United States
                 Environmental Protection
                                Pollution Prevention
                                and Toxics
    December 1994
    EPA 749-F-95-002a
wEPA      OPPT  Chemical  Fact Sheets
                    Aniline Fact Sheet: Support Document
                    (CAS  No.  62-53-3)

  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 These sources include online databases, unpublished EPA information, government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 was done in
  February of 1995.  No attempt has been made to verify information from these databases or secondary
         The chemical identity and physical/chemical properties of aniline are summarized in Table 1.

  CAS No.

  Common Synonyms

  Molecular Formula

  Chemical Structure

  Physical State

  Molecular Weight

  Melting Point

  Boiling Point

  Water Solubility

  Specific Gravity

  Vapor Density (air = 1)


  Log Kom

  Vapor Pressure


  Flash Point

  Henry's Law Constant

  Fish Bioconcentration Factor

  Odor Threshold

  Conversion Factors (in air)

                        aminobenzene; aminophen; phenylamine;




                        184.4C@ 1 atm

                        34 g/L @ 20 C; 35 g/L @ 25 C

                        1.02173 @ 20/4 C


                        3870 @ pH 6.5 (measured)


                        0.3 mm Hg @ 20 C; 0.67 mm Hg @ 25 C


                        76C (closed cup)

                        1.9x10'6 atm-m3/mole @ 25 C

                        3.0 (calculated)

                        perception, 0.34 mg/m3

                        1 ppm = 3.87 mg/m3; 1 mg/m3 = 0.259 ppm
U.S. EPA 1994
U.S. EPA 1985

U.S. EPA 1985

U.S. EPA 1985

U.S. EPA 1985

U.S. EPA 1985

U.S. EPA 1985

Verschueren 1983

U.S. EPA 1985

U.S. EPA 1985

U.S. EPA 1985

U.S. EPA 1985;
Budavari 1989
U.S. EPA 1985

U.S. EPA 1985

U.S. EPA 1985

Verschueren 1983

U.S. EPA 1985



       In 1992, the estimated total United States production capacity of aniline was 1,380 million pounds.
       The 1994 capacity was expected to remain the same (Mannsville 1992).  Table 2 shows the plant
       locations and plant capacities of producers of aniline in 1992.  In 1992, the production volume of
       aniline was estimated to be 1,005 million pounds (457 million kilograms) (USITC 1994). The U.S.
       imported four million pounds of aniline in 1991, and was expected to import the same amount in
       1992. In 1991, the U.S. exported 55 million pounds of aniline, but it is expected to export only 40
       million pounds in  1992.  Table 2 lists six producers of aniline in 1992  (Mannsville 1993). USITC
       (1994) lists an additional producer as Malinckrodt  Specialty Chemicals Company of Raleigh, North
BASF Corporation-?
First Chemical Corporation
Miles, Inc. (formerly Mobay;
now Bayer)
Rubicon (ICI/Uniroyal
Plant Location
Haverhill, OH
Geismar, LA
Beaumont, TX
Pascaqoula, MS
New Martinsville, WV
Geismar, LA
Plant Capacity
(Millions of Pounds)
Source:  Mannsville 1992.
1USITC (1994) lists Malinckrodt Specialty Chemicals Company of Raleigh, NC as an additional producer
of aniline.

2USITC's list (1994) was drafted before the opening of BASF Corporation's new 170 milliopounds per
year plant at Geismar, Louisiana in 1992.
3Rubicon is an affiliate of ICI and Uniroyal (Mannsville 1992).
       B. USES

       Isocyanate production accounts for approximately two-thirds of total U.S. demand for aniline (see Table
       3). Isocyanates derived from anilines are used to produce urethanes (Mannsville 1992).  The production
       of methyl diphenyl diisocyanate, an intermediate for the production of urethanes, is the largest end use
       for aniline (Windholz 1983).

       Other principal applications of aniline include production of rubber accelerators and antioxidants to
       vulcanize rubber; the manufacture  of intermediates for herbicides and other pesticides, especially
       fungicides; and the manufacture of dyes and pigments, especially azo dyes (Mannsville 1992; Sax and
       Lewis 1987; Windholz 1983) Aniline is also used to produce medicinals and pharmaceuticals, resins,

       varnishes, perfumes, shoe blacks, photographic chemicals (hydroquinone), explosives, petroleum
       refining chemicals, diphenylamine, and phenolics (Mannsville 1992; Sax and Lewis 1987; Windholz
       1983). Table 3 shows the end use pattern of aniline in 1992.
(Typical Standard Industrial Classification
(SIC) Code)4
(SIC 2865)
Rubber Chemicals
(SIC 2869)
(SIC 2879)
Dyes and Pigments
(SIC 2865)
(Various SICs)
U.S. Consumption
(Millions of Pounds)
Percentage of U.S.
Source: Mannsville 1992.
4 The Standard Industrial Classification (SIC) code is the statistical classification standard for all Federal
economic statistics. The code provides a convenient way to reference economic data on industriesfo
interest to the researcher.  SIC codes presented here are not intended to be an exhaustive listing; rather,
the codes listed should povide an  indication of where a chemical may be likely to be found in commerce.

