United States
Environmental Protection
Agency
Pollution Prevention
and Toxics
(7407)
November 1994
EPA 749-F-95-020a
f/EPA OPPT Chemical Fact Sheets
1,2,4-Trichlorobenzene (TCB) Fact Sheet:
Support Document (CAS No. 120-82-1)
This summary is based on information retrieved from a systematic search limited to secondary sources (see Appendix
A). These sources include online databases, unpublished EPA information, government publications, review
documents, and standard reference materials. The literature search done in January of 1995. No attempt has been
made to verify information in these databases and secondary sources.
I. CHEMICAL IDENTITY AND PHYSICAL/CHEMICAL PROPERTIES
The chemical identity and physical/chemical properties of 1,2,4-trichlorobenzene (TCB) are summarized in Table 1.
TABLE 1. CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL PROPERTIES OF 1,2, 4-TRICHLOROBENZENE
Characteristic/Property
Data
Reference
CAS No.
Common Synonyms
Molecular Formula
Chemical Structure
Physical State
Molecular Weight
Melting Point
Boiling Point
Water Solubility
Density
Vapor Density (air =1)
KOC
Log Kow
Vapor Pressure
Reactivity
Flash Point
Henry's Law Constant
Fish Bioconcentration Factor
Odor Threshold
Conversion Factors (in air)
120-82-1
TCB; Unsym-trichlorobenzene
C6H3C13
colorless liquid
181.46
17°C
213°C
31mg/Lat25°C
1.46 at 25"
6.26
6350
4.12
0.27mmHgat20°C
110°C
4.33 x m3atm-m3/mol
182-815 (bluegill)
1200-3200 (rainbow trout)
3 ppm
1 ppm = 7.41 mg/rrf
1 mg/rrf = 0.135 ppm
U.S. Air Force 1989
Budavari et al. 1989
Budavari et al. 1989
Keith and Walters 1985
Budavari et al. 1989
Budavari et al. 1989
Budavari et al. 1989
Darling 1995
Budavari et al. 1989
Keith and Walters 1985
U.S. Air Force 1989
U.S. Air Force 1989
U.S. Air Force 1989
Budavari et al. 1989
U.S. Air Force 1989
U.S. EPA 1987
U.S. Air Force 1989
U.S. Air Force 1989
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II. PRODUCTION, USE, AND TRENDS
A. Production
In 1990, the total United States production and import volume of 1,2,4-trichlorobenzene was between 22
million and 32 million pounds. More exact figures on production and import volume are not available. Table
2 lists the two producers of 1,2,4-trichlorobenzene in 1992 (PPG Industries, Inc. and Standard Chlorine
Chemical Company Inc. of Delaware) along with their plant locations. In 1990, the importers of 1,2,4-
trichlorobenzene included Mobay, Inc. and Sandoz Crop Protection of Beaumont, Texas. The TCB production
capacity of these two companies are not available.
TABLE 2. UNITED STATES PRODUCERS OF 1,2,4-TRICHLOROBENZENE IN 1992
Company Name
PPG Industries, Inc.
Standard Chlorine Chemical Company
Plant Site
New Martinsville, WV
Delaware City, DE
Source: USITC 1994
B. Uses
Major applications of 1,2,4-trichlorobenzene include its use as a solvent in chemical manufacturing, dyes and
intermediates, as a dielectric fluid, as a component of synthetic transformer oils, as a component of lubricants,
as a heat-transfer medium, as an ingredient in insecticides and herbicides, as degreasing agents, as septic tank
and drain cleaners, as an ingredient in wood preservatives, and as an ingredient in abrasive formulations
(HSDB 1994; Sax and Lewis 1987). It is also used as a comonomer with p-dichlorobenzene in the production
of arylene sulfide polymers (HSDB 1994).
C. Trends
The use of chlorinated hydrocarbon solvents, of which 1,2,4-trichlorobenzene is one, is being phased out due
to more stringent environmental standards. U.S. demand is expected to decrease in the near future (The
Freedonia Group, Inc. 1990).
