United States                 Pollution Prevention         December 1994
Environmental Protection      and Toxics                   EPA 749-F-95-002a
Agency  (7407)
             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unpublished EPA information, government publications, review documents, and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 sources.
I. CHEMICAL IDENTITY AND PHYSICAL/CHEMICAL PROPERTIES
   The chemical identity and physical/chemical properties of aniline are summarized in
   Table 1.
TABLE 1.  CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL PROPERTIES OF ANILINE
__________________________________________________________________________________
Characteristic/Property     Reference                  		Data
__________________________________________________________________________________
CAS No.                     62-53-3
Common Synonyms             aminobenzene; aminophen;   		U.S. EPA 1994
                            phenylamine; benzeneamine
Molecular Formula           C6H7N
Chemical Structure
Physical State              liquid                     		U.S. EPA 1985
Molecular Weight            93.12                      		U.S. EPA 1985
Melting Point               6.15C                     		U.S. EPA 1985
Boiling Point               184.4C @ 1 atm            		U.S. EPA 1985
Water Solubility            34 g/L @ 20C; 35 g/L @ 25C  	U.S. EPA 1985
Specific Gravity            1.02173 @ 20/4C           		U.S. EPA 1985
Vapor Density (air = 1)     3.22                       		Verschueren 1983
KOC                         3870 @ pH 6.5 (measured)   		U.S. EPA 1985
Log KOW                     0.90                       		U.S. EPA 1985
Vapor Pressure              0.3 mm Hg @ 20C; 0.67 mm Hg @ 25C  U.S. EPA 1985
Reactivity                  flammable                  		U.S. EPA 1985;
                                                       		Budavari 1989
Flash Point                 76C (closed cup)          		U.S. EPA 1985
Henry's Law Constant        1.9 x 10-6 atm-m3/mole @ 25C       U.S. EPA 1985
Fish Bioconcentration Factor  3.0 (calculated)    		U.S. EPA 1985
Odor Threshold              perception, 0.34 mg/m3     		Verschueren 1983
Conversion Factors (in air) 1 ppm = 3.87 mg/m3; 1
			    mg/m3 = 0.259 ppm           	U.S. EPA 1985
___________________________________________________________________________________
II.  PRODUCTION, USE, AND TRENDS
     A.  PRODUCTION
     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 Carolina.
TABLE 2.  U.S. PRODUCERS OF ANILINE AND THEIR CAPACITIES IN 1992
_____________________________________________________________________
Producer1                Plant Location      Plant Capacity
                                             (Millions of Pounds)
_____________________________________________________________________
Aristech                 Haverhill, OH            200
BASF Corporation2        Geismar, LA              170
DuPont                   Beaumont, TX             270
First Chemical           Pascaqoula, MS           300
Corporation
Miles, Inc.              New Martinsville, WV     40
(formerly Mobay; now Bayer)
Rubicon                  Geismar, LA              400
(ICI/Uniroyal affiliate)3
_____________________________________________________________________
TOTAL                                             1,380
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 million pounds 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.
TABLE 3.  END USE PATTERN OF ANILINE IN THE UNITED STATES (1992)
_____________________________________________________________________
Derivative                    U.S. Consumption         Percentage of
(Typical Standard             (Millions of Pounds)     U.S. Use
Industrial Classification
(SIC) Code)4
_____________________________________________________________________
Isocyanates
(SIC 2865)                    659                      68
Rubber Chemicals
(SIC 2869)                    155                      16
Agricultural-Pesticides
(SIC 2879)                    68                       7
Dyes and Pigments
(SIC 2865)                    39                       4
Miscellaneous
(Various SICs)                48                       5
_____________________________________________________________________
TOTAL                         964                      100
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 industries of
interest to the researcher.  SIC codes presented here are not intended
to be an exhaustive listing; rather, the codes listed should provide an
indication of where a chemical may be likely to be found in commerce.
     C.  TRENDS
     United States demand for aniline is expected to increase three to
     four percent per year (Mannsville 1992).  Increases in demand for
     aniline is dependent on increased demand for methyl diphenyl
     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 expected to 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.
III. ENVIRONMENTAL FATE
     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 @ 25C) 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).
IV.  HUMAN HEALTH EFFECTS
     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 p-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 1985).
          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) 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 RfC  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).
          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) 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).  B6C3F1 mice were fed
               diets containing 0, 6000, or 12,000 ppm  (480 or 960
               mg/kg) 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 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 B6C3F1 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 with
          E. 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-1 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.
V.   ENVIRONMENTAL EFFECTS
     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).
VI.  EPA/OTHER FEDERAL/OTHER GROUP ACTIVITY
     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.
TABLE 4.  EPA OFFICES AND CONTACT NUMBERS INFORMATION ON ANILINE
____________________________________________________________________________
EPA Office                         Statute                 Contact Number
____________________________________________________________________________
Pollution Prevention & Toxics  PPAa                        (202) 260-1023
                                   EPCRA (313/TRI)b        (800) 424-9346
                                   TSCA (4, 8D)c          (202) 554-1404
Air                                Clean Air Act           (919) 541-0888
                                   (111, 112B)d
Water                              Clean Water Act (311)e  (202) 260-7588
Solid Waste &                     RCRA (Action levels:     (800) 424-9346
Emergency Response                 water,6E-3 mg/L; soils, 1E+2 mg/kg)f
                                  CERCLA (RQ: 5000 pounds)g(800) 424-9346
___________________________________________________________________________
aPPA:  Pollution Prevention Act
bEPCRA:  Emergency Planning and Community Right to Know Act of 1986
cTSCA: Toxic Substances Control Act
dListed 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)].
fRCRA: 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).
gCERCLA: 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)].
TABLE 5.  OTHER FEDERAL OFFICES/CONTACT NUMBERS FOR INFORMATION ON
ANILINE
______________________________________________________________________
Other Agency/Department/Group  				Contact Number
______________________________________________________________________
American Conference of
  Governmental Industrial Hygienists                 	(513) 742-2020
  [TLV-TWA, 2 ppm (7.6 mg/m3); skin exposure]a
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/m3); IDLH, 100 ppm; skin exposure, Ca, LF]b
Occupational Safety & Health Administration
  [TWA, 5 ppm (19 mg/m3 ]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 1993-1994).
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).
cTWA: 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 1993).
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Grayson, M. (ed.).  Kirk-Othmer Concise Encyclopedia of Chemical
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Howard PH.  1989.  Handbook of Environmental Fate and Exposure Data
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Newsome L. 1995.  Memorandum from Larry Newsome, HERD/EEB, to Richard
Wormell, CSRAD/AIMB.  Subject:  Comments on OPPT Fact Sheet for
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