       C.  TRENDS

       United States demand for aniline is expected to incease three to four percent per year (Mannsville
       1 992).  Increases in demand for aniline is dependent on increased demand for methyl dipheitiy
       diisocyanate (MDI). MDI demand is dependent on general economic conditions due to its heavy
       use in the production of construction and transportation materials. MDI demand is expecteobt
       increase at four to five percent annually (Mannsville 1992). U.S. demand for rubber, agricultural
       chemicals, and dyes has  moderated over the last several years.


A.     Environmental Release

       Aniline is a colorless, oily liquid at room temperature that darkens on exposure to air and light.
       It has a characteristic pungent odor and burning taste (U.S. EPA  1985; Budavari 1989). It
       occurs naturally in some foods  (e.g., in corn, grains, beans, and tea).  It is released into the
       environment primarily from industrial uses. The largest sources of aniline release are from its
       primary  uses  as  a chemical  intermediate in the production  of polymers,  pesticides,
       Pharmaceuticals and  dyes (U.S.  EPA 1985).   The chemical  has  been  detected, but not
       quantified, in ground water in a shallow aquifer known to be contaminated by coal-tar wastes.
       It has been measured at a  maximum  of 36 parts  per  billion (ppb) in an aquifer near an
       underground coal gasification  site in Wyoming.  Aniline  has  been found in industrial
       wastewater and leachates from  disposal sites.  One of two soil samples collected near the
       Buffalo River in New York contained 5 parts per million (ppm) aniline.  One air sample near
       Raleigh, NC was found to contain 90 ppb aniline, and it has been detected  in air about 4000
       meters from a chemical factory (Howard 1989).

       In 1992, releases of aniline to environmental media, as reported to the Toxic Chemical Release
       Inventory by certain types of U.S. industries, totaled about  1.6 million pounds. Of this amount,
       400 thousand pounds (25%) were  released to the atmosphere;  16 thousand pounds were released
       to surface water; 1.2 million pounds (74%) were released in underground injection sites; and
       11 hundred pounds were released to land (TRI92 1994).

B.     Transport

       Aniline in solution adsorbs strongly to colloidal organic matter, which effectively increases its
       solubility and movement into ground water.  It is also  moderately adsorbed to organic material
       in the soil; adsorption is dependent upon soil pH (pKa of 4.596)  (Howard 1989).  It will slowly
       volatilize from soil and surface water (vapor  pressure 0.67 mm Hg @ 25 C) and is subject to
       biodegradation.  Although rapidly degraded in the atmosphere, aniline can be deposited in the
       soil by wet and dry deposition, and by adsorption on aerosol particles (U.S.  EPA 1985).

C.     Transformation/Persistence

       1.     Air  Aniline reacts with any free radicals  produced  by sunlight in the atmosphere.
              This radical scavenging reactivity  has  been shown to inhibit the production of
              photochemical smog by sunlight. Aniline apparently undergoes direct photolysis and
              has considerable  absorption of wavelengths above 290  nanometers.  Photoproducts
              formed from aniline in the atmosphere include N-methylaniline, N,N-dimethylaniline,
              isomeric hydroxyanilines, and phenols (U.S. EPA 1985).  The half-life of atmospheric
              aniline due to photodegradation has been estimated at  3.3 hours (Howard  1989).

       2.     Soil  A number of microorganisms in soil can use aniline as a sole  carbon and
              nitrogen source. Degradation of 44.2% of the incubated aniline to CO2 in 10 days and
              12% in 20 days, respectively,  by different isolated  soil microorganisms has  been
              demonstrated in the laboratory (U.S. EPA 1985).   Aniline bound to humic materials in
              the soil is subject to oxidation (U.S. EPA 1985; Howard 1989).