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ENVIRONMENTAL FATE
A. Environmental Release
Of the total 420 thousand pounds of 1,2,4-trichlorobenzene released to the environment in 1992, as
reported to the Toxics Release Inventory by certain types of U.S. industries, 415 thousand pounds
were released into the atmosphere, 1 thousand pounds each into surface waters and underground
injection sites, and 2.7 thousand pounds onto land (TRI92 1994). As much as 0.25 micrograms/m3 of
TCB has been measured in the air of Los Angeles (IPCS 1991). Concentrations ranging from 0.007
to 275 micrograms/L (ppb) have been measured in the drinking water supplies of U.S. cities (IPCS
1991).
B. Transport
TCB is classified as a bioaccumulator and is persistent in the environment (TRI92 1994). The
chemical strongly adsorbs to soils with 1 -2% organic content, as predicted by its Koc value, but
leaching into ground waters can occur from deep soils (U.S. Air Force 1989). Slow evaporation into
the atmosphere occurs from surface water and, to a lesser extent, from soils (IPCS 1991).
C. Transformation/Persistence
1. Air — In the atmosphere, TCB reacts with photochemically produced hydroxyl radicals with
an estimated half-life of approximately 18.8 days (U.S. EPA 1987).
2. Soil — One study suggests that TCB may be biodegraded slowly in aerobic soils (U.S. EPA
1987). In another report, a degradation rate of only 1.0 nmole/day per 20 g of soil was
measured (IPCS 1991). Generally, the chemical is expected to persist adsorbed to soils
(U.S. EPA 1987; U.S. Air Force 1989).
3. Water — Half-lives of TCB in water range from 1 day in rivers to 10 days in lakes and 100
days in ground waters (IPCS 1991). A volatilization half-life of 11 to 22 days has been
measured for aerated seawater (U.S. EPA 1987). Biodegradation of TCB in water is not an
important removal route (U.S. EPA 1987; IPCS 1991).
4. Biota — Based on the bioconcentration factor of TCB in fish (ranging from 182 to 3200), the
chemical is expected to bioaccumulate in aquatic organisms. Biomagnification of
trichlorobenzene in the food chain has not been investigated (IPCS 1991).
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IV. HUMAN HEALTH EFFECTS
A. Pharmacokinetics
1. Absorption — TCB is readily absorbed following oral, inhalation, and dermal exposure
(IPCS 1991). Based on recovery in the feces and urine of radioactivity associated with a
single oral dose of TCB to rats or monkeys, these species absorbed 89 and 99%,
respectively, of the administered dose (U.S. EPA 1987).
2. Distribution — TCB is preferentially distributed to the fat and liver following oral
administration to rats. Starvation of rats for 4 days had no effect on TCB concentrations in
fat (IPCS 1991).
3. Metabolism — Metabolism of TCB is mediated by microsomal oxidation to form
chlorophenols which are conjugated to glutathione, glucuronic acid or sulfate (IPCS 1991).
Following oral administration of 10 mg/kg to rats, 60% of the urinary metabolites consisted
of isomers of N-acetyl-S-(trichlorophenyl)-L-cysteine and 33% consisted of isomers of
tnchlorothiophenol (IPCS 1991).
4. Excretion — Rats and monkeys were given an oral dose of 10 mg/kg radiolabled TCB. In
24 hours, rats had excreted 84 and 11% of the dose in urine and feces, respectively, while
monkeys had excreted 40 and 1% of the dose in urine and feces, respectively (U.S. EPA
1987). The half-life of TCB has been reported as 93 hours in the rat (IPCS 1991).
B. Acute Toxicity
TCB is irritating to the eye and respiratory tract. Altered liver enzymes and hepatic porphyria occurs
in experimental animals after oral exposure to relatively high doses. At high doses, death can occur
following either oral or dermal exposure.
