United States
Environmental Protection
Agency
Pollution Prevention
and Toxics
(7407)
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 These sources include online databases, unpublished EPA information, government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
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
CAS No.
Common Synonyms
Molecular Formula
Chemical Structure
Physical State
Molecular Weight
Melting Point
Boiling Point
Water Solubility
Specific Gravity
Vapor Density (air = 1)
KOC
Log Kom
Vapor Pressure
Reactivity
Flash Point
Henry's Law Constant
Fish Bioconcentration Factor
Odor Threshold
Conversion Factors (in air)
Data
62-53-3
aminobenzene; aminophen; phenylamine;
benzeneamine
C6H7N
liquid
93.12
6.15°C
184.4°C@ 1 atm
34 g/L @ 20 °C; 35 g/L @ 25 °C
1.02173 @ 20/4 °C
3.22
3870 @ pH 6.5 (measured)
0.90
0.3 mm Hg @ 20 °C; 0.67 mm Hg @ 25 °C
flammable
76°C (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
Reference
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
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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
Aristech
BASF Corporation-?
DuPont
First Chemical Corporation
Miles, Inc. (formerly Mobay;
now Bayer)
Rubicon (ICI/Uniroyal
affiliate)3
Plant Location
Haverhill, OH
Geismar, LA
Beaumont, TX
Pascaqoula, MS
New Martinsville, WV
Geismar, LA
TOTAL
Plant Capacity
(Millions of Pounds)
200
170
270
300
40
400
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 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,
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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
(Typical Standard Industrial Classification
(SIC) Code)4
Isocyanates
(SIC 2865)
Rubber Chemicals
(SIC 2869)
Agricultural-Pesticides
(SIC 2879)
Dyes and Pigments
(SIC 2865)
Miscellaneous
(Various SICs)
TOTAL
U.S. Consumption
(Millions of Pounds)
659
155
68
39
48
964
Percentage of U.S.
Use
68
16
7
4
5
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 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.
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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 @ 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
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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 /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
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
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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)
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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.
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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).
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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.
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
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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
Air
Water
Solid Waste & Emergency Response
PPAa
EPCRA(§313/TRi;P
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
(202)260-1023
(800) 535-0202
(202)554-1404
(919)541-0888
(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)].
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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/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-
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).
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
1993).
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VII. CITED REFERENCES
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.
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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).
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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.
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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
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Washington, D.C., pp. 21,22. OHEA-C-073.
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30867.
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.
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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
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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.
Howard, P.H., Ed. 1989. Handbook of Environmental Fate and Exposure Data. Lewis Publishers, Chelsea,
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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
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IPCS. 19.... International Programme on Chemical Safety. Environmental Health Criteria. World Health
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NIOSH (National Institute for Occupational Safety and Health). 1992. NIOSH Recommendations for
Occupational Safety and Health. Compendium of Policy Documents and Statements. Cincinnati, OH:
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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
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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.
A-1
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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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