              Products  apparently  formed from  oxidation include azobenzene, azoxybenzene,
              phenazine, formanilide, and acetanilide (U.S. EPA 1985).  Photodegradation of aniline
              on the soil surface is also  thought to be an environmentally important removal process
              (U.S. EPA 1985).   The combination of these  processes eventually  results in the
              degradation of aniline to CO2. The half-life for the  mineralization of aniline to CO2 has
              been estimated at 4 days, utilizing a model soil ecosystem. Information from studies

                      done obtained under environmental conditions indicate that the half-life of aniline in
                      the soil is less than one week (U.S. EPA 1985).

              3.      Water   Aniline in water is subject  to  biodegradation, photodegradation,  and
                      adsorption to sediment and humic materials.  Low pH will increase the removal of
                      aniline by adsorption; however, the adsorption to colloidal particles can extend the
                      persistence  of aniline  in the aquatic environment (Howard 1989; U.S. EPA 1985).
                      Although subject to oxidation when adsorbed to humic materials, aniline is resistant to
                      hydrolysis.  A half-life for aniline of 2.3 days has been reported in an industrial river
                      (Howard 1989). The presence of humic acids and various species of algae  in the water
                      can increase the photodegradation rates of aniline up to 50 fold (Howard  1989).

              4.      Biota  The bioconcentration factor in two species of fish has been estimated at 0.78
                      and less than 1 (Howard 1989). A bioconcentration factor of 3 has also been calculated
                      for fish (U.S. EPA 1985). Aniline is not expected to accumulate significantly in aquatic
                      organisms; however, it is absorbed and metabolized by fish (Howard 1989).

       A.     Pharmacokinetics
               1.      Absorption  Studies in humans and animals have  demonstrated that aniline is
                      absorbed through the gastrointestinal tract and the lungs (see Sections IV.B. and C.);
                      however, the only quantitative information found for the rates of absorption in humans
                      were based on dermal exposures. Volunteers were exposed to solutions of 1-2% aniline
                      for 30 or 60 minutes. The amount of aniline absorbed was quantitated by measuring
                      the amount of /7-aminophenol excreted in the urine in 24 hours. The absorption rates
                      were  0.15-1.38  mg/cm2/hour.   The absorption  rates increased with increasing
                      concentrations and  decreased  with longer  exposure  times  (U.S  EPA  1985).
                      Experiments with rats demonstrated that peak plasma levels of aniline were reached in
                      0.5, 1.0, and 2.0 hours following gavage administration of 10, 30, and 100 mg/kg 14[C]-
                      aniline hydrochloride, respectively (U.S. EPA  1985)

               2.      Distribution  The distribution of radioactivity  after  oral administration of 14[C]-
                      aniline to rats was highest in the kidney, liver, plasma, lung, heart, spleen, and brain.
                      However, some radioactivity was reported in all tissues examined.  Different doses of
                      14[C]-aniline  (10,  30,  and 100  mg/kg)  did  not alter the  distribution pattern  of
                      radioactivity (U.S. EPA 1985).

               3.      Metabolism  The primary  metabolic route for aniline has been shown in several
                      species to involve ring hydroxylation forming 4-aminophenol and 2-aminophenol, and
                      N-hydroxylation forming phenylhydroxylamine. Other metabolites identified in a rat
                      liver perfusate include acetanilide, 4-acetamidophenol, and nitrosobenzene (U.S. EPA

               4.      Excretion   Aniline metabolites  are  excreted  in  the  urine.    Conjugates of  4-
                      aminophenol and glucuronic or sulfuric acid have been identified in the urine of all
                      species tested.  Phenylhydroxylamine may also be conjugated with glucuronate or
                      sulfate, or it may form a mercapturic acid conjugate after reacting with cysteine. Forty-
                      eight hours following oral administration of 10, 30 or 100 mg/kg body weight 14[C]-
                      aniline to rats, 96, 91, and 77%, respectively, of the radioactivity was recovered in the
                      urine (U.S. EPA 1985).
       B.     Acute Toxicity

          The primary toxic effect resulting from acute exposure to aniline by inhalation, oral or dermal
          routes  is methemoglobinemia and accompanying anoxia, erythrocyte damage, and spleen
          effects.  Adverse effects on the liver and spleen have also been reported.

          1.      Humans  Volunteers given single oral doses of 5, 15, 25, 35, 45, 55, and 65 mg of
                 aniline developed increased methemoglobin formation at doses 25 mg or higher.  The
                 authors concluded that humans were much more sensitive to aniline exposure than rats,
                 judging from methemoglobin formation (U.S.  EPA  1994;  U.S. EPA  1985). Liver
                 cirrhosis and atrophy were  reported in at least one fatal case  of aniline exposure
                 (ACGIH 1991). Inhalation exposure to 7-53 ppm aniline for several hours resulted in
                 slight symptoms; exposure to 100-160 ppm for 1 hour (6.91-11.06 mg/kg)5 resulted in
                 (unspecified) serious disturbances (ACGIH 1991). Sitting in a car seat contaminated
                 with aniline resulted in a methemoglobin level of 53% with cyanosis, dyspnea, fatigue,
                 and dizziness in one individual. Recovery occurred within 24 hours following medical
                 treatment (U.S. EPA 1985).