1. Humans — An individual developed eye and respiratory tract irritation from exposure to 3-5
ppm TCB for an unspecified duration (U.S. Air force 1989). The concentration of 4 ppm is
roughly equivalent to 4.24 mg/kg over an eight-hour period1.
2. Animals — Acute oral LD50 values of 756 and 766 mg/kg have been reported for rats and
mice, respectively. Death occurred within 3 days for mice and 5 days for rats (U.S. Air
Force 1989). Reversible hepatic porphyria was induced in rats fed 730 mg/kg/day for 15
days and in rats exposed to 30-100 ppm 7 hours/ day, 5 days/week, for 30 days (U.S. Air
Force 1989).
The acute dermal LD50 for TCB in rats is >5 mg/kg. Focal necrosis of the liver of guinea
pigs resulted from dermal application of 0.5 mL, 5 days/week, and death of all animals
occurred within 3 weeks (IPCS 1991).
dose comparison purposes this has been calculated using the factor 7.41 (U.S. Air
Force 1989) to convert 4 ppm to 29.64 mg/m3. This value is multiplied by 0.143 (the
occupational standard 8-hour breathing rate, 10 m3, divided by the assumed adult body
weight, 70 kg and assuming 100% absorption) to obtain the dose in mg/kg (U.S. EPA 1988).
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C. Subchronic/Chronic Toxicity
Chronic dermal contact with TCB can cause dermatitis in humans. Increased liver weights and
altered hepatic enzymes occurred in animals after chronic oral or inhalation exposure to moderate to
high levels of TCB.
1. Humans — Prolonged dermal contact with TCB can cause dermatitis (IPCS 1991). Anemia
has been reported in two individuals chronically exposed to TCB, although the possibility
exists that the workers were exposed to multiple chemicals (U.S. Air Force 1989).
2. Animals — Male and female rats were given 53 mg/kg/day for 1 month by gavage.
Increased adrenal gland weight was associated with vacuolization of the zona f asciculata
(U.S. EPA 1994a). Rats exposed orally to 40 mg/kg for 90 days had altered hepatic enzyme
activities and increased liver weights (U.S. EPA 1987). Female rats were given TCB by
gavage for up to 120 days. After 30 days, increased liver porphyrins were observed at ^ 100
mg/kg and increased liver weights were observed at 200 mg/kg. After 120 days, increased
liver porphyrins were observed at 2:50 mg/kg (U.S. EPA 1987).
Rats, rabbits, and monkeys were exposed to 0, 25, 50, or 100 ppm, 7 hours/day, 5
days/week, for up to 26 weeks. No effects were observed in rabbits or monkeys. Rats had a
dose-related hepatocytomegaly and vacuolization of hepatocytes, granuloma formation,
biliary hyperplasia, and hyaline degeneration of the kidney after 4 and 13 weeks but not after
26 weeks of exposure (U.S. EPA 1994a). Rats, rabbits, and dogs were exposed to 0, 30, or
100 ppm, 7 hours/day, 5 days/week, for 30 exposures in 44 days. At 100 ppm, increased
liver weights were observed for rats and dogs and increased kidney weights were observed
in rats (U.S. EPA 1987). Urinary porphyrin excretion was elevated in rats exposed to 10
ppm, 6 hours/day, 5 days/week, for 3 months (IPCS 1991).
D. Carcinogenicity
The chlorinated benzene industry has completed cancer studies on TCB in animals in response to an
EPA request for testing. 1,2,4-Trichlorobenzene in the diet of animals causes cancer in mice but not
in rats. The significance of these results in assessing the potential for TCB to cause cancer in humans
is not known.
1. Humans — No information was found in the secondary sources searched concerning the
carcinogenicity of TCB in humans.
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2. Animals — In 1986, EPA issued a final rule under section 4 of the Toxic Substances Control
Act that manufacturers and processors of TCB conduct oncogenicity tests (U.S. EPA 1986).
