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 These sources include online databases, unpublished EPA information, government publications, review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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VII.  CITED REFERENCES

Budavari S, O'Neil MJ, Smith A, Hickelman PE (Eds.). 1989. The Merck Index, 11thed. Merck & Co., Inc., Rahway, NJ, pp. 1515-1516.

Darling D.  1995.  Memorandum from Diana Darling (Environmental Exposure and Technology Division) to Sylvon Von Der Pool (Chemical
Screening and Risk Assessment Division).  Subject:  Chemicals in the Environment-1,2,4-Trichlorobenzene.  June 8, 1995.

HSDB. 1994. Hazardous Substances Database. Printout retrieved August 1994.

IPCS. 1991. International Programme on Chemical Safety. Environmental Health Criteria 128. Chlorobenzenes other than
Hexachlorobenzene. World Health Organization, Geneva, Switzerland, 252 pp.

Keith LH and Walters DB (Eds.).  1985. Compendium of Safety Data Sheets for Research and Industrial Chemicals, Part III. VCH Publishers,
Deerfield Beach, pp. 1642-1643.

Lai D. 1994a. Memorandum from David Lai (Health and Environmental Review Division) to Roger Nelson (Chemical Control Division).
Subject: Reviews of TSCA Section 4 Carcinogenicity Studies on 1,2,4-Trichlorobenzene in Rats. August 23, 1994.

Lai D. 1994b. Memorandum from David Lai (Health and Environmental Review Division) to Roger Nelson (Chemical Control Division).
Subject: Reviews of TSCA Section 4 Carcinogenicity Studies on 1,2,4-Trichlorobenzene in Mice. September 9, 1994.

Newsome L. 1995.  Memorandum from Larry Newsome (Health and Environmental Review Division) to Richard Wormell (Chemical
Screening and Risk Assessment Division).  Subject:  Comments on OPPT Fact Sheets on Aniline and Others. July 13, 1995.

NTP. 1994. National Toxicology Program. Management Status Report produced from Chemtrack System, National Library of Medicine.

Sax, N.I., and R.J. Lewis, Sr. (eds.). Hawley's Condensed Chemical Dictionary, Eleventh edition. New York:  Van Nostrand Reinhold
Company,  1987.

The Freedonia Group, Inc.  "Chlorinated Hydrocarbons." November 1990.

TRI92. 1994. 1992 Toxics Release  Inventory. Office of Pollution Prevention and Toxics, U.S. EPA, Washington, D.C., pp. 84, 94.

U.S. Air Force. 1989. The Installation Restoration Program Guide, Vol. 2. Wright-Patterson Air Force Base, OH, pp. 28-1 - 28-30.

U.S. EPA. 1986. U.S. Environmental Protection Agency. Chlorinated benzenes; Final test rule. Fed. Reg. 51:24657.

U.S. EPA. 1987. U.S. Environmental Protection Agency. Health Effects Assessment for 1,2,4-Trichlorobenzene. Office of Research and
Development, U.S. EPA, Washington, D.C., 22 pp. ECAO-CIN-H093.

U.S. EPA. 1988. U.S. Environmental Protection Agency. Methodology for Evaluating Potential Carcinogenicity in Support of Reportable
Quantity Adjustments Pursuant to CERCLA Section 102.  Carcinogen Assessment Group, Office of Health and Environmental Assessment,
U.S. EPA, Washington, D.C., pp. 21, 22. OHEA-C-073.

U.S. EPA. 1994a. U.S. Environmental Protection Agency. Integrated Risk Information  System (IRIS) Online.  1,2,4-Trichlorobenzene. Office
of Health and Environmental Assessment, USEPA, Cincinnati, OH.