          2.      Animals  Increased spleen weight, splenic erythropoietic activity, splenic sinusoidal
                 engorgement, and splenic hemosiderin content were reported in Colworth-Wistar male
                 rats 12 days after receiving aniline in single oral doses of 20 mg/kg or above.  A slight
                 increase in hepatic hemosiderin content and erythropoietic activity was also reported
                 but no gross  pathological changes in the liver were seen (U.S. EPA 1985).

                 Oral LD50 values of 440 mg/kg  (males) and 1072 mg/kg have been reported for rats,
                 and an oral LD50 of 841 mg/kg was reported for mice.  An inhalation LC50 value of 950
                 mg/m3 (250 ppm) for 4 hours was reported for rats, and a dermal  LD50 of 1320 mg/kg
                 was reported for guinea pigs (U.S. EPA 1985).
   C.     Subchronic/Chronic Effects

          Increased methemoglobin production and adverse splenic effects are the major non-neoplastic
          effects reported with extended exposure to aniline. Adverse effects on the liver and kidneys
          have been reported in some studies.  A no-observed-adverse-effect level of 3.4 mg/m3 was
          determined for continuous inhalation exposure in rats, dogs, mice, and guinea pigs.  A lowest-
          observed-adverse-effect level of 64.7 mg/m3 was identified in rats exposed by inhalation for 2
          weeks based on increased methemoglobin production. EPA has derived an inhalation RfC6  of
          0.001 mg/m3 for aniline exposure.

          1.      Humans  Increased methemoglobin and decreased hemoglobin, erythrocyte count,
                 and coagulative factors were reported in an occupational study on workers exposed to
                 1.3 to 2.75 mg/m3 (0.19-0.39 mg/kg/day) aniline  for 3 to 5 years compared to  an
                 unexposed control  group.   An  increase in  methemoglobin was  reported on
                 reexamination after one year, however no numerical data were given (U.S. EPA 1994).
5 For dose comparison purposes, this has been calculated using the factor, 3.87, to convert ppm to
mg/m3, which is multiplied by 0.0179 (the calculated occupational 1-hour breathing  rate, I^S'rri
divided by the assumed adult body weight, 70 kg) to obtain the dose in mg/kg/hr assuming 100%
absorption (U.S. EPA 1988).

6 For dose comparison purposes, this has been calculated by multiplying by 0.143 (the adult
occupational breathing rate, 10 mVday, divided by the assumed adult body weight, 70 kg) to obtain the
dose in mg/kg/day assuming 100% absorption (U.S. EPA 1988)

          2.      Animals  Nine male Wistar rats, 2 dogs, 20 female albino mice, and 10 guinea pigs
                 were exposed to 5 ppm (19 mg/m3) aniline, 6 hours/day, 5 days/week for 26 weeks.
                 The continuous exposure level was calculated to be 3.4 mg/m3. Methemoglobin was
                 slightly increased only in rats, but there were no pathological changes in any organs in
                 any species tested attributed to aniline exposure. Although only one dose level was
                 given in this study, it was identified as a no-observed-adverse-effect level (NOAEL)
                 (U.S. EPA 1994). This value together with a 2-week study (see below for  discussion)
                 LOAEL  of 17 ppm (64.7 mg/m3) for increased methemoglobin levels and minimal
                 splenic effects in rats were utilized by the U.S. EPA (1994) to calculate a chronic
                 inhalation RfC of 0.001 mg/m3 for aniline.