The tests were conducted in B6C3F[ mice (groups of 50/sex) and in F344 rats (groups of
50/sex). 1,2,4-trichlorobenzene was administered for 104 weeks in the diet at 150 ppm, 700
ppm, and 3200 ppm in mice; for 104 weeks in the diet at 100 ppm, 350 ppm, and 1200 ppm
in rats (Lai 1994a and 1994b). Results have been submitted to EPA and reviewed. The
design and conduct of the studies appear adequate. Under conditions of the test TCB was
carcinogenic to mice, inducing liver tumors (hepatocellular adenomas and carcinomas) in
both males and females. The incidences of hepatocellular carcinomas (malignant liver
tumors) was 8/49, 50/50, 27/50, and 50/50 in the control, low dose, mid dose and high dose
male mouse. They were 1/50, 1/50, 28/50, and 46/50, respectively, in the female mouse.
For hepatocellular adenomas (benign liver tumors) the incidences were 4/49, 7/50, 16/50,
2/50 for male mice and 3/50, 4/50, 16/50, and 8/50 for female mice. The increased
incidences of these liver tumors combined appeared to be statistically significant for the
mid-and high-dose male and female mice. TCB was not carcinogenic in either sex of rats.
The validity of these findings for assessing human cancer risk is questionable. The mouse
liver tumors could have been caused by a secondary mechanism due to liver toxicity (Lai
1994b).
In another study 0.03 mL of a TCB solution was applied to the skin of male and female mice
at concentrations of 30 or 60% twice a week for 2 years. No increase in a specific tumor
type was observed in either sex (U.S. EPA 1987, 1994a). The chemical is not listed among
the chemicals studied or to be studied by the National Toxicology Program (NTP 1994).
E. Genotoxicity
Results of short-term mutation tests are mixed. The chlorinated benzene industry has completed an
unscheduled DNA synthesis study on 1,2,4 trichlorobenzene in response to an EPA request for
testing. Results show that TCB does not induce in vitro DNA repair at concentrations up to 1%
(v/v). Other studies with up to seven strains of Salmonella typhimurium were negative for mutation
with or without metabolic activation (U.S. EPA 1987; U.S. Air Force 1989). Eight-week-old mice
injected i.p. with up to 420 mg/kg of TCB had a dose-related increase in the number of
micronucleated cells in the bone marrow (U.S. Air Force 1989).
F. Developmental/Reproductive Toxicity
EPA has derived an oral reference dose (RfD2) for TCB of 0.01 mg/kg/day, based on increased
adrenal gland weights observed in a multigeneration reproductive study in rats exposed to 400 ppm in
the drinking water. No information was found on the developmental or reproductive toxicity of TCB
to humans. Developmental toxicity, such as growth retardation, occurred in experimental animals
only at maternally toxic doses.
1. Humans — No information was found in the secondary sources searched concerning the
developmental or reproductive toxicity of TCB to humans.
2. Animals — The derivation of the oral RfD is based on a multigeneration reproductive study.
Male and female rats were exposed to TCB in the drinking water at concentrations of 0, 25,
100, or 400 ppm. At the highest concentration, a significant increase in adrenal gland weight
occurred in males and females of the FO and Fl generations; a no-observed-adverse-effect
level (NOAEL) for the study was 100 ppm. No effect was seen in gestation index, fertility,
2The RfD is an estimate (with uncertainty spanning perhaps an order of magnitude) of the
daily exposure level for the human population, including sensitive subpopulations, that is
likely to be without an appreciable risk of deleterious effects during the time period of
concern.
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neonate weight, maternal weight, litter size, viability, or growth in either the FO or Fl
generations (U.S. EPA 1994a). Based on these data for the effects on the adrenal gland, the
U.S. EPA (1994a) calculated a chronic RfD for TCB of 0.01 mg/kg/day.
Retarded embryonic development associated with maternal toxicity was observed in rat pups
following maternal oral doses of 360 mg/kg on gestation days 9-13 (U.S. EPA 1987; U.S.
