for drawing
conclusions as to carcinogenicity in humans.
__II.A.2. Human Carcinogenicity Data
None.
__II.A.3. Animal Carcinogenicity Data
Inadequate. Yamamoto et al. (1982) applied 1,2,4-trichlorobenzene in
acetone to the dorsal skin of Slc.ddy mice twice weekly for 2 years. The
solution of 1,2,4-trichlorobenzene was 60% for the high dose and 30% for the
low dose and the volume applied was 0.03 mL/application. Each treated group
contained 75 animals of each sex. There were 50 vehicle control animals for
each sex. Growth rates in treated and control mice were comparable through 83
weeks. Mean survival days were significantly reduced in the 60% 1,2,4-
trichlorobenzene groups of males and females and also in the 30% treatment
group of females. All males and treated females showed as poor as 60%
survival by week 40.
Histopathology showed some organ sites had increased nonneoplastic
lesions. All 75 animals in the treated groups and all 50 in the control
groups appear to have been examined. Increases in nonneoplastic lesions
(i.e., amyloid) were reported in lung, liver, kidney, adrenal, spleen and
lymph node of the male high-dose group and in all these organs except lymph
node of the female high-dose group.
No single tumor type was increased significantly over the control
incidence; there was no significant difference in total tumor incidence
between treated and control groups. Among males, nine different tumors were
found in the high-dose group as compared with two in the low-dose and two in
the control group. In females there were 11 different tumors in the high-dose
group as compared with 3 in the low-dose and 8 in the control group. However,
no adjustment was made for reduced survival, and there was no indication of
the time to first tumor appearance. The authors do not state whether these
tumors were all found in different individual animals or whether these were
multiple tumors in the same animal. This study has several limitations.
Although male mice were housed individually, female mice were group-housed.
The animals were only treated twice a week, and no pharmacokinetic studies
were performed. There was a low survival rate; 80% of the control mice and
90% of the treated mice died before the end of the study.
__II.A.4. Supporting Data for Carcinogenicity
Results of two reports on mutagenicity tests with Salmonella typhimurium test strains were negative (Schoeny et al., 1979; Lawlor et al., 1979). Grover and Sims (1965) reported trichlorobenzene to be a metabolite of gamma- hexachlorocyclohexane (Lindane) which is a possible or probable human carcinogen. The authors isolated 2,4,5- and 2,3,5-trichlorophenol, which are metabolites of trichlorobenzene, from urine of Lindane treated rats. This suggested that dehydrochlorination via trichlorobenzene is one metabolic pathway of gamma-hexachlorocyclohexane.
_II.B. Quantitative Estimate of Carcinogenic Risk from Oral Exposure
Not available.
_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, 1988
__II.D.2. EPA Review (Carcinogenicity Assessment)
Agency Work Group Review — 10/19/1988
Verification Date — 10/19/1988
Screening-Level Literature Review Findings — A screening-level review conducted by an EPA contractor of the more recent toxicology literature pertinent to the cancer assessment for 1,2,4-Trichlorobenzene conducted in November 2001 identified one or more significant new studies. IRIS users may request the references for those studies from the IRIS Hotline at hotline.iris@epa.gov or (202)566-1676.
__II.D.3. EPA Contacts (Carcinogenicity Assessment)
Please contact the IRIS Hotline for all questions concerning this assessment or IRIS, in general, at (202)566-1676 (phone), (202)566-1749 (FAX) or hotline.iris@epa.gov (internet address).
_III.
[reserved]
_IV. [reserved]
_V. [reserved]
_VI. Bibliography
Substance Name — 1,2,4-Trichlorobenzene
CASRN — 120-82-1
Last Revised — 07/01/1993
_VI.A. Oral RfD References
Black, W.D., V.E.O. Valli, J.A. Ruddick and D.C. Villeneuve. 1983.
The toxicity of three trichlorobenzene isomers in pregnant rats.
Toxicologist. 3(1): 30. (Abstract)
Carlson, G.P. 1977. Chlorinated benzene induction of hepatic porphyria.
Experientia. 33(12): 1627-1629.
Carlson, G.P and R.G. Tardiff. 1976. Effect of chlorinated benzenes on the
metabolism of foreign organic compounds. Toxicol. Appl. Pharmacol. 36:
383-394.
Cicmanec, J. 1991. U.S. EPA, Cincinnati, OH. Memorandum to the RfD/RfC
Work Group, U.S. EPA. November 15.
Coate, W.B., T.R. Lewis, W.M. Busey and W.H. Schoenfisch. 1977. Chronic
inhalation exposure of rats, rabbits, and monkeys to 1,2,4-trichlorobenzene.
Arch. Environ. Health. 32(6): 249-255.
Dilley, J.V. 1977. Toxic evaluation of inhaled chlorobenzene
(monochlorobenzene). Prepared by Stanford Research Institute for NIOSH, DHEW,
Cincinnati, OH. NTIS PB 276 623.
Kitchin, K.T. and M.T. Ebron. 1983. Maternal hepatic and embryonic effects
of 1,2,4-trichlorobenzene in the rat. Environ. Res. 31: 362-373.
Kociba, R.J., B.K.J. Leong and R.E. Hefner, Jr. 1981. Subchronic toxicity
study of 1,2,4-trichlorobenzene in the rat, rabbit and beagle dog. Drug Chem.
Toxicol. 4(3): 229-249.