                 Male Crl:CD rats were exposed in an inhalation study to 0, 17, 45, or 87 ppm aniline
                 vapors,   6  hours/day,  5 days/week  for 2 weeks.  A dose-related  increase  in
                 methemoglobin level at 17 ppm and above was reported. The increase seen at 17 ppm
                 (64.7 mg/m3) was not  statistically significant, compared to controls,  and  spleen
                 histopathology was judged to be minimal.  The higher doses resulted in cyanosis,
                 anemia,  increased relative  spleen weight, and increases  in  erythropoietin foci,
                 reticuloendothelial cell hypertrophy and hemosiderin deposition. The 17 ppm (64.7
                 mg/m3) dose was identified as a lowest-observed-adverse-effect level (LOAEL) by
                 U.S. EPA 1994

                 Dietary exposure of Fischer 344 rats to 3000 or 6000 ppm (150 or 300 mg/kg)7 aniline
                 hydrochloride for 103 weeks resulted in an increased incidence of splenic hyperplasia
                 and erythropoiesis, and renal and hepatic hemosiderosis in both sexes (U.S. EPA  1985).
                 B6C3FJ mice were fed diets containing 0, 6000, or 12,000 ppm  (480 or 960 mg/kg)8
                 aniline hydrochloride for 103 weeks. Males developed diffuse inflammation of the bile
                 duct at both dose levels, and females were found to have an increased incidence of
                 splenic erythropoiesis  and an accumulation of serous fluid  in the uterine  cavity at
                 12,000 ppm (U.S. EPA 1985).

                 Wistar rats were given 300-1200 ppm aniline in their drinking water for 80  weeks.  No
                 changes in body weight or liver weight were reported; however, there were slight but
                 dose-related decreases  in erythrocyte  counts, hemoglobin levels, and hematocrits of
                 treated rats (U.S. EPA 1985).

                 Daily oral doses of 110 mg aniline/kg for 5, 10, or 20 days resulted in increased  spleen
                 weight, splenic congestion, and hematopoiesis in Fischer 344 rats. Increased cellularity
                 in bone marrow was also reported at all time points.  Increased splenic hemosiderosis
                 was seen but only after 20 days of exposure. No adverse effects  were reported in the
                 livers of the animals in this study (U.S. EPA 1985).

   D.     Carcinogenicity

          Tumors of the spleen and body cavity were induced in two strains of rats in separate dietary
          studies. This information and the genotoxicity evidence of aniline were used by U.S. EPA as
          a basis for classifying aniline as a B2, probable human carcinogen.

          1.      Humans  The incidence of bladder tumors was investigated  in British chemical dye
                 workers exposed to aniline and other aromatic amines. There was inadequate  evidence
7 For dose comparison purposes this has been calculated by multiplying the ppm value by a factor
of 0.05. the food consumption conversion factor for the rat.

8 For dose comparison purposes this has been calculated by multiplying the ppm value by a factor
of 0.13, the food conversion factor for the mouse.

              to conclude that aniline alone was a cause of bladder tumors (U.S. EPA 1994).

       2.     Animals  Groups of 130 CD-F rats per sex were fed diets containing 0, 200, 600, or
              2000 ppm (10, 30, or 100 mg/kg)4 aniline hydrochloride for two years.  An increased
              incidence of primary splenic sarcomas was reported in male rats at the 2000 ppm dose.
              Stromal hyperplasia and splenic red pulp fibrosis, probable precursors of sarcoma, were
              observed in both sexes at the high dose (U.S. EPA 1994).

              Groups of 50 Fischer 344 rats per sex were given aniline hydrochloride in the diet at
              0, 3000, or 6000 ppm for 103 weeks (Section IV.C.2).  The animals were killed and
              examined after a 4-7 week observation period.  Significant, dose-related increases in
              the  incidence  of splenic hemangiosarcomas,  multiple  organ  fibrosarcomas, and
              malignant pheochromocytomas were reported in treated males compared to controls.
              The incidences of splenic sarcomas and fibromas were also increased but were not dose
              dependent.   Splenic sarcomas were  slightly (3/50 at high  dose,  0/24 in control)
              increased at the high dose in females. The incidence of sarcomas in a pooled group of
              control  female  Fisher  344  rats  was  0/249.    Likewise,  the  incidence   of
              hemangiosarcomas, fibrosarcomas, and sarcomas in a pooled group of control male
              Fisher 344 rats was 0/250 (U.S. EPA 1994; 1985; NCI 1978). A parallel study was also
              conducted with B6C3Fj mice in which the mice were fed diets containing 0, 6000, or
              12,000 ppm  aniline hydrochloride for 103 weeks.  No  significant increase in  the
              incidence of any type of tumor was observed in either sex (U.S. EPA 1985; NCI 1978).
E.     Genotoxicity
       Results of short term mutagenicity testing of aniline are mixed. Positive results of a mouse
       bone marrow micronucleus assay of aniline have been submitted to EPA (Federal Register
       1989b) in response to a request for testing under Section 4 of the Toxic Substances Control Act
       (TSCA). Aniline was positive in the mouse lymphoma forward mutation test and for sister-
       chromatid exchanges (SCE) in Chinese hamster ovary cells (ACGIH  1991) and in Swiss mice
       bone marrow cells (U.S. EPA 1985). Aniline did not increase the SCE in human fibroblasts;
       however, both 2-aminophenol and N-phenylhydroxylamine, potential metabolites of aniline,
       were positive for SCE (U.S. EPA 1985). Aniline was positive in the cell transformation assay
       in mouse Balb/3T3 cells, but was negative with Syrian hamster embryo cells or Fischer 344 rat
       embryo cells infected with murine leukemia virus (U.S. EPA 1994). Aniline has generally been
       reported negative in reverse mutation tests in multiple strains of Salmonella typhimurium with
       or without metabolic  activation.   In one assay, a weakly positive result was reported in S.
       typhimurium strains TA98 and/or TA100 with metabolic activation. Results of DNA interaction
       tests withE. coli are negative (U.S. EPA 1985).
F.     Developmental/Reproductive Toxicity