U.S. EPA. 1994b. Inhalation four-hour single exposure. Doc #878220476. (Cited in TSCATS 1994)

USITC.  1994. United States International Trade Commission.  Synthetic Organic  Chemicals: United States  Production and Sales, 1992,
76th edition.  USITC Publication
2720, February 1994.
                                                           A-1

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APPENDIX A.  SOURCES SEARCHED FOR FACT SHEET PREPARATION

ACGIH.  Most recent. American Conference for Governmental Industrial Hygienists, Inc. TLVs®.  Documentation of the Threshold Limit
Values and  Biological Exposure Indices, ... ed. ACGIH, Cincinnati, OH.

AQUIRE. 1994. Aquatic Information Retrieval online data base. Chemical Information Systems, Inc., a subsidiary of Fein-Marquart
Assoc.

ATSDR. 1989-1994. Agency for Toxic Substances and Disease Registry. Toxicological Profiles. Chamblee, GA: ATSDR.

Budavari S, O'Neil MJ, Smith A, Heckelman PE (Eds.). 1989. The Merck Index, 11th ed. Rahway, N.J.:  Merck & Co., Inc.

Clayton GD, Clayton FE. 1981-1982. Patty's  Industrial Hygiene and Toxicology, 3rd ed., Vol. 2C. New York: John Wiley & Sons.
(Soon to be updated)

Clean Air Act. 1990. As amended. 42 U.S.C. 7412.

GENETOX. 1994. U.S. EPA GENETOX Program, computerized database.

HSDB. 1994. Hazardous Substances Data Bank. MEDLARS Online Information Retrieval System, National Library of Medicine.

IARC. 1979-1994. International Agency for Research on Cancer.  IARC Monographs on the Evaluation of Carcinogenic Risk of
Chemicals to Man.  Lyon: IARC.

IPCS. 19....  International Programme on Chemical Safety.  Environmental Health Criteria. World Health Organization, Geneva,
Switzerland.

NIOSH (National Institute for Occupational Safety and Health). 1992. NIOSH Recommendations for Occupational Safety and Health.
Compendium of Policy Documents and Statements. Cincinnati, OH: NIOSH.

NTP.  199...  National Toxicology Program.  Toxicology and  Carcinogenesis Studies. Tech Rep Ser.

NTP.  199...  National Toxicology Program.  Management Status Report.  Produced from NTP Chemtrack system.  Aprils, 1994.
National Toxicology Program, Research Triangle Park, NC.

OSHA. 1993. Occupational Safety and Health Administration. Table Z-2. Limits for Air Contaminants.

RTECS. 199... Registry of Toxic Effects of Chemical Substances. MEDLARS Online Information Retrieval System, National Library of
Medicine.

TRI92. 1994. 1992  Toxics Release Inventory. Office of Pollution Prevention and Toxics, U.S. EPA, Washington, D.C.,  pp. 84, 94.

TSCATS. 199... MEDLARS Online Information Retrieval System, National Library of Medicine.

U.S. Air Force.  1989. The Installation Restoration Toxicology Guide, Vols. 1-5. Wright-Patterson Air Force Base, OH.

U.S. EPA .  1991. U.S. Environmental Protection Agency. Table 302.4 List of Hazardous Substances and Reportable Quantities 40
CFR, part 302.4:3-271.

U.S. EPA.  U.S. Environmental Protection Agency. Appendix A. Examples of Concentrations Meeting Criteria for Action Levels. 40
CFR Part 264.521 (a)(2)(i-iv). Fed. Reg. 55:30865-30867.

U.S. EPA.  Most current. Drinking Water Regulations and Health Advisories. Office of Drinking Water, U.S. Environmental Protection
Agency, Washington, D.C.

U.S. EPA.  Most Current.  Health Effects Assessment Summary Tables. Cincinnati, OH: Environmental Criteria and Assessment
Office, U.S.EPA.

U.S. EPA reviews such as Health and Environmental Effects Documents, Health and Environmental Effect Profiles, and Health and
Environmental Assessments, HERD Analogue Profiles, ITC  Documents.

U.S. EPA.  1994. Integrated Risk Information System (IRIS) Online. Cincinnati, OH:  Office of Health and Environmental Assessment.
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