Air Force 1989). No effects were observed on offspring from mice given 130 mg/kg by
gavage on gestation days 8-12 (U.S. Air Force 1989).
G. Neurotoxicity
At lethal doses to experimental animals, TCB causes tremors and convulsions.
1. Humans — No information was found in the secondary sources searched concerning the
neurotoxicity of TCB to humans.
2. Animals — During LD50 studies, rats and mice had symptoms of depressed activity at lower
doses and extensor convulsions at lethal doses (IPCS 1991). Tremors followed by death
within 20-30 days occurred in monkeys exposed orally to 174 mg/kg/day (U.S. EPA 1994a).
No mortality was observed in rats exposed by inhalation to 418 ppm TCB for 4 hours,
however, clinical signs included lacrimation, salivation, pink ears, labored breathing, and
discoordination (U.S. EPA 1994b).
V. ENVIRONMENTAL EFFECTS
The chlorinated benzene industry has submitted to EPA results of aquatic toxicity testing on 1,2,4-
trichlorobenzene. Results show that TCB is highly toxic to aquatic organisms. Based on studies in laboratory
animals, it is unlikely that TCB would be toxic to terrestrial animals at environmental levels.
A. Toxicity to Aquatic Organisms
TCB is moderately to highly toxicity to aquatic organisms. The high toxicity is based on a measured
algal 96-h EC50 value of 0.37 mg/L (Newsome 1995). The chlorinated benzene industry has
completed aquatic toxicity studies in response to an EPA request for testing. Results show that the
96-hr LC50 for TCB in mysid shrimp is 0.49 mg/L. TCB adversely affects survival, growth, and
reproduction in mysid shrimp. The 28-day chronic toxicity value for mysid shrimp is 0.06 mg/L
(Newsome 1995).
Ninety-six-hour LC50 values for Cyprinodon variegatus (sheepshead minnow) and Lepomis
macrochirus (bluegill) are 10 mg/L and 3.4 mg/L, respectively. The 48-hour LC50 for Salmo
gairdneri (rainbow trout) is 1.95 mg/L (IPCS 1991). Based on the bioconcentration factor in fish
(182-3200), TCB also has the potential to bioconcentrate in the tissues of aquatic organisms (U.S. Air
Force 1989).
B. Toxicity to Terrestrial Organisms
No information was found in the secondary sources searched concerning the toxicity of TCB to
terrestrial organisms. However based on the LD50 values of 756 mg/kg and 766 mg/kg for rats and
mice, respectively (U.S. Air Force 1989) it is unlikely that TCB would be toxic to terrestrial animals
at environmental levels. Developmental toxicity, such as growth retardation, occurred in
experimental animals at maternally toxic doses (U.S. Air Force 1989; U.S. EPA 1987) which are
unlikely to occur in the environment.
C. Abiotic Effects
Most TCB in the atmosphere is removed by reaction with photochemically produced hydroxyl
radicals (U.S. EPA 1987). TCB is not expected to react to an appreciable amount with ozone (IPCS
1991).
VI. EPA/OTHER FEDERAL/OTHER GROUP ACTIVITY
The Clean Air Act Amendments of 1990 list TCB as a hazardous air pollutant. Federal agencies and groups
may develop recommendations to assist in controlling workplace exposure. These agencies and groups (listed
in Tables 3 and 4) should be contacted regarding workplace exposures and for additional information on TCB.