       Conclusive information on human and animal developmental/reproductive effects of aniline is
       not available. Limited evidence from animal and human studies suggest that repeat exposure
       to aniline may cause adverse effects on the reproductive system in female workers and fetal
       toxicity in animals.

       1.       Humans  A possible correlation has been reported between exposure to aniline and
               other organics encountered by Russian aniline dye industry workers and the incidence
               of menstrual disturbances and ovarian dysfunction. However, the effect was dependent
               on the nutritional status of the exposed individuals.  The dye workers also experienced
               an increase in abortion rates, but  the strenuous physical exertion required for the job
               complicates the interpretation of these results (U.S. EPA 1985).

              2.     Animals  Daily treatment of 50 pregnant CD-I mice from day 7 to 14 of gestation
                     with 560 mg/kg/day aniline by gavage resulted in slightly decreased pup weight gain
                     and pup survival during the first 3 days postpartum. The average number of pups per
                     litter  was the same in the  control  and  treated groups, however fewer litters were
                     produced in the treated group. There was evidence of maternal toxicity.  Six dams died
                     and the mean weight gain was significantly decreased during treatment compared to
                     control dams (U.S. EPA 1985).

                     Aniline has been shown to cause malformations following injection into the inner shell
                     membrane of 3-day-old chick embryos (U.S. EPA 1985).  Embryonic malformations
                     occurred when eggs from bass, goldfish, and catfish were exposed to aniline at 34-100
                     mg/L for 4 days. Exposure of clawed toad eggs to 10 mg aniline/L for 4 days resulted
                     in 11% abnormal embryos and 28% mortality. No abnormalities or deaths were seen
                     in the control animals (U.S. EPA 1985).

       G.     Neurotoxicity

              Central nervous system effects following aniline exposure are secondary to effects associated
              with the anoxia resulting from methemoglobinemia.

              1.     Humans  Exposure to aniline caused central nervous  system  symptoms such as
                     euphoria  and headache.    Continued  exposure  increases  the   symptoms  to
                     lightheadedness, ataxia, and weakness. These symptoms are concurrent with signs of
                     anoxia resulting from methemoglobinemia (Beard and Noe 1981).

              2.     Animals  No information was found in  the secondary sources searched on the
                     neurotoxicity of aniline in animals.


       The aniline industry has completed aquatic toxicity studies in response to an EPA request for testing.
       These tests show that aniline is highly toxic to aquatic life. Reported LC50 values for daphnids are less
       than 1 mg/L.  Reported chronic values for daphnids are less than 0.1 mg/L.

       A.     Toxicity to Aquatic Organisms

              Ninety-six-hour LC50 values for fish are: 41 mg/L in hard water and 20 mg/L in soft water for
              Salmo gairdneri (rainbow trout), and 32-53 mg/L for Brachydanio rerio (zebrafish).  Forty-
              eight-hour LC50 values for fish are: 43 mg/L for Salmo  gairdneri,  100 mg/L for Poecilia
              reticulata (guppy), 165 mg/L for Oryzias latipes (medaka),  65 mg/L for Pimephales promelas
              (fathead minnow), and 61-78 mg/L for Leuciscus idus (golden orfe) (U.S.  EPA 1985).  A 96-
              hour EC50 for aniline in algae  is 19 mg/L; a 48-hour EC50 for aniline in daphnids is 0.65 mg/L
              (Rabert 1991).  The geometric average concentration 48-hour LC50 for aniline in daphnids is
              0.57 mg/L, based on three tests (Newsome 1995).