Linder, R., T. Scotti, J. Goldstein and K. McElroy. 1980. Acute and
subchronic toxicity of pentachlorobenzene. J. Environ. Pathol. Toxicol. 4:
183-196.
Robinson, K.S., R.J. Kavlock, N. Chernoff and L.E. Gray. 1981.
Multigeneration study of 1,2,4-trichlorobenzene in rats. J. Toxicol. Environ.
Health. 8: 489-500.
Smith, E.N. and G.P. Carlson. 1980. Various pharmacokinetic parameters in
relation to enzyme-inducing abilities of 1,2,4-trichlorobenzene and 1,2,4-
tribromobenzene. J. Toxicol. Environ. Health. 6(4): 737-749.
Smith, C.C., S.T. Cragg and G.F. Wolfe. 1978. Subacute toxicity of 1,2,4-
trichlorobenzene (TCB) in sub-human primates. Fed. Proc. Fed. Am. Soc. Exp.
Biol. 37(3): 248. (Abstract)
U.S. EPA. 1985. Health Assessment Document for Chlorinated Benzenes.
Prepared by the Environmental Criteria and Assessment Office, Cincinnati, OH
for the Office of Air Quality Planning and Standards, Washington, DC. EPA
600/8-84-015F.
U.S. EPA. 1988. Drinking Water Criteria Document for Trichlorobenzenes.
Prepared by the Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH for the Office of Drinking
Water, Washington, DC.
Wantanabe, P.G., H.O. Yankel and R.J. Kociba. 1977. Subchronic Toxicity
Study of Inhaled 1,2,4-Trichlorobenzene in Rats. Internal Report. Toxicology
Research Laboratory. Dow Chemical Co., Midland, MI.
_VI.B. Inhalation RfC References
None.
_VI.C. Carcinogenicity Assessment References
Grover, P.L. and P. Sims. 1965. The metabolism of gamma-2,3,4,5,6-
pentachlorocyclohex-1-ene and gamma-hexachlorocyclohexane in rats. Biochem.
J. 96: 521-525.
Lawlor, T., S.R. Haworth and P. Voytek. 1979. Evaluation of the genetic
activity of nine chlorinated phenols, seven chlorinated benzenes, and three
chlorinated hexanes. Environ. Mutagen. 1: 143. (Abstract)
Schoeny, R.S., C.C. Smith and J.C. Loper. 1979. Non-mutagenicity for
Salmonella of the chlorinated hydrocarbons Arochlor 1254, 1,2,4-
trichlorobenzene, mirex and kepone. Mutat. Res. 68(2): 125-132.
U.S. EPA. 1988. Drinking Water Criteria Document for Trichlorobenzenes.
Prepared by the Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH for the Office of Drinking
Water, Washington, DC. Final Draft.
Yamamoto, H., Y. Ohno, K. Nakamori, T. Okuyama, S. Imai and Y. Tsubura. 1982.
Chronic toxicity and carcinogenicity test of 1,2,4-trichlorobenzene on mice by
dermal painting. J. Nara. Med. Assoc. 33: 132-145. (Eng. translation)
_VII. Revision History
Substance Name — 1,2,4-Trichlorobenzene
CASRN — 120-82-1
Date |
Section | Description |
03/31/1987 | I.A.6. | Documentation corrected |
03/01/1988 | I.A.2. | Paragraph 1 deleted |
06/30/1988 | I.A. | RfD noted as pending change |
06/01/1989 | II. | Carcinogen summary on-line |
06/01/1989 | VI. | Bibliography on-line |
10/01/1989 | I.A. | Oral RfD withdrawn pending further review |
06/01/1990 | IV.A.1. | Area code for EPA contact corrected |
06/01/1990 | IV.F.1. | EPA contact changed |
08/01/1990 | III.A. | Health Advisory on-line |
08/01/1990 | VI.D. | Health Advisory references added |
03/01/1991 | II.D.3. | Secondary contact changed |
01/01/1992 | IV. | Regulatory actions updated |
04/01/1992 | IV.A.1. | CAA regulatory action withdrawn |
05/01/1992 | I.A. | Oral RfD summary replaced; RfD changed |
05/01/1992 | VI.A. | Oral RfD references replaced |
03/01/1993 | I.B. | Inhalation RfC now under review |
07/01/1993 | VI.C. | References alphabetized correctly |
08/01/1993 | I.B. | Work group review date added |
08/01/1995 | I.B. | EPA's RfD/RfC and CRAVE workgroups were discontinued in May, 1995. Chemical substance reviews that were not completed by September 1995 were taken out of IRIS review. The IRIS Pilot Program replaced the workgroup functions beginning in September, 1995. |
11/01/1996 | I.A.7. | Primary contact's office changed |
04/01/1997 | III., IV., V. | Drinking Water Health Advisories, EPA Regulatory Actions, and Supplementary Data were removed from IRIS on or before April 1997. IRIS users were directed to the appropriate EPA Program Offices for this information. |
12/03/2002 | I.A.6., II.D.2. | Screening-Level Literature Review Findings message has been added. |
_VIII. Synonyms
Substance Name — 1,2,4-Trichlorobenzene
CASRN — 120-82-1
Last Revised — 01/31/1987
- 120-82-1
- BENZENE, 1,2,4-TRICHLORO-
- 1,2,4-Trichlorobenzene
- Trichlorobenzene, 1,2,4-
- TROJCHLOROBENZEN
- UN 2321
- unsym-TRICHLOROBENZENE