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TABLE 3. EPA OFFICES AND CONTACT NUMBERS FOR INFORMATION ON TCB
EPA Office Statute Contact Number
Pollution Prevention & Toxics PPAa (202)260-1023
EPCRA(§313/TRI)b (800)535-0202
TSCA (§4, 8A, 8D)C (800)554-1404
Air Clean Air Act (§111.112B)d (919)541-0888
Solid Waste & RCRAe (Action levels: (800) 535-0202
Emergency Response air, 1E+01 |jg/m3
water, 7E-01 mg/L
soil, 2E+03 mg/kg)
CERCLA' (RQ: 100 pounds) (800) 535-0202
Water Safe Drinking Water Act9 (800) 426-4791
(MCL: 70 ug/L; MCLG:
0.07 ug/L; Health
Advisories: 0.01 mg/L [ch/1d];
0.01 mg/L [ch/10d]; 0.1 mg/L [ch/lt];
0.5 mg/L [a/It]); 0.07 mg/L [lifetime])
Clean Water Act(§304B, (202) 260-7588
§307A)h
Pesticides FIFRA1 (800) 858-7378
aPPA: Pollution Prevention Act
bEPCRA: Emergency Planning and Community Right to Know Act of 1986
TSCA: Toxic Substances Control Act
dl_isted as hazardous air pollutant under §112 of Clean Air Act [42 U.S.C. 7401 etseq. (1990)]
eRCRA: Resource Conservation and Recovery Act [40 CFR §264.94 (1990)]. Action Levels = Health and
environmental-based levels used by the EPA as indicators for the protection of human health and the
environment and as triggers for a Corrective Measure Study.
'CERCLA: Comprehensive Environmental Response, Compensation, and Liability Act of 1980, as amended;
RQ: level of hazardous substance, which, if equaled or exceeded in a spill or release, necessitates the
immediate reporting of that release to the National Response Center [40 CFR Part 302 (1991)].
9MCL: Maximum contaminant level [40 CFR Part 141 (1994)]; MCLG: Maximum contaminant level goal [40
CFR Part 141 (1994)]; Drinking Water Health Advisories. Estimated for a 10-kg child or a 70-kg adult
consuming 2 L of water per day. (ch/1d): Child, one-day health advisory = the concentration of a chemical in
drinking water that is not expected to cause any adverse noncarcinogenic effects for up to 5 consecutive days
of exposure, with a margin of safety. (ch/10d): Child, ten-day health advisory = the concentration of a
chemical in drinking water that is not expected to cause any adverse noncarcinogenic effects up to 14
consecutive days of exposure, with a margin of safety, (ch/lt): Child, longer-term health advisory = the
concentration of a chemical in drinking water that is not expected to cause any adverse noncarcinogenic
effects up to approximately 7 yr (10% of an individual's lifetime) of exposure, with a margin of safety. (a/It):
Adult, longer-term health advisory. Lifetime: lifetime health advisory, the concentration of a chemical in
drinking water that is not expected to cause any adverse noncarcinogenic effects over a lifetime of exposure,
with a margin of safety.
hClean Water Act; regulates waters of the United States, including surface waters, ground waters, and
wetlands [40 CFR Part 131 (1994)].
'FIFRA: Federal Insecticide, Fungicide, and Rodenticide Act
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TABLE 4. OTHER FEDERAL OFFICES/CONTACT NUMBERS FOR INFORMATION ON 1,2,4-
TRICHLOROBENZENE
Other Agency/Department/Group Contact Number
Agency of Toxic Substances & Disease Registry (404) 639-6000
American Conference of Governmental Industrial Hygienists (513) 742-2020
(Ceiling limit: 5 ppm [37 mg/m3])3
Consumer Product Safety Commission (301) 504-0994
Food & Drug Administration (301) 443-3170
National Institute for Occupational Safety & Health (800) 356-4674
(Ceiling limit: 5 ppm [40 mg/m3])3
Occupational Safety & Health Administration [TWAb: 1ppm (7 mg/m3)]
(Check local phone book for phone number under Department of Labor)
a Ceiling limit: concentration that should not be exceeded during any part of the working exposure.
b TWA: Time-weighted-average that must not be exceeded during any 8-hour work shift of a 40-hour
workweek. Standard promulgated pursuant to the Occupational Safety and Health Act, 29 CFR 1910
(OSHA1993).
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A-1
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U.S. EPA. 1994. Integrated Risk Information System (IRIS) Online. Cincinnati, OH: Office of Health and Environmental Assessment.
A-2
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