              Results of acute and  chronic aquatic testing of aniline in invertebrates have been submitted to
              EPA (Federal Register 1989a and 1989c) in response to a  request for testing under Section 4
              of The Toxic Substance Control Act.  The 96-hour LC50 of aniline is 2.3 mg/L in the amphipod
              Gammarus fasciatus.  Results of a 21-day chronic  flow  through assay of daphnids  shows
              decreased reproductive capacity at 0.027 mg/L. Test results from the chronic daphind toxicity
              study have been described as unreliable because of several deficiencies, including unstable test
              concentrations and poor replication of test results (Rabert 1991).

       B.     Toxicity to Terrestrial Organisms

              Aniline is unlikely to exist in U.S. terrestrial environments in sufficient concentrations to cause
              serious acute or chronic effects to terrestrial organisms.  The toxicity data reported for rats,
              mice, and guinea pigs (see sections IV.B.2. and IV.C.2.) suggest that no effects would be seen
              at normally expected U.S. environmental concentrations.

       C.     Abiotic Effects

              Aniline  acts as  a  radical scavenger in the atmosphere and inhibits the formation of
              photochemical smog (Howard 1989).


       The Clean Air Act Amendments of 1990 list aniline as a hazardous air pollutant.  Occupational exposure
       to aniline is regulated by the Occupational Safety and Health Administration (OSHA).  The OSHA
       permissible exposure limit (PEL) is 5 parts per million parts of air (ppm) as an 8-hour time-weighted
       average (TWA)  (29 CFR 1910.1000).  In addition to OSHA, other federal agencies and groups may
       develop recommendations to assist in controlling workplace exposure. These agencies and other groups
       (listed in Tables 4 and 5) should be contacted regarding  workplace  exposures, and for  additional
       information on aniline.

EPA Office
Contact Number
Pollution Prevention & Toxics



Solid Waste & Emergency Response
TSCA (4, 80)=

Clean Air Act (111, 112B)1

Clean Water Act (311|

RCRA (Action levels: water,
6E-3 mg/L; soils, 1E+2 mg/kg)f
CERCLA(RQ: 5000 pounds)9
(800) 535-0202


(202) 260-7588

(800) 535-0202

(800) 535-0202
aPPA:  Pollution Prevention Act

"EPCRA: Emergency Planning and Community Right to Know Act of 1986

TSCA: Toxic Substances Control Act

"Listed as hazardous air pollutant under  112 of Clean Air Act [42 U.S.C. 7401 et seq.]

eCWA: Clean Water Act; regulates waters of the United States, including surface waters, ground waters, and wetlands [40
CFR Part 131 (1994)].

'RCRA: Resource Conservation and Recovery Act of 1976, (codified as amended at 42 U.S.C. 6901 et seq).  Action
Level: 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 Measures Study (U.S. EPA 1990).

9CERCLA: Comprehensive Environmental Response, Conpensation, 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 Naltional Response Center [40 CFR Part 302 (1991)].


Other Agency/Department/Group                                  Contact Number

American Conference of Governmental Industrial Hygienists           (513) 742-2020
 [TLV-TWA, 2 ppm (7.6 mg/rrl); skin exposure]3
Consumer Product Safety Commission                               (301) 504-0994
Food & Drug Administration                                          (301) 443-3170
National Institute for Occupational Safety & Health                    (800) 356-4674
 [TWA, 2 ppm (8 mg/rrr);  IDLH, 100 ppm; skin exposure, Ca,  LF*]
Occupational Safety & Health Administration
 [TWA, 5 ppm (19mg/rrr]c
 Check local phone book for phone number under Department of Labor

aTLV-TWA: Time-Weighted-Average concentration for a normal 8-hr workday and a 40-hr workweek to which nearly all
workers may be repeatedly exposed without adverse effects. Skin exposure : air sampling alone is insufficient to
accurately quantitate exposure. Measures to prevent significant cutaneous absorption may be required (ACGIH 1993-

bTWA: Time-Weighted-Average concentration for up to a 10-hour workday during a 40-hour workweek. IDLH: immediate
danger to life and health. Ca: potential human carcinogens.  LF: reduce exposure to lowest feasible concentration; when
Ca designation accompanies lowest feasible designation, use of only the most reliable and protective respirators is
recommended. Skin exposure : air sampling alone is insufficient to accurately quantitate exposure.  Measures to prevent
significant cutaneous absorption may be required (NIOSH 1990, 1992).

TWA: Time-Weighted-Average concentrations that must not be exceeded during any 8-hour work shift of a 40-hour
workweek.  OSHA standards promulgated pursuant to the Occupational Safety and Health Act, 29 CFR 1910 (OSHA


ACGIH.  1991.  Documentation of the Threshold Limit Values and Biological Exposure Indices, Sixth
edition. American Conference of Governmental Industrial Hygienists, Inc., Cincinnati, OH, pp. 256-257.

ACGIH.  1993-1994.  American Conference of Governmental Industrial Hygienists. Threshold Limit
Values for Chemical Substances and Physical Agents and Biological Exposure Indices.  ACGIH,
Cincinnati, OH.

Beard RR and Noe JT.  1981.  Aromatic Nitro and Amino Compounds. In: Clayton GEJIayton FE.
1981-1982. Patty's Industrial Hygiene and Toxicology, 3rd ed., Vol. 2A. John Wiley & Sons, New York,
pp. 2413-2446.

Budavari S, O'Neil MJ, Smith A, Heckelman PE (Eds.). 1989.  The Merck Index,  11th ed. Merck & Co.,
Inc., Rahway, N.J., p. 686.

Federal  Register. 1989a. 54 FR 25167. June 13, 1989.

Federal  Register. 1989b. 54 FR32117. August 4, 1989.

Federal  Register. 1989c. 54 FR 33773. August 16, 1989.

Grayson, M. (ed.). Kirk-Othmer Concise Encyclopedia of Chemical Technology, Third edition.  New
York:  John Wiley and Sons, 1985.

Howard  PH. 1989. Handbook of Environmental Fate and Exposure Data for Organic Chemicals, Vol. I,
Large Production and Priority Pollutants. Lewis Publishers, Inc., Chelsea, Ml. pp. 44-52.

Mannsville. 1992. Mannsville Chemical Products Corporation. Aniline.  Chemical Products Synopsis,
December 1992.

Newsome L. 1995. Memorandum from Larry  Newsome, HERD/EEB, to Richard Wormell,
CSRAD/AIMB.  Subject: Comments on OPPT Fact Sheet for Aniline and Others.  July 13, 1995.

NCI.  1978.  National Cancer Institute. Bioassay of Aniline Hydrochloride for Possible Carcinogenicity.
CAS No.: 142-04-1. ITS Carcinogenesis Technical Report Series 130. U.S.  DHEW, PHS, NIH,
Bethesda, MD.  DHEW Publ. No. (NIH) 78 to 1385. (as cited in U.S. EPA 1985).

NIOSH.  1990.  National Institute for Occupational Safety and Health.  Pocket Guide to Chemical
Hazards. NIOSH, Cincinnati, OH.

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

OSHA. 1993. Occupational Safety and Health Administration.  Air Contaminants. Final Rule.  29 CFR
part 1910. Fed. Reg.  58:35338-35351.

Rabert WS. 1991. Memorandum from William Rabert, Environmental Effects Branch, to John Harris,
Chemical Testing Branch. Subject:  Review oDaphnia magna 21-Day Life Cycle Toxicity Test on
Aniline.  Jan 8,  1991.

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

TRI92. 1994.  1992 Toxics Release Inventory, Public Data Release. Office of Pollution Prevention and
Toxics, U.S. EPA, Washington, D.C., p. 87.

U.S. EPA. 1985  Health and Environmental Effects Profile for Aniline. U.S. Environmental Protection
Agency, Office of Solid Waste and Emergency Response Washington, D.C., Environmental Criteria and
Assessment Office, Cincinnati, OH. ECAO-CIN-P136.

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. 1990.  Examples of concentrations meeting criteria for action levels. Fed. Reg. 55:30865-

U.S. EPA. 1994.  U.S. Environmental Protection Agency.  Integrated  Risk Information System (IRIS)
Online. Coversheet for Aniline. Office of Health and Environmental Assessment, U.S. EPA, Cincinnati,
OH.  Retrieved 10/94.

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

Verschueren,  K.  1983. Aniline. In: Handbook of Environmental Data on Organic Chemicals, Second
Edition. Van Nostrand Reinhold Co., New York, pp. 201-203.

Windholz, M. (ed.).  The Merck Index, Tenth edition. Rahway, N.J.: Merck and Company, Inc., 1983.


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,

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.

Howard, P.H., Ed. 1989. Handbook of Environmental Fate and Exposure Data.  Lewis Publishers, Chelsea,

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:

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. April 8, 1994. National Toxicology Program, Research Triangle Park, NC.

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

TRI92.  1994. 1992 Toxics Release Inventory.  Public Data Release. Office of Pollution Prevention and
Toxics  (7408), U.S. Environmental Protection Agency, Washington,  D.